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Preservation of the Anterior Cruciate Ligament: A Treatment Algorithm Based on Tear Location and Tissue Quality
Injury of the anterior cruciate ligament (ACL) is very common with over 200,000 annual injuries in the United Status.1,2 There is a general consensus that these injuries should not be treated conservatively in patients that are younger, or who wish to remain active.3,4 Reconstructive surgery is currently the preferred treatment in these patients, and anatomic single-bundle reconstruction with autografts is considered the gold standard.5,6
Reconstruction of the ACL is, however, not a perfect treatment. Following single-bundle autograft reconstruction, revision rates of 3% to 8%,6-9 contralateral injury rates of 3% to 8%,10,11 and infection rates of 0.5% to 3%7,12,13 have been reported. Furthermore, due to the invasive nature of graft harvesting and the surgical procedure, 10% to 25% of the patients are not satisfied following ACL reconstruction.14,15 This can often be explained by common complaints, such as anterior knee pain (13%-43%), kneeling pain (12%-54%), quadriceps muscle atrophy (20%-30%),16,17 and loss of range of motion (ROM) (12%-23%).7,9,18,19 Furthermore, as a result of the invasive nature of reconstructive surgery, revisions can be difficult due to complications, such as tunnel widening, tunnel malpositioning, and preexisting hardware.20-22 This can lead to inferior outcomes and higher rates (13%) of revision surgery compared to primary reconstruction.23-26 Finally, reconstructive surgery does not restore native kinematics of the ACL,27-29 which may partially explain why reconstructive surgery has not been shown to prevent osteoarthritis.28-31
Over the past decades, there has been an increasing interest in the preservation of the ACL in an attempt to ameliorate these issues.32-37 Ligament preservation focuses on preserving the native tissues and biology, while minimizing the surgical morbidity to the patients.
Some authors have recently reported on arthroscopic primary repair of proximal ACL tears in which the ligament is reattached onto the femoral wall using modern-day suture anchor technology.32,38 Others have augmented this repair technique with an internal brace39,40 or with a synthetic device.33,41 When performing primary repair, it is believed that proprioception is maintained,42-44 while experimental studies have suggested that primary repair also restores the native kinematics,45 and may prevent osteoarthritis.46 Furthermore, primary repair is a conservative approach in that no grafts need to be harvested, no tunnels need to be drilled, and revision surgery, if necessary, is more analogous to primary reconstructions.32In patients with partial tears, some surgeons have advocated preserving the anteromedial (AM) or posterolateral (PL) bundle and performing selective single-bundle augmentation.34,35 In addition, several authors have used remnant tensioning36,47 or remnant preservation37,48 in combination with reconstructive surgery in order to benefit from the biological characteristics of the remnant. These techniques lead to better proprioceptive function,44,49,50 vascularization and ligamentization of the graft,50-52 provide an optical guide for anatomic tunnel placement,53 and decrease the incidence of tunnel widening.54,55The feasibility and applicability of these surgical techniques mainly depends on the tear type and tissue quality of the torn ligament. In this article we (I) discuss the history of ACL preservation, (II) discuss how modern advances alter the risk-benefit ratio for ACL preservation, and (III) propose a treatment algorithm for ACL injuries that is based on tear location and tissue quality.
History of ACL Preservation
The history of the surgical treatment of ACL injuries started in 1895 when Robson56 treated a 41-year-old male who tore both cruciate ligaments from the femoral wall. Performing primary repair with catgut ligatures, both cruciate ligaments were preserved and the patients had resolution of pain symptoms and full function at 6-year follow-up. Over the following decades, Palmer57,58 and O’Donoghue59,60 further popularized open primary repair for the treatment of ACL injuries, and this technique was the most commonly performed treatment in the 1970s and early 1980s.61-65 The initial short-term results of primary repair were excellent,61,62 but Feagin and Curl66 were the first to note that the results deteriorated at mid-term follow-up. Despite improvements in the surgical technique of repairing the ACL, such as the usage of nonabsorbable sutures and directly tying the sutures over bone,63,67 the results remained disappointing at longer-term follow-up.68-70
In response to these disappointing results, surgeons sought to improve the surgical treatment by either augmenting the primary repair with a semitendinosus, a patella tendon graft or an augmentation device,71-74 or by performing primary reconstruction.75-77 At the end of the 1980s and early 1990s, several randomized and prospective clinical trials were performed in order to compare the outcomes of these techniques.74,78-82 Many studies showed that results of augmented repair were more reliable when compared to primary repair, which led to the abandonment of primary repair in favor of augmented repair, and eventually primary reconstruction.65
The Important Role of Tear Location in Ligament Preservation
When taking a closer look at the outcomes of primary repair and augmented repair, it seems that the results of these preservation techniques were not as disappointing as was suggested. This can be explained, in large part, by the fact that the important roles of tear location and tissue quality were not widely recognized.
Sherman and colleagues70 reported in 1991 their mid-term results of open primary repair. Similar to others, they noted a deterioration of their results at mid-term follow-up. However, they uniquely performed an extensive subgroup analysis in order to find an explanation for this. In their study, considered a landmark paper on primary repair,65,70 they concluded that, “poor tissue quality is typical for midsubstance tears and that a repair of these injuries will predictably fail while type I tears (proximal), with better tissue quality, show a definite trend towards better results.”70 With these findings, they confirmed the findings of others that had recognized a trend of better outcomes with proximal tears.64,67,83-85
A majority of the historical studies that were published before 1991 had not considered the role of tear location and tissue quality on outcomes of open primary repair. This was also true for the aforementioned randomized studies that compared primary repair with augmented repair and primary reconstruction. Because these studies randomized patients and did not take tear location into account, it can be expected that patients with midsubstance tears were included in the cohorts of primary repair and the outcomes of these studies were therefore confounded.74,78-82 If these studies would have been aware of the role that tear location plays on primary repair outcomes, different outcomes may have been found and different conclusions on the optimal treatment for different tear types may have been drawn.86
Open Primary ACL Repair Outcomes Stratified by Tear Location
When reviewing the literature of open primary repair outcomes stratified by tear location, it is noted that multiple studies reported excellent outcomes following primary repair of proximal ACL tears.73,83,84,87-90 Weaver and colleagues64 were among the first to stratify their results by tear location, and they found that more patients with proximal tears (52 of 66; 79%) were satisfied after the procedure when compared to patients with midsubstance tears (3 of 13; 23%) at 3.5-year follow-up. They concluded that, “selection can be made with some predictability of the type of injury to the ligament as to which patients will do better.”64 Kühne and colleagues89 reported the outcomes of 75 patients with proximal tears treated with open primary repair and noted no failures, negative pivot shift in 88% of patients, stable or nearly stable Lachman test in 87% of patients, and 89% return to sports rate at 4-year follow-up. Raunest and colleagues91 reported a negative pivot shift and negative anterior drawer test in 84%, return to sports in 71%, and satisfaction in 75% of 51 patients that underwent open primary repair of proximal tears at 3.5-year follow-up.
Interestingly, and in contrast to the findings of Feagin and Curl,66 no deterioration of the outcomes at mid-term follow-up was noted in patients with proximal tears. Genelin and colleagues88 reported their results of 42 patients with proximal tears treated with open primary repair at 5- to 7-year follow-up. They found a negative pivot shift in 81%, stable or nearly stable Lachman test in 81%, and patient satisfaction in 86% of patients. Similarly, Bräm and colleagues87 found good results at mid-term follow-up with a good-excellent Lysholm score in 79%, return to a similar level of sports in 76%, stable or nearly stable Lachman test in 91%, and anterior drawer test in 94% of patients, along with an 88% satisfaction rate and 7% failure rate in patients who underwent open primary repair of proximal tears.
On the contrary, when the outcomes of studies that performed open primary repair in mainly, or only, patients with midsubstance tears are reviewed, significantly inferior results are found. Frank and colleagues92 reported outcomes in 42 patients with midsubstance tears at 4-year follow-up. They reported that 56% had a stable or nearly stable anterior drawer test, 78% had a positive pivot shift, and that only 61% were satisfied with the procedure. Odensten and colleagues78 reported outcomes of open primary repair in a subgroup of 22 patients with midsubstance tears at 1.5-year follow-up, and noted a 14% failure rate.
When reviewing the mid-term results in patients with midsubstance tears, it seems that there was more deterioration in outcomes.69,70 Firstly, the aforementioned study by Sherman and colleagues70 showed poor results in the patients with (type IV) midsubstance tears at mid-term follow-up. Furthermore, Kaplan and colleagues69 reported the mid-term outcomes of 70 patients, of which 56 patients had midsubstance tears. After having reported good outcomes at short-term follow-up,63,67 they noted that 42% of patients had >3 mm anteroposterior stability when compared to the contralateral leg, only a 62% return to sport rate, and a 17% failure rate. They concluded that, “Although … primary repair of the anterior cruciate may work in some patients, it is an unpredictable operative procedure.”
These studies showed that the outcomes of open primary repair were significantly better in patients with proximal ACL tears and sufficient tissue quality when compared to midsubstance tears. This suggests that open primary ACL repair may have been prematurely abandoned as a treatment option for patients with proximal tears.
Augmented ACL Repair
There were several reasons why augmented repair became the preferred treatment in the early and mid 1990s. First of all, the results of augmented repair were more consistent compared to primary repair in the aforementioned randomized and prospective studies,74,78-82 which is not surprising given the fact that the role of tear location was not widely recognized at the time. Secondly, in the 1970s and early 1980s, patients were treated postoperatively in a cast for 6 weeks, which led to problems, such as loss of ROM, pain, and decreased function.93,94 At the end of the1980s and 1990s, the focus shifted from prolonged joint immobilization towards early postoperative ROM.95-97 Since many authors believed that primary repair of the ACL was not strong enough to tolerate early mobilization, an augmentation was added to the technique in order to fortify the repair and enable early ROM.98
Interestingly, augmented repair, which is essentially a combination of primary ACL repair and ACL reconstruction, was mainly performed in the 1990s and many surgeons did recognize the role of tear location in this treatment at this point.73,98-103 In these years, the treatment algorithm consisted of augmented ACL repair in patients with proximal tears in the acute setting and ACL reconstruction in patients with midsubstance or chronic tears. Several different augmentation techniques were used to reinforce the primary repair in these years including autograft tissues (semitendinosus tendon,102-104 patellar tendon,100 or iliotibial band [ITB]105) synthetic materials (polydioxanone [PDS],101,102,106 carbon fibre,74 and polyester [Trevira]97), augmentation devices (Kennedy Ligament Augmentation Device [LAD]98-100) and extra-articular augmentations.73
When reviewing the outcomes of augmented repair of the ACL, good to excellent results can be found in studies that used this technique in patients with proximal tears.73,98-106 Kdolsky and colleagues98 were in one of the first groups that reported their results of augmented repair in only patients with proximal tears. In 1993, they reported their mid-term outcomes (5 to 8 years) in 66 patients who underwent primary repair and augmentation with the Kennedy LAD and found that 97% of patients had stable knees (<3 mm on KT-1000 examination), 98% had a negative pivot shift, and 76% returned to previous level of sports. However, often-reported problems with the augmentation devices were found in this study with rupture of the device (12%) and decreased ROM (14%).98 In 1995, Grøntvedt and Engebretsen100 compared augmentation with the Kennedy LAD to patellar tendon augmentation in a randomized study of patients with acute proximal tears. They noted that 50% of the patients in the Kennedy LAD group had a positive pivot shift compared to 23% in the patellar tendon group. Furthermore, they found KT-1000 leg differences of <3 mm in 92% of the patellar tendon group and 54% of the Kennedy LAD group. Because the authors found significant differences between both groups at 1- and 2-year follow-up, they stopped the clinical trial.
Several authors in the following years reported good results of augmented repair using autograft tissues. Natri and colleagues105 reported the outcomes of 72 patients treated with primary repair of proximal tears augmented with the ITB at 3.5-year follow-up. They found 89% negative pivot shift rate, 93% stable or nearly stable Lachman test, 99% stable or nearly stable anterior drawer test, 79% satisfaction rate, and 91% return to previous level of sports rate. Krueger-Franke and colleagues104 reported the outcomes of primary repair of proximal tears with augmentation using the semitendinosus tendon. In a retrospective study of 76 patients, they noted that 96% of patients had a negative pivot shift, 75% of patients had stable or nearly stable Lachman test, 93% were satisfied with the procedure, a mean Lysholm score of 92, a Tegner score that only decreased from 7.2 to 7.1, and KT-1000 testing with 78% <4 mm leg difference with the contralateral leg. The authors concluded that patients with femoral ruptures could be treated with augmented repair when performed in the acute setting. As this study was published in 1998, they stated that magnetic resonance imaging and arthroscopy could be helpful in identifying the tear location.
Final Abandonment of ACL Preservation
Reviewing these outcomes raises the question as to why these techniques were ultimately abandoned in the treatment algorithm of proximal ACL injuries, especially given the aforementioned advantages of ACL preservation. One of the possible answers can be found in a landmark study on ACL reconstruction and rehabilitation published by Shelbourne and colleagues107 in 1991. At that time, arthrofibrosis and knee stiffness were frequently reported problems following ACL surgery, which could partially be explained by the standard conservative rehabilitation using postoperative joint immobilization.67,70,80,88
Shelbourne and colleagues107 aimed to assess the cause of arthrofibrosis and knee stiffness, and divided the patients into groups by number of days between injury and surgery (<7, 7 to 21 days, and >21 days between injury and surgery). Furthermore, patients within these groups underwent either a conventional or accelerated rehabilitation program. The authors not only found that patients undergoing accelerated rehabilitation had less arthrofibrosis, but they also noted that less arthrofibrosis was seen when surgery was delayed. These findings, however, contrasted with the general perception that the ACL should be repaired in the first 3 weeks postinjury to ensure optimal tissue quality with an augmented approach. As a result, the treatment of ACL injuries shifted towards ACL reconstruction after these findings. Krueger-Franke and colleagues104 commented on the trend after the study of Shelbourne and colleagues:107 “Less consideration has been given to the importance of the proprioceptive receptors in the tibial remnants of the torn ACL and the value of their preservation as part of a primary reconstruction.”
In addition to the trend away from an augmented repair approach due to the novel understanding of the importance of early mobilization, some discussion should focus on the technical limitations of arthroscopy at that time. While arthroscopy had been around for several decades, fluid management and arthroscopic instrumentation was slow to develop. All of the repair and augmentation techniques previously discussed had been performed via an open arthrotomy. Arthroscopic technologies of the time were not refined enough to enable surgeons to perform such complex, intra-articular techniques that would enable suturing of the ligament remnant. In this regard, arthroscopic ACL reconstruction was a much simpler technique to accomplish, and this also likely contributed to the final abandonment of the ligament preservation approach.
Role for ACL Preservation with Modern Advances
As stated in the introduction, there has been a recent resurgence of interest in preservation of the native ligament.32-37 With the passage of time, many technologic advances have been made, which has allowed surgeons to reconsider the concept of ligament preservation.
First of all, appropriate patient selection was not applied historically, as the critical factors of tear location and tissue quality were not recognized in the era of open primary repair. In modern days, however, advances such as MRI have been developed, which can give the surgeon an idea of the status, and tear type of the ACL pre-operatively.108 This may help the orthopaedic surgeon to plan the surgery and make an assessment as to whether ACL preservation is possible. Secondly, in the historic literature the postoperative regimen consisted of casting for 5 or 6 weeks,67,70,80,88 while the focus later shifted towards early ROM.95-97Modern day ACL rehabilitation focuses on immediate ROM to avoid the complications stiffness, pain and decreased function that plagued the outcomes when immobilization was used.93,94 Thirdly, historically small tunnels were drilled with primary repair and sutures had to be tied over bone,57,67 whereas currently suture anchors are available that prevent the need for tunnel drilling and enable direct suture tensioning.32,38 Finally, and most importantly, in the historic literature patients were treated with an invasive arthrotomy technique, while modern day arthroscopic techniques readily enable the surgeon to effectively suture the remnant arthroscopically. Interestingly, in 2005, in their 20-year follow-up of primary repair surgeries, Strand and colleagues109 stated, “if the same results could be accomplished by a smaller, arthroscopic procedure, primary repair might reduce the number of patients needing later reconstructions with small ‘costs’ in the way of risk and inconvenience for the patients. We therefore believe that further research and development of methods for closed (arthroscopic) repair are justified.”
Altered Risk-Benefit Ratio
Historically, the treatments of open primary repair and open ACL reconstruction were both invasive surgeries with an arthrotomy, drilling of bone tunnels, and postoperative joint immobilization for 4 to 6 weeks. However, with the modern-day advances, the risk-benefit ratio of both treatments has changed, as Strand and colleagues109 had already suggested. Although ACL reconstruction can be performed arthroscopically, it remains an invasive procedure, in which tunnels are drilled, patellar tendons or hamstring tendons are harvested, and complications, such as knee pain and quadriceps atrophy, are common. The surgery of primary ACL repair, however, has benefited significantly from the modern developments.32,38 Primary ACL repair can now be performed arthroscopically, and by using suture anchors no tunnels need to be drilled and the remnant can be tensioned directly. An additional benefit of the use of suture anchors is that revision surgery of a failed primary repair is analogous to primary reconstruction, whereas revision surgery of a failed ACL reconstruction can be problematic due to tunnel widening, tunnel malpositioning, and preexisting hardware.20-22
Reviewing the differences between arthroscopic primary ACL repair and ACL reconstruction, it becomes clear that primary repair has benefited significantly from the modern advances and that the risk-benefit ratio for primary repair has been altered. This means that patients with proximal tears can be treated with a relatively straight forward, minimally invasive surgery, which has been shown to be effective in 85% to 90% of patients.32,38
Treatment Algorithm Based on Tear Location
Since 2008, in the practice of the senior author (GSD), the surgical treatment algorithm for ACL injuries is completely based on the tear location and tissue quality of the ligament.110,111 To describe the different tear types, we use the modified Sherman classification in which we extended his classification towards the tibial side whereas Sherman and colleagues70 only described the femoral side of the tears (Figures A-F, Table).
Type I Tears: Primary Repair
Type I tears are soft tissue avulsion type tears that can be easily treated with arthroscopic primary repair.107 The length of the distal remnant has to be at least 90% and the tissue quality has to be good to excellent in order to approximate the remnant towards the femoral wall (Table).112 The incidence of type I tears was 26% in the study of Sherman and colleagues,70 although recent studies showed a lower incidence (6% to 10%) in a larger population.32,38 Certainly, individual practices will see different percentages of type I tears based upon the mix of injury mechanisms they see most frequently. Over the last 2 years, with the recognition of the importance of tear type and tissue quality, there has been a renewed interest in arthroscopic primary ACL repair.32,38
DiFelice and colleagues32 were the first to arthroscopically perform primary repair of the ACL in proximal tears using suture anchors. They reported the outcomes of the first 11 consecutive patients that underwent primary repair in a previously described technique.113 At mean 3.5-year follow-up, they noted only 1 failure (9%) due to re-injury; mean Lysholm score of 93.2; mean modified Cincinnati score of 91.5; pre- and postoperative Tegner score of 7.3 and 6.9, respectively; SANE score of 91.8; and subjective International Knee Documentation Committee (IKDC) score of 86.4. Of the patients with an intact repair, 9 patients had an objective IKDC rating A and 1 patient had B and all patients had KT-1000 leg differences of <3 mm with the contralateral side (three patients were not available for KT-1000 testing). The authors concluded that arthroscopic primary ACL repair could achieve short-term clinical success in a selected group of patients with proximal avulsion tears and excellent tissue quality. They further noted that mid-term outcomes are necessary given that the results of open primary repair deteriorated at longer-term follow-up in the historical literature. Recently, the senior author (GSD) has added an Internal Brace (Arthrex) to the primary repair with the goal of protecting the ligament in the first weeks to further promote healing of the ligament.39,40,114
More recently, Achtnich and colleagues38 compared the treatment of arthroscopic primary ACL repair with primary ACL reconstruction in 41 patients with type I tears at 2.3-years follow-up. Twenty-one patients consented for primary repair while 20 patients declined this procedure and underwent primary reconstruction. They noted no significant differences in Lachman test, pivot shift test, objective IKDC score, and KT-1000 scores. Although not significant, the clinical failure rate in the primary repair group (15%) was higher than the reconstruction group (0%). Interestingly, despite the higher failure rate in the repair group, the authors concluded that primary ACL repair is recommended in a carefully selected group of patients with type I tears and excellent tissue quality, which can likely be explained by the differences in the risk-benefit ratio between both procedures.
Over the last decade, the research group led by Murray46,115,116 has performed experimental research on primary repair with a biological scaffold and reported many interesting findings that could be extrapolated to primary ACL repair. First of all, they compared bioenhanced primary repair with bioenhanced primary reconstruction in 64 Yucutan pigs and noted that there was significantly less macroscopic cartilage damage in the primary repair group at 1-year follow-up.46 They concluded that bioenhanced ACL repair may provide a new, less invasive treatment option that reduces cartilage damage following joint injury. This may suggest that primary repair may have a lower incidence of osteoarthritis when compared to ACL reconstruction, which is interesting as osteoarthritis is very common after ACL reconstruction. Further research in this area is certainly warranted.
In another study they compared bioenhanced primary repair in juvenile, adolescent and mature Yucutan pigs and noted that functional healing depended on the level of skeletal maturity with immature animals having a more productive healing response.116 This indicates that primary repair might be a good treatment option in skeletally immature patients, especially since reconstruction increases the risk of premature closure of the epiphysis117,118 and delaying treatment increases the risk of meniscus injury.119 Interestingly, a recent meta-analysis showed indeed that the risk of epiphysis closure was lower in primary repair when compared to ACL reconstruction and the rupture rate was also lower.118 Primary repair may be a good treatment option in children as the procedure has all the attributes that should be applicable to children: it is minimally morbid, tissue sparing, and it is a conservative approach that does not burn any surgical bridges for future reconstructive surgery if necessary.
Finally, the research group of Murray115 assessed the effect of surgical delay of primary repair following injury in Yucutan pigs and noted that better biomechanical outcomes were noted after delaying surgery for 2 weeks when compared to 6 weeks. This suggests that primary repair should preferably be performed in the acute setting, which has also been shown in historical studies since the ligament in the acute setting has optimal tissue quality and the ligament is less likely to be retracted or reabsorbed.59,60,115
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the tear locations of the AM and PL bundle are not at the same location and Zantop and colleagues120 reported in an arthroscopic study that this could be as frequent as in 30% of all complete tears. In some of these tears, one of the bundles can be avulsed of the femoral wall (type I tear) while the other bundle is not directly repairable (non-type I tear). In these cases, the senior author (GSD) will repair the type I tear bundle, whereas a hamstring augmentation is placed at the location of the other bundle. When reviewing the literature, a combination of primary repair of one bundle and reconstruction of the second bundle has not been described before. However, over the last decade several surgeons have performed augmentation of one bundle in the setting of partial tears.34,35,121-124
Buda and colleagues34 were the first to perform selective AM or PL bundle reconstruction in the setting of partial tears.34 At 5-year follow-up, they reported no reruptures and only 1 patient with an IKDC C-score, although reoperation was necessary in 4 out of 47 patients (9%). Following this publication, many others reported on selective bundle reconstruction.35,121-124 However, with partial tears, the knee is often stable and a selective augmentation technique is utilized to prevent complete rupture of the ligament. The application of this technique is essentially different from reconstruction for complete ACL tears in which the knee is unstable, there is a giving way sensation and patients have problems participating in sports.
Type II Tears: Augmented Repair
Type II tears often have good or excellent tissue quality and can be pulled up towards the femoral footprint, but are too short to be firmly attached. Sherman and colleagues70 reported that approximately 22% patients had a type II tear, which corresponds to a tear located in the proximal part of the ligament. With this technique, multiple suture passes are used to stitch the remnant and, in addition, a smaller hamstring autograft or allograft is passed through the middle of the tibial remnant. A suture button is used proximally for the graft, and the tensioning repair sutures through the remnant are also passed through the suture button. The suture button is passed through the femoral tunnel and flipped so that the graft is proximally fixed. Then, the repair sutures of the remnant are tensioned, and the ligament is pulled towards the femoral wall as a sleeve around the graft. When the ligament is approximated to the femoral wall, the sutures are tied over the suture button. The graft is then tensioned distally to complete the augmented repair.
In the recent literature, the technique of augmentation of a primary repair using autograft tissue has not been reported. However, augmented repair using an internal brace39,40 or augmentation devices33,41 have been recently performed. MacKay and colleagues39 reported good outcomes of arthroscopic primary repair of proximal tears using an internal brace. Eggli and colleagues33 reported the results of the first 10 patients treated with ACL preservation using primary repair of the ligament with the addition of a dynamic screw-spring mechanism. The authors reported good preliminary results with one failure (10%) and good objective and subjective outcomes. In a next study, they reported the outcomes of 278 patients and although they reported good clinical outcomes and a revision rate of 4%, the reoperation rate for removal of the screw-spring mechanism was high (24%).41 This is not surprising when reviewing the historical literature in which high complication rates of the augmentation devices were reported.99,100 We were unable to identify any other studies reporting surgical techniques of augmenting primary repair in the literature.
Type III Tears: Reconstruction With Remnant Tensioning
In patients with type III tears, the ligament cannot be approximated to the wall and reconstruction is necessary in order to restore knee stability. However, in these cases the ligament has sufficient length (25%-75%) and can be tensioned along or around the graft. Preservation of the ligament remnant has several (theoretical) advantages, such as better proprioceptive function,42,49,50 vascularization and ligamentization of the graft,50-52 an optical guide for anatomic tunnel placement,53 and a decreased incidence of tunnel widening.54,55 Furthermore, tensioning of the remnant is thought to lower the risk of cyclops lesions when compared to remnant preservation.125 Although the difference between augmented repair and remnant tensioning seems small, the purpose of surgery is different. With augmented repair, the ligament can be approximated close to the femoral wall and the goal of surgery is to use the healing capacity that the ACL has in the proximal part of the ligament,126 while with remnant tensioning the goal is only to benefit from some of the aforementioned advantages. Ahn and colleagues36 were the first to perform this technique and stated, “Our concept is that the remnant tissue has only an additive effect.” Furthermore, with augmented repair multiple sutures are passed through the AM and PL bundle in order to sufficiently approximate the ligament to the femoral wall, while with the remnant tensioning technique generally one or a few sutures or lasso loop are passed through the proximal part to tension the ligament, prevent sagging of the remnant, and decrease the risk of cyclops lesions.127,128
Several authors have recently performed remnant tensioning during ACL.36,47,125-127 Ahn and colleagues47 reported excellent objective and subjective outcomes following this procedure and found that with re-arthroscopy nearly all patients had fair synovialization of the graft. Others have reported similarly good outcomes of these techniques.125,129,130 However, studies comparing this treatment with normal ACL reconstruction and assessing outcomes, failure rates and proprioception are lacking.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some patients the ligament is torn distally or the tissue quality is not optimal. In these patients, the remnant can be debrided to the part of good tissue quality in order to preserve the biology and minimize the risk for cyclops lesions. A standard reconstruction needs to be performed to restore the instability, but by preserving the remnant, advantages, such as proprioception,44,49,50 graft vascularization,50-52 an optical guide for tibial tunnel placement,53 and a decreased incidence of tunnel widening54,55 can be expected.
Lee and colleagues37 presented the tibial remnant technique in which standard reconstruction was performed, and the tibial tunnel was drilled through the center of the remnant. In a later study, they compared remnant preservation with a remnant of <20% of the total ACL length with >20% of the length and found that proprioception was better with more remnant volume.48 Similarly, Muneta and colleagues131 assessed the role of remnant length and found that remnant length is positively correlated with better stability measured on KT-1000 anteroposterior stability.
Several studies compared ACL reconstruction with remnant preservation vs conventional ACL reconstruction.52,54,129 Takazawa and colleagues52 performed a retrospective study of 183 patients and found that patients in the remnant preservation group had significantly better KT-2000 stability, while they also reported a significantly lower graft rupture rate in this group (1.1% vs 7.1%) at 2-year follow-up. Hong and colleagues129 performed a randomized clinical trial of 80 patients and did not find these differences, although there was a trend towards higher Lysholm scores in the remnant preservation group. Finally, Zhang and colleagues54 performed a randomized clinical trial and found a lower incidence and amount of tibial tunnel widening in the preserving-remnant group when compared to the removing-remnant group. These studies show that there is likely a role for remnant preservation.
Type V Tears: Primary Repair
In some patients, the ligament is torn in the distal 10% of the ligament, which can occur as a distal avulsion tear or as a distal bony avulsion fracture.132 Bony avulsion fractures are most commonly seen in children whereas true distal soft tissue avulsion tears are very rare.132
Treatments of these tear types include antegrade screw fixation, pullout sutures or the use of suture anchors in case of bony avulsion fractures and pullout sutures with tying over a bony bridge or ligament button in case of soft tissue avulsions. Leeberg and colleagues132 recently performed a systematic review of all studies reporting on treatment of distal avulsion fractures.They noted that most treatments were currently performed arthroscopically and that outcomes were generally good. Another recent biomechanical study compared antegrade screw fixation with suture anchor fixation and pullout suture fixation.133 The authors noted that suture anchor fixation has slightly less displacement of the bony fragment when compared to screw fixation and pull-out sutures, and that the strength to failure was higher in the suture anchor fixation when compared to the pullout suture fixation. The outcomes of this study suggest that screw fixation and suture anchor fixation might be superior to pullout suture fixation, which might be interesting as with pullout suture fixation the ligament cannot be directly tensioned to the tibial footprint, which can lead to anteroposterior laxity.132 Clinical studies are necessary to assess the preferred treatment in these tear types but it seems that screw fixation is preferred in large bony avulsion fractures, while suture anchor fixation or pullout suture fixation can be used for soft tissue avulsion tears.
Complex Tears or Poor Tissue Quality: Reconstruction
If the tear is complex, multiple tears are present, or the tissue quality is poor, then preservation of the ligament is not possible, and in these cases a standard reconstruction should be performed.
Conclusion
When reviewing the literature of ACL preservation, it becomes clear that the evolution of surgical treatment of ACL injuries was biased. Preservation of the native ligament has many advantages, such as better proprioception, graft vascularization, an optical guide for tibial tunnel placement, and a decreased incidence of tunnel widening that can be expected. Furthermore, arthroscopic primary ACL repair is minimally invasive and does not burn any bridges for future reconstructions, if necessary. This is in addition to the other (theoretical) advantages of primary repair, such as restoration of native kinematics and a decreased risk of osteoarthritis. Modern advances have significantly changed the risk-benefit ratio that should make us reconsider ACL preservation approaches. Certainly, further research in this area is warranted. In this article we have presented a treatment algorithm for ACL preservation, which is based on tear location and remnant tissue quality.
Am J Orthop. 2016;45(7):E393-E405. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Mall NA, Chalmers PN, Moric M, et al. Incidence and trends of anterior cruciate ligament reconstruction in the United States. Am J Sports Med. 2014;42(10):2363-2370.
2. Sanders TL, Maradit Kremers H, Bryan AJ, et al. Incidence of anterior cruciate ligament tears and reconstruction: a 21-year population-based study. Am J Sports Med. 2016;44(6):1502-1507.
3. Ciccotti MG, Lombardo SJ, Nonweiler B, Pink M. Non-operative treatment of ruptures of the anterior cruciate ligament in middle-aged patients. Results after long-term follow-up. J Bone Joint Surg Am. 1994;76(9):1315-1321.
4. Sanders TL, Pareek A, Kremers HM, et al. Long-term follow-up of isolated ACL tears treated without ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2016 May 24. [Epub ahead of print]
5. Irarrázaval S, Kurosaka M, Cohen M, Fu FH. Anterior cruciate ligament reconstruction. J ISAKOS. 2016;1(1):38-52.
6. Gabler CM, Jacobs CA, Howard JS, Mattacola CG, Johnson DL. Comparison of graft failure rate between autografts placed via an anatomic anterior cruciate ligament reconstruction technique: a systematic review, meta-analysis, and meta-regression. Am J Sports Med. 2016;44(4):1069-1079.
7. Li S, Chen Y, Lin Z, Cui W, Zhao J, Su W. A systematic review of randomized controlled clinical trials comparing hamstring autografts versus bone-patellar tendon-bone autografts for the reconstruction of the anterior cruciate ligament. Arch Orthop Trauma Surg. 2012;132(9):1287-1297.
8. Rahr-Wagner L, Thillemann TM, Pedersen AB, Lind M. Comparison of hamstring tendon and patellar tendon grafts in anterior cruciate ligament reconstruction in a nationwide population-based cohort study: results from the danish registry of knee ligament reconstruction. Am J Sports Med. 2014;42(2):278-284.
9. Xie X, Liu X, Chen Z, Yu Y, Peng S, Li Q. A meta-analysis of bone-patellar tendon-bone autograft versus four-strand hamstring tendon autograft for anterior cruciate ligament reconstruction. Knee. 2015;22(2):100-110.
10. Andernord D, Desai N, Björnsson H, Gillén S, Karlsson J, Samuelsson K. Predictors of contralateral anterior cruciate ligament reconstruction: a cohort study of 9061 patients with 5-year follow-up. Am J Sports Med. 2015;43(2):295-302.
11. Maletis GB, Inacio MC, Funahashi TT. Risk factors associated with revision and contralateral anterior cruciate ligament reconstructions in the Kaiser Permanente ACLR registry. Am J Sports Med. 2015;43(3):641-647.
12. Kim SJ, Postigo R, Koo S, Kim JH. Infection after arthroscopic anterior cruciate ligament reconstruction. Orthopedics. 2014;37(7):477-484.
13. Makhni EC, Steinhaus ME, Mehran N, Schulz BS, Ahmad CS. Functional outcome and graft retention in patients with septic arthritis after anterior cruciate ligament reconstruction: a systematic review. Arthroscopy. 2015;31(7):1392-1401.
14. Kocher MS, Steadman JR, Briggs K, Zurakowski D, Sterett WI, Hawkins RJ. Determinants of patient satisfaction with outcome after anterior cruciate ligament reconstruction. J Bone Joint Surg Am. 2002;84-A(9):1560-1572.
15. Ardern CL, Österberg A, Sonesson S, Gauffin H, Webster KE, Kvist J. Satisfaction with knee function after primary anterior cruciate ligament reconstruction is associated with self-efficacy, quality of life, and returning to the preinjury physical activity. Arthroscopy. 2016;32(8):1631-1638.e3.
16. Grant JA, Mohtadi NG, Maitland ME, Zernicke RF. Comparison of home versus physical therapy-supervised rehabilitation programs after anterior cruciate ligament reconstruction: a randomized clinical trial. Am J Sports Med. 2005;33(9):1288-1297.
17. Lindström M, Strandberg S, Wredmark T, Fell änder-Tsai L, Henriksson M. Functional and muscle morphometric effects of ACL reconstruction. A prospective CT study with 1 year follow-up. Scand J Med Sci Sports. 2013;23(4):431-442.
18. Biau DJ, Tournoux C, Katsahian S, Schranz PJ, Nizard RS. Bone-patellar tendon-bone autografts versus hamstring autografts for reconstruction of anterior cruciate ligament: meta-analysis. BMJ. 2006;332(7548):995-1001.
19. Spindler KP, Kuhn JE, Freedman KB, Matthews CE, Dittus RS, Harrell FE Jr. Anterior cruciate ligament reconstruction autograft choice: bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med. 2004;32(8):1986-1995.
20. Aga C, Wilson KJ, Johansen S, Dornan G, La Prade RF, Engebretsen L. Tunnel widening in single- versus double-bundle anterior cruciate ligament reconstructed knees. Knee Surg Sports Traumatol Arthrosc. 2016 Jun 21. [Epub ahead of print]
21. Maak TG, Voos JE, Wickiewicz TL, Warren RF. Tunnel widening in revision anterior cruciate ligament reconstruction. J Am Acad Orthop Surg. 2010;18(11):695-706.
22. Cheatham SA, Johnson DL. Anticipating problems unique to revision ACL surgery. Sports Med Arthrosc. 2013;21(2):129-134.
23. Kamath GV, Redfern JC, Greis PE, Burks RT. Revision anterior cruciate ligament reconstruction. Am J Sports Med. 2011;39(1):199-217.
24. Wright RW, Gill CS, Chen L, et al. Outcome of revision anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg Am. 2012;94(6):531-536.
25. Andriolo L, Filardo G, Kon E, et al. Revision anterior cruciate ligament reconstruction: clinical outcome and evidence for return to sport. Knee Surg Sports Traumatol Arthrosc. 2015;23(10):2825-2845.
26. Grassi A, Ardern CL, Marcheggiani Muccioli GM, Neri MP, Marcacci M, Zaffagnini S. Does revision ACL reconstruction measure up to primary surgery? A meta-analysis comparing patient-reported and clinician-reported outcomes, and radiographic results. Br J Sports Med. 2016;50(12):716-724.
27. Ristanis S, Stergiou N, Patras K, Vasiliadis HS, Giakas G, Georgoulis AD. Excessive tibial rotation during high-demand activities is not restored by anterior cruciate ligament reconstruction. Arthroscopy. 2005;21(11):1323-1329.
28. Andriacchi TP, Mündermann A, Smith RL, Alexander EJ, Dyrby CO, Koo S. A framework for the in vivo pathomechanics of osteoarthritis at the knee. Ann Biomed Eng. 2004;32(3):447-457.
29. Imhauser C, Mauro C, Choi D, et al. Abnormal tibiofemoral contact stress and its association with altered kinematics after center-center anterior cruciate ligament reconstruction: an in vitro study. Am J Sports Med. 2013;41(4):815-825.
30. Ajuied A, Wong F, Smith C, et al. Anterior cruciate ligament injury and radiologic progression of knee osteoarthritis: a systematic review and meta-analysis. Am J Sports Med. 2014;42(9):2242-2252.
31. Chalmers PN, Mall NA, Moric M, et al. Does ACL reconstruction alter natural history?: A systematic literature review of long-term outcomes. J Bone Joint Surg Am. 2014;96(4):292-300.
32. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
33. Eggli S, Kohlhof H, Zumstein M, et al. Dynamic intraligamentary stabilization: novel technique for preserving the ruptured ACL. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1215-1221.
34. Buda R, Ferruzzi A, Vannini F, Zambelli L, Di Caprio F. Augmentation technique with semitendinosus and gracilis tendons in chronic partial lesions of the ACL: clinical and arthrometric analysis. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1101-1107.
35. Ochi M, Adachi N, Uchio Y, et al. A minimum 2-year follow-up after selective anteromedial or posterolateral bundle anterior cruciate ligament reconstruction. Arthroscopy. 2009;25(2):117-122.
36. Ahn JH, Lee YS, Ha HC. Anterior cruciate ligament reconstruction with preservation of remnant bundle using hamstring autograft: technical note. Arch Orthop Trauma Surg. 2009;129(8):1011-1015.
37. Lee BI, Min KD, Choi HS, Kim JB, Kim ST. Arthroscopic anterior cruciate ligament reconstruction with the tibial-remnant preserving technique using a hamstring graft. Arthroscopy. 2006;22(3):340.e1-e7.
38. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016 Jun 17. [Epub ahead of print]
39. MacKay G, Anthony IC, Jenkins PJ, Blyth M. Anterior cruciate ligament repair revisited. Preliminary results of primary repair with internal brace ligament augmentation: a case series. Orthop Muscul Syst. 2015;4:188.
40. Mackay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
41. Henle P, Röder C, Perler G, Heitkemper S, Eggli S. Dynamic intraligamentary stabilization (DIS) for treatment of acute anterior cruciate ligament ruptures: case series experience of the first three years. BMC Musculoskelet Disord. 2015;16:27.
42. Adachi N, Ochi M, Uchio Y, Iwasa J, Ryoke K, Kuriwaka M. Mechanoreceptors in the anterior cruciate ligament contribute to the joint position sense. Acta Orthop Scand. 2002;73(3):330-334.
43. Gao F, Zhou J, He C, et al. A morphologic and quantitative study of mechanoreceptors in the remnant stump of the human anterior cruciate ligament. Arthroscopy. 2016;32(2):273-280.
44. Georgoulis AD, Pappa L, Moebius U, et al. The presence of proprioceptive mechanoreceptors in the remnants of the ruptured ACL as a possible source of re-innervation of the ACL autograft. Knee Surg Sports Traumatol Arthrosc. 2001;9(6):364-368.
45. Fleming BC, Carey JL, Spindler KP, Murray MM. Can suture repair of ACL transection restore normal anteroposterior laxity of the knee? An ex vivo study. J Orthop Res. 2008;26(11):1500-1505.
46. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
47. Ahn JH, Wang JH, Lee YS, Kim JG, Kang JH, Koh KH. Anterior cruciate ligament reconstruction using remnant preservation and a femoral tensioning technique: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(8):1079-1089.
48. Lee BI, Kwon SW, Kim JB, Choi HS, Min KD. Comparison of clinical results according to amount of preserved remnant in arthroscopic anterior cruciate ligament reconstruction using quadrupled hamstring graft. Arthroscopy. 2008;24(5):560-568.
49. Lee BI, Min KD, Choi HS, et al. Immunohistochemical study of mechanoreceptors in the tibial remnant of the ruptured anterior cruciate ligament in human knees. Knee Surg Sports Traumatol Arthrosc. 2009;17(9):1095-1101.
50. Takahashi T, Kondo E, Yasuda K, et al. Effects of remnant tissue preservation on the tendon graft in anterior cruciate ligament reconstruction: a biomechanical and histological study. Am J Sports Med. 2016;44(7):1708-1716.
51. Dong S, Xie G, Zhang Y, Shen P, Huangfu X, Zhao J. Ligamentization of autogenous hamstring grafts after anterior cruciate ligament reconstruction: midterm versus long-term results. Am J Sports Med. 2015;43(8):1908-1917.
52. Takazawa Y, Ikeda H, Kawasaki T, et al. ACL reconstruction preserving the ACL remnant achieves good clinical outcomes and can reduce subsequent graft rupture. Orthop J Sports Med. 2013;1(4):2325967113505076.
53. Shimodaira H, Tensho K, Akaoka Y, Takanashi S, Kato H, Saito N. Remnant-preserving tibial tunnel positioning using anatomic landmarks in double-bundle anterior cruciate ligament reconstruction. Arthroscopy. 2016;32(9):1822-1830.
54. Zhang Q, Zhang S, Cao X, Liu L, Liu Y, Li R. The effect of remnant preservation on tibial tunnel enlargement in ACL reconstruction with hamstring autograft: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):166-173.
55. Tie K, Chen L, Hu D, Wang H. The difference in clinical outcome of single-bundle anterior cruciate ligament reconstructions with and without remnant preservation: A meta-analysis. Knee. 2016;23(4):566-574.
56. Robson AW. VI. Ruptured crucial ligaments and their repair by operation. Ann Surg. 1903;37(5):716-718.
57. Palmer I. On the injuries to the ligaments of the knee joint. Acta Orthop Scand. 1938;53.
58. Palmer I. On the injuries to the ligaments of the knee joint: a clinical study. 1938. Clin Orthop Relat Res. 2007;454:17-22.
59 O’Donoghue DH. An analysis of end results of surgical treatment of major injuries to the ligaments of the knee. J Bone Joint Surg Am. 1955;37-A(1):1-13.
60. O’Donoghue DH. Surgical treatment of fresh injuries to the major ligaments of the knee. J Bone Joint Surg Am. 1950;32 A(4):721-738.
61. Feagin JA, Abbott HG, Rokous JR. The isolated tear of the anterior cruciate ligament. J Bone Joint Surg Am. 1972;54-A:1340-1341.
62. England RL. Repair of the ligaments about the knee. Orthop Clin North Am. 1976;7(1):195-204.
63. Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.
64. Weaver JK, Derkash RS, Freeman JR, Kirk RE, Oden RR, Matyas J. Primary knee ligament repair--revisited. Clin Orthop Relat Res. 1985;(199):185-191.
65. Nogalski MP, Bach BR Jr. A review of early anterior cruciate ligament surgical repair or reconstruction. Results and caveats. Orthop Rev. 1993;22(11):1213-1223.
66. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
67. Marshall JL, Warren RF, Wickiewicz TL. Primary surgical treatment of anterior cruciate ligament lesions. Am J Sports Med. 1982;10(2):103-107.
68. Straub T, Hunter RE. Acute anterior cruciate ligament repair. Clin Orthop Relat Res. 1988;227:238-250.
69. Kaplan N, Wickiewicz TL, Warren RF. Primary surgical treatment of anterior cruciate ligament ruptures. A long-term follow-up study. Am J Sports Med. 1990;18(4):354-358.
70. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
71. Paar O. Use of semitendinosus tendon to strengthen a freshly repaired anterior cruciate ligament. Chirurg. 1985;56(11):728-734.
72. Aglietti P, Buzzi R, Pisaneschi A, Salvi M. Comparison between suture and augmentation with the semitendinosus tendon in the repair of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1986;8(4):217-231.
73. Higgins RW, Steadman JR. Anterior cruciate ligament repairs in world class skiers. Am J Sports Med. 1987;15(5):439-447.
74. Harilainen A, Myllynen P. Treatment of fresh tears of the anterior cruciate ligament. A comparison of primary suture and augmentation with carbon fibre. Injury. 1987;18(6):396-400.
75. Jones KG. Results of use of the central one-third of the patellar ligament to compensate for anterior cruciate ligament deficiency. Clin Orthop Relat Res. 1980;(147):39-44.
76. Puddu G. Method for reconstruction of the anterior cruciate ligament using the semitendinosus tendon. Am J Sports Med. 1980;8(6):402-404.
77. Hefti F, Gächter A, Jenny H, Morscher E. Replacement of the anterior cruciate ligament. a comparative study of four different methods of reconstruction. Arch Orthop Trauma Surg. 1982;100(2):83-94.
78. Odensten M, Hamberg P, Nordin M, Lysholm J, Gillquist J. Surgical or conservative treatment of the acutely torn anterior cruciate ligament. A randomized study with short-term follow-up observations. Clin Orthop Relat Res. 1985;(198):87-93.
79. Andersson C, Odensten M, Good L, Gillquist J. Surgical or non-surgical treatment of acute rupture of the anterior cruciate ligament. A randomized study with long-term follow-up. J Bone Joint Surg Am. 1989;71(7):965-974.
80. Engebretsen L, Benum P, Fasting O, Mølster A, Strand T. A prospective, randomized study of three surgical techniques for treatment of acute ruptures of the anterior cruciate ligament. Am J Sports Med. 1990;18(6):585-590.
81. Jonsson T, Peterson L, Renström P. Anterior cruciate ligament repair with and without augmentation. A prospective 7-year study of 51 patients. Acta Orthop Scand. 1990;61(6):562-566.
82. Andersson C, Odensten M, Gillquist J. Knee function after surgical or nonsurgical treatment of acute rupture of the anterior cruciate ligament: a randomized study with a long-term follow-up period. Clin Orthop Relat Res. 1991;(264):255-263.
83. Heim U, Bachmann B, Infanger K. Reinsertion of the anterior cruciate ligament or primary ligamentous plasty? Helv Chir Acta. 1982;48(5):703-708.
84. Strand T, Engesaeter LB, Mølster AO, et al. Knee function following suture of fresh tear of the anterior cruciate ligament. Acta Orthop Scand. 1984;55(2):181-184.
85. Marcacci M, Spinelli M, Chiellini F, Buccolieri V. Notes on 53 cases of immediate suture of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1985;7(2):69-79.
86. van der List JP, DiFelice GS. Primary repair of the anterior cruciate ligament: a paradigm shift. Surgeon. 2016 Oct 6. [Epub ahead of print]
87. Bräm J, Plaschy S, Lütolf M, Leutenegger A. [The primary cruciate ligament suture--is the method outdated? Results in follow-up of 58 patients]. Z Unfallchir Versicherungsmed. 1994;87(2):91-109.
88. Genelin F, Trost A, Primavesi C, Knoll P. Late results following proximal reinsertion of isolated ruptured ACL ligaments. Knee Surg Sports Traumatol Arthrosc. 1993;1(1):17-19.
89. Kühne JH, Theermann R, Neumann R, Sagasser J. [Acute uncomplicated anterior knee instability. 2-5 year follow-up of surgical treatment]. Unfallchirurg. 1991;94(2):81-87.
90. Simonet WT, Sim FH. Repair and reconstruction of rotatory instability of the knee. Am J Sports Med. 1984;12(2):89-97.
91. Raunest J, Derra E, Ohmann C. [Clinical results of Palmer’s primary cruciate ligament insertion without augmentation]. Unfallchirurgie. 1991;17(3):166-174.
92. Frank C, Beaver P, Rademaker F, Becker K, Schachar N, Edwards G. A computerized study of knee-ligament injuries: repair versus removal of the torn anterior cruciate ligament. Can J Surg. 1982;25(4):454-458.
93. Enneking WF, Horowitz M. The intra-articular effects of immobilization on the human knee. J Bone Joint Surg Am. 1972;54(5):973-985.
94. Millett PJ, Wickiewicz TL, Warren RF. Motion loss after ligament injuries to the knee. Part I: causes. Am J Sports Med. 2001;29(5):664-675.
95. Bilko TE, Paulos LE, Feagin JA Jr, Lambert KL, Cunningham HR. Current trends in repair and rehabilitation of complete (acute) anterior cruciate ligament injuries. Analysis of 1984 questionnaire completed by ACL Study Group. Am J Sports Med. 1986;14(2):143-147.
96. Paulos L, Noyes FR, Grood E, Butler DL. Knee rehabilitation after anterior cruciate ligament reconstruction and repair. J Orthop Sports Phys Ther. 1991;13(2):60-70.
97. Paessler HH, Deneke J, Dahners LE. Augmented repair and early mobilization of acute anterior cruciate ligament injuries. Am J Sports Med. 1992;20(6):667-674.
98.
99. Kdolsky RK, Gibbons DF, Kwasny O, Schabus R, Plenk H Jr. Braided polypropylene augmentation device in reconstructive surgery of the anterior cruciate ligament: long-term clinical performance of 594 patients and short-term arthroscopic results, failure analysis by scanning electron microscopy, and synovial histomorphology. J Orthop Res. 1997;15(1):1-10.
100. Grøntvedt T, Engebretsen L. Comparison between two techniques for surgical repair of the acutely torn anterior cruciate ligament. A prospective, randomized follow-up study of 48 patients. Scand J Med Sci Sports. 1995;5(6):358-363.
101. Hehl G, Strecker W, Richter M, Kiefer H, Wissmeyer T. Clinical experience with PDS II augmentation for operative treatment of acute proximal ACL ruptures--2-year follow-up. Knee Surg Sports Traumatol Arthrosc. 1999;7(2):102-106.
102. Schenk S, Landsiedl F, Enenkel M. Arthroscopic single-stranded semitendinosus tendon- versus PDS-augmentation of reinserted acute femoral anterior cruciate ligament tears: 7 year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2006;14(4):318-324.
103. Zysk SP, Refior HJ. Operative or conservative treatment of the acutely torn anterior cruciate ligament in middle-aged patients. A follow-up study of 133 patients between the ages of 40 and 59 years. Arch Orthop Trauma Surg. 2000;120(1-2):59-64.
104. Krueger-Franke M, Siebert CH, Schupp A. Refixation of femoral anterior cruciate ligament tears combined with a semitendinosus tendon augmentation. Technique and results. Arch Orthop Trauma Surg. 1998;117(1-2):68-72.
105. Natri A, Järvinen M, Kannus P. Primary repair plus intra-articular iliotibial band augmentation in the treatment of an acute anterior cruciate ligament rupture. A follow-up study of 70 patients. Arch Orthop Trauma Surg. 1996;115(1):22-27.
106. Träger D, Pohle K, Tschirner W. Anterior cruciate ligament suture in comparison with plasty. A 5-year follow-up study. Arch Orthop Trauma Surg. 1995;114(5):278-280.
107. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M. Arthrofibrosis in acute anterior cruciate ligament reconstruction. The effect of timing of reconstruction and rehabilitation. Am J Sports Med. 1991;19(4):332-336.
108. Volokhina YV, Syed HM, Pham PH, Blackburn AK. Two helpful MRI signs for evaluation of posterolateral bundle tears of the anterior cruciate ligament: a pilot study. Orthop J Sports Med. 2015;3(8):2325967115597641.
109. Strand T, Mølster A, Hordvik M, Krukhaug Y. Long-term follow-up after primary repair of the anterior cruciate ligament: clinical and radiological evaluation 15-23 years postoperatively. Arch Orthop Trauma Surg. 2005;125(4):217-221.
110. van der List JP, DiFelice GS. Successful arthroscopic primary repair of a chronic anterior cruciate ligament tear 11 years following injury. HSS J. 2016. In press.
111. van der List JP, DiFelice GS. The role of ligament repair in anterior cruciate ligament surgery. In: Mascarenhas R, Bhatia S, Lowe WR, eds. Ligamentous Injuries of the Knee. 1st ed. Houston: Nova Science Publishers; 2016:199-220.
112. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
113. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
114. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
115. Magarian EM, Fleming BC, Harrison SL, Mastrangelo AN, Badger GJ, Murray MM. Delay of 2 or 6 weeks adversely affects the functional outcome of augmented primary repair of the porcine anterior cruciate ligament. Am J Sports Med. 2010;38(12):2528-2534.
116. Murray MM, Magarian EM, Harrison SL, Mastrangelo AN, Zurakowski D, Fleming BC. The effect of skeletal maturity on functional healing of the anterior cruciate ligament. J Bone Joint Surg Am. 2010;92(11):2039-2049.
117. Werner BC, Yang S, Looney AM, Gwathmey FW Jr. Trends in pediatric and adolescent anterior cruciate ligament iInjury and reconstruction. J Pediatr Orthop. 2016;36(5):447-452.
118. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
119. Ramski DE, Kanj WW, Franklin CC, Baldwin KD, Ganley TJ. Anterior cruciate ligament tears in children and adolescents: a meta-analysis of nonoperative versus operative treatment. Am J Sports Med. 2014;42(11):2769-2776.
120. Zantop T, Brucker PU, Vidal A, Zelle BA, Fu FH. Intraarticular rupture pattern of the ACL. Clin Orthop Relat Res. 2007;454:48-53.
121. Yoon KH, Bae DK, Cho SM, Park SY, Lee JH. Standard anterior cruciate ligament reconstruction versus isolated single-bundle augmentation with hamstring autograft. Arthroscopy. 2009;25(11):1265-1274.
122 Demirağ B, Ermutlu C, Aydemir F, Durak K. A comparison of clinical outcome of augmentation and standard reconstruction techniques for partial anterior cruciate ligament tears. Eklem Hastalik Cerrahisi. 2012;23(3):140-144.
123. Sonnery-Cottet B, Zayni R, Conteduca J, et al. Posterolateral bundle reconstruction with anteromedial bundle remnant preservation in ACL tears: clinical and MRI evaluation of 39 patients with 24-month follow-up. Orthop J Sports Med. 2013;1(3):2325967113501624.
124. Sabat D, Kumar V. Partial tears of anterior cruciate ligament: results of single bundle augmentation. Indian J Orthop. 2015;49(2):129-135.
125. Jung YB, Jung HJ, Siti HT, et al. Comparison of anterior cruciate ligament reconstruction with preservation only versus remnant tensioning technique. Arthroscopy. 2011;27(9):1252-1258.
126. Nguyen DT, Ramwadhdoebe TH, van der Hart CP, Blankevoort L, Tak PP, van Dijk CN. Intrinsic healing response of the human anterior cruciate ligament: an histological study of reattached ACL remnants. J Orthop Res. 2014;32(2):296-301.
127. Boutsiadis A, Karampalis C, Tzavelas A, Vraggalas V, Christodoulou P, Bisbinas I. Anterior cruciate ligament remnant-preserving reconstruction using a “lasso-loop” knot configuration. Arthrosc Tech. 2015;4(6):e741-e746.
128. Noh JH, Yoon KH, Song SJ, Roh YH. Re-tensioning technique to cover the graft with remnant in anterior cruciate ligament reconstruction. Arthrosc Tech. 2014;3(6):e679-e682.
129. Hong L, Li X, Zhang H, et al. Anterior cruciate ligament reconstruction with remnant preservation: a prospective, randomized controlled study. Am J Sports Med. 2012;40(12):2747-2755.
130. Noh JH, Kyung HS, Roh YH, Kang TS. Remnant-preserving and re-tensioning technique to cover the graft in anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 12. [Epub ahead of print]
131. Muneta T, Koga H, Ju YJ, Horie M, Nakamura T, Sekiya I. Remnant volume of anterior cruciate ligament correlates preoperative patients’ status and postoperative outcome. Knee Surg Sports Traumatol Arthrosc. 2013;21(4):906-913.
132. Leeberg V, Lekdorf J, Wong C, Sonne-Holm S. Tibial eminentia avulsion fracture in children - a systematic review of the current literature. Dan Med J. 2014;61(3):A4792.
133. In Y, Kwak DS, Moon CW, Han SH, Choi NY. Biomechanical comparison of three techniques for fixation of tibial avulsion fractures of the anterior cruciate ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1470-1478.
Injury of the anterior cruciate ligament (ACL) is very common with over 200,000 annual injuries in the United Status.1,2 There is a general consensus that these injuries should not be treated conservatively in patients that are younger, or who wish to remain active.3,4 Reconstructive surgery is currently the preferred treatment in these patients, and anatomic single-bundle reconstruction with autografts is considered the gold standard.5,6
Reconstruction of the ACL is, however, not a perfect treatment. Following single-bundle autograft reconstruction, revision rates of 3% to 8%,6-9 contralateral injury rates of 3% to 8%,10,11 and infection rates of 0.5% to 3%7,12,13 have been reported. Furthermore, due to the invasive nature of graft harvesting and the surgical procedure, 10% to 25% of the patients are not satisfied following ACL reconstruction.14,15 This can often be explained by common complaints, such as anterior knee pain (13%-43%), kneeling pain (12%-54%), quadriceps muscle atrophy (20%-30%),16,17 and loss of range of motion (ROM) (12%-23%).7,9,18,19 Furthermore, as a result of the invasive nature of reconstructive surgery, revisions can be difficult due to complications, such as tunnel widening, tunnel malpositioning, and preexisting hardware.20-22 This can lead to inferior outcomes and higher rates (13%) of revision surgery compared to primary reconstruction.23-26 Finally, reconstructive surgery does not restore native kinematics of the ACL,27-29 which may partially explain why reconstructive surgery has not been shown to prevent osteoarthritis.28-31
Over the past decades, there has been an increasing interest in the preservation of the ACL in an attempt to ameliorate these issues.32-37 Ligament preservation focuses on preserving the native tissues and biology, while minimizing the surgical morbidity to the patients.
Some authors have recently reported on arthroscopic primary repair of proximal ACL tears in which the ligament is reattached onto the femoral wall using modern-day suture anchor technology.32,38 Others have augmented this repair technique with an internal brace39,40 or with a synthetic device.33,41 When performing primary repair, it is believed that proprioception is maintained,42-44 while experimental studies have suggested that primary repair also restores the native kinematics,45 and may prevent osteoarthritis.46 Furthermore, primary repair is a conservative approach in that no grafts need to be harvested, no tunnels need to be drilled, and revision surgery, if necessary, is more analogous to primary reconstructions.32In patients with partial tears, some surgeons have advocated preserving the anteromedial (AM) or posterolateral (PL) bundle and performing selective single-bundle augmentation.34,35 In addition, several authors have used remnant tensioning36,47 or remnant preservation37,48 in combination with reconstructive surgery in order to benefit from the biological characteristics of the remnant. These techniques lead to better proprioceptive function,44,49,50 vascularization and ligamentization of the graft,50-52 provide an optical guide for anatomic tunnel placement,53 and decrease the incidence of tunnel widening.54,55The feasibility and applicability of these surgical techniques mainly depends on the tear type and tissue quality of the torn ligament. In this article we (I) discuss the history of ACL preservation, (II) discuss how modern advances alter the risk-benefit ratio for ACL preservation, and (III) propose a treatment algorithm for ACL injuries that is based on tear location and tissue quality.
History of ACL Preservation
The history of the surgical treatment of ACL injuries started in 1895 when Robson56 treated a 41-year-old male who tore both cruciate ligaments from the femoral wall. Performing primary repair with catgut ligatures, both cruciate ligaments were preserved and the patients had resolution of pain symptoms and full function at 6-year follow-up. Over the following decades, Palmer57,58 and O’Donoghue59,60 further popularized open primary repair for the treatment of ACL injuries, and this technique was the most commonly performed treatment in the 1970s and early 1980s.61-65 The initial short-term results of primary repair were excellent,61,62 but Feagin and Curl66 were the first to note that the results deteriorated at mid-term follow-up. Despite improvements in the surgical technique of repairing the ACL, such as the usage of nonabsorbable sutures and directly tying the sutures over bone,63,67 the results remained disappointing at longer-term follow-up.68-70
In response to these disappointing results, surgeons sought to improve the surgical treatment by either augmenting the primary repair with a semitendinosus, a patella tendon graft or an augmentation device,71-74 or by performing primary reconstruction.75-77 At the end of the 1980s and early 1990s, several randomized and prospective clinical trials were performed in order to compare the outcomes of these techniques.74,78-82 Many studies showed that results of augmented repair were more reliable when compared to primary repair, which led to the abandonment of primary repair in favor of augmented repair, and eventually primary reconstruction.65
The Important Role of Tear Location in Ligament Preservation
When taking a closer look at the outcomes of primary repair and augmented repair, it seems that the results of these preservation techniques were not as disappointing as was suggested. This can be explained, in large part, by the fact that the important roles of tear location and tissue quality were not widely recognized.
Sherman and colleagues70 reported in 1991 their mid-term results of open primary repair. Similar to others, they noted a deterioration of their results at mid-term follow-up. However, they uniquely performed an extensive subgroup analysis in order to find an explanation for this. In their study, considered a landmark paper on primary repair,65,70 they concluded that, “poor tissue quality is typical for midsubstance tears and that a repair of these injuries will predictably fail while type I tears (proximal), with better tissue quality, show a definite trend towards better results.”70 With these findings, they confirmed the findings of others that had recognized a trend of better outcomes with proximal tears.64,67,83-85
A majority of the historical studies that were published before 1991 had not considered the role of tear location and tissue quality on outcomes of open primary repair. This was also true for the aforementioned randomized studies that compared primary repair with augmented repair and primary reconstruction. Because these studies randomized patients and did not take tear location into account, it can be expected that patients with midsubstance tears were included in the cohorts of primary repair and the outcomes of these studies were therefore confounded.74,78-82 If these studies would have been aware of the role that tear location plays on primary repair outcomes, different outcomes may have been found and different conclusions on the optimal treatment for different tear types may have been drawn.86
Open Primary ACL Repair Outcomes Stratified by Tear Location
When reviewing the literature of open primary repair outcomes stratified by tear location, it is noted that multiple studies reported excellent outcomes following primary repair of proximal ACL tears.73,83,84,87-90 Weaver and colleagues64 were among the first to stratify their results by tear location, and they found that more patients with proximal tears (52 of 66; 79%) were satisfied after the procedure when compared to patients with midsubstance tears (3 of 13; 23%) at 3.5-year follow-up. They concluded that, “selection can be made with some predictability of the type of injury to the ligament as to which patients will do better.”64 Kühne and colleagues89 reported the outcomes of 75 patients with proximal tears treated with open primary repair and noted no failures, negative pivot shift in 88% of patients, stable or nearly stable Lachman test in 87% of patients, and 89% return to sports rate at 4-year follow-up. Raunest and colleagues91 reported a negative pivot shift and negative anterior drawer test in 84%, return to sports in 71%, and satisfaction in 75% of 51 patients that underwent open primary repair of proximal tears at 3.5-year follow-up.
Interestingly, and in contrast to the findings of Feagin and Curl,66 no deterioration of the outcomes at mid-term follow-up was noted in patients with proximal tears. Genelin and colleagues88 reported their results of 42 patients with proximal tears treated with open primary repair at 5- to 7-year follow-up. They found a negative pivot shift in 81%, stable or nearly stable Lachman test in 81%, and patient satisfaction in 86% of patients. Similarly, Bräm and colleagues87 found good results at mid-term follow-up with a good-excellent Lysholm score in 79%, return to a similar level of sports in 76%, stable or nearly stable Lachman test in 91%, and anterior drawer test in 94% of patients, along with an 88% satisfaction rate and 7% failure rate in patients who underwent open primary repair of proximal tears.
On the contrary, when the outcomes of studies that performed open primary repair in mainly, or only, patients with midsubstance tears are reviewed, significantly inferior results are found. Frank and colleagues92 reported outcomes in 42 patients with midsubstance tears at 4-year follow-up. They reported that 56% had a stable or nearly stable anterior drawer test, 78% had a positive pivot shift, and that only 61% were satisfied with the procedure. Odensten and colleagues78 reported outcomes of open primary repair in a subgroup of 22 patients with midsubstance tears at 1.5-year follow-up, and noted a 14% failure rate.
When reviewing the mid-term results in patients with midsubstance tears, it seems that there was more deterioration in outcomes.69,70 Firstly, the aforementioned study by Sherman and colleagues70 showed poor results in the patients with (type IV) midsubstance tears at mid-term follow-up. Furthermore, Kaplan and colleagues69 reported the mid-term outcomes of 70 patients, of which 56 patients had midsubstance tears. After having reported good outcomes at short-term follow-up,63,67 they noted that 42% of patients had >3 mm anteroposterior stability when compared to the contralateral leg, only a 62% return to sport rate, and a 17% failure rate. They concluded that, “Although … primary repair of the anterior cruciate may work in some patients, it is an unpredictable operative procedure.”
These studies showed that the outcomes of open primary repair were significantly better in patients with proximal ACL tears and sufficient tissue quality when compared to midsubstance tears. This suggests that open primary ACL repair may have been prematurely abandoned as a treatment option for patients with proximal tears.
Augmented ACL Repair
There were several reasons why augmented repair became the preferred treatment in the early and mid 1990s. First of all, the results of augmented repair were more consistent compared to primary repair in the aforementioned randomized and prospective studies,74,78-82 which is not surprising given the fact that the role of tear location was not widely recognized at the time. Secondly, in the 1970s and early 1980s, patients were treated postoperatively in a cast for 6 weeks, which led to problems, such as loss of ROM, pain, and decreased function.93,94 At the end of the1980s and 1990s, the focus shifted from prolonged joint immobilization towards early postoperative ROM.95-97 Since many authors believed that primary repair of the ACL was not strong enough to tolerate early mobilization, an augmentation was added to the technique in order to fortify the repair and enable early ROM.98
Interestingly, augmented repair, which is essentially a combination of primary ACL repair and ACL reconstruction, was mainly performed in the 1990s and many surgeons did recognize the role of tear location in this treatment at this point.73,98-103 In these years, the treatment algorithm consisted of augmented ACL repair in patients with proximal tears in the acute setting and ACL reconstruction in patients with midsubstance or chronic tears. Several different augmentation techniques were used to reinforce the primary repair in these years including autograft tissues (semitendinosus tendon,102-104 patellar tendon,100 or iliotibial band [ITB]105) synthetic materials (polydioxanone [PDS],101,102,106 carbon fibre,74 and polyester [Trevira]97), augmentation devices (Kennedy Ligament Augmentation Device [LAD]98-100) and extra-articular augmentations.73
When reviewing the outcomes of augmented repair of the ACL, good to excellent results can be found in studies that used this technique in patients with proximal tears.73,98-106 Kdolsky and colleagues98 were in one of the first groups that reported their results of augmented repair in only patients with proximal tears. In 1993, they reported their mid-term outcomes (5 to 8 years) in 66 patients who underwent primary repair and augmentation with the Kennedy LAD and found that 97% of patients had stable knees (<3 mm on KT-1000 examination), 98% had a negative pivot shift, and 76% returned to previous level of sports. However, often-reported problems with the augmentation devices were found in this study with rupture of the device (12%) and decreased ROM (14%).98 In 1995, Grøntvedt and Engebretsen100 compared augmentation with the Kennedy LAD to patellar tendon augmentation in a randomized study of patients with acute proximal tears. They noted that 50% of the patients in the Kennedy LAD group had a positive pivot shift compared to 23% in the patellar tendon group. Furthermore, they found KT-1000 leg differences of <3 mm in 92% of the patellar tendon group and 54% of the Kennedy LAD group. Because the authors found significant differences between both groups at 1- and 2-year follow-up, they stopped the clinical trial.
Several authors in the following years reported good results of augmented repair using autograft tissues. Natri and colleagues105 reported the outcomes of 72 patients treated with primary repair of proximal tears augmented with the ITB at 3.5-year follow-up. They found 89% negative pivot shift rate, 93% stable or nearly stable Lachman test, 99% stable or nearly stable anterior drawer test, 79% satisfaction rate, and 91% return to previous level of sports rate. Krueger-Franke and colleagues104 reported the outcomes of primary repair of proximal tears with augmentation using the semitendinosus tendon. In a retrospective study of 76 patients, they noted that 96% of patients had a negative pivot shift, 75% of patients had stable or nearly stable Lachman test, 93% were satisfied with the procedure, a mean Lysholm score of 92, a Tegner score that only decreased from 7.2 to 7.1, and KT-1000 testing with 78% <4 mm leg difference with the contralateral leg. The authors concluded that patients with femoral ruptures could be treated with augmented repair when performed in the acute setting. As this study was published in 1998, they stated that magnetic resonance imaging and arthroscopy could be helpful in identifying the tear location.
Final Abandonment of ACL Preservation
Reviewing these outcomes raises the question as to why these techniques were ultimately abandoned in the treatment algorithm of proximal ACL injuries, especially given the aforementioned advantages of ACL preservation. One of the possible answers can be found in a landmark study on ACL reconstruction and rehabilitation published by Shelbourne and colleagues107 in 1991. At that time, arthrofibrosis and knee stiffness were frequently reported problems following ACL surgery, which could partially be explained by the standard conservative rehabilitation using postoperative joint immobilization.67,70,80,88
Shelbourne and colleagues107 aimed to assess the cause of arthrofibrosis and knee stiffness, and divided the patients into groups by number of days between injury and surgery (<7, 7 to 21 days, and >21 days between injury and surgery). Furthermore, patients within these groups underwent either a conventional or accelerated rehabilitation program. The authors not only found that patients undergoing accelerated rehabilitation had less arthrofibrosis, but they also noted that less arthrofibrosis was seen when surgery was delayed. These findings, however, contrasted with the general perception that the ACL should be repaired in the first 3 weeks postinjury to ensure optimal tissue quality with an augmented approach. As a result, the treatment of ACL injuries shifted towards ACL reconstruction after these findings. Krueger-Franke and colleagues104 commented on the trend after the study of Shelbourne and colleagues:107 “Less consideration has been given to the importance of the proprioceptive receptors in the tibial remnants of the torn ACL and the value of their preservation as part of a primary reconstruction.”
In addition to the trend away from an augmented repair approach due to the novel understanding of the importance of early mobilization, some discussion should focus on the technical limitations of arthroscopy at that time. While arthroscopy had been around for several decades, fluid management and arthroscopic instrumentation was slow to develop. All of the repair and augmentation techniques previously discussed had been performed via an open arthrotomy. Arthroscopic technologies of the time were not refined enough to enable surgeons to perform such complex, intra-articular techniques that would enable suturing of the ligament remnant. In this regard, arthroscopic ACL reconstruction was a much simpler technique to accomplish, and this also likely contributed to the final abandonment of the ligament preservation approach.
Role for ACL Preservation with Modern Advances
As stated in the introduction, there has been a recent resurgence of interest in preservation of the native ligament.32-37 With the passage of time, many technologic advances have been made, which has allowed surgeons to reconsider the concept of ligament preservation.
First of all, appropriate patient selection was not applied historically, as the critical factors of tear location and tissue quality were not recognized in the era of open primary repair. In modern days, however, advances such as MRI have been developed, which can give the surgeon an idea of the status, and tear type of the ACL pre-operatively.108 This may help the orthopaedic surgeon to plan the surgery and make an assessment as to whether ACL preservation is possible. Secondly, in the historic literature the postoperative regimen consisted of casting for 5 or 6 weeks,67,70,80,88 while the focus later shifted towards early ROM.95-97Modern day ACL rehabilitation focuses on immediate ROM to avoid the complications stiffness, pain and decreased function that plagued the outcomes when immobilization was used.93,94 Thirdly, historically small tunnels were drilled with primary repair and sutures had to be tied over bone,57,67 whereas currently suture anchors are available that prevent the need for tunnel drilling and enable direct suture tensioning.32,38 Finally, and most importantly, in the historic literature patients were treated with an invasive arthrotomy technique, while modern day arthroscopic techniques readily enable the surgeon to effectively suture the remnant arthroscopically. Interestingly, in 2005, in their 20-year follow-up of primary repair surgeries, Strand and colleagues109 stated, “if the same results could be accomplished by a smaller, arthroscopic procedure, primary repair might reduce the number of patients needing later reconstructions with small ‘costs’ in the way of risk and inconvenience for the patients. We therefore believe that further research and development of methods for closed (arthroscopic) repair are justified.”
Altered Risk-Benefit Ratio
Historically, the treatments of open primary repair and open ACL reconstruction were both invasive surgeries with an arthrotomy, drilling of bone tunnels, and postoperative joint immobilization for 4 to 6 weeks. However, with the modern-day advances, the risk-benefit ratio of both treatments has changed, as Strand and colleagues109 had already suggested. Although ACL reconstruction can be performed arthroscopically, it remains an invasive procedure, in which tunnels are drilled, patellar tendons or hamstring tendons are harvested, and complications, such as knee pain and quadriceps atrophy, are common. The surgery of primary ACL repair, however, has benefited significantly from the modern developments.32,38 Primary ACL repair can now be performed arthroscopically, and by using suture anchors no tunnels need to be drilled and the remnant can be tensioned directly. An additional benefit of the use of suture anchors is that revision surgery of a failed primary repair is analogous to primary reconstruction, whereas revision surgery of a failed ACL reconstruction can be problematic due to tunnel widening, tunnel malpositioning, and preexisting hardware.20-22
Reviewing the differences between arthroscopic primary ACL repair and ACL reconstruction, it becomes clear that primary repair has benefited significantly from the modern advances and that the risk-benefit ratio for primary repair has been altered. This means that patients with proximal tears can be treated with a relatively straight forward, minimally invasive surgery, which has been shown to be effective in 85% to 90% of patients.32,38
Treatment Algorithm Based on Tear Location
Since 2008, in the practice of the senior author (GSD), the surgical treatment algorithm for ACL injuries is completely based on the tear location and tissue quality of the ligament.110,111 To describe the different tear types, we use the modified Sherman classification in which we extended his classification towards the tibial side whereas Sherman and colleagues70 only described the femoral side of the tears (Figures A-F, Table).
Type I Tears: Primary Repair
Type I tears are soft tissue avulsion type tears that can be easily treated with arthroscopic primary repair.107 The length of the distal remnant has to be at least 90% and the tissue quality has to be good to excellent in order to approximate the remnant towards the femoral wall (Table).112 The incidence of type I tears was 26% in the study of Sherman and colleagues,70 although recent studies showed a lower incidence (6% to 10%) in a larger population.32,38 Certainly, individual practices will see different percentages of type I tears based upon the mix of injury mechanisms they see most frequently. Over the last 2 years, with the recognition of the importance of tear type and tissue quality, there has been a renewed interest in arthroscopic primary ACL repair.32,38
DiFelice and colleagues32 were the first to arthroscopically perform primary repair of the ACL in proximal tears using suture anchors. They reported the outcomes of the first 11 consecutive patients that underwent primary repair in a previously described technique.113 At mean 3.5-year follow-up, they noted only 1 failure (9%) due to re-injury; mean Lysholm score of 93.2; mean modified Cincinnati score of 91.5; pre- and postoperative Tegner score of 7.3 and 6.9, respectively; SANE score of 91.8; and subjective International Knee Documentation Committee (IKDC) score of 86.4. Of the patients with an intact repair, 9 patients had an objective IKDC rating A and 1 patient had B and all patients had KT-1000 leg differences of <3 mm with the contralateral side (three patients were not available for KT-1000 testing). The authors concluded that arthroscopic primary ACL repair could achieve short-term clinical success in a selected group of patients with proximal avulsion tears and excellent tissue quality. They further noted that mid-term outcomes are necessary given that the results of open primary repair deteriorated at longer-term follow-up in the historical literature. Recently, the senior author (GSD) has added an Internal Brace (Arthrex) to the primary repair with the goal of protecting the ligament in the first weeks to further promote healing of the ligament.39,40,114
More recently, Achtnich and colleagues38 compared the treatment of arthroscopic primary ACL repair with primary ACL reconstruction in 41 patients with type I tears at 2.3-years follow-up. Twenty-one patients consented for primary repair while 20 patients declined this procedure and underwent primary reconstruction. They noted no significant differences in Lachman test, pivot shift test, objective IKDC score, and KT-1000 scores. Although not significant, the clinical failure rate in the primary repair group (15%) was higher than the reconstruction group (0%). Interestingly, despite the higher failure rate in the repair group, the authors concluded that primary ACL repair is recommended in a carefully selected group of patients with type I tears and excellent tissue quality, which can likely be explained by the differences in the risk-benefit ratio between both procedures.
Over the last decade, the research group led by Murray46,115,116 has performed experimental research on primary repair with a biological scaffold and reported many interesting findings that could be extrapolated to primary ACL repair. First of all, they compared bioenhanced primary repair with bioenhanced primary reconstruction in 64 Yucutan pigs and noted that there was significantly less macroscopic cartilage damage in the primary repair group at 1-year follow-up.46 They concluded that bioenhanced ACL repair may provide a new, less invasive treatment option that reduces cartilage damage following joint injury. This may suggest that primary repair may have a lower incidence of osteoarthritis when compared to ACL reconstruction, which is interesting as osteoarthritis is very common after ACL reconstruction. Further research in this area is certainly warranted.
In another study they compared bioenhanced primary repair in juvenile, adolescent and mature Yucutan pigs and noted that functional healing depended on the level of skeletal maturity with immature animals having a more productive healing response.116 This indicates that primary repair might be a good treatment option in skeletally immature patients, especially since reconstruction increases the risk of premature closure of the epiphysis117,118 and delaying treatment increases the risk of meniscus injury.119 Interestingly, a recent meta-analysis showed indeed that the risk of epiphysis closure was lower in primary repair when compared to ACL reconstruction and the rupture rate was also lower.118 Primary repair may be a good treatment option in children as the procedure has all the attributes that should be applicable to children: it is minimally morbid, tissue sparing, and it is a conservative approach that does not burn any surgical bridges for future reconstructive surgery if necessary.
Finally, the research group of Murray115 assessed the effect of surgical delay of primary repair following injury in Yucutan pigs and noted that better biomechanical outcomes were noted after delaying surgery for 2 weeks when compared to 6 weeks. This suggests that primary repair should preferably be performed in the acute setting, which has also been shown in historical studies since the ligament in the acute setting has optimal tissue quality and the ligament is less likely to be retracted or reabsorbed.59,60,115
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the tear locations of the AM and PL bundle are not at the same location and Zantop and colleagues120 reported in an arthroscopic study that this could be as frequent as in 30% of all complete tears. In some of these tears, one of the bundles can be avulsed of the femoral wall (type I tear) while the other bundle is not directly repairable (non-type I tear). In these cases, the senior author (GSD) will repair the type I tear bundle, whereas a hamstring augmentation is placed at the location of the other bundle. When reviewing the literature, a combination of primary repair of one bundle and reconstruction of the second bundle has not been described before. However, over the last decade several surgeons have performed augmentation of one bundle in the setting of partial tears.34,35,121-124
Buda and colleagues34 were the first to perform selective AM or PL bundle reconstruction in the setting of partial tears.34 At 5-year follow-up, they reported no reruptures and only 1 patient with an IKDC C-score, although reoperation was necessary in 4 out of 47 patients (9%). Following this publication, many others reported on selective bundle reconstruction.35,121-124 However, with partial tears, the knee is often stable and a selective augmentation technique is utilized to prevent complete rupture of the ligament. The application of this technique is essentially different from reconstruction for complete ACL tears in which the knee is unstable, there is a giving way sensation and patients have problems participating in sports.
Type II Tears: Augmented Repair
Type II tears often have good or excellent tissue quality and can be pulled up towards the femoral footprint, but are too short to be firmly attached. Sherman and colleagues70 reported that approximately 22% patients had a type II tear, which corresponds to a tear located in the proximal part of the ligament. With this technique, multiple suture passes are used to stitch the remnant and, in addition, a smaller hamstring autograft or allograft is passed through the middle of the tibial remnant. A suture button is used proximally for the graft, and the tensioning repair sutures through the remnant are also passed through the suture button. The suture button is passed through the femoral tunnel and flipped so that the graft is proximally fixed. Then, the repair sutures of the remnant are tensioned, and the ligament is pulled towards the femoral wall as a sleeve around the graft. When the ligament is approximated to the femoral wall, the sutures are tied over the suture button. The graft is then tensioned distally to complete the augmented repair.
In the recent literature, the technique of augmentation of a primary repair using autograft tissue has not been reported. However, augmented repair using an internal brace39,40 or augmentation devices33,41 have been recently performed. MacKay and colleagues39 reported good outcomes of arthroscopic primary repair of proximal tears using an internal brace. Eggli and colleagues33 reported the results of the first 10 patients treated with ACL preservation using primary repair of the ligament with the addition of a dynamic screw-spring mechanism. The authors reported good preliminary results with one failure (10%) and good objective and subjective outcomes. In a next study, they reported the outcomes of 278 patients and although they reported good clinical outcomes and a revision rate of 4%, the reoperation rate for removal of the screw-spring mechanism was high (24%).41 This is not surprising when reviewing the historical literature in which high complication rates of the augmentation devices were reported.99,100 We were unable to identify any other studies reporting surgical techniques of augmenting primary repair in the literature.
Type III Tears: Reconstruction With Remnant Tensioning
In patients with type III tears, the ligament cannot be approximated to the wall and reconstruction is necessary in order to restore knee stability. However, in these cases the ligament has sufficient length (25%-75%) and can be tensioned along or around the graft. Preservation of the ligament remnant has several (theoretical) advantages, such as better proprioceptive function,42,49,50 vascularization and ligamentization of the graft,50-52 an optical guide for anatomic tunnel placement,53 and a decreased incidence of tunnel widening.54,55 Furthermore, tensioning of the remnant is thought to lower the risk of cyclops lesions when compared to remnant preservation.125 Although the difference between augmented repair and remnant tensioning seems small, the purpose of surgery is different. With augmented repair, the ligament can be approximated close to the femoral wall and the goal of surgery is to use the healing capacity that the ACL has in the proximal part of the ligament,126 while with remnant tensioning the goal is only to benefit from some of the aforementioned advantages. Ahn and colleagues36 were the first to perform this technique and stated, “Our concept is that the remnant tissue has only an additive effect.” Furthermore, with augmented repair multiple sutures are passed through the AM and PL bundle in order to sufficiently approximate the ligament to the femoral wall, while with the remnant tensioning technique generally one or a few sutures or lasso loop are passed through the proximal part to tension the ligament, prevent sagging of the remnant, and decrease the risk of cyclops lesions.127,128
Several authors have recently performed remnant tensioning during ACL.36,47,125-127 Ahn and colleagues47 reported excellent objective and subjective outcomes following this procedure and found that with re-arthroscopy nearly all patients had fair synovialization of the graft. Others have reported similarly good outcomes of these techniques.125,129,130 However, studies comparing this treatment with normal ACL reconstruction and assessing outcomes, failure rates and proprioception are lacking.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some patients the ligament is torn distally or the tissue quality is not optimal. In these patients, the remnant can be debrided to the part of good tissue quality in order to preserve the biology and minimize the risk for cyclops lesions. A standard reconstruction needs to be performed to restore the instability, but by preserving the remnant, advantages, such as proprioception,44,49,50 graft vascularization,50-52 an optical guide for tibial tunnel placement,53 and a decreased incidence of tunnel widening54,55 can be expected.
Lee and colleagues37 presented the tibial remnant technique in which standard reconstruction was performed, and the tibial tunnel was drilled through the center of the remnant. In a later study, they compared remnant preservation with a remnant of <20% of the total ACL length with >20% of the length and found that proprioception was better with more remnant volume.48 Similarly, Muneta and colleagues131 assessed the role of remnant length and found that remnant length is positively correlated with better stability measured on KT-1000 anteroposterior stability.
Several studies compared ACL reconstruction with remnant preservation vs conventional ACL reconstruction.52,54,129 Takazawa and colleagues52 performed a retrospective study of 183 patients and found that patients in the remnant preservation group had significantly better KT-2000 stability, while they also reported a significantly lower graft rupture rate in this group (1.1% vs 7.1%) at 2-year follow-up. Hong and colleagues129 performed a randomized clinical trial of 80 patients and did not find these differences, although there was a trend towards higher Lysholm scores in the remnant preservation group. Finally, Zhang and colleagues54 performed a randomized clinical trial and found a lower incidence and amount of tibial tunnel widening in the preserving-remnant group when compared to the removing-remnant group. These studies show that there is likely a role for remnant preservation.
Type V Tears: Primary Repair
In some patients, the ligament is torn in the distal 10% of the ligament, which can occur as a distal avulsion tear or as a distal bony avulsion fracture.132 Bony avulsion fractures are most commonly seen in children whereas true distal soft tissue avulsion tears are very rare.132
Treatments of these tear types include antegrade screw fixation, pullout sutures or the use of suture anchors in case of bony avulsion fractures and pullout sutures with tying over a bony bridge or ligament button in case of soft tissue avulsions. Leeberg and colleagues132 recently performed a systematic review of all studies reporting on treatment of distal avulsion fractures.They noted that most treatments were currently performed arthroscopically and that outcomes were generally good. Another recent biomechanical study compared antegrade screw fixation with suture anchor fixation and pullout suture fixation.133 The authors noted that suture anchor fixation has slightly less displacement of the bony fragment when compared to screw fixation and pull-out sutures, and that the strength to failure was higher in the suture anchor fixation when compared to the pullout suture fixation. The outcomes of this study suggest that screw fixation and suture anchor fixation might be superior to pullout suture fixation, which might be interesting as with pullout suture fixation the ligament cannot be directly tensioned to the tibial footprint, which can lead to anteroposterior laxity.132 Clinical studies are necessary to assess the preferred treatment in these tear types but it seems that screw fixation is preferred in large bony avulsion fractures, while suture anchor fixation or pullout suture fixation can be used for soft tissue avulsion tears.
Complex Tears or Poor Tissue Quality: Reconstruction
If the tear is complex, multiple tears are present, or the tissue quality is poor, then preservation of the ligament is not possible, and in these cases a standard reconstruction should be performed.
Conclusion
When reviewing the literature of ACL preservation, it becomes clear that the evolution of surgical treatment of ACL injuries was biased. Preservation of the native ligament has many advantages, such as better proprioception, graft vascularization, an optical guide for tibial tunnel placement, and a decreased incidence of tunnel widening that can be expected. Furthermore, arthroscopic primary ACL repair is minimally invasive and does not burn any bridges for future reconstructions, if necessary. This is in addition to the other (theoretical) advantages of primary repair, such as restoration of native kinematics and a decreased risk of osteoarthritis. Modern advances have significantly changed the risk-benefit ratio that should make us reconsider ACL preservation approaches. Certainly, further research in this area is warranted. In this article we have presented a treatment algorithm for ACL preservation, which is based on tear location and remnant tissue quality.
Am J Orthop. 2016;45(7):E393-E405. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Injury of the anterior cruciate ligament (ACL) is very common with over 200,000 annual injuries in the United Status.1,2 There is a general consensus that these injuries should not be treated conservatively in patients that are younger, or who wish to remain active.3,4 Reconstructive surgery is currently the preferred treatment in these patients, and anatomic single-bundle reconstruction with autografts is considered the gold standard.5,6
Reconstruction of the ACL is, however, not a perfect treatment. Following single-bundle autograft reconstruction, revision rates of 3% to 8%,6-9 contralateral injury rates of 3% to 8%,10,11 and infection rates of 0.5% to 3%7,12,13 have been reported. Furthermore, due to the invasive nature of graft harvesting and the surgical procedure, 10% to 25% of the patients are not satisfied following ACL reconstruction.14,15 This can often be explained by common complaints, such as anterior knee pain (13%-43%), kneeling pain (12%-54%), quadriceps muscle atrophy (20%-30%),16,17 and loss of range of motion (ROM) (12%-23%).7,9,18,19 Furthermore, as a result of the invasive nature of reconstructive surgery, revisions can be difficult due to complications, such as tunnel widening, tunnel malpositioning, and preexisting hardware.20-22 This can lead to inferior outcomes and higher rates (13%) of revision surgery compared to primary reconstruction.23-26 Finally, reconstructive surgery does not restore native kinematics of the ACL,27-29 which may partially explain why reconstructive surgery has not been shown to prevent osteoarthritis.28-31
Over the past decades, there has been an increasing interest in the preservation of the ACL in an attempt to ameliorate these issues.32-37 Ligament preservation focuses on preserving the native tissues and biology, while minimizing the surgical morbidity to the patients.
Some authors have recently reported on arthroscopic primary repair of proximal ACL tears in which the ligament is reattached onto the femoral wall using modern-day suture anchor technology.32,38 Others have augmented this repair technique with an internal brace39,40 or with a synthetic device.33,41 When performing primary repair, it is believed that proprioception is maintained,42-44 while experimental studies have suggested that primary repair also restores the native kinematics,45 and may prevent osteoarthritis.46 Furthermore, primary repair is a conservative approach in that no grafts need to be harvested, no tunnels need to be drilled, and revision surgery, if necessary, is more analogous to primary reconstructions.32In patients with partial tears, some surgeons have advocated preserving the anteromedial (AM) or posterolateral (PL) bundle and performing selective single-bundle augmentation.34,35 In addition, several authors have used remnant tensioning36,47 or remnant preservation37,48 in combination with reconstructive surgery in order to benefit from the biological characteristics of the remnant. These techniques lead to better proprioceptive function,44,49,50 vascularization and ligamentization of the graft,50-52 provide an optical guide for anatomic tunnel placement,53 and decrease the incidence of tunnel widening.54,55The feasibility and applicability of these surgical techniques mainly depends on the tear type and tissue quality of the torn ligament. In this article we (I) discuss the history of ACL preservation, (II) discuss how modern advances alter the risk-benefit ratio for ACL preservation, and (III) propose a treatment algorithm for ACL injuries that is based on tear location and tissue quality.
History of ACL Preservation
The history of the surgical treatment of ACL injuries started in 1895 when Robson56 treated a 41-year-old male who tore both cruciate ligaments from the femoral wall. Performing primary repair with catgut ligatures, both cruciate ligaments were preserved and the patients had resolution of pain symptoms and full function at 6-year follow-up. Over the following decades, Palmer57,58 and O’Donoghue59,60 further popularized open primary repair for the treatment of ACL injuries, and this technique was the most commonly performed treatment in the 1970s and early 1980s.61-65 The initial short-term results of primary repair were excellent,61,62 but Feagin and Curl66 were the first to note that the results deteriorated at mid-term follow-up. Despite improvements in the surgical technique of repairing the ACL, such as the usage of nonabsorbable sutures and directly tying the sutures over bone,63,67 the results remained disappointing at longer-term follow-up.68-70
In response to these disappointing results, surgeons sought to improve the surgical treatment by either augmenting the primary repair with a semitendinosus, a patella tendon graft or an augmentation device,71-74 or by performing primary reconstruction.75-77 At the end of the 1980s and early 1990s, several randomized and prospective clinical trials were performed in order to compare the outcomes of these techniques.74,78-82 Many studies showed that results of augmented repair were more reliable when compared to primary repair, which led to the abandonment of primary repair in favor of augmented repair, and eventually primary reconstruction.65
The Important Role of Tear Location in Ligament Preservation
When taking a closer look at the outcomes of primary repair and augmented repair, it seems that the results of these preservation techniques were not as disappointing as was suggested. This can be explained, in large part, by the fact that the important roles of tear location and tissue quality were not widely recognized.
Sherman and colleagues70 reported in 1991 their mid-term results of open primary repair. Similar to others, they noted a deterioration of their results at mid-term follow-up. However, they uniquely performed an extensive subgroup analysis in order to find an explanation for this. In their study, considered a landmark paper on primary repair,65,70 they concluded that, “poor tissue quality is typical for midsubstance tears and that a repair of these injuries will predictably fail while type I tears (proximal), with better tissue quality, show a definite trend towards better results.”70 With these findings, they confirmed the findings of others that had recognized a trend of better outcomes with proximal tears.64,67,83-85
A majority of the historical studies that were published before 1991 had not considered the role of tear location and tissue quality on outcomes of open primary repair. This was also true for the aforementioned randomized studies that compared primary repair with augmented repair and primary reconstruction. Because these studies randomized patients and did not take tear location into account, it can be expected that patients with midsubstance tears were included in the cohorts of primary repair and the outcomes of these studies were therefore confounded.74,78-82 If these studies would have been aware of the role that tear location plays on primary repair outcomes, different outcomes may have been found and different conclusions on the optimal treatment for different tear types may have been drawn.86
Open Primary ACL Repair Outcomes Stratified by Tear Location
When reviewing the literature of open primary repair outcomes stratified by tear location, it is noted that multiple studies reported excellent outcomes following primary repair of proximal ACL tears.73,83,84,87-90 Weaver and colleagues64 were among the first to stratify their results by tear location, and they found that more patients with proximal tears (52 of 66; 79%) were satisfied after the procedure when compared to patients with midsubstance tears (3 of 13; 23%) at 3.5-year follow-up. They concluded that, “selection can be made with some predictability of the type of injury to the ligament as to which patients will do better.”64 Kühne and colleagues89 reported the outcomes of 75 patients with proximal tears treated with open primary repair and noted no failures, negative pivot shift in 88% of patients, stable or nearly stable Lachman test in 87% of patients, and 89% return to sports rate at 4-year follow-up. Raunest and colleagues91 reported a negative pivot shift and negative anterior drawer test in 84%, return to sports in 71%, and satisfaction in 75% of 51 patients that underwent open primary repair of proximal tears at 3.5-year follow-up.
Interestingly, and in contrast to the findings of Feagin and Curl,66 no deterioration of the outcomes at mid-term follow-up was noted in patients with proximal tears. Genelin and colleagues88 reported their results of 42 patients with proximal tears treated with open primary repair at 5- to 7-year follow-up. They found a negative pivot shift in 81%, stable or nearly stable Lachman test in 81%, and patient satisfaction in 86% of patients. Similarly, Bräm and colleagues87 found good results at mid-term follow-up with a good-excellent Lysholm score in 79%, return to a similar level of sports in 76%, stable or nearly stable Lachman test in 91%, and anterior drawer test in 94% of patients, along with an 88% satisfaction rate and 7% failure rate in patients who underwent open primary repair of proximal tears.
On the contrary, when the outcomes of studies that performed open primary repair in mainly, or only, patients with midsubstance tears are reviewed, significantly inferior results are found. Frank and colleagues92 reported outcomes in 42 patients with midsubstance tears at 4-year follow-up. They reported that 56% had a stable or nearly stable anterior drawer test, 78% had a positive pivot shift, and that only 61% were satisfied with the procedure. Odensten and colleagues78 reported outcomes of open primary repair in a subgroup of 22 patients with midsubstance tears at 1.5-year follow-up, and noted a 14% failure rate.
When reviewing the mid-term results in patients with midsubstance tears, it seems that there was more deterioration in outcomes.69,70 Firstly, the aforementioned study by Sherman and colleagues70 showed poor results in the patients with (type IV) midsubstance tears at mid-term follow-up. Furthermore, Kaplan and colleagues69 reported the mid-term outcomes of 70 patients, of which 56 patients had midsubstance tears. After having reported good outcomes at short-term follow-up,63,67 they noted that 42% of patients had >3 mm anteroposterior stability when compared to the contralateral leg, only a 62% return to sport rate, and a 17% failure rate. They concluded that, “Although … primary repair of the anterior cruciate may work in some patients, it is an unpredictable operative procedure.”
These studies showed that the outcomes of open primary repair were significantly better in patients with proximal ACL tears and sufficient tissue quality when compared to midsubstance tears. This suggests that open primary ACL repair may have been prematurely abandoned as a treatment option for patients with proximal tears.
Augmented ACL Repair
There were several reasons why augmented repair became the preferred treatment in the early and mid 1990s. First of all, the results of augmented repair were more consistent compared to primary repair in the aforementioned randomized and prospective studies,74,78-82 which is not surprising given the fact that the role of tear location was not widely recognized at the time. Secondly, in the 1970s and early 1980s, patients were treated postoperatively in a cast for 6 weeks, which led to problems, such as loss of ROM, pain, and decreased function.93,94 At the end of the1980s and 1990s, the focus shifted from prolonged joint immobilization towards early postoperative ROM.95-97 Since many authors believed that primary repair of the ACL was not strong enough to tolerate early mobilization, an augmentation was added to the technique in order to fortify the repair and enable early ROM.98
Interestingly, augmented repair, which is essentially a combination of primary ACL repair and ACL reconstruction, was mainly performed in the 1990s and many surgeons did recognize the role of tear location in this treatment at this point.73,98-103 In these years, the treatment algorithm consisted of augmented ACL repair in patients with proximal tears in the acute setting and ACL reconstruction in patients with midsubstance or chronic tears. Several different augmentation techniques were used to reinforce the primary repair in these years including autograft tissues (semitendinosus tendon,102-104 patellar tendon,100 or iliotibial band [ITB]105) synthetic materials (polydioxanone [PDS],101,102,106 carbon fibre,74 and polyester [Trevira]97), augmentation devices (Kennedy Ligament Augmentation Device [LAD]98-100) and extra-articular augmentations.73
When reviewing the outcomes of augmented repair of the ACL, good to excellent results can be found in studies that used this technique in patients with proximal tears.73,98-106 Kdolsky and colleagues98 were in one of the first groups that reported their results of augmented repair in only patients with proximal tears. In 1993, they reported their mid-term outcomes (5 to 8 years) in 66 patients who underwent primary repair and augmentation with the Kennedy LAD and found that 97% of patients had stable knees (<3 mm on KT-1000 examination), 98% had a negative pivot shift, and 76% returned to previous level of sports. However, often-reported problems with the augmentation devices were found in this study with rupture of the device (12%) and decreased ROM (14%).98 In 1995, Grøntvedt and Engebretsen100 compared augmentation with the Kennedy LAD to patellar tendon augmentation in a randomized study of patients with acute proximal tears. They noted that 50% of the patients in the Kennedy LAD group had a positive pivot shift compared to 23% in the patellar tendon group. Furthermore, they found KT-1000 leg differences of <3 mm in 92% of the patellar tendon group and 54% of the Kennedy LAD group. Because the authors found significant differences between both groups at 1- and 2-year follow-up, they stopped the clinical trial.
Several authors in the following years reported good results of augmented repair using autograft tissues. Natri and colleagues105 reported the outcomes of 72 patients treated with primary repair of proximal tears augmented with the ITB at 3.5-year follow-up. They found 89% negative pivot shift rate, 93% stable or nearly stable Lachman test, 99% stable or nearly stable anterior drawer test, 79% satisfaction rate, and 91% return to previous level of sports rate. Krueger-Franke and colleagues104 reported the outcomes of primary repair of proximal tears with augmentation using the semitendinosus tendon. In a retrospective study of 76 patients, they noted that 96% of patients had a negative pivot shift, 75% of patients had stable or nearly stable Lachman test, 93% were satisfied with the procedure, a mean Lysholm score of 92, a Tegner score that only decreased from 7.2 to 7.1, and KT-1000 testing with 78% <4 mm leg difference with the contralateral leg. The authors concluded that patients with femoral ruptures could be treated with augmented repair when performed in the acute setting. As this study was published in 1998, they stated that magnetic resonance imaging and arthroscopy could be helpful in identifying the tear location.
Final Abandonment of ACL Preservation
Reviewing these outcomes raises the question as to why these techniques were ultimately abandoned in the treatment algorithm of proximal ACL injuries, especially given the aforementioned advantages of ACL preservation. One of the possible answers can be found in a landmark study on ACL reconstruction and rehabilitation published by Shelbourne and colleagues107 in 1991. At that time, arthrofibrosis and knee stiffness were frequently reported problems following ACL surgery, which could partially be explained by the standard conservative rehabilitation using postoperative joint immobilization.67,70,80,88
Shelbourne and colleagues107 aimed to assess the cause of arthrofibrosis and knee stiffness, and divided the patients into groups by number of days between injury and surgery (<7, 7 to 21 days, and >21 days between injury and surgery). Furthermore, patients within these groups underwent either a conventional or accelerated rehabilitation program. The authors not only found that patients undergoing accelerated rehabilitation had less arthrofibrosis, but they also noted that less arthrofibrosis was seen when surgery was delayed. These findings, however, contrasted with the general perception that the ACL should be repaired in the first 3 weeks postinjury to ensure optimal tissue quality with an augmented approach. As a result, the treatment of ACL injuries shifted towards ACL reconstruction after these findings. Krueger-Franke and colleagues104 commented on the trend after the study of Shelbourne and colleagues:107 “Less consideration has been given to the importance of the proprioceptive receptors in the tibial remnants of the torn ACL and the value of their preservation as part of a primary reconstruction.”
In addition to the trend away from an augmented repair approach due to the novel understanding of the importance of early mobilization, some discussion should focus on the technical limitations of arthroscopy at that time. While arthroscopy had been around for several decades, fluid management and arthroscopic instrumentation was slow to develop. All of the repair and augmentation techniques previously discussed had been performed via an open arthrotomy. Arthroscopic technologies of the time were not refined enough to enable surgeons to perform such complex, intra-articular techniques that would enable suturing of the ligament remnant. In this regard, arthroscopic ACL reconstruction was a much simpler technique to accomplish, and this also likely contributed to the final abandonment of the ligament preservation approach.
Role for ACL Preservation with Modern Advances
As stated in the introduction, there has been a recent resurgence of interest in preservation of the native ligament.32-37 With the passage of time, many technologic advances have been made, which has allowed surgeons to reconsider the concept of ligament preservation.
First of all, appropriate patient selection was not applied historically, as the critical factors of tear location and tissue quality were not recognized in the era of open primary repair. In modern days, however, advances such as MRI have been developed, which can give the surgeon an idea of the status, and tear type of the ACL pre-operatively.108 This may help the orthopaedic surgeon to plan the surgery and make an assessment as to whether ACL preservation is possible. Secondly, in the historic literature the postoperative regimen consisted of casting for 5 or 6 weeks,67,70,80,88 while the focus later shifted towards early ROM.95-97Modern day ACL rehabilitation focuses on immediate ROM to avoid the complications stiffness, pain and decreased function that plagued the outcomes when immobilization was used.93,94 Thirdly, historically small tunnels were drilled with primary repair and sutures had to be tied over bone,57,67 whereas currently suture anchors are available that prevent the need for tunnel drilling and enable direct suture tensioning.32,38 Finally, and most importantly, in the historic literature patients were treated with an invasive arthrotomy technique, while modern day arthroscopic techniques readily enable the surgeon to effectively suture the remnant arthroscopically. Interestingly, in 2005, in their 20-year follow-up of primary repair surgeries, Strand and colleagues109 stated, “if the same results could be accomplished by a smaller, arthroscopic procedure, primary repair might reduce the number of patients needing later reconstructions with small ‘costs’ in the way of risk and inconvenience for the patients. We therefore believe that further research and development of methods for closed (arthroscopic) repair are justified.”
Altered Risk-Benefit Ratio
Historically, the treatments of open primary repair and open ACL reconstruction were both invasive surgeries with an arthrotomy, drilling of bone tunnels, and postoperative joint immobilization for 4 to 6 weeks. However, with the modern-day advances, the risk-benefit ratio of both treatments has changed, as Strand and colleagues109 had already suggested. Although ACL reconstruction can be performed arthroscopically, it remains an invasive procedure, in which tunnels are drilled, patellar tendons or hamstring tendons are harvested, and complications, such as knee pain and quadriceps atrophy, are common. The surgery of primary ACL repair, however, has benefited significantly from the modern developments.32,38 Primary ACL repair can now be performed arthroscopically, and by using suture anchors no tunnels need to be drilled and the remnant can be tensioned directly. An additional benefit of the use of suture anchors is that revision surgery of a failed primary repair is analogous to primary reconstruction, whereas revision surgery of a failed ACL reconstruction can be problematic due to tunnel widening, tunnel malpositioning, and preexisting hardware.20-22
Reviewing the differences between arthroscopic primary ACL repair and ACL reconstruction, it becomes clear that primary repair has benefited significantly from the modern advances and that the risk-benefit ratio for primary repair has been altered. This means that patients with proximal tears can be treated with a relatively straight forward, minimally invasive surgery, which has been shown to be effective in 85% to 90% of patients.32,38
Treatment Algorithm Based on Tear Location
Since 2008, in the practice of the senior author (GSD), the surgical treatment algorithm for ACL injuries is completely based on the tear location and tissue quality of the ligament.110,111 To describe the different tear types, we use the modified Sherman classification in which we extended his classification towards the tibial side whereas Sherman and colleagues70 only described the femoral side of the tears (Figures A-F, Table).
Type I Tears: Primary Repair
Type I tears are soft tissue avulsion type tears that can be easily treated with arthroscopic primary repair.107 The length of the distal remnant has to be at least 90% and the tissue quality has to be good to excellent in order to approximate the remnant towards the femoral wall (Table).112 The incidence of type I tears was 26% in the study of Sherman and colleagues,70 although recent studies showed a lower incidence (6% to 10%) in a larger population.32,38 Certainly, individual practices will see different percentages of type I tears based upon the mix of injury mechanisms they see most frequently. Over the last 2 years, with the recognition of the importance of tear type and tissue quality, there has been a renewed interest in arthroscopic primary ACL repair.32,38
DiFelice and colleagues32 were the first to arthroscopically perform primary repair of the ACL in proximal tears using suture anchors. They reported the outcomes of the first 11 consecutive patients that underwent primary repair in a previously described technique.113 At mean 3.5-year follow-up, they noted only 1 failure (9%) due to re-injury; mean Lysholm score of 93.2; mean modified Cincinnati score of 91.5; pre- and postoperative Tegner score of 7.3 and 6.9, respectively; SANE score of 91.8; and subjective International Knee Documentation Committee (IKDC) score of 86.4. Of the patients with an intact repair, 9 patients had an objective IKDC rating A and 1 patient had B and all patients had KT-1000 leg differences of <3 mm with the contralateral side (three patients were not available for KT-1000 testing). The authors concluded that arthroscopic primary ACL repair could achieve short-term clinical success in a selected group of patients with proximal avulsion tears and excellent tissue quality. They further noted that mid-term outcomes are necessary given that the results of open primary repair deteriorated at longer-term follow-up in the historical literature. Recently, the senior author (GSD) has added an Internal Brace (Arthrex) to the primary repair with the goal of protecting the ligament in the first weeks to further promote healing of the ligament.39,40,114
More recently, Achtnich and colleagues38 compared the treatment of arthroscopic primary ACL repair with primary ACL reconstruction in 41 patients with type I tears at 2.3-years follow-up. Twenty-one patients consented for primary repair while 20 patients declined this procedure and underwent primary reconstruction. They noted no significant differences in Lachman test, pivot shift test, objective IKDC score, and KT-1000 scores. Although not significant, the clinical failure rate in the primary repair group (15%) was higher than the reconstruction group (0%). Interestingly, despite the higher failure rate in the repair group, the authors concluded that primary ACL repair is recommended in a carefully selected group of patients with type I tears and excellent tissue quality, which can likely be explained by the differences in the risk-benefit ratio between both procedures.
Over the last decade, the research group led by Murray46,115,116 has performed experimental research on primary repair with a biological scaffold and reported many interesting findings that could be extrapolated to primary ACL repair. First of all, they compared bioenhanced primary repair with bioenhanced primary reconstruction in 64 Yucutan pigs and noted that there was significantly less macroscopic cartilage damage in the primary repair group at 1-year follow-up.46 They concluded that bioenhanced ACL repair may provide a new, less invasive treatment option that reduces cartilage damage following joint injury. This may suggest that primary repair may have a lower incidence of osteoarthritis when compared to ACL reconstruction, which is interesting as osteoarthritis is very common after ACL reconstruction. Further research in this area is certainly warranted.
In another study they compared bioenhanced primary repair in juvenile, adolescent and mature Yucutan pigs and noted that functional healing depended on the level of skeletal maturity with immature animals having a more productive healing response.116 This indicates that primary repair might be a good treatment option in skeletally immature patients, especially since reconstruction increases the risk of premature closure of the epiphysis117,118 and delaying treatment increases the risk of meniscus injury.119 Interestingly, a recent meta-analysis showed indeed that the risk of epiphysis closure was lower in primary repair when compared to ACL reconstruction and the rupture rate was also lower.118 Primary repair may be a good treatment option in children as the procedure has all the attributes that should be applicable to children: it is minimally morbid, tissue sparing, and it is a conservative approach that does not burn any surgical bridges for future reconstructive surgery if necessary.
Finally, the research group of Murray115 assessed the effect of surgical delay of primary repair following injury in Yucutan pigs and noted that better biomechanical outcomes were noted after delaying surgery for 2 weeks when compared to 6 weeks. This suggests that primary repair should preferably be performed in the acute setting, which has also been shown in historical studies since the ligament in the acute setting has optimal tissue quality and the ligament is less likely to be retracted or reabsorbed.59,60,115
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the tear locations of the AM and PL bundle are not at the same location and Zantop and colleagues120 reported in an arthroscopic study that this could be as frequent as in 30% of all complete tears. In some of these tears, one of the bundles can be avulsed of the femoral wall (type I tear) while the other bundle is not directly repairable (non-type I tear). In these cases, the senior author (GSD) will repair the type I tear bundle, whereas a hamstring augmentation is placed at the location of the other bundle. When reviewing the literature, a combination of primary repair of one bundle and reconstruction of the second bundle has not been described before. However, over the last decade several surgeons have performed augmentation of one bundle in the setting of partial tears.34,35,121-124
Buda and colleagues34 were the first to perform selective AM or PL bundle reconstruction in the setting of partial tears.34 At 5-year follow-up, they reported no reruptures and only 1 patient with an IKDC C-score, although reoperation was necessary in 4 out of 47 patients (9%). Following this publication, many others reported on selective bundle reconstruction.35,121-124 However, with partial tears, the knee is often stable and a selective augmentation technique is utilized to prevent complete rupture of the ligament. The application of this technique is essentially different from reconstruction for complete ACL tears in which the knee is unstable, there is a giving way sensation and patients have problems participating in sports.
Type II Tears: Augmented Repair
Type II tears often have good or excellent tissue quality and can be pulled up towards the femoral footprint, but are too short to be firmly attached. Sherman and colleagues70 reported that approximately 22% patients had a type II tear, which corresponds to a tear located in the proximal part of the ligament. With this technique, multiple suture passes are used to stitch the remnant and, in addition, a smaller hamstring autograft or allograft is passed through the middle of the tibial remnant. A suture button is used proximally for the graft, and the tensioning repair sutures through the remnant are also passed through the suture button. The suture button is passed through the femoral tunnel and flipped so that the graft is proximally fixed. Then, the repair sutures of the remnant are tensioned, and the ligament is pulled towards the femoral wall as a sleeve around the graft. When the ligament is approximated to the femoral wall, the sutures are tied over the suture button. The graft is then tensioned distally to complete the augmented repair.
In the recent literature, the technique of augmentation of a primary repair using autograft tissue has not been reported. However, augmented repair using an internal brace39,40 or augmentation devices33,41 have been recently performed. MacKay and colleagues39 reported good outcomes of arthroscopic primary repair of proximal tears using an internal brace. Eggli and colleagues33 reported the results of the first 10 patients treated with ACL preservation using primary repair of the ligament with the addition of a dynamic screw-spring mechanism. The authors reported good preliminary results with one failure (10%) and good objective and subjective outcomes. In a next study, they reported the outcomes of 278 patients and although they reported good clinical outcomes and a revision rate of 4%, the reoperation rate for removal of the screw-spring mechanism was high (24%).41 This is not surprising when reviewing the historical literature in which high complication rates of the augmentation devices were reported.99,100 We were unable to identify any other studies reporting surgical techniques of augmenting primary repair in the literature.
Type III Tears: Reconstruction With Remnant Tensioning
In patients with type III tears, the ligament cannot be approximated to the wall and reconstruction is necessary in order to restore knee stability. However, in these cases the ligament has sufficient length (25%-75%) and can be tensioned along or around the graft. Preservation of the ligament remnant has several (theoretical) advantages, such as better proprioceptive function,42,49,50 vascularization and ligamentization of the graft,50-52 an optical guide for anatomic tunnel placement,53 and a decreased incidence of tunnel widening.54,55 Furthermore, tensioning of the remnant is thought to lower the risk of cyclops lesions when compared to remnant preservation.125 Although the difference between augmented repair and remnant tensioning seems small, the purpose of surgery is different. With augmented repair, the ligament can be approximated close to the femoral wall and the goal of surgery is to use the healing capacity that the ACL has in the proximal part of the ligament,126 while with remnant tensioning the goal is only to benefit from some of the aforementioned advantages. Ahn and colleagues36 were the first to perform this technique and stated, “Our concept is that the remnant tissue has only an additive effect.” Furthermore, with augmented repair multiple sutures are passed through the AM and PL bundle in order to sufficiently approximate the ligament to the femoral wall, while with the remnant tensioning technique generally one or a few sutures or lasso loop are passed through the proximal part to tension the ligament, prevent sagging of the remnant, and decrease the risk of cyclops lesions.127,128
Several authors have recently performed remnant tensioning during ACL.36,47,125-127 Ahn and colleagues47 reported excellent objective and subjective outcomes following this procedure and found that with re-arthroscopy nearly all patients had fair synovialization of the graft. Others have reported similarly good outcomes of these techniques.125,129,130 However, studies comparing this treatment with normal ACL reconstruction and assessing outcomes, failure rates and proprioception are lacking.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some patients the ligament is torn distally or the tissue quality is not optimal. In these patients, the remnant can be debrided to the part of good tissue quality in order to preserve the biology and minimize the risk for cyclops lesions. A standard reconstruction needs to be performed to restore the instability, but by preserving the remnant, advantages, such as proprioception,44,49,50 graft vascularization,50-52 an optical guide for tibial tunnel placement,53 and a decreased incidence of tunnel widening54,55 can be expected.
Lee and colleagues37 presented the tibial remnant technique in which standard reconstruction was performed, and the tibial tunnel was drilled through the center of the remnant. In a later study, they compared remnant preservation with a remnant of <20% of the total ACL length with >20% of the length and found that proprioception was better with more remnant volume.48 Similarly, Muneta and colleagues131 assessed the role of remnant length and found that remnant length is positively correlated with better stability measured on KT-1000 anteroposterior stability.
Several studies compared ACL reconstruction with remnant preservation vs conventional ACL reconstruction.52,54,129 Takazawa and colleagues52 performed a retrospective study of 183 patients and found that patients in the remnant preservation group had significantly better KT-2000 stability, while they also reported a significantly lower graft rupture rate in this group (1.1% vs 7.1%) at 2-year follow-up. Hong and colleagues129 performed a randomized clinical trial of 80 patients and did not find these differences, although there was a trend towards higher Lysholm scores in the remnant preservation group. Finally, Zhang and colleagues54 performed a randomized clinical trial and found a lower incidence and amount of tibial tunnel widening in the preserving-remnant group when compared to the removing-remnant group. These studies show that there is likely a role for remnant preservation.
Type V Tears: Primary Repair
In some patients, the ligament is torn in the distal 10% of the ligament, which can occur as a distal avulsion tear or as a distal bony avulsion fracture.132 Bony avulsion fractures are most commonly seen in children whereas true distal soft tissue avulsion tears are very rare.132
Treatments of these tear types include antegrade screw fixation, pullout sutures or the use of suture anchors in case of bony avulsion fractures and pullout sutures with tying over a bony bridge or ligament button in case of soft tissue avulsions. Leeberg and colleagues132 recently performed a systematic review of all studies reporting on treatment of distal avulsion fractures.They noted that most treatments were currently performed arthroscopically and that outcomes were generally good. Another recent biomechanical study compared antegrade screw fixation with suture anchor fixation and pullout suture fixation.133 The authors noted that suture anchor fixation has slightly less displacement of the bony fragment when compared to screw fixation and pull-out sutures, and that the strength to failure was higher in the suture anchor fixation when compared to the pullout suture fixation. The outcomes of this study suggest that screw fixation and suture anchor fixation might be superior to pullout suture fixation, which might be interesting as with pullout suture fixation the ligament cannot be directly tensioned to the tibial footprint, which can lead to anteroposterior laxity.132 Clinical studies are necessary to assess the preferred treatment in these tear types but it seems that screw fixation is preferred in large bony avulsion fractures, while suture anchor fixation or pullout suture fixation can be used for soft tissue avulsion tears.
Complex Tears or Poor Tissue Quality: Reconstruction
If the tear is complex, multiple tears are present, or the tissue quality is poor, then preservation of the ligament is not possible, and in these cases a standard reconstruction should be performed.
Conclusion
When reviewing the literature of ACL preservation, it becomes clear that the evolution of surgical treatment of ACL injuries was biased. Preservation of the native ligament has many advantages, such as better proprioception, graft vascularization, an optical guide for tibial tunnel placement, and a decreased incidence of tunnel widening that can be expected. Furthermore, arthroscopic primary ACL repair is minimally invasive and does not burn any bridges for future reconstructions, if necessary. This is in addition to the other (theoretical) advantages of primary repair, such as restoration of native kinematics and a decreased risk of osteoarthritis. Modern advances have significantly changed the risk-benefit ratio that should make us reconsider ACL preservation approaches. Certainly, further research in this area is warranted. In this article we have presented a treatment algorithm for ACL preservation, which is based on tear location and remnant tissue quality.
Am J Orthop. 2016;45(7):E393-E405. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Mall NA, Chalmers PN, Moric M, et al. Incidence and trends of anterior cruciate ligament reconstruction in the United States. Am J Sports Med. 2014;42(10):2363-2370.
2. Sanders TL, Maradit Kremers H, Bryan AJ, et al. Incidence of anterior cruciate ligament tears and reconstruction: a 21-year population-based study. Am J Sports Med. 2016;44(6):1502-1507.
3. Ciccotti MG, Lombardo SJ, Nonweiler B, Pink M. Non-operative treatment of ruptures of the anterior cruciate ligament in middle-aged patients. Results after long-term follow-up. J Bone Joint Surg Am. 1994;76(9):1315-1321.
4. Sanders TL, Pareek A, Kremers HM, et al. Long-term follow-up of isolated ACL tears treated without ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2016 May 24. [Epub ahead of print]
5. Irarrázaval S, Kurosaka M, Cohen M, Fu FH. Anterior cruciate ligament reconstruction. J ISAKOS. 2016;1(1):38-52.
6. Gabler CM, Jacobs CA, Howard JS, Mattacola CG, Johnson DL. Comparison of graft failure rate between autografts placed via an anatomic anterior cruciate ligament reconstruction technique: a systematic review, meta-analysis, and meta-regression. Am J Sports Med. 2016;44(4):1069-1079.
7. Li S, Chen Y, Lin Z, Cui W, Zhao J, Su W. A systematic review of randomized controlled clinical trials comparing hamstring autografts versus bone-patellar tendon-bone autografts for the reconstruction of the anterior cruciate ligament. Arch Orthop Trauma Surg. 2012;132(9):1287-1297.
8. Rahr-Wagner L, Thillemann TM, Pedersen AB, Lind M. Comparison of hamstring tendon and patellar tendon grafts in anterior cruciate ligament reconstruction in a nationwide population-based cohort study: results from the danish registry of knee ligament reconstruction. Am J Sports Med. 2014;42(2):278-284.
9. Xie X, Liu X, Chen Z, Yu Y, Peng S, Li Q. A meta-analysis of bone-patellar tendon-bone autograft versus four-strand hamstring tendon autograft for anterior cruciate ligament reconstruction. Knee. 2015;22(2):100-110.
10. Andernord D, Desai N, Björnsson H, Gillén S, Karlsson J, Samuelsson K. Predictors of contralateral anterior cruciate ligament reconstruction: a cohort study of 9061 patients with 5-year follow-up. Am J Sports Med. 2015;43(2):295-302.
11. Maletis GB, Inacio MC, Funahashi TT. Risk factors associated with revision and contralateral anterior cruciate ligament reconstructions in the Kaiser Permanente ACLR registry. Am J Sports Med. 2015;43(3):641-647.
12. Kim SJ, Postigo R, Koo S, Kim JH. Infection after arthroscopic anterior cruciate ligament reconstruction. Orthopedics. 2014;37(7):477-484.
13. Makhni EC, Steinhaus ME, Mehran N, Schulz BS, Ahmad CS. Functional outcome and graft retention in patients with septic arthritis after anterior cruciate ligament reconstruction: a systematic review. Arthroscopy. 2015;31(7):1392-1401.
14. Kocher MS, Steadman JR, Briggs K, Zurakowski D, Sterett WI, Hawkins RJ. Determinants of patient satisfaction with outcome after anterior cruciate ligament reconstruction. J Bone Joint Surg Am. 2002;84-A(9):1560-1572.
15. Ardern CL, Österberg A, Sonesson S, Gauffin H, Webster KE, Kvist J. Satisfaction with knee function after primary anterior cruciate ligament reconstruction is associated with self-efficacy, quality of life, and returning to the preinjury physical activity. Arthroscopy. 2016;32(8):1631-1638.e3.
16. Grant JA, Mohtadi NG, Maitland ME, Zernicke RF. Comparison of home versus physical therapy-supervised rehabilitation programs after anterior cruciate ligament reconstruction: a randomized clinical trial. Am J Sports Med. 2005;33(9):1288-1297.
17. Lindström M, Strandberg S, Wredmark T, Fell änder-Tsai L, Henriksson M. Functional and muscle morphometric effects of ACL reconstruction. A prospective CT study with 1 year follow-up. Scand J Med Sci Sports. 2013;23(4):431-442.
18. Biau DJ, Tournoux C, Katsahian S, Schranz PJ, Nizard RS. Bone-patellar tendon-bone autografts versus hamstring autografts for reconstruction of anterior cruciate ligament: meta-analysis. BMJ. 2006;332(7548):995-1001.
19. Spindler KP, Kuhn JE, Freedman KB, Matthews CE, Dittus RS, Harrell FE Jr. Anterior cruciate ligament reconstruction autograft choice: bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med. 2004;32(8):1986-1995.
20. Aga C, Wilson KJ, Johansen S, Dornan G, La Prade RF, Engebretsen L. Tunnel widening in single- versus double-bundle anterior cruciate ligament reconstructed knees. Knee Surg Sports Traumatol Arthrosc. 2016 Jun 21. [Epub ahead of print]
21. Maak TG, Voos JE, Wickiewicz TL, Warren RF. Tunnel widening in revision anterior cruciate ligament reconstruction. J Am Acad Orthop Surg. 2010;18(11):695-706.
22. Cheatham SA, Johnson DL. Anticipating problems unique to revision ACL surgery. Sports Med Arthrosc. 2013;21(2):129-134.
23. Kamath GV, Redfern JC, Greis PE, Burks RT. Revision anterior cruciate ligament reconstruction. Am J Sports Med. 2011;39(1):199-217.
24. Wright RW, Gill CS, Chen L, et al. Outcome of revision anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg Am. 2012;94(6):531-536.
25. Andriolo L, Filardo G, Kon E, et al. Revision anterior cruciate ligament reconstruction: clinical outcome and evidence for return to sport. Knee Surg Sports Traumatol Arthrosc. 2015;23(10):2825-2845.
26. Grassi A, Ardern CL, Marcheggiani Muccioli GM, Neri MP, Marcacci M, Zaffagnini S. Does revision ACL reconstruction measure up to primary surgery? A meta-analysis comparing patient-reported and clinician-reported outcomes, and radiographic results. Br J Sports Med. 2016;50(12):716-724.
27. Ristanis S, Stergiou N, Patras K, Vasiliadis HS, Giakas G, Georgoulis AD. Excessive tibial rotation during high-demand activities is not restored by anterior cruciate ligament reconstruction. Arthroscopy. 2005;21(11):1323-1329.
28. Andriacchi TP, Mündermann A, Smith RL, Alexander EJ, Dyrby CO, Koo S. A framework for the in vivo pathomechanics of osteoarthritis at the knee. Ann Biomed Eng. 2004;32(3):447-457.
29. Imhauser C, Mauro C, Choi D, et al. Abnormal tibiofemoral contact stress and its association with altered kinematics after center-center anterior cruciate ligament reconstruction: an in vitro study. Am J Sports Med. 2013;41(4):815-825.
30. Ajuied A, Wong F, Smith C, et al. Anterior cruciate ligament injury and radiologic progression of knee osteoarthritis: a systematic review and meta-analysis. Am J Sports Med. 2014;42(9):2242-2252.
31. Chalmers PN, Mall NA, Moric M, et al. Does ACL reconstruction alter natural history?: A systematic literature review of long-term outcomes. J Bone Joint Surg Am. 2014;96(4):292-300.
32. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
33. Eggli S, Kohlhof H, Zumstein M, et al. Dynamic intraligamentary stabilization: novel technique for preserving the ruptured ACL. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1215-1221.
34. Buda R, Ferruzzi A, Vannini F, Zambelli L, Di Caprio F. Augmentation technique with semitendinosus and gracilis tendons in chronic partial lesions of the ACL: clinical and arthrometric analysis. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1101-1107.
35. Ochi M, Adachi N, Uchio Y, et al. A minimum 2-year follow-up after selective anteromedial or posterolateral bundle anterior cruciate ligament reconstruction. Arthroscopy. 2009;25(2):117-122.
36. Ahn JH, Lee YS, Ha HC. Anterior cruciate ligament reconstruction with preservation of remnant bundle using hamstring autograft: technical note. Arch Orthop Trauma Surg. 2009;129(8):1011-1015.
37. Lee BI, Min KD, Choi HS, Kim JB, Kim ST. Arthroscopic anterior cruciate ligament reconstruction with the tibial-remnant preserving technique using a hamstring graft. Arthroscopy. 2006;22(3):340.e1-e7.
38. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016 Jun 17. [Epub ahead of print]
39. MacKay G, Anthony IC, Jenkins PJ, Blyth M. Anterior cruciate ligament repair revisited. Preliminary results of primary repair with internal brace ligament augmentation: a case series. Orthop Muscul Syst. 2015;4:188.
40. Mackay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
41. Henle P, Röder C, Perler G, Heitkemper S, Eggli S. Dynamic intraligamentary stabilization (DIS) for treatment of acute anterior cruciate ligament ruptures: case series experience of the first three years. BMC Musculoskelet Disord. 2015;16:27.
42. Adachi N, Ochi M, Uchio Y, Iwasa J, Ryoke K, Kuriwaka M. Mechanoreceptors in the anterior cruciate ligament contribute to the joint position sense. Acta Orthop Scand. 2002;73(3):330-334.
43. Gao F, Zhou J, He C, et al. A morphologic and quantitative study of mechanoreceptors in the remnant stump of the human anterior cruciate ligament. Arthroscopy. 2016;32(2):273-280.
44. Georgoulis AD, Pappa L, Moebius U, et al. The presence of proprioceptive mechanoreceptors in the remnants of the ruptured ACL as a possible source of re-innervation of the ACL autograft. Knee Surg Sports Traumatol Arthrosc. 2001;9(6):364-368.
45. Fleming BC, Carey JL, Spindler KP, Murray MM. Can suture repair of ACL transection restore normal anteroposterior laxity of the knee? An ex vivo study. J Orthop Res. 2008;26(11):1500-1505.
46. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
47. Ahn JH, Wang JH, Lee YS, Kim JG, Kang JH, Koh KH. Anterior cruciate ligament reconstruction using remnant preservation and a femoral tensioning technique: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(8):1079-1089.
48. Lee BI, Kwon SW, Kim JB, Choi HS, Min KD. Comparison of clinical results according to amount of preserved remnant in arthroscopic anterior cruciate ligament reconstruction using quadrupled hamstring graft. Arthroscopy. 2008;24(5):560-568.
49. Lee BI, Min KD, Choi HS, et al. Immunohistochemical study of mechanoreceptors in the tibial remnant of the ruptured anterior cruciate ligament in human knees. Knee Surg Sports Traumatol Arthrosc. 2009;17(9):1095-1101.
50. Takahashi T, Kondo E, Yasuda K, et al. Effects of remnant tissue preservation on the tendon graft in anterior cruciate ligament reconstruction: a biomechanical and histological study. Am J Sports Med. 2016;44(7):1708-1716.
51. Dong S, Xie G, Zhang Y, Shen P, Huangfu X, Zhao J. Ligamentization of autogenous hamstring grafts after anterior cruciate ligament reconstruction: midterm versus long-term results. Am J Sports Med. 2015;43(8):1908-1917.
52. Takazawa Y, Ikeda H, Kawasaki T, et al. ACL reconstruction preserving the ACL remnant achieves good clinical outcomes and can reduce subsequent graft rupture. Orthop J Sports Med. 2013;1(4):2325967113505076.
53. Shimodaira H, Tensho K, Akaoka Y, Takanashi S, Kato H, Saito N. Remnant-preserving tibial tunnel positioning using anatomic landmarks in double-bundle anterior cruciate ligament reconstruction. Arthroscopy. 2016;32(9):1822-1830.
54. Zhang Q, Zhang S, Cao X, Liu L, Liu Y, Li R. The effect of remnant preservation on tibial tunnel enlargement in ACL reconstruction with hamstring autograft: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):166-173.
55. Tie K, Chen L, Hu D, Wang H. The difference in clinical outcome of single-bundle anterior cruciate ligament reconstructions with and without remnant preservation: A meta-analysis. Knee. 2016;23(4):566-574.
56. Robson AW. VI. Ruptured crucial ligaments and their repair by operation. Ann Surg. 1903;37(5):716-718.
57. Palmer I. On the injuries to the ligaments of the knee joint. Acta Orthop Scand. 1938;53.
58. Palmer I. On the injuries to the ligaments of the knee joint: a clinical study. 1938. Clin Orthop Relat Res. 2007;454:17-22.
59 O’Donoghue DH. An analysis of end results of surgical treatment of major injuries to the ligaments of the knee. J Bone Joint Surg Am. 1955;37-A(1):1-13.
60. O’Donoghue DH. Surgical treatment of fresh injuries to the major ligaments of the knee. J Bone Joint Surg Am. 1950;32 A(4):721-738.
61. Feagin JA, Abbott HG, Rokous JR. The isolated tear of the anterior cruciate ligament. J Bone Joint Surg Am. 1972;54-A:1340-1341.
62. England RL. Repair of the ligaments about the knee. Orthop Clin North Am. 1976;7(1):195-204.
63. Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.
64. Weaver JK, Derkash RS, Freeman JR, Kirk RE, Oden RR, Matyas J. Primary knee ligament repair--revisited. Clin Orthop Relat Res. 1985;(199):185-191.
65. Nogalski MP, Bach BR Jr. A review of early anterior cruciate ligament surgical repair or reconstruction. Results and caveats. Orthop Rev. 1993;22(11):1213-1223.
66. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
67. Marshall JL, Warren RF, Wickiewicz TL. Primary surgical treatment of anterior cruciate ligament lesions. Am J Sports Med. 1982;10(2):103-107.
68. Straub T, Hunter RE. Acute anterior cruciate ligament repair. Clin Orthop Relat Res. 1988;227:238-250.
69. Kaplan N, Wickiewicz TL, Warren RF. Primary surgical treatment of anterior cruciate ligament ruptures. A long-term follow-up study. Am J Sports Med. 1990;18(4):354-358.
70. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
71. Paar O. Use of semitendinosus tendon to strengthen a freshly repaired anterior cruciate ligament. Chirurg. 1985;56(11):728-734.
72. Aglietti P, Buzzi R, Pisaneschi A, Salvi M. Comparison between suture and augmentation with the semitendinosus tendon in the repair of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1986;8(4):217-231.
73. Higgins RW, Steadman JR. Anterior cruciate ligament repairs in world class skiers. Am J Sports Med. 1987;15(5):439-447.
74. Harilainen A, Myllynen P. Treatment of fresh tears of the anterior cruciate ligament. A comparison of primary suture and augmentation with carbon fibre. Injury. 1987;18(6):396-400.
75. Jones KG. Results of use of the central one-third of the patellar ligament to compensate for anterior cruciate ligament deficiency. Clin Orthop Relat Res. 1980;(147):39-44.
76. Puddu G. Method for reconstruction of the anterior cruciate ligament using the semitendinosus tendon. Am J Sports Med. 1980;8(6):402-404.
77. Hefti F, Gächter A, Jenny H, Morscher E. Replacement of the anterior cruciate ligament. a comparative study of four different methods of reconstruction. Arch Orthop Trauma Surg. 1982;100(2):83-94.
78. Odensten M, Hamberg P, Nordin M, Lysholm J, Gillquist J. Surgical or conservative treatment of the acutely torn anterior cruciate ligament. A randomized study with short-term follow-up observations. Clin Orthop Relat Res. 1985;(198):87-93.
79. Andersson C, Odensten M, Good L, Gillquist J. Surgical or non-surgical treatment of acute rupture of the anterior cruciate ligament. A randomized study with long-term follow-up. J Bone Joint Surg Am. 1989;71(7):965-974.
80. Engebretsen L, Benum P, Fasting O, Mølster A, Strand T. A prospective, randomized study of three surgical techniques for treatment of acute ruptures of the anterior cruciate ligament. Am J Sports Med. 1990;18(6):585-590.
81. Jonsson T, Peterson L, Renström P. Anterior cruciate ligament repair with and without augmentation. A prospective 7-year study of 51 patients. Acta Orthop Scand. 1990;61(6):562-566.
82. Andersson C, Odensten M, Gillquist J. Knee function after surgical or nonsurgical treatment of acute rupture of the anterior cruciate ligament: a randomized study with a long-term follow-up period. Clin Orthop Relat Res. 1991;(264):255-263.
83. Heim U, Bachmann B, Infanger K. Reinsertion of the anterior cruciate ligament or primary ligamentous plasty? Helv Chir Acta. 1982;48(5):703-708.
84. Strand T, Engesaeter LB, Mølster AO, et al. Knee function following suture of fresh tear of the anterior cruciate ligament. Acta Orthop Scand. 1984;55(2):181-184.
85. Marcacci M, Spinelli M, Chiellini F, Buccolieri V. Notes on 53 cases of immediate suture of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1985;7(2):69-79.
86. van der List JP, DiFelice GS. Primary repair of the anterior cruciate ligament: a paradigm shift. Surgeon. 2016 Oct 6. [Epub ahead of print]
87. Bräm J, Plaschy S, Lütolf M, Leutenegger A. [The primary cruciate ligament suture--is the method outdated? Results in follow-up of 58 patients]. Z Unfallchir Versicherungsmed. 1994;87(2):91-109.
88. Genelin F, Trost A, Primavesi C, Knoll P. Late results following proximal reinsertion of isolated ruptured ACL ligaments. Knee Surg Sports Traumatol Arthrosc. 1993;1(1):17-19.
89. Kühne JH, Theermann R, Neumann R, Sagasser J. [Acute uncomplicated anterior knee instability. 2-5 year follow-up of surgical treatment]. Unfallchirurg. 1991;94(2):81-87.
90. Simonet WT, Sim FH. Repair and reconstruction of rotatory instability of the knee. Am J Sports Med. 1984;12(2):89-97.
91. Raunest J, Derra E, Ohmann C. [Clinical results of Palmer’s primary cruciate ligament insertion without augmentation]. Unfallchirurgie. 1991;17(3):166-174.
92. Frank C, Beaver P, Rademaker F, Becker K, Schachar N, Edwards G. A computerized study of knee-ligament injuries: repair versus removal of the torn anterior cruciate ligament. Can J Surg. 1982;25(4):454-458.
93. Enneking WF, Horowitz M. The intra-articular effects of immobilization on the human knee. J Bone Joint Surg Am. 1972;54(5):973-985.
94. Millett PJ, Wickiewicz TL, Warren RF. Motion loss after ligament injuries to the knee. Part I: causes. Am J Sports Med. 2001;29(5):664-675.
95. Bilko TE, Paulos LE, Feagin JA Jr, Lambert KL, Cunningham HR. Current trends in repair and rehabilitation of complete (acute) anterior cruciate ligament injuries. Analysis of 1984 questionnaire completed by ACL Study Group. Am J Sports Med. 1986;14(2):143-147.
96. Paulos L, Noyes FR, Grood E, Butler DL. Knee rehabilitation after anterior cruciate ligament reconstruction and repair. J Orthop Sports Phys Ther. 1991;13(2):60-70.
97. Paessler HH, Deneke J, Dahners LE. Augmented repair and early mobilization of acute anterior cruciate ligament injuries. Am J Sports Med. 1992;20(6):667-674.
98.
99. Kdolsky RK, Gibbons DF, Kwasny O, Schabus R, Plenk H Jr. Braided polypropylene augmentation device in reconstructive surgery of the anterior cruciate ligament: long-term clinical performance of 594 patients and short-term arthroscopic results, failure analysis by scanning electron microscopy, and synovial histomorphology. J Orthop Res. 1997;15(1):1-10.
100. Grøntvedt T, Engebretsen L. Comparison between two techniques for surgical repair of the acutely torn anterior cruciate ligament. A prospective, randomized follow-up study of 48 patients. Scand J Med Sci Sports. 1995;5(6):358-363.
101. Hehl G, Strecker W, Richter M, Kiefer H, Wissmeyer T. Clinical experience with PDS II augmentation for operative treatment of acute proximal ACL ruptures--2-year follow-up. Knee Surg Sports Traumatol Arthrosc. 1999;7(2):102-106.
102. Schenk S, Landsiedl F, Enenkel M. Arthroscopic single-stranded semitendinosus tendon- versus PDS-augmentation of reinserted acute femoral anterior cruciate ligament tears: 7 year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2006;14(4):318-324.
103. Zysk SP, Refior HJ. Operative or conservative treatment of the acutely torn anterior cruciate ligament in middle-aged patients. A follow-up study of 133 patients between the ages of 40 and 59 years. Arch Orthop Trauma Surg. 2000;120(1-2):59-64.
104. Krueger-Franke M, Siebert CH, Schupp A. Refixation of femoral anterior cruciate ligament tears combined with a semitendinosus tendon augmentation. Technique and results. Arch Orthop Trauma Surg. 1998;117(1-2):68-72.
105. Natri A, Järvinen M, Kannus P. Primary repair plus intra-articular iliotibial band augmentation in the treatment of an acute anterior cruciate ligament rupture. A follow-up study of 70 patients. Arch Orthop Trauma Surg. 1996;115(1):22-27.
106. Träger D, Pohle K, Tschirner W. Anterior cruciate ligament suture in comparison with plasty. A 5-year follow-up study. Arch Orthop Trauma Surg. 1995;114(5):278-280.
107. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M. Arthrofibrosis in acute anterior cruciate ligament reconstruction. The effect of timing of reconstruction and rehabilitation. Am J Sports Med. 1991;19(4):332-336.
108. Volokhina YV, Syed HM, Pham PH, Blackburn AK. Two helpful MRI signs for evaluation of posterolateral bundle tears of the anterior cruciate ligament: a pilot study. Orthop J Sports Med. 2015;3(8):2325967115597641.
109. Strand T, Mølster A, Hordvik M, Krukhaug Y. Long-term follow-up after primary repair of the anterior cruciate ligament: clinical and radiological evaluation 15-23 years postoperatively. Arch Orthop Trauma Surg. 2005;125(4):217-221.
110. van der List JP, DiFelice GS. Successful arthroscopic primary repair of a chronic anterior cruciate ligament tear 11 years following injury. HSS J. 2016. In press.
111. van der List JP, DiFelice GS. The role of ligament repair in anterior cruciate ligament surgery. In: Mascarenhas R, Bhatia S, Lowe WR, eds. Ligamentous Injuries of the Knee. 1st ed. Houston: Nova Science Publishers; 2016:199-220.
112. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
113. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
114. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
115. Magarian EM, Fleming BC, Harrison SL, Mastrangelo AN, Badger GJ, Murray MM. Delay of 2 or 6 weeks adversely affects the functional outcome of augmented primary repair of the porcine anterior cruciate ligament. Am J Sports Med. 2010;38(12):2528-2534.
116. Murray MM, Magarian EM, Harrison SL, Mastrangelo AN, Zurakowski D, Fleming BC. The effect of skeletal maturity on functional healing of the anterior cruciate ligament. J Bone Joint Surg Am. 2010;92(11):2039-2049.
117. Werner BC, Yang S, Looney AM, Gwathmey FW Jr. Trends in pediatric and adolescent anterior cruciate ligament iInjury and reconstruction. J Pediatr Orthop. 2016;36(5):447-452.
118. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
119. Ramski DE, Kanj WW, Franklin CC, Baldwin KD, Ganley TJ. Anterior cruciate ligament tears in children and adolescents: a meta-analysis of nonoperative versus operative treatment. Am J Sports Med. 2014;42(11):2769-2776.
120. Zantop T, Brucker PU, Vidal A, Zelle BA, Fu FH. Intraarticular rupture pattern of the ACL. Clin Orthop Relat Res. 2007;454:48-53.
121. Yoon KH, Bae DK, Cho SM, Park SY, Lee JH. Standard anterior cruciate ligament reconstruction versus isolated single-bundle augmentation with hamstring autograft. Arthroscopy. 2009;25(11):1265-1274.
122 Demirağ B, Ermutlu C, Aydemir F, Durak K. A comparison of clinical outcome of augmentation and standard reconstruction techniques for partial anterior cruciate ligament tears. Eklem Hastalik Cerrahisi. 2012;23(3):140-144.
123. Sonnery-Cottet B, Zayni R, Conteduca J, et al. Posterolateral bundle reconstruction with anteromedial bundle remnant preservation in ACL tears: clinical and MRI evaluation of 39 patients with 24-month follow-up. Orthop J Sports Med. 2013;1(3):2325967113501624.
124. Sabat D, Kumar V. Partial tears of anterior cruciate ligament: results of single bundle augmentation. Indian J Orthop. 2015;49(2):129-135.
125. Jung YB, Jung HJ, Siti HT, et al. Comparison of anterior cruciate ligament reconstruction with preservation only versus remnant tensioning technique. Arthroscopy. 2011;27(9):1252-1258.
126. Nguyen DT, Ramwadhdoebe TH, van der Hart CP, Blankevoort L, Tak PP, van Dijk CN. Intrinsic healing response of the human anterior cruciate ligament: an histological study of reattached ACL remnants. J Orthop Res. 2014;32(2):296-301.
127. Boutsiadis A, Karampalis C, Tzavelas A, Vraggalas V, Christodoulou P, Bisbinas I. Anterior cruciate ligament remnant-preserving reconstruction using a “lasso-loop” knot configuration. Arthrosc Tech. 2015;4(6):e741-e746.
128. Noh JH, Yoon KH, Song SJ, Roh YH. Re-tensioning technique to cover the graft with remnant in anterior cruciate ligament reconstruction. Arthrosc Tech. 2014;3(6):e679-e682.
129. Hong L, Li X, Zhang H, et al. Anterior cruciate ligament reconstruction with remnant preservation: a prospective, randomized controlled study. Am J Sports Med. 2012;40(12):2747-2755.
130. Noh JH, Kyung HS, Roh YH, Kang TS. Remnant-preserving and re-tensioning technique to cover the graft in anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 12. [Epub ahead of print]
131. Muneta T, Koga H, Ju YJ, Horie M, Nakamura T, Sekiya I. Remnant volume of anterior cruciate ligament correlates preoperative patients’ status and postoperative outcome. Knee Surg Sports Traumatol Arthrosc. 2013;21(4):906-913.
132. Leeberg V, Lekdorf J, Wong C, Sonne-Holm S. Tibial eminentia avulsion fracture in children - a systematic review of the current literature. Dan Med J. 2014;61(3):A4792.
133. In Y, Kwak DS, Moon CW, Han SH, Choi NY. Biomechanical comparison of three techniques for fixation of tibial avulsion fractures of the anterior cruciate ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1470-1478.
1. Mall NA, Chalmers PN, Moric M, et al. Incidence and trends of anterior cruciate ligament reconstruction in the United States. Am J Sports Med. 2014;42(10):2363-2370.
2. Sanders TL, Maradit Kremers H, Bryan AJ, et al. Incidence of anterior cruciate ligament tears and reconstruction: a 21-year population-based study. Am J Sports Med. 2016;44(6):1502-1507.
3. Ciccotti MG, Lombardo SJ, Nonweiler B, Pink M. Non-operative treatment of ruptures of the anterior cruciate ligament in middle-aged patients. Results after long-term follow-up. J Bone Joint Surg Am. 1994;76(9):1315-1321.
4. Sanders TL, Pareek A, Kremers HM, et al. Long-term follow-up of isolated ACL tears treated without ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2016 May 24. [Epub ahead of print]
5. Irarrázaval S, Kurosaka M, Cohen M, Fu FH. Anterior cruciate ligament reconstruction. J ISAKOS. 2016;1(1):38-52.
6. Gabler CM, Jacobs CA, Howard JS, Mattacola CG, Johnson DL. Comparison of graft failure rate between autografts placed via an anatomic anterior cruciate ligament reconstruction technique: a systematic review, meta-analysis, and meta-regression. Am J Sports Med. 2016;44(4):1069-1079.
7. Li S, Chen Y, Lin Z, Cui W, Zhao J, Su W. A systematic review of randomized controlled clinical trials comparing hamstring autografts versus bone-patellar tendon-bone autografts for the reconstruction of the anterior cruciate ligament. Arch Orthop Trauma Surg. 2012;132(9):1287-1297.
8. Rahr-Wagner L, Thillemann TM, Pedersen AB, Lind M. Comparison of hamstring tendon and patellar tendon grafts in anterior cruciate ligament reconstruction in a nationwide population-based cohort study: results from the danish registry of knee ligament reconstruction. Am J Sports Med. 2014;42(2):278-284.
9. Xie X, Liu X, Chen Z, Yu Y, Peng S, Li Q. A meta-analysis of bone-patellar tendon-bone autograft versus four-strand hamstring tendon autograft for anterior cruciate ligament reconstruction. Knee. 2015;22(2):100-110.
10. Andernord D, Desai N, Björnsson H, Gillén S, Karlsson J, Samuelsson K. Predictors of contralateral anterior cruciate ligament reconstruction: a cohort study of 9061 patients with 5-year follow-up. Am J Sports Med. 2015;43(2):295-302.
11. Maletis GB, Inacio MC, Funahashi TT. Risk factors associated with revision and contralateral anterior cruciate ligament reconstructions in the Kaiser Permanente ACLR registry. Am J Sports Med. 2015;43(3):641-647.
12. Kim SJ, Postigo R, Koo S, Kim JH. Infection after arthroscopic anterior cruciate ligament reconstruction. Orthopedics. 2014;37(7):477-484.
13. Makhni EC, Steinhaus ME, Mehran N, Schulz BS, Ahmad CS. Functional outcome and graft retention in patients with septic arthritis after anterior cruciate ligament reconstruction: a systematic review. Arthroscopy. 2015;31(7):1392-1401.
14. Kocher MS, Steadman JR, Briggs K, Zurakowski D, Sterett WI, Hawkins RJ. Determinants of patient satisfaction with outcome after anterior cruciate ligament reconstruction. J Bone Joint Surg Am. 2002;84-A(9):1560-1572.
15. Ardern CL, Österberg A, Sonesson S, Gauffin H, Webster KE, Kvist J. Satisfaction with knee function after primary anterior cruciate ligament reconstruction is associated with self-efficacy, quality of life, and returning to the preinjury physical activity. Arthroscopy. 2016;32(8):1631-1638.e3.
16. Grant JA, Mohtadi NG, Maitland ME, Zernicke RF. Comparison of home versus physical therapy-supervised rehabilitation programs after anterior cruciate ligament reconstruction: a randomized clinical trial. Am J Sports Med. 2005;33(9):1288-1297.
17. Lindström M, Strandberg S, Wredmark T, Fell änder-Tsai L, Henriksson M. Functional and muscle morphometric effects of ACL reconstruction. A prospective CT study with 1 year follow-up. Scand J Med Sci Sports. 2013;23(4):431-442.
18. Biau DJ, Tournoux C, Katsahian S, Schranz PJ, Nizard RS. Bone-patellar tendon-bone autografts versus hamstring autografts for reconstruction of anterior cruciate ligament: meta-analysis. BMJ. 2006;332(7548):995-1001.
19. Spindler KP, Kuhn JE, Freedman KB, Matthews CE, Dittus RS, Harrell FE Jr. Anterior cruciate ligament reconstruction autograft choice: bone-tendon-bone versus hamstring: does it really matter? A systematic review. Am J Sports Med. 2004;32(8):1986-1995.
20. Aga C, Wilson KJ, Johansen S, Dornan G, La Prade RF, Engebretsen L. Tunnel widening in single- versus double-bundle anterior cruciate ligament reconstructed knees. Knee Surg Sports Traumatol Arthrosc. 2016 Jun 21. [Epub ahead of print]
21. Maak TG, Voos JE, Wickiewicz TL, Warren RF. Tunnel widening in revision anterior cruciate ligament reconstruction. J Am Acad Orthop Surg. 2010;18(11):695-706.
22. Cheatham SA, Johnson DL. Anticipating problems unique to revision ACL surgery. Sports Med Arthrosc. 2013;21(2):129-134.
23. Kamath GV, Redfern JC, Greis PE, Burks RT. Revision anterior cruciate ligament reconstruction. Am J Sports Med. 2011;39(1):199-217.
24. Wright RW, Gill CS, Chen L, et al. Outcome of revision anterior cruciate ligament reconstruction: a systematic review. J Bone Joint Surg Am. 2012;94(6):531-536.
25. Andriolo L, Filardo G, Kon E, et al. Revision anterior cruciate ligament reconstruction: clinical outcome and evidence for return to sport. Knee Surg Sports Traumatol Arthrosc. 2015;23(10):2825-2845.
26. Grassi A, Ardern CL, Marcheggiani Muccioli GM, Neri MP, Marcacci M, Zaffagnini S. Does revision ACL reconstruction measure up to primary surgery? A meta-analysis comparing patient-reported and clinician-reported outcomes, and radiographic results. Br J Sports Med. 2016;50(12):716-724.
27. Ristanis S, Stergiou N, Patras K, Vasiliadis HS, Giakas G, Georgoulis AD. Excessive tibial rotation during high-demand activities is not restored by anterior cruciate ligament reconstruction. Arthroscopy. 2005;21(11):1323-1329.
28. Andriacchi TP, Mündermann A, Smith RL, Alexander EJ, Dyrby CO, Koo S. A framework for the in vivo pathomechanics of osteoarthritis at the knee. Ann Biomed Eng. 2004;32(3):447-457.
29. Imhauser C, Mauro C, Choi D, et al. Abnormal tibiofemoral contact stress and its association with altered kinematics after center-center anterior cruciate ligament reconstruction: an in vitro study. Am J Sports Med. 2013;41(4):815-825.
30. Ajuied A, Wong F, Smith C, et al. Anterior cruciate ligament injury and radiologic progression of knee osteoarthritis: a systematic review and meta-analysis. Am J Sports Med. 2014;42(9):2242-2252.
31. Chalmers PN, Mall NA, Moric M, et al. Does ACL reconstruction alter natural history?: A systematic literature review of long-term outcomes. J Bone Joint Surg Am. 2014;96(4):292-300.
32. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
33. Eggli S, Kohlhof H, Zumstein M, et al. Dynamic intraligamentary stabilization: novel technique for preserving the ruptured ACL. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1215-1221.
34. Buda R, Ferruzzi A, Vannini F, Zambelli L, Di Caprio F. Augmentation technique with semitendinosus and gracilis tendons in chronic partial lesions of the ACL: clinical and arthrometric analysis. Knee Surg Sports Traumatol Arthrosc. 2006;14(11):1101-1107.
35. Ochi M, Adachi N, Uchio Y, et al. A minimum 2-year follow-up after selective anteromedial or posterolateral bundle anterior cruciate ligament reconstruction. Arthroscopy. 2009;25(2):117-122.
36. Ahn JH, Lee YS, Ha HC. Anterior cruciate ligament reconstruction with preservation of remnant bundle using hamstring autograft: technical note. Arch Orthop Trauma Surg. 2009;129(8):1011-1015.
37. Lee BI, Min KD, Choi HS, Kim JB, Kim ST. Arthroscopic anterior cruciate ligament reconstruction with the tibial-remnant preserving technique using a hamstring graft. Arthroscopy. 2006;22(3):340.e1-e7.
38. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016 Jun 17. [Epub ahead of print]
39. MacKay G, Anthony IC, Jenkins PJ, Blyth M. Anterior cruciate ligament repair revisited. Preliminary results of primary repair with internal brace ligament augmentation: a case series. Orthop Muscul Syst. 2015;4:188.
40. Mackay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
41. Henle P, Röder C, Perler G, Heitkemper S, Eggli S. Dynamic intraligamentary stabilization (DIS) for treatment of acute anterior cruciate ligament ruptures: case series experience of the first three years. BMC Musculoskelet Disord. 2015;16:27.
42. Adachi N, Ochi M, Uchio Y, Iwasa J, Ryoke K, Kuriwaka M. Mechanoreceptors in the anterior cruciate ligament contribute to the joint position sense. Acta Orthop Scand. 2002;73(3):330-334.
43. Gao F, Zhou J, He C, et al. A morphologic and quantitative study of mechanoreceptors in the remnant stump of the human anterior cruciate ligament. Arthroscopy. 2016;32(2):273-280.
44. Georgoulis AD, Pappa L, Moebius U, et al. The presence of proprioceptive mechanoreceptors in the remnants of the ruptured ACL as a possible source of re-innervation of the ACL autograft. Knee Surg Sports Traumatol Arthrosc. 2001;9(6):364-368.
45. Fleming BC, Carey JL, Spindler KP, Murray MM. Can suture repair of ACL transection restore normal anteroposterior laxity of the knee? An ex vivo study. J Orthop Res. 2008;26(11):1500-1505.
46. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
47. Ahn JH, Wang JH, Lee YS, Kim JG, Kang JH, Koh KH. Anterior cruciate ligament reconstruction using remnant preservation and a femoral tensioning technique: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(8):1079-1089.
48. Lee BI, Kwon SW, Kim JB, Choi HS, Min KD. Comparison of clinical results according to amount of preserved remnant in arthroscopic anterior cruciate ligament reconstruction using quadrupled hamstring graft. Arthroscopy. 2008;24(5):560-568.
49. Lee BI, Min KD, Choi HS, et al. Immunohistochemical study of mechanoreceptors in the tibial remnant of the ruptured anterior cruciate ligament in human knees. Knee Surg Sports Traumatol Arthrosc. 2009;17(9):1095-1101.
50. Takahashi T, Kondo E, Yasuda K, et al. Effects of remnant tissue preservation on the tendon graft in anterior cruciate ligament reconstruction: a biomechanical and histological study. Am J Sports Med. 2016;44(7):1708-1716.
51. Dong S, Xie G, Zhang Y, Shen P, Huangfu X, Zhao J. Ligamentization of autogenous hamstring grafts after anterior cruciate ligament reconstruction: midterm versus long-term results. Am J Sports Med. 2015;43(8):1908-1917.
52. Takazawa Y, Ikeda H, Kawasaki T, et al. ACL reconstruction preserving the ACL remnant achieves good clinical outcomes and can reduce subsequent graft rupture. Orthop J Sports Med. 2013;1(4):2325967113505076.
53. Shimodaira H, Tensho K, Akaoka Y, Takanashi S, Kato H, Saito N. Remnant-preserving tibial tunnel positioning using anatomic landmarks in double-bundle anterior cruciate ligament reconstruction. Arthroscopy. 2016;32(9):1822-1830.
54. Zhang Q, Zhang S, Cao X, Liu L, Liu Y, Li R. The effect of remnant preservation on tibial tunnel enlargement in ACL reconstruction with hamstring autograft: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):166-173.
55. Tie K, Chen L, Hu D, Wang H. The difference in clinical outcome of single-bundle anterior cruciate ligament reconstructions with and without remnant preservation: A meta-analysis. Knee. 2016;23(4):566-574.
56. Robson AW. VI. Ruptured crucial ligaments and their repair by operation. Ann Surg. 1903;37(5):716-718.
57. Palmer I. On the injuries to the ligaments of the knee joint. Acta Orthop Scand. 1938;53.
58. Palmer I. On the injuries to the ligaments of the knee joint: a clinical study. 1938. Clin Orthop Relat Res. 2007;454:17-22.
59 O’Donoghue DH. An analysis of end results of surgical treatment of major injuries to the ligaments of the knee. J Bone Joint Surg Am. 1955;37-A(1):1-13.
60. O’Donoghue DH. Surgical treatment of fresh injuries to the major ligaments of the knee. J Bone Joint Surg Am. 1950;32 A(4):721-738.
61. Feagin JA, Abbott HG, Rokous JR. The isolated tear of the anterior cruciate ligament. J Bone Joint Surg Am. 1972;54-A:1340-1341.
62. England RL. Repair of the ligaments about the knee. Orthop Clin North Am. 1976;7(1):195-204.
63. Marshall JL, Warren RF, Wickiewicz TL, Reider B. The anterior cruciate ligament: a technique of repair and reconstruction. Clin Orthop Relat Res. 1979;(143):97-106.
64. Weaver JK, Derkash RS, Freeman JR, Kirk RE, Oden RR, Matyas J. Primary knee ligament repair--revisited. Clin Orthop Relat Res. 1985;(199):185-191.
65. Nogalski MP, Bach BR Jr. A review of early anterior cruciate ligament surgical repair or reconstruction. Results and caveats. Orthop Rev. 1993;22(11):1213-1223.
66. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
67. Marshall JL, Warren RF, Wickiewicz TL. Primary surgical treatment of anterior cruciate ligament lesions. Am J Sports Med. 1982;10(2):103-107.
68. Straub T, Hunter RE. Acute anterior cruciate ligament repair. Clin Orthop Relat Res. 1988;227:238-250.
69. Kaplan N, Wickiewicz TL, Warren RF. Primary surgical treatment of anterior cruciate ligament ruptures. A long-term follow-up study. Am J Sports Med. 1990;18(4):354-358.
70. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
71. Paar O. Use of semitendinosus tendon to strengthen a freshly repaired anterior cruciate ligament. Chirurg. 1985;56(11):728-734.
72. Aglietti P, Buzzi R, Pisaneschi A, Salvi M. Comparison between suture and augmentation with the semitendinosus tendon in the repair of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1986;8(4):217-231.
73. Higgins RW, Steadman JR. Anterior cruciate ligament repairs in world class skiers. Am J Sports Med. 1987;15(5):439-447.
74. Harilainen A, Myllynen P. Treatment of fresh tears of the anterior cruciate ligament. A comparison of primary suture and augmentation with carbon fibre. Injury. 1987;18(6):396-400.
75. Jones KG. Results of use of the central one-third of the patellar ligament to compensate for anterior cruciate ligament deficiency. Clin Orthop Relat Res. 1980;(147):39-44.
76. Puddu G. Method for reconstruction of the anterior cruciate ligament using the semitendinosus tendon. Am J Sports Med. 1980;8(6):402-404.
77. Hefti F, Gächter A, Jenny H, Morscher E. Replacement of the anterior cruciate ligament. a comparative study of four different methods of reconstruction. Arch Orthop Trauma Surg. 1982;100(2):83-94.
78. Odensten M, Hamberg P, Nordin M, Lysholm J, Gillquist J. Surgical or conservative treatment of the acutely torn anterior cruciate ligament. A randomized study with short-term follow-up observations. Clin Orthop Relat Res. 1985;(198):87-93.
79. Andersson C, Odensten M, Good L, Gillquist J. Surgical or non-surgical treatment of acute rupture of the anterior cruciate ligament. A randomized study with long-term follow-up. J Bone Joint Surg Am. 1989;71(7):965-974.
80. Engebretsen L, Benum P, Fasting O, Mølster A, Strand T. A prospective, randomized study of three surgical techniques for treatment of acute ruptures of the anterior cruciate ligament. Am J Sports Med. 1990;18(6):585-590.
81. Jonsson T, Peterson L, Renström P. Anterior cruciate ligament repair with and without augmentation. A prospective 7-year study of 51 patients. Acta Orthop Scand. 1990;61(6):562-566.
82. Andersson C, Odensten M, Gillquist J. Knee function after surgical or nonsurgical treatment of acute rupture of the anterior cruciate ligament: a randomized study with a long-term follow-up period. Clin Orthop Relat Res. 1991;(264):255-263.
83. Heim U, Bachmann B, Infanger K. Reinsertion of the anterior cruciate ligament or primary ligamentous plasty? Helv Chir Acta. 1982;48(5):703-708.
84. Strand T, Engesaeter LB, Mølster AO, et al. Knee function following suture of fresh tear of the anterior cruciate ligament. Acta Orthop Scand. 1984;55(2):181-184.
85. Marcacci M, Spinelli M, Chiellini F, Buccolieri V. Notes on 53 cases of immediate suture of acute lesions of the anterior cruciate ligament. Ital J Orthop Traumatol. 1985;7(2):69-79.
86. van der List JP, DiFelice GS. Primary repair of the anterior cruciate ligament: a paradigm shift. Surgeon. 2016 Oct 6. [Epub ahead of print]
87. Bräm J, Plaschy S, Lütolf M, Leutenegger A. [The primary cruciate ligament suture--is the method outdated? Results in follow-up of 58 patients]. Z Unfallchir Versicherungsmed. 1994;87(2):91-109.
88. Genelin F, Trost A, Primavesi C, Knoll P. Late results following proximal reinsertion of isolated ruptured ACL ligaments. Knee Surg Sports Traumatol Arthrosc. 1993;1(1):17-19.
89. Kühne JH, Theermann R, Neumann R, Sagasser J. [Acute uncomplicated anterior knee instability. 2-5 year follow-up of surgical treatment]. Unfallchirurg. 1991;94(2):81-87.
90. Simonet WT, Sim FH. Repair and reconstruction of rotatory instability of the knee. Am J Sports Med. 1984;12(2):89-97.
91. Raunest J, Derra E, Ohmann C. [Clinical results of Palmer’s primary cruciate ligament insertion without augmentation]. Unfallchirurgie. 1991;17(3):166-174.
92. Frank C, Beaver P, Rademaker F, Becker K, Schachar N, Edwards G. A computerized study of knee-ligament injuries: repair versus removal of the torn anterior cruciate ligament. Can J Surg. 1982;25(4):454-458.
93. Enneking WF, Horowitz M. The intra-articular effects of immobilization on the human knee. J Bone Joint Surg Am. 1972;54(5):973-985.
94. Millett PJ, Wickiewicz TL, Warren RF. Motion loss after ligament injuries to the knee. Part I: causes. Am J Sports Med. 2001;29(5):664-675.
95. Bilko TE, Paulos LE, Feagin JA Jr, Lambert KL, Cunningham HR. Current trends in repair and rehabilitation of complete (acute) anterior cruciate ligament injuries. Analysis of 1984 questionnaire completed by ACL Study Group. Am J Sports Med. 1986;14(2):143-147.
96. Paulos L, Noyes FR, Grood E, Butler DL. Knee rehabilitation after anterior cruciate ligament reconstruction and repair. J Orthop Sports Phys Ther. 1991;13(2):60-70.
97. Paessler HH, Deneke J, Dahners LE. Augmented repair and early mobilization of acute anterior cruciate ligament injuries. Am J Sports Med. 1992;20(6):667-674.
98.
99. Kdolsky RK, Gibbons DF, Kwasny O, Schabus R, Plenk H Jr. Braided polypropylene augmentation device in reconstructive surgery of the anterior cruciate ligament: long-term clinical performance of 594 patients and short-term arthroscopic results, failure analysis by scanning electron microscopy, and synovial histomorphology. J Orthop Res. 1997;15(1):1-10.
100. Grøntvedt T, Engebretsen L. Comparison between two techniques for surgical repair of the acutely torn anterior cruciate ligament. A prospective, randomized follow-up study of 48 patients. Scand J Med Sci Sports. 1995;5(6):358-363.
101. Hehl G, Strecker W, Richter M, Kiefer H, Wissmeyer T. Clinical experience with PDS II augmentation for operative treatment of acute proximal ACL ruptures--2-year follow-up. Knee Surg Sports Traumatol Arthrosc. 1999;7(2):102-106.
102. Schenk S, Landsiedl F, Enenkel M. Arthroscopic single-stranded semitendinosus tendon- versus PDS-augmentation of reinserted acute femoral anterior cruciate ligament tears: 7 year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2006;14(4):318-324.
103. Zysk SP, Refior HJ. Operative or conservative treatment of the acutely torn anterior cruciate ligament in middle-aged patients. A follow-up study of 133 patients between the ages of 40 and 59 years. Arch Orthop Trauma Surg. 2000;120(1-2):59-64.
104. Krueger-Franke M, Siebert CH, Schupp A. Refixation of femoral anterior cruciate ligament tears combined with a semitendinosus tendon augmentation. Technique and results. Arch Orthop Trauma Surg. 1998;117(1-2):68-72.
105. Natri A, Järvinen M, Kannus P. Primary repair plus intra-articular iliotibial band augmentation in the treatment of an acute anterior cruciate ligament rupture. A follow-up study of 70 patients. Arch Orthop Trauma Surg. 1996;115(1):22-27.
106. Träger D, Pohle K, Tschirner W. Anterior cruciate ligament suture in comparison with plasty. A 5-year follow-up study. Arch Orthop Trauma Surg. 1995;114(5):278-280.
107. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M. Arthrofibrosis in acute anterior cruciate ligament reconstruction. The effect of timing of reconstruction and rehabilitation. Am J Sports Med. 1991;19(4):332-336.
108. Volokhina YV, Syed HM, Pham PH, Blackburn AK. Two helpful MRI signs for evaluation of posterolateral bundle tears of the anterior cruciate ligament: a pilot study. Orthop J Sports Med. 2015;3(8):2325967115597641.
109. Strand T, Mølster A, Hordvik M, Krukhaug Y. Long-term follow-up after primary repair of the anterior cruciate ligament: clinical and radiological evaluation 15-23 years postoperatively. Arch Orthop Trauma Surg. 2005;125(4):217-221.
110. van der List JP, DiFelice GS. Successful arthroscopic primary repair of a chronic anterior cruciate ligament tear 11 years following injury. HSS J. 2016. In press.
111. van der List JP, DiFelice GS. The role of ligament repair in anterior cruciate ligament surgery. In: Mascarenhas R, Bhatia S, Lowe WR, eds. Ligamentous Injuries of the Knee. 1st ed. Houston: Nova Science Publishers; 2016:199-220.
112. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
113. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
114. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
115. Magarian EM, Fleming BC, Harrison SL, Mastrangelo AN, Badger GJ, Murray MM. Delay of 2 or 6 weeks adversely affects the functional outcome of augmented primary repair of the porcine anterior cruciate ligament. Am J Sports Med. 2010;38(12):2528-2534.
116. Murray MM, Magarian EM, Harrison SL, Mastrangelo AN, Zurakowski D, Fleming BC. The effect of skeletal maturity on functional healing of the anterior cruciate ligament. J Bone Joint Surg Am. 2010;92(11):2039-2049.
117. Werner BC, Yang S, Looney AM, Gwathmey FW Jr. Trends in pediatric and adolescent anterior cruciate ligament iInjury and reconstruction. J Pediatr Orthop. 2016;36(5):447-452.
118. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
119. Ramski DE, Kanj WW, Franklin CC, Baldwin KD, Ganley TJ. Anterior cruciate ligament tears in children and adolescents: a meta-analysis of nonoperative versus operative treatment. Am J Sports Med. 2014;42(11):2769-2776.
120. Zantop T, Brucker PU, Vidal A, Zelle BA, Fu FH. Intraarticular rupture pattern of the ACL. Clin Orthop Relat Res. 2007;454:48-53.
121. Yoon KH, Bae DK, Cho SM, Park SY, Lee JH. Standard anterior cruciate ligament reconstruction versus isolated single-bundle augmentation with hamstring autograft. Arthroscopy. 2009;25(11):1265-1274.
122 Demirağ B, Ermutlu C, Aydemir F, Durak K. A comparison of clinical outcome of augmentation and standard reconstruction techniques for partial anterior cruciate ligament tears. Eklem Hastalik Cerrahisi. 2012;23(3):140-144.
123. Sonnery-Cottet B, Zayni R, Conteduca J, et al. Posterolateral bundle reconstruction with anteromedial bundle remnant preservation in ACL tears: clinical and MRI evaluation of 39 patients with 24-month follow-up. Orthop J Sports Med. 2013;1(3):2325967113501624.
124. Sabat D, Kumar V. Partial tears of anterior cruciate ligament: results of single bundle augmentation. Indian J Orthop. 2015;49(2):129-135.
125. Jung YB, Jung HJ, Siti HT, et al. Comparison of anterior cruciate ligament reconstruction with preservation only versus remnant tensioning technique. Arthroscopy. 2011;27(9):1252-1258.
126. Nguyen DT, Ramwadhdoebe TH, van der Hart CP, Blankevoort L, Tak PP, van Dijk CN. Intrinsic healing response of the human anterior cruciate ligament: an histological study of reattached ACL remnants. J Orthop Res. 2014;32(2):296-301.
127. Boutsiadis A, Karampalis C, Tzavelas A, Vraggalas V, Christodoulou P, Bisbinas I. Anterior cruciate ligament remnant-preserving reconstruction using a “lasso-loop” knot configuration. Arthrosc Tech. 2015;4(6):e741-e746.
128. Noh JH, Yoon KH, Song SJ, Roh YH. Re-tensioning technique to cover the graft with remnant in anterior cruciate ligament reconstruction. Arthrosc Tech. 2014;3(6):e679-e682.
129. Hong L, Li X, Zhang H, et al. Anterior cruciate ligament reconstruction with remnant preservation: a prospective, randomized controlled study. Am J Sports Med. 2012;40(12):2747-2755.
130. Noh JH, Kyung HS, Roh YH, Kang TS. Remnant-preserving and re-tensioning technique to cover the graft in anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 12. [Epub ahead of print]
131. Muneta T, Koga H, Ju YJ, Horie M, Nakamura T, Sekiya I. Remnant volume of anterior cruciate ligament correlates preoperative patients’ status and postoperative outcome. Knee Surg Sports Traumatol Arthrosc. 2013;21(4):906-913.
132. Leeberg V, Lekdorf J, Wong C, Sonne-Holm S. Tibial eminentia avulsion fracture in children - a systematic review of the current literature. Dan Med J. 2014;61(3):A4792.
133. In Y, Kwak DS, Moon CW, Han SH, Choi NY. Biomechanical comparison of three techniques for fixation of tibial avulsion fractures of the anterior cruciate ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1470-1478.
Preservation of the Anterior Cruciate Ligament: Surgical Techniques
In the first part of this series, “Preservation of the Anterior Cruciate Ligament: A Treatment Algorithm Based on Tear Location and Tissue Quality” we discussed the history of anterior cruciate ligament (ACL) preservation, and the historical outcomes of both open primary repair and augmented repair. We also presented our surgical treatment algorithm for ACL preservation, which is based on the tear location and tissue quality of the ligament remnant. In this article, we propose a modification of the Sherman classification1 to identify the different tear types, and we will discuss the different surgical techniques that can be used for each one. Furthermore, we aim to provide an overview of the variations of these techniques that are seen in the literature. It is important to emphasize that these tear types and corresponding surgical techniques are to be seen as guidelines, rather than strict criteria, and that significant overlap between these tear types and surgical indications exist.
Assessment of Tear Type and Tissue Quality
The first assessment of the tear location and tissue quality is made using magnetic resonance imaging (MRI). Although MRI can give you an idea of where the tear is located, the final assessment for eligibility of each specific preservation technique is made during arthroscopy. Therefore, the routine preoperative discussion and informed consent process with the patient should encompass the gamut of surgical possibilities ranging from repair to reconstruction.
The Table shows our tear type classification, along with the corresponding preservation surgical techniques.
Surgical Preparation
In the operating room, the patient is placed in supine position on a standard operative table, such that the knee can be moved freely through its range of motion (ROM). The operative leg is then prepped and draped in standard fashion for knee arthroscopy. Standard knee arthroscopy equipment and implants are used, although some instruments from the standard shoulder set are also utilized. Anteromedial and anterolateral portals are created, and a general inspection of the knee is performed. By pulling the remnant ligament proximally using a broad tissue gasper, the available length of the remnant can be assessed. It is important to reduce possible anterior tibial subluxation in the sagittal plane in order to prevent “false” shortening of the distal ligament remnant. Once the length of the remnant tissue is assessed and the tissue quality is determined, the surgical preservation technique can be chosen (Table).
Type I Tears: Primary Repair
In order to be a candidate for arthroscopic primary repair, sufficient tissue length and tissue quality are necessary (Figures 1A and 1B, Table).
Sutures are then passed through the anteromedial bundle using the Scorpion Suture Passer (Arthrex) with a No. 2 FiberWire suture (Arthrex) (Figure 1C). Suturing is commenced at the intact distal end of the anteromedial bundle and is advanced in an alternating, interlocking Bunnell-type pattern towards the avulsed proximal end with approximately 4 mm to 5 mm between each pass. In general, 3 to 4 passes can be made before the final pass exits via the avulsed end of the ligament towards the femur (Figure 1D). The same process is then repeated for the posterolateral bundle of the ACL remnant with a No. 2 TigerWire suture (Arthrex) to optimize suture management. With each subsequent pass of the sutures, it is important to assess tissue resistance to prevent perforation of a previous stitch. Mild resistance is normal, but the suture-passing device should be repositioned when notably increased resistance is encountered. In addition, placing all of the bites in the same plane should be avoided since this can allow the sutures to “cheese cut” along the collagen fibers of the ligament remnant rather than holding firm.
After passing the sutures through both bundles, the sutures are guided outside the knee using an accessory stab incision situated just above the medial portal. Using this portal, the ligament can be retracted away from the femoral footprint for optimal visibility. The femoral footprint is then roughed using a shaver or burr, and bleeding is induced to stimulate a local healing response,2 while the sutures and the ACL are protected via the portal. With the knee in flexion, an accessory inferomedial portal is then created under direct visualization using a spinal needle for localization. Care should be taken to enable the appropriate trajectory for anchor placement to be achieved.
Many different techniques can be used to provide fixation of the ACL repair to the femoral footprint; the 2 most straightforward techniques are presented here. The first technique provides fixation with knotless suture anchors,3,4 whereas in the second technique the sutures are transosseously passed, and tied over a bone bridge, as was performed in the 1970s and 1980s.
Suture Anchor Fixation
With the suture anchor fixation technique, the knee is flexed in 90°, the anteromedial bundle origin within the femoral footprint is identified, and a 4.5-mm x 20-mm hole is drilled, punched, or tapped, in the case of high bone density. The FiberWire sutures are then retrieved through the accessory portal and passed through a 4.75-mm Vented BioComposite SwiveLock suture anchor (Arthrex). The suture anchor for the anteromedial bundle is then deployed into the hole within the anteromedial footprint, while tensioning the ACL remnant to the wall with a visual gap of <1 mm (Figure 1E).5 The procedure is then repeated using another suture anchor with TigerWire sutures for the posterolateral bundle with the knee flexed at 110° to 115°. This ensures an optimal angle of approach and avoids perforating the posterior condyle with the anchor. The drill hole and anchor are placed into the origin of the posterolateral bundle within the femoral footprint. The order of bundle tensioning and repair may be varied depending on the particulars of each case.
Once the anchors are fully deployed and flush with the femoral footprint, the handle is removed and the additional core stitches are unloaded. Occasionally, the core stitches can be passed from lateral to medial through the proximal ligament remnant and tied down with an arthroscopic knot pusher to add extra compression of the remnant to the origin. The free ends of the repair sutures are cut with an Open Ended Suture Cutter (Arthrex) so that they are flush with the notch. The repair is now complete (Figure 1F). Using a probe, the ACL remnant is tested for tension and stiffness. Finally, cycling of the knee through the full ROM confirms anatomic positioning without impingement of the graft. Manual laxity testing should reveal minimal anteroposterior translation with a firm endpoint on Lachman examination intraoperatively.
Bone Bridge Fixation
With this technique, parallel drill holes are created exiting at each bundle origin. The repair stitches can then be retrieved and tensioned proximally. One way to accomplish this is by using an ACL femoral guide (Arthrex) that is placed via the anterolateral portal and is centered on the anteromedial bundle insertion. This device guides a cannulated RetroDrill (Arthrex) to drill through the lateral femoral condyle towards the anteromedial footprint. A passing wire can then be delivered through the cannulation and used to retrieve that anteromedial bundle repair stitches. This process can then be repeated for the posterolateral bundle and the associated repair stitches. Drill holes can also be made retrograde from a low anteromedial accessory portal using a slotted pit that can be used to shuttle the repair stitches. When all the repair sutures are passed, the ligament is tensioned while being visualized arthroscopically. The knee is held at 20° of flexion and a posterior drawer force can be applied, if necessary, to reduce the tibia to its anatomic position. The suture limbs are then tensioned and can be fixated using any of a multitude of techniques, including tying over a bony bridge, tying over a 4-hole ligament button, and tying to a post.
One disadvantage of the bone bridge fixation technique, however, is the suspensory fixation that is not as stiff as tensioning and fixating with suture anchors. Despite this disadvantage, however, the senior author (GSD) has achieved excellent results with this technique at longer-term follow-up in a small group of patients. One advantage of the bone bridge fixation technique is that the procedure has lower costs than fixation with suture anchors.
One Anchor Repair Fixation
Achtnich and colleagues6 recently published a slightly different technique for repairing type I tears. The authors passed a No. 2 FiberWire suture through the midsubstance of both bundles of the ACL remnant to create a modified Mason-Allen stitch configuration. Subsequently, they tensioned the remnant towards the middle of the ACL footprint (between the anteromedial and posterolateral footprint) using one PushLock suture anchor (Arthrex). They hypothesized that using 1 anchor would be enough fixation for tears amenable to repair, and that doing so would minimize the invasion of the bone.
The preference of the senior author (GSD) is, however, to use 2 suture anchors for each bundle in order to more anatomically and biomechanically repair the remnant, since both bundles have different biomechanical characteristics.7 Similarly, the preference of the senior author is to commence the suturing as distal as possible and pass multiple sutures towards the proximal end. This ensures that the last suture pass is exited very proximally, and ensures that the proximal end is approximated towards the femoral wall. One suture passed at the midsubstance portion of the remnant might cause a different tension pattern and prevent optimal re-approximation of the most proximal part towards the femoral wall. Future studies are necessary to assess the efficacy of different suture and fixation techniques as these are currently lacking.
Addition of Internal Brace
Over the last few years, the senior author has added an internal brace (FiberTape, Arthrex) to the repair technique, which was first performed by MacKay and colleagues.8 The added internal brace protects the repair and the healing process in the first few weeks and enables early ROM.
With this technique, the previously described arthroscopic primary repair technique is performed with suturing of both bundles. However, after punching, tapping, or drilling a hole in the anteromedial origin of the femoral footprint, the anteromedial anchor is first loaded with the FiberTape in addition to the repair stitches. After placing the anteromedial suture anchor in the femoral footprint, the internal brace is fixated proximally with the suture anchor into the femoral wall.
Others, however, have advocated fixing the internal brace independently of the repaired ligament and suture anchors.9 With this technique, tunnels are drilled in the femur and tibia and the internal brace construct is fixed proximally using a RetroButton (Arthrex) and fixed distally in the tibial metaphysis using a suture anchor. A disadvantage of this technique is that an extra femoral tunnel needs to be drilled, which is especially important in pediatric patients with the increased risk for growth disturbances.10
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the anteromedial or posterolateral bundle is a type I tear with good or excellent tissue quality, whereas the other bundle is not a type I tear or has poor tissue quality (Figure 3A). In these cases, a primary repair of one bundle is performed with a hamstring reconstruction of the other bundle.
First, a No. 2 FiberWire is used to make 4 to 5 passes from distal to proximal, as previously described. Then, the remnants of the irreparable bundle are debrided (Figure 3B). Subsequently, the semitendinosus tendon is harvested in standard fashion, or soft tissue allografts can be used.
Type II Tears: Augmented Repair
In patients with type II tears, primary repair is not possible as the length of the remnant is too short to firmly approximate the remnant towards the femoral wall (75%-90% of native tissue length) (Figure 4A). In these patients, an augmented repair of the entire ACL is performed using hamstring autograft or soft tissue allograft.
With this technique, repair stitches are passed into the anteromedial bundle of the remnant as previously described (Figure 4B). Keeping the repair stitches anteriorly in the anteromedial bundle tends to prevent entanglement during graft passage later in the case.
Once the repair stitches are in place, a small accessory stab incision is made just above the medial portal. The repair stitches are parked here to keep them out of harms way. Traction on the repair stitches will retract the ACL away from the lateral wall of the notch and allow work to be performed here. A small opening notchplasty is generally performed to enhance visualization and to add a bleeding surface for enhanced healing. Next, the arthroscope is placed into the medial portal, which allows the femoral guide to be placed into the lateral portal. The femoral guide is positioned to optimize the femoral tunnel location in the center of the footprint. A small incision is made laterally over the condyle and through the iliotibial band to allow access to the lateral cortex of the lateral femoral condyle. The FlipCutter is then used to back-cut the femoral socket as described above. A FiberStick (Arthrex) passing suture is then placed in the femoral tunnel and brought out through the anteromedial portal.
Next, the tibial tunnel is drilled with a tibial guide at 55° inclination. The pin is drilled up into the center of the tibial footprint and this is over-reamed with a reamer. The reaming is stopped precisely upon breaking to proximal tibial cortex so as to minimize soft tissue damage of the ACL insertion fibers that are typically pristine. Then, a grasper is passed up and through the tunnel to retrieve the repair stitches and bring them out distally for later use. At the same time, the passing suture in the femoral is also retrieved distally. The soft tissue graft is proximally prepared with a TightRope RT button, and the repair stitches are passed through the button. The passing suture from the femoral socket is then used to shuttle the draw sutures and repair stitches up through the tibia, through the ACL remnant, and out the femoral socket (Figure 4C). The TightRope RT button is then engaged on the lateral femoral cortex in standard fashion. Using the cinch stitches, the graft is delivered through the tibia, up and through the center of the ACL remnant, and into the femoral socket. The knee is then cycled and the graft is tensioned distally in standard fashion, and fixed using a BioComposite interference screw. Finally, the repair stitches can be tensioned pulling the ligament remnant up as a sleeve around the hamstring graft (Figure 4D). They are then tied over the TightRope RT button using alternating half hitches tied with a knot pusher from laterally.
Type III Tears: Reconstruction With Remnant Tensioning
The previously discussed techniques have the goals of preserving as much native ligament remnant as possible, approximating the ligament remnant towards the femoral wall, and promoting healing of the ligament. In some cases, however, the ligament remnant is too short for healing (Figure 5A). Although the ligament cannot be approximated to the femoral wall in these cases, there is still an argument for ACL preservation, as was discussed in the first article of this series.
If the ligament length is between 25% and 75% of the native tissue length, the senior author performs a remnant tensioning technique.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some cases, the distal remnant is small or the tissue quality in the largest part of the remnant is poor, and after debriding back to good tissue quality, only 10% to 25% of the native tissue length is left (Figure 6A). In these cases, the remnant is preserved, however, tensioning of the remnant with sutures is usually not necessary for the prevention of cyclops lesions. Nonetheless, it is important to debride the parts of the remnant ligament with poor tissue quality as mop-end patterns of the remnant may increase the chance of these lesions (Figure 6B).
In this situation, any of the standard ACL reconstruction techniques can be performed with simple attention being paid to preserving what is left of the tibial insertion site. At the very least, the small insertion remnant guides the anatomic placement of the graft, and prevents egress of joint fluid into the tibial tunnel and could minimize tunnel widening.
Type V Tears: Primary Repair
Finally, in some patients a soft tissue avulsion (Figure 7A) or bony avulsion of the distal attachment of the ACL can be seen. Both injuries are relatively rare, although bony avulsions are frequently seen in children, especially those younger than 12 years old. In these cases, the same techniques and theory that are applied to proximal avulsion type tears can be used and applied to distal avulsion type tears.
First, No. 2 FiberWire sutures are passed from proximal towards the distal end of the ligament in the anteromedial bundle, and the same process is then repeated for No. 2 TigerWire sutures for the posterolateral bundle. Then both sutures are exited at the distal avulsed end at the locations of the anteromedial and posterolateral footprints (Figure 7B). A 2.4-mm ACL guide wire and a Ninitol wire are used to drill 2 tunnels from the tibia towards the tibial footprint. The repair sutures are then retrieved through both tunnels (Figure 7C) and the sutures are tied distally over a ligament button after cycling of the knee (Figure 7D). This technique is very useful for soft tissue avulsions, or when there are only small flecks of bone or when the avulsed bone is significantly comminuted. If a large bony avulsion fragment is present, this technique can also be applied with some modification, although there have been multiple other techniques described in the literature that work well in this situation including fixation with screw and washer, or with suture anchors.
Complex Tear or Poor Tissue Quality: Reconstruction
In some cases, the tissue quality is poor, or the ligament has complex or multiple tears. Essentially, in these cases, there is nothing to preserve and a standard reconstruction approach is performed in these cases.
Conclusion
The uniform gold standard for all ACL tear types is currently primary reconstruction. However, several disadvantages of ACL reconstruction exist, while there are multiple advantages to the concept of ACL preservation. In this surgical technique article, we have discussed our tear type classification and the recommended surgical techniques for each. With this treatment algorithm, which is based on tear location and tissue quality, an optimal and minimally invasive treatment can be chosen for each individual patient. Future studies are needed to compare and contrast these treatments with the current gold standard of ACL reconstruction.
Am J Orthop. 2016;45(7):E406-E414. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
2. Steadman JR, Matheny LM, Briggs KK, Rodkey WG, Carreira DS. Outcomes following healing response in older, active patients: a primary anterior cruciate ligament repair technique. J Knee Surg. 2012;25(3):255-260.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
5. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
6. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016. [Epub ahead of print]
7. Amis AA. The functions of the fibre bundles of the anterior cruciate ligament in anterior drawer, rotational laxity and the pivot shift. Knee Surg Sports Traumatol Arthrosc. 2012;20(4):613-620.
8. MacKay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
9. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
10. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
11. Crain EH, Fithian DC, Paxton EW, Luetzow WF. Variation in anterior cruciate ligament scar pattern: does the scar pattern affect anterior laxity in anterior cruciate ligament-deficient knees? Arthroscopy. 2005;21(1):19-24.
In the first part of this series, “Preservation of the Anterior Cruciate Ligament: A Treatment Algorithm Based on Tear Location and Tissue Quality” we discussed the history of anterior cruciate ligament (ACL) preservation, and the historical outcomes of both open primary repair and augmented repair. We also presented our surgical treatment algorithm for ACL preservation, which is based on the tear location and tissue quality of the ligament remnant. In this article, we propose a modification of the Sherman classification1 to identify the different tear types, and we will discuss the different surgical techniques that can be used for each one. Furthermore, we aim to provide an overview of the variations of these techniques that are seen in the literature. It is important to emphasize that these tear types and corresponding surgical techniques are to be seen as guidelines, rather than strict criteria, and that significant overlap between these tear types and surgical indications exist.
Assessment of Tear Type and Tissue Quality
The first assessment of the tear location and tissue quality is made using magnetic resonance imaging (MRI). Although MRI can give you an idea of where the tear is located, the final assessment for eligibility of each specific preservation technique is made during arthroscopy. Therefore, the routine preoperative discussion and informed consent process with the patient should encompass the gamut of surgical possibilities ranging from repair to reconstruction.
The Table shows our tear type classification, along with the corresponding preservation surgical techniques.
Surgical Preparation
In the operating room, the patient is placed in supine position on a standard operative table, such that the knee can be moved freely through its range of motion (ROM). The operative leg is then prepped and draped in standard fashion for knee arthroscopy. Standard knee arthroscopy equipment and implants are used, although some instruments from the standard shoulder set are also utilized. Anteromedial and anterolateral portals are created, and a general inspection of the knee is performed. By pulling the remnant ligament proximally using a broad tissue gasper, the available length of the remnant can be assessed. It is important to reduce possible anterior tibial subluxation in the sagittal plane in order to prevent “false” shortening of the distal ligament remnant. Once the length of the remnant tissue is assessed and the tissue quality is determined, the surgical preservation technique can be chosen (Table).
Type I Tears: Primary Repair
In order to be a candidate for arthroscopic primary repair, sufficient tissue length and tissue quality are necessary (Figures 1A and 1B, Table).
Sutures are then passed through the anteromedial bundle using the Scorpion Suture Passer (Arthrex) with a No. 2 FiberWire suture (Arthrex) (Figure 1C). Suturing is commenced at the intact distal end of the anteromedial bundle and is advanced in an alternating, interlocking Bunnell-type pattern towards the avulsed proximal end with approximately 4 mm to 5 mm between each pass. In general, 3 to 4 passes can be made before the final pass exits via the avulsed end of the ligament towards the femur (Figure 1D). The same process is then repeated for the posterolateral bundle of the ACL remnant with a No. 2 TigerWire suture (Arthrex) to optimize suture management. With each subsequent pass of the sutures, it is important to assess tissue resistance to prevent perforation of a previous stitch. Mild resistance is normal, but the suture-passing device should be repositioned when notably increased resistance is encountered. In addition, placing all of the bites in the same plane should be avoided since this can allow the sutures to “cheese cut” along the collagen fibers of the ligament remnant rather than holding firm.
After passing the sutures through both bundles, the sutures are guided outside the knee using an accessory stab incision situated just above the medial portal. Using this portal, the ligament can be retracted away from the femoral footprint for optimal visibility. The femoral footprint is then roughed using a shaver or burr, and bleeding is induced to stimulate a local healing response,2 while the sutures and the ACL are protected via the portal. With the knee in flexion, an accessory inferomedial portal is then created under direct visualization using a spinal needle for localization. Care should be taken to enable the appropriate trajectory for anchor placement to be achieved.
Many different techniques can be used to provide fixation of the ACL repair to the femoral footprint; the 2 most straightforward techniques are presented here. The first technique provides fixation with knotless suture anchors,3,4 whereas in the second technique the sutures are transosseously passed, and tied over a bone bridge, as was performed in the 1970s and 1980s.
Suture Anchor Fixation
With the suture anchor fixation technique, the knee is flexed in 90°, the anteromedial bundle origin within the femoral footprint is identified, and a 4.5-mm x 20-mm hole is drilled, punched, or tapped, in the case of high bone density. The FiberWire sutures are then retrieved through the accessory portal and passed through a 4.75-mm Vented BioComposite SwiveLock suture anchor (Arthrex). The suture anchor for the anteromedial bundle is then deployed into the hole within the anteromedial footprint, while tensioning the ACL remnant to the wall with a visual gap of <1 mm (Figure 1E).5 The procedure is then repeated using another suture anchor with TigerWire sutures for the posterolateral bundle with the knee flexed at 110° to 115°. This ensures an optimal angle of approach and avoids perforating the posterior condyle with the anchor. The drill hole and anchor are placed into the origin of the posterolateral bundle within the femoral footprint. The order of bundle tensioning and repair may be varied depending on the particulars of each case.
Once the anchors are fully deployed and flush with the femoral footprint, the handle is removed and the additional core stitches are unloaded. Occasionally, the core stitches can be passed from lateral to medial through the proximal ligament remnant and tied down with an arthroscopic knot pusher to add extra compression of the remnant to the origin. The free ends of the repair sutures are cut with an Open Ended Suture Cutter (Arthrex) so that they are flush with the notch. The repair is now complete (Figure 1F). Using a probe, the ACL remnant is tested for tension and stiffness. Finally, cycling of the knee through the full ROM confirms anatomic positioning without impingement of the graft. Manual laxity testing should reveal minimal anteroposterior translation with a firm endpoint on Lachman examination intraoperatively.
Bone Bridge Fixation
With this technique, parallel drill holes are created exiting at each bundle origin. The repair stitches can then be retrieved and tensioned proximally. One way to accomplish this is by using an ACL femoral guide (Arthrex) that is placed via the anterolateral portal and is centered on the anteromedial bundle insertion. This device guides a cannulated RetroDrill (Arthrex) to drill through the lateral femoral condyle towards the anteromedial footprint. A passing wire can then be delivered through the cannulation and used to retrieve that anteromedial bundle repair stitches. This process can then be repeated for the posterolateral bundle and the associated repair stitches. Drill holes can also be made retrograde from a low anteromedial accessory portal using a slotted pit that can be used to shuttle the repair stitches. When all the repair sutures are passed, the ligament is tensioned while being visualized arthroscopically. The knee is held at 20° of flexion and a posterior drawer force can be applied, if necessary, to reduce the tibia to its anatomic position. The suture limbs are then tensioned and can be fixated using any of a multitude of techniques, including tying over a bony bridge, tying over a 4-hole ligament button, and tying to a post.
One disadvantage of the bone bridge fixation technique, however, is the suspensory fixation that is not as stiff as tensioning and fixating with suture anchors. Despite this disadvantage, however, the senior author (GSD) has achieved excellent results with this technique at longer-term follow-up in a small group of patients. One advantage of the bone bridge fixation technique is that the procedure has lower costs than fixation with suture anchors.
One Anchor Repair Fixation
Achtnich and colleagues6 recently published a slightly different technique for repairing type I tears. The authors passed a No. 2 FiberWire suture through the midsubstance of both bundles of the ACL remnant to create a modified Mason-Allen stitch configuration. Subsequently, they tensioned the remnant towards the middle of the ACL footprint (between the anteromedial and posterolateral footprint) using one PushLock suture anchor (Arthrex). They hypothesized that using 1 anchor would be enough fixation for tears amenable to repair, and that doing so would minimize the invasion of the bone.
The preference of the senior author (GSD) is, however, to use 2 suture anchors for each bundle in order to more anatomically and biomechanically repair the remnant, since both bundles have different biomechanical characteristics.7 Similarly, the preference of the senior author is to commence the suturing as distal as possible and pass multiple sutures towards the proximal end. This ensures that the last suture pass is exited very proximally, and ensures that the proximal end is approximated towards the femoral wall. One suture passed at the midsubstance portion of the remnant might cause a different tension pattern and prevent optimal re-approximation of the most proximal part towards the femoral wall. Future studies are necessary to assess the efficacy of different suture and fixation techniques as these are currently lacking.
Addition of Internal Brace
Over the last few years, the senior author has added an internal brace (FiberTape, Arthrex) to the repair technique, which was first performed by MacKay and colleagues.8 The added internal brace protects the repair and the healing process in the first few weeks and enables early ROM.
With this technique, the previously described arthroscopic primary repair technique is performed with suturing of both bundles. However, after punching, tapping, or drilling a hole in the anteromedial origin of the femoral footprint, the anteromedial anchor is first loaded with the FiberTape in addition to the repair stitches. After placing the anteromedial suture anchor in the femoral footprint, the internal brace is fixated proximally with the suture anchor into the femoral wall.
Others, however, have advocated fixing the internal brace independently of the repaired ligament and suture anchors.9 With this technique, tunnels are drilled in the femur and tibia and the internal brace construct is fixed proximally using a RetroButton (Arthrex) and fixed distally in the tibial metaphysis using a suture anchor. A disadvantage of this technique is that an extra femoral tunnel needs to be drilled, which is especially important in pediatric patients with the increased risk for growth disturbances.10
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the anteromedial or posterolateral bundle is a type I tear with good or excellent tissue quality, whereas the other bundle is not a type I tear or has poor tissue quality (Figure 3A). In these cases, a primary repair of one bundle is performed with a hamstring reconstruction of the other bundle.
First, a No. 2 FiberWire is used to make 4 to 5 passes from distal to proximal, as previously described. Then, the remnants of the irreparable bundle are debrided (Figure 3B). Subsequently, the semitendinosus tendon is harvested in standard fashion, or soft tissue allografts can be used.
Type II Tears: Augmented Repair
In patients with type II tears, primary repair is not possible as the length of the remnant is too short to firmly approximate the remnant towards the femoral wall (75%-90% of native tissue length) (Figure 4A). In these patients, an augmented repair of the entire ACL is performed using hamstring autograft or soft tissue allograft.
With this technique, repair stitches are passed into the anteromedial bundle of the remnant as previously described (Figure 4B). Keeping the repair stitches anteriorly in the anteromedial bundle tends to prevent entanglement during graft passage later in the case.
Once the repair stitches are in place, a small accessory stab incision is made just above the medial portal. The repair stitches are parked here to keep them out of harms way. Traction on the repair stitches will retract the ACL away from the lateral wall of the notch and allow work to be performed here. A small opening notchplasty is generally performed to enhance visualization and to add a bleeding surface for enhanced healing. Next, the arthroscope is placed into the medial portal, which allows the femoral guide to be placed into the lateral portal. The femoral guide is positioned to optimize the femoral tunnel location in the center of the footprint. A small incision is made laterally over the condyle and through the iliotibial band to allow access to the lateral cortex of the lateral femoral condyle. The FlipCutter is then used to back-cut the femoral socket as described above. A FiberStick (Arthrex) passing suture is then placed in the femoral tunnel and brought out through the anteromedial portal.
Next, the tibial tunnel is drilled with a tibial guide at 55° inclination. The pin is drilled up into the center of the tibial footprint and this is over-reamed with a reamer. The reaming is stopped precisely upon breaking to proximal tibial cortex so as to minimize soft tissue damage of the ACL insertion fibers that are typically pristine. Then, a grasper is passed up and through the tunnel to retrieve the repair stitches and bring them out distally for later use. At the same time, the passing suture in the femoral is also retrieved distally. The soft tissue graft is proximally prepared with a TightRope RT button, and the repair stitches are passed through the button. The passing suture from the femoral socket is then used to shuttle the draw sutures and repair stitches up through the tibia, through the ACL remnant, and out the femoral socket (Figure 4C). The TightRope RT button is then engaged on the lateral femoral cortex in standard fashion. Using the cinch stitches, the graft is delivered through the tibia, up and through the center of the ACL remnant, and into the femoral socket. The knee is then cycled and the graft is tensioned distally in standard fashion, and fixed using a BioComposite interference screw. Finally, the repair stitches can be tensioned pulling the ligament remnant up as a sleeve around the hamstring graft (Figure 4D). They are then tied over the TightRope RT button using alternating half hitches tied with a knot pusher from laterally.
Type III Tears: Reconstruction With Remnant Tensioning
The previously discussed techniques have the goals of preserving as much native ligament remnant as possible, approximating the ligament remnant towards the femoral wall, and promoting healing of the ligament. In some cases, however, the ligament remnant is too short for healing (Figure 5A). Although the ligament cannot be approximated to the femoral wall in these cases, there is still an argument for ACL preservation, as was discussed in the first article of this series.
If the ligament length is between 25% and 75% of the native tissue length, the senior author performs a remnant tensioning technique.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some cases, the distal remnant is small or the tissue quality in the largest part of the remnant is poor, and after debriding back to good tissue quality, only 10% to 25% of the native tissue length is left (Figure 6A). In these cases, the remnant is preserved, however, tensioning of the remnant with sutures is usually not necessary for the prevention of cyclops lesions. Nonetheless, it is important to debride the parts of the remnant ligament with poor tissue quality as mop-end patterns of the remnant may increase the chance of these lesions (Figure 6B).
In this situation, any of the standard ACL reconstruction techniques can be performed with simple attention being paid to preserving what is left of the tibial insertion site. At the very least, the small insertion remnant guides the anatomic placement of the graft, and prevents egress of joint fluid into the tibial tunnel and could minimize tunnel widening.
Type V Tears: Primary Repair
Finally, in some patients a soft tissue avulsion (Figure 7A) or bony avulsion of the distal attachment of the ACL can be seen. Both injuries are relatively rare, although bony avulsions are frequently seen in children, especially those younger than 12 years old. In these cases, the same techniques and theory that are applied to proximal avulsion type tears can be used and applied to distal avulsion type tears.
First, No. 2 FiberWire sutures are passed from proximal towards the distal end of the ligament in the anteromedial bundle, and the same process is then repeated for No. 2 TigerWire sutures for the posterolateral bundle. Then both sutures are exited at the distal avulsed end at the locations of the anteromedial and posterolateral footprints (Figure 7B). A 2.4-mm ACL guide wire and a Ninitol wire are used to drill 2 tunnels from the tibia towards the tibial footprint. The repair sutures are then retrieved through both tunnels (Figure 7C) and the sutures are tied distally over a ligament button after cycling of the knee (Figure 7D). This technique is very useful for soft tissue avulsions, or when there are only small flecks of bone or when the avulsed bone is significantly comminuted. If a large bony avulsion fragment is present, this technique can also be applied with some modification, although there have been multiple other techniques described in the literature that work well in this situation including fixation with screw and washer, or with suture anchors.
Complex Tear or Poor Tissue Quality: Reconstruction
In some cases, the tissue quality is poor, or the ligament has complex or multiple tears. Essentially, in these cases, there is nothing to preserve and a standard reconstruction approach is performed in these cases.
Conclusion
The uniform gold standard for all ACL tear types is currently primary reconstruction. However, several disadvantages of ACL reconstruction exist, while there are multiple advantages to the concept of ACL preservation. In this surgical technique article, we have discussed our tear type classification and the recommended surgical techniques for each. With this treatment algorithm, which is based on tear location and tissue quality, an optimal and minimally invasive treatment can be chosen for each individual patient. Future studies are needed to compare and contrast these treatments with the current gold standard of ACL reconstruction.
Am J Orthop. 2016;45(7):E406-E414. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
In the first part of this series, “Preservation of the Anterior Cruciate Ligament: A Treatment Algorithm Based on Tear Location and Tissue Quality” we discussed the history of anterior cruciate ligament (ACL) preservation, and the historical outcomes of both open primary repair and augmented repair. We also presented our surgical treatment algorithm for ACL preservation, which is based on the tear location and tissue quality of the ligament remnant. In this article, we propose a modification of the Sherman classification1 to identify the different tear types, and we will discuss the different surgical techniques that can be used for each one. Furthermore, we aim to provide an overview of the variations of these techniques that are seen in the literature. It is important to emphasize that these tear types and corresponding surgical techniques are to be seen as guidelines, rather than strict criteria, and that significant overlap between these tear types and surgical indications exist.
Assessment of Tear Type and Tissue Quality
The first assessment of the tear location and tissue quality is made using magnetic resonance imaging (MRI). Although MRI can give you an idea of where the tear is located, the final assessment for eligibility of each specific preservation technique is made during arthroscopy. Therefore, the routine preoperative discussion and informed consent process with the patient should encompass the gamut of surgical possibilities ranging from repair to reconstruction.
The Table shows our tear type classification, along with the corresponding preservation surgical techniques.
Surgical Preparation
In the operating room, the patient is placed in supine position on a standard operative table, such that the knee can be moved freely through its range of motion (ROM). The operative leg is then prepped and draped in standard fashion for knee arthroscopy. Standard knee arthroscopy equipment and implants are used, although some instruments from the standard shoulder set are also utilized. Anteromedial and anterolateral portals are created, and a general inspection of the knee is performed. By pulling the remnant ligament proximally using a broad tissue gasper, the available length of the remnant can be assessed. It is important to reduce possible anterior tibial subluxation in the sagittal plane in order to prevent “false” shortening of the distal ligament remnant. Once the length of the remnant tissue is assessed and the tissue quality is determined, the surgical preservation technique can be chosen (Table).
Type I Tears: Primary Repair
In order to be a candidate for arthroscopic primary repair, sufficient tissue length and tissue quality are necessary (Figures 1A and 1B, Table).
Sutures are then passed through the anteromedial bundle using the Scorpion Suture Passer (Arthrex) with a No. 2 FiberWire suture (Arthrex) (Figure 1C). Suturing is commenced at the intact distal end of the anteromedial bundle and is advanced in an alternating, interlocking Bunnell-type pattern towards the avulsed proximal end with approximately 4 mm to 5 mm between each pass. In general, 3 to 4 passes can be made before the final pass exits via the avulsed end of the ligament towards the femur (Figure 1D). The same process is then repeated for the posterolateral bundle of the ACL remnant with a No. 2 TigerWire suture (Arthrex) to optimize suture management. With each subsequent pass of the sutures, it is important to assess tissue resistance to prevent perforation of a previous stitch. Mild resistance is normal, but the suture-passing device should be repositioned when notably increased resistance is encountered. In addition, placing all of the bites in the same plane should be avoided since this can allow the sutures to “cheese cut” along the collagen fibers of the ligament remnant rather than holding firm.
After passing the sutures through both bundles, the sutures are guided outside the knee using an accessory stab incision situated just above the medial portal. Using this portal, the ligament can be retracted away from the femoral footprint for optimal visibility. The femoral footprint is then roughed using a shaver or burr, and bleeding is induced to stimulate a local healing response,2 while the sutures and the ACL are protected via the portal. With the knee in flexion, an accessory inferomedial portal is then created under direct visualization using a spinal needle for localization. Care should be taken to enable the appropriate trajectory for anchor placement to be achieved.
Many different techniques can be used to provide fixation of the ACL repair to the femoral footprint; the 2 most straightforward techniques are presented here. The first technique provides fixation with knotless suture anchors,3,4 whereas in the second technique the sutures are transosseously passed, and tied over a bone bridge, as was performed in the 1970s and 1980s.
Suture Anchor Fixation
With the suture anchor fixation technique, the knee is flexed in 90°, the anteromedial bundle origin within the femoral footprint is identified, and a 4.5-mm x 20-mm hole is drilled, punched, or tapped, in the case of high bone density. The FiberWire sutures are then retrieved through the accessory portal and passed through a 4.75-mm Vented BioComposite SwiveLock suture anchor (Arthrex). The suture anchor for the anteromedial bundle is then deployed into the hole within the anteromedial footprint, while tensioning the ACL remnant to the wall with a visual gap of <1 mm (Figure 1E).5 The procedure is then repeated using another suture anchor with TigerWire sutures for the posterolateral bundle with the knee flexed at 110° to 115°. This ensures an optimal angle of approach and avoids perforating the posterior condyle with the anchor. The drill hole and anchor are placed into the origin of the posterolateral bundle within the femoral footprint. The order of bundle tensioning and repair may be varied depending on the particulars of each case.
Once the anchors are fully deployed and flush with the femoral footprint, the handle is removed and the additional core stitches are unloaded. Occasionally, the core stitches can be passed from lateral to medial through the proximal ligament remnant and tied down with an arthroscopic knot pusher to add extra compression of the remnant to the origin. The free ends of the repair sutures are cut with an Open Ended Suture Cutter (Arthrex) so that they are flush with the notch. The repair is now complete (Figure 1F). Using a probe, the ACL remnant is tested for tension and stiffness. Finally, cycling of the knee through the full ROM confirms anatomic positioning without impingement of the graft. Manual laxity testing should reveal minimal anteroposterior translation with a firm endpoint on Lachman examination intraoperatively.
Bone Bridge Fixation
With this technique, parallel drill holes are created exiting at each bundle origin. The repair stitches can then be retrieved and tensioned proximally. One way to accomplish this is by using an ACL femoral guide (Arthrex) that is placed via the anterolateral portal and is centered on the anteromedial bundle insertion. This device guides a cannulated RetroDrill (Arthrex) to drill through the lateral femoral condyle towards the anteromedial footprint. A passing wire can then be delivered through the cannulation and used to retrieve that anteromedial bundle repair stitches. This process can then be repeated for the posterolateral bundle and the associated repair stitches. Drill holes can also be made retrograde from a low anteromedial accessory portal using a slotted pit that can be used to shuttle the repair stitches. When all the repair sutures are passed, the ligament is tensioned while being visualized arthroscopically. The knee is held at 20° of flexion and a posterior drawer force can be applied, if necessary, to reduce the tibia to its anatomic position. The suture limbs are then tensioned and can be fixated using any of a multitude of techniques, including tying over a bony bridge, tying over a 4-hole ligament button, and tying to a post.
One disadvantage of the bone bridge fixation technique, however, is the suspensory fixation that is not as stiff as tensioning and fixating with suture anchors. Despite this disadvantage, however, the senior author (GSD) has achieved excellent results with this technique at longer-term follow-up in a small group of patients. One advantage of the bone bridge fixation technique is that the procedure has lower costs than fixation with suture anchors.
One Anchor Repair Fixation
Achtnich and colleagues6 recently published a slightly different technique for repairing type I tears. The authors passed a No. 2 FiberWire suture through the midsubstance of both bundles of the ACL remnant to create a modified Mason-Allen stitch configuration. Subsequently, they tensioned the remnant towards the middle of the ACL footprint (between the anteromedial and posterolateral footprint) using one PushLock suture anchor (Arthrex). They hypothesized that using 1 anchor would be enough fixation for tears amenable to repair, and that doing so would minimize the invasion of the bone.
The preference of the senior author (GSD) is, however, to use 2 suture anchors for each bundle in order to more anatomically and biomechanically repair the remnant, since both bundles have different biomechanical characteristics.7 Similarly, the preference of the senior author is to commence the suturing as distal as possible and pass multiple sutures towards the proximal end. This ensures that the last suture pass is exited very proximally, and ensures that the proximal end is approximated towards the femoral wall. One suture passed at the midsubstance portion of the remnant might cause a different tension pattern and prevent optimal re-approximation of the most proximal part towards the femoral wall. Future studies are necessary to assess the efficacy of different suture and fixation techniques as these are currently lacking.
Addition of Internal Brace
Over the last few years, the senior author has added an internal brace (FiberTape, Arthrex) to the repair technique, which was first performed by MacKay and colleagues.8 The added internal brace protects the repair and the healing process in the first few weeks and enables early ROM.
With this technique, the previously described arthroscopic primary repair technique is performed with suturing of both bundles. However, after punching, tapping, or drilling a hole in the anteromedial origin of the femoral footprint, the anteromedial anchor is first loaded with the FiberTape in addition to the repair stitches. After placing the anteromedial suture anchor in the femoral footprint, the internal brace is fixated proximally with the suture anchor into the femoral wall.
Others, however, have advocated fixing the internal brace independently of the repaired ligament and suture anchors.9 With this technique, tunnels are drilled in the femur and tibia and the internal brace construct is fixed proximally using a RetroButton (Arthrex) and fixed distally in the tibial metaphysis using a suture anchor. A disadvantage of this technique is that an extra femoral tunnel needs to be drilled, which is especially important in pediatric patients with the increased risk for growth disturbances.10
One Bundle Type I Tears: Single Bundle Augmented Repair
In some cases, the anteromedial or posterolateral bundle is a type I tear with good or excellent tissue quality, whereas the other bundle is not a type I tear or has poor tissue quality (Figure 3A). In these cases, a primary repair of one bundle is performed with a hamstring reconstruction of the other bundle.
First, a No. 2 FiberWire is used to make 4 to 5 passes from distal to proximal, as previously described. Then, the remnants of the irreparable bundle are debrided (Figure 3B). Subsequently, the semitendinosus tendon is harvested in standard fashion, or soft tissue allografts can be used.
Type II Tears: Augmented Repair
In patients with type II tears, primary repair is not possible as the length of the remnant is too short to firmly approximate the remnant towards the femoral wall (75%-90% of native tissue length) (Figure 4A). In these patients, an augmented repair of the entire ACL is performed using hamstring autograft or soft tissue allograft.
With this technique, repair stitches are passed into the anteromedial bundle of the remnant as previously described (Figure 4B). Keeping the repair stitches anteriorly in the anteromedial bundle tends to prevent entanglement during graft passage later in the case.
Once the repair stitches are in place, a small accessory stab incision is made just above the medial portal. The repair stitches are parked here to keep them out of harms way. Traction on the repair stitches will retract the ACL away from the lateral wall of the notch and allow work to be performed here. A small opening notchplasty is generally performed to enhance visualization and to add a bleeding surface for enhanced healing. Next, the arthroscope is placed into the medial portal, which allows the femoral guide to be placed into the lateral portal. The femoral guide is positioned to optimize the femoral tunnel location in the center of the footprint. A small incision is made laterally over the condyle and through the iliotibial band to allow access to the lateral cortex of the lateral femoral condyle. The FlipCutter is then used to back-cut the femoral socket as described above. A FiberStick (Arthrex) passing suture is then placed in the femoral tunnel and brought out through the anteromedial portal.
Next, the tibial tunnel is drilled with a tibial guide at 55° inclination. The pin is drilled up into the center of the tibial footprint and this is over-reamed with a reamer. The reaming is stopped precisely upon breaking to proximal tibial cortex so as to minimize soft tissue damage of the ACL insertion fibers that are typically pristine. Then, a grasper is passed up and through the tunnel to retrieve the repair stitches and bring them out distally for later use. At the same time, the passing suture in the femoral is also retrieved distally. The soft tissue graft is proximally prepared with a TightRope RT button, and the repair stitches are passed through the button. The passing suture from the femoral socket is then used to shuttle the draw sutures and repair stitches up through the tibia, through the ACL remnant, and out the femoral socket (Figure 4C). The TightRope RT button is then engaged on the lateral femoral cortex in standard fashion. Using the cinch stitches, the graft is delivered through the tibia, up and through the center of the ACL remnant, and into the femoral socket. The knee is then cycled and the graft is tensioned distally in standard fashion, and fixed using a BioComposite interference screw. Finally, the repair stitches can be tensioned pulling the ligament remnant up as a sleeve around the hamstring graft (Figure 4D). They are then tied over the TightRope RT button using alternating half hitches tied with a knot pusher from laterally.
Type III Tears: Reconstruction With Remnant Tensioning
The previously discussed techniques have the goals of preserving as much native ligament remnant as possible, approximating the ligament remnant towards the femoral wall, and promoting healing of the ligament. In some cases, however, the ligament remnant is too short for healing (Figure 5A). Although the ligament cannot be approximated to the femoral wall in these cases, there is still an argument for ACL preservation, as was discussed in the first article of this series.
If the ligament length is between 25% and 75% of the native tissue length, the senior author performs a remnant tensioning technique.
Type IV Tears: Reconstruction With Remnant Preservation
Finally, in some cases, the distal remnant is small or the tissue quality in the largest part of the remnant is poor, and after debriding back to good tissue quality, only 10% to 25% of the native tissue length is left (Figure 6A). In these cases, the remnant is preserved, however, tensioning of the remnant with sutures is usually not necessary for the prevention of cyclops lesions. Nonetheless, it is important to debride the parts of the remnant ligament with poor tissue quality as mop-end patterns of the remnant may increase the chance of these lesions (Figure 6B).
In this situation, any of the standard ACL reconstruction techniques can be performed with simple attention being paid to preserving what is left of the tibial insertion site. At the very least, the small insertion remnant guides the anatomic placement of the graft, and prevents egress of joint fluid into the tibial tunnel and could minimize tunnel widening.
Type V Tears: Primary Repair
Finally, in some patients a soft tissue avulsion (Figure 7A) or bony avulsion of the distal attachment of the ACL can be seen. Both injuries are relatively rare, although bony avulsions are frequently seen in children, especially those younger than 12 years old. In these cases, the same techniques and theory that are applied to proximal avulsion type tears can be used and applied to distal avulsion type tears.
First, No. 2 FiberWire sutures are passed from proximal towards the distal end of the ligament in the anteromedial bundle, and the same process is then repeated for No. 2 TigerWire sutures for the posterolateral bundle. Then both sutures are exited at the distal avulsed end at the locations of the anteromedial and posterolateral footprints (Figure 7B). A 2.4-mm ACL guide wire and a Ninitol wire are used to drill 2 tunnels from the tibia towards the tibial footprint. The repair sutures are then retrieved through both tunnels (Figure 7C) and the sutures are tied distally over a ligament button after cycling of the knee (Figure 7D). This technique is very useful for soft tissue avulsions, or when there are only small flecks of bone or when the avulsed bone is significantly comminuted. If a large bony avulsion fragment is present, this technique can also be applied with some modification, although there have been multiple other techniques described in the literature that work well in this situation including fixation with screw and washer, or with suture anchors.
Complex Tear or Poor Tissue Quality: Reconstruction
In some cases, the tissue quality is poor, or the ligament has complex or multiple tears. Essentially, in these cases, there is nothing to preserve and a standard reconstruction approach is performed in these cases.
Conclusion
The uniform gold standard for all ACL tear types is currently primary reconstruction. However, several disadvantages of ACL reconstruction exist, while there are multiple advantages to the concept of ACL preservation. In this surgical technique article, we have discussed our tear type classification and the recommended surgical techniques for each. With this treatment algorithm, which is based on tear location and tissue quality, an optimal and minimally invasive treatment can be chosen for each individual patient. Future studies are needed to compare and contrast these treatments with the current gold standard of ACL reconstruction.
Am J Orthop. 2016;45(7):E406-E414. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
2. Steadman JR, Matheny LM, Briggs KK, Rodkey WG, Carreira DS. Outcomes following healing response in older, active patients: a primary anterior cruciate ligament repair technique. J Knee Surg. 2012;25(3):255-260.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
5. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
6. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016. [Epub ahead of print]
7. Amis AA. The functions of the fibre bundles of the anterior cruciate ligament in anterior drawer, rotational laxity and the pivot shift. Knee Surg Sports Traumatol Arthrosc. 2012;20(4):613-620.
8. MacKay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
9. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
10. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
11. Crain EH, Fithian DC, Paxton EW, Luetzow WF. Variation in anterior cruciate ligament scar pattern: does the scar pattern affect anterior laxity in anterior cruciate ligament-deficient knees? Arthroscopy. 2005;21(1):19-24.
1. Sherman MF, Lieber L, Bonamo JR, Podesta L, Reiter I. The long-term followup of primary anterior cruciate ligament repair. Defining a rationale for augmentation. Am J Sports Med. 1991;19(3):243-255.
2. Steadman JR, Matheny LM, Briggs KK, Rodkey WG, Carreira DS. Outcomes following healing response in older, active patients: a primary anterior cruciate ligament repair technique. J Knee Surg. 2012;25(3):255-260.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. DiFelice GS, van der List JP. Arthroscopic primary repair of proximal anterior cruciate ligament tears. Arthrosc Tech. 2016. In press.
5. van der List JP, DiFelice GS. Gap formation following primary anterior cruciate ligament repair: a biomechanical study. Knee. 2016. In press.
6. Achtnich A, Herbst E, Forkel P, et al. Acute proximal anterior cruciate ligament tears: outcomes after arthroscopic suture anchor repair versus anatomic single-bundle reconstruction. Arthroscopy. 2016. [Epub ahead of print]
7. Amis AA. The functions of the fibre bundles of the anterior cruciate ligament in anterior drawer, rotational laxity and the pivot shift. Knee Surg Sports Traumatol Arthrosc. 2012;20(4):613-620.
8. MacKay GM, Blyth MJ, Anthony I, Hopper GP, Ribbans WJ. A review of ligament augmentation with the InternalBrace™: the surgical principle is described for the lateral ankle ligament and ACL repair in particular, and a comprehensive review of other surgical applications and techniques is presented. Surg Technol Int. 2015;26:239-255.
9. Smith JO, Yasen SK, Palmer HC, Lord BR, Britton EM, Wilson AJ. Paediatric ACL repair reinforced with temporary internal bracing. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1845-1851.
10. Frosch KH, Stengel D, Brodhun T, et al. Outcomes and risks of operative treatment of rupture of the anterior cruciate ligament in children and adolescents. Arthroscopy. 2010;26(11):1539-1550.
11. Crain EH, Fithian DC, Paxton EW, Luetzow WF. Variation in anterior cruciate ligament scar pattern: does the scar pattern affect anterior laxity in anterior cruciate ligament-deficient knees? Arthroscopy. 2005;21(1):19-24.
Why Do Lateral Unicompartmental Knee Arthroplasties Fail Today?
In 1975, Skolnick and colleagues1 introduced unicompartmental knee arthroplasty (UKA) for patients with isolated unicompartmental osteoarthritis (OA). They reported a study of 14 UKA procedures, of which 12 were at the medial and 2 at the lateral side. Forty years since this procedure was introduced, UKA is used in 8% to 12% of all knee arthroplasties.2-6 A minority of these procedures are performed at the lateral side (5%-10%).6-8
The considerable anatomical and kinematical differences between compartments9-14 make it impossible to directly compare outcomes of medial and lateral UKA. For example, a greater degree of femoral roll and more posterior translation at the lateral side in flexion9,10,13 can contribute to different pattern and volume differences of cartilage wear.15 Because of these differences, and because of implant design factors and lower surgical volume, lateral UKA is considered a technically more challenging surgery compared to medial UKA.12,16,17
Since isolated lateral compartment OA is relatively scarce, current literature on lateral UKA is limited, and most studies combine medial and lateral outcomes to report UKA outcomes and failure modes.3,4,18-20 However, as the UKA has grown in popularity over the last decade,2,21-25 the number of reports about the lateral UKA also has increased. Recent studies reported excellent short-term survivorship results of the lateral UKA (96%-99%)26,27 and smaller lateral UKA studies reported the 10-year survivorship with varying outcomes from good (84%)14,28-30 to excellent (94%-100%).8,31,32 Indeed, a recent systematic review showed survivorship of lateral UKA at 5, 10, and 15 years of 93%, 91%, and 89%, respectively.33Because of the differences between the medial and lateral compartment, it is important to know the failure modes of lateral UKA in order to improve clinical outcomes and revision rates. We performed a systematic review of cohort studies and registry-based studies that reported lateral UKA failure to assess the causes of lateral UKA failure. In addition, we compared the failure modes in cohort studies with those found in registry-based studies.
Patients and Methods
Search Strategy and Criteria
Databases of PubMed, Embase, and Cochrane (Cochrane Central Register of Clinical Trials) were searched with the terms “knee, arthroplasty, replacement,” “unicompartmental,” “unicondylar,” “partial,” “UKA,” “UKR,” “UCA,” “UCR,” “PKA,” “PKR,” “PCA,” “prosthesis failure,” “reoperation,” “survivorship,” and “treatment failure.” After removal of duplicates, 2 authors (JPvdL and HAZ) scanned the articles for their title and abstract to assess eligibility for the study.
Inclusion criteria were: (I) English language articles describing studies in humans published in the last 25 years, (II) retrospective and prospective studies, (III) featured lateral UKA, (IV) OA was indication for surgery, and (V) included failure modes data. The exclusion criteria were studies that featured: (I) only a specific group of failure (eg, bearing dislocations only), (II) previous surgery in ipsilateral knee (high tibial osteotomy, medial UKA), (III) acute concurrent knee diagnoses (acute anterior cruciate ligament rupture, acute meniscal tear), (IV) combined reporting of medial and lateral UKA, or (V) multiple studies with the same patient database.
Data Collection
All studies that reported modes of failure were used in this study and these failure modes were noted in a datasheet in Microsoft Excel 2011 (Microsoft).
Statistical Analysis
For this systematic review, statistical analysis was performed with IBM SPSS Statistics 22 (SPSS Inc.). We performed chi square tests and Fisher’s exact tests to assess a difference between cohort studies and registry-based studies with the null hypothesis of no difference between both groups. A difference was considered significant when P < .05.
Results
Through the search of the databases, 1294 studies were identified and 26 handpicked studies were added. Initially, based on the title and abstract, 184 of these studies were found eligible.
A total of 366 lateral UKA failures were included. The most common failure modes were progression of OA (29%), aseptic loosening (23%), and bearing dislocation (10%). Infection (6%), instability (6%), unexplained pain (6%), and fractures (4%) were less common causes of failure of lateral UKA (Table 2).
One hundred fifty-five of these failures were reported in the cohort studies. The most common modes of failure were OA progression (36%), bearing dislocation (17%) and aseptic loosening (16%). Less common were infection (10%), fractures (5%), pain (5%), and other causes (6%). In registry-based studies, with 211 lateral UKA failures, the most common modes of failure were aseptic loosening (28%), OA progression (24%), other causes (12%), instability (10%), pain (7%), bearing dislocation (5%), and polyethylene wear (4%) (Table 2).
When pooling cohort and registry-based studies, progression of OA was significantly more common than aseptic loosening (29% vs 23%, respectively; P < .01). It was also significantly more common in the cohort studies (36% vs 16%, respectively; P < .01) but no significant difference was found between progression of OA and aseptic loosening in registry-based studies (24% and 28%, respectively; P = .16) (Table 2).
When comparing cohort with registry-based studies, progression of OA was higher in cohort studies (36% vs. 24%; P < .01). Other failures modes that were more common in cohort studies compared with registry-based studies were bearing dislocation (17% vs 5%, respectively; P < .01) and infections (10% vs 3%, P < .01). Failure modes that were more common in registry-based studies than cohort studies were aseptic loosening (28% vs 16%, respectively; P < .01), other causes (12% vs 6%, respectively, P = .02), and instability (10% vs 1%, respectively, P < .01) (Table 2).
Discussion
In this systematic review, the most common failure modes in lateral UKA review were OA progression (29%), aseptic loosening (23%), and bearing dislocation (10%). Progression of OA and bearing dislocation were the most common modes of failure in cohort studies (36% and 17%, respectively), while aseptic loosening and OA progression were the most common failure modes in registry-based studies (28% and 24%, respectively).
As mentioned above, there are differences in anatomy and kinematics between the medial and lateral compartment. When the lateral UKA failure modes are compared with studies reporting medial UKA failure modes, differences in failure modes are seen.34 Siddiqui and Ahmad35 performed a systematic review of outcomes after UKA revision and presented a table with the failure modes of included studies. Unfortunately they did not report the ratio of medial and lateral UKA. However, when assuming an average percentage of 90% to 95% of medial UKA,6,7,36 the main failure mode in their review in 17 out of 21 studies was aseptic loosening. Indeed, a recent systematic review on medial UKA failure modes showed that aseptic loosening is the most common cause of failure following this procedure.34 Similarly, a search through registry-based studies6,7 and large cohort studies37-40 that only reported medial UKA failures showed that the majority of these studies7,37-39 also reported aseptic loosening as the main cause of failure in medial UKA. When comparing the results of our systematic review of lateral UKA failures with the results of these studies of medial UKA failures, it seems that OA progression seems to play a more dominant role in failures of lateral UKA, while aseptic loosening seems to be more common in medial UKA.
Differences in anatomy and kinematics of the medial and lateral compartment can explain this. Malalignment of the joint is an important factor in the etiology of OA41,42 and biomechanical studies showed that this malalignment can cause decreased viability and further degenerative changes of cartilage of the knee.43 Hernigou and Deschamps44 showed that the alignment of the knee after medial UKA is an important factor in postoperative joint changes. They found that overcorrection of varus deformity during medial UKA surgery, measured by the hip-knee-ankle (HKA) angle, was associated with increased OA at the lateral condyle and less tibial wear of the medial UKA. Undercorrection of the varus caused an increase in tibial wear of polyethylene. Chatellard and colleagues45 found the same results in the correction of varus, measured by HKA. In addition, they found that when the prosthetic (medial) joint space was smaller than healthy (lateral) joint space, this was correlated with lower prosthesis survival. A smaller joint space at the healthy side was correlated with OA progression at the lateral compartment and tibial component wear.
These studies explain the mechanism of progression of OA and aseptic loosening. Harrington46 assessed the load in patients with valgus and varus deformity. Patients with a valgus deformity have high mechanical load on the lateral condyle during the static phase, but during the dynamic phase, a major part of this load shifts to the medial condyle. In the patients with varus deformity, the mechanical load was noted on the medial condyle during both the static and dynamic phase. Ohdera and colleagues47 advised, based on this biomechanical study and their own experiences, to correct the knee during lateral UKA to a slight valgus angle (5°-7°) to prevent OA progression at the medial side. van der List and colleagues48 similarly showed that undercorrection of 3° to 7° was correlated with better functional outcomes when compared to more neutral alignment. Moreover, Khamaisy and colleagues49 recently showed that overcorrection during UKA surgery is more common in lateral than medial UKA.
These studies are important to understanding why OA progression is more common as a failure mode in lateral UKA. The shift of mechanical load from the lateral to medial epicondyle during the dynamic phase also could explain why aseptic loosening is less common in lateral UKA. As Hernigou and Deschamps44 and Chatellard and colleagues45 stated, undercorrection of varus deformity in medial UKA is associated with higher mechanical load on the medial prosthesis side and smaller joint space width. These factors are correlated with mechanical failure of medial UKA. We think this process can be applied to lateral UKA, with the addition that the mechanical load is higher on the healthy medial compartment during the dynamic phase. This causes more forces on the healthy (medial) side in lateral UKA, and in medial UKA more forces on the prosthesis (medial) side, which results in more OA progression in lateral UKA and more aseptic loosening in medial UKA. This finding is consistent with the results of our review of more OA progression and less aseptic loosening in lateral UKA. This study also suggests that medial and lateral UKA should not be reported together in studies that present survivorship, failure modes, or clinical outcomes.
A large discrepancy was seen in bearing dislocation between cohort studies (17%) and registry-based studies (5%). When we take a closer look to the bearing dislocation failures in the cohort studies, most of the failures were reported in only 2 cohort studies.50,51 In a study by Pandit and colleagues,50 3 different prosthesis designs were used in 3 different time periods. In the first series of lateral UKA (1983-1991), 6 out of 51 (12%) bearings dislocated. In the second series (1998-2004), a modified technique was used and 3 out of 65 (5%) bearings dislocated. In the third series (2004-2008), a modified technique and a domed tibial component was used and only 1 out of 68 bearings dislocated (1%). In a study published in 1996, Gunther and colleagues51 also used surgical techniques and implants that were modified over the course of the study period. Because of these modified techniques, different implant designs, and year of publication, bearing dislocation most likely plays a smaller role than the 17% reported in the cohort studies. This discrepancy is a good example of the important role for the registries and registry-based studies in reporting failure modes and survivorship, especially in lateral UKA due to the low surgical frequency. Pabinger and colleagues52 recently performed a systematic review of cohort studies and registry-based studies in which they stated that the reliability in non-registry-based studies should be questioned and they considered registry-based studies superior in reporting UKA outcomes and revision rates. Furthermore, given the differences in anatomic and kinematic differences between the medial and lateral compartment and different failure modes between medial and lateral UKA, it would be better if future studies presented the medial and lateral failures separately. As stated above, most large cohort studies and especially annual registries currently do not report modes of failure of medial and lateral UKA separately.3,4,18-20
There are limitations in this study. First, this systematic review is not a full meta-analysis but a pooled analysis of collected study series and retrospective studies. Therefore, we cannot exclude sampling bias, confounders, and selection bias from the literature. We included all studies reporting failure modes of lateral UKA and excluded all case reports. We made a conscious choice about including all lateral UKA failures because this is the first systematic review of lateral UKA failure modes. Another limitation is that the follow-up period of the studies differed (Table 1) and we did not correct for the follow-up period. As stated in the example of bearing dislocations, some of these studies reported old or different techniques, while other, more recently published studies used more modified techniques11,29,53-56 Unfortunately, most studies did not report the time of arthroplasty survival and therefore we could not correct for the follow-up period.
In conclusion, progression of OA is the most common failure mode in lateral UKA, followed by aseptic loosening. Anatomic and kinematic factors such as alignment, mechanical forces during dynamic phase, and correction of valgus seem to play important roles in failure modes of lateral UKA. In the future, failure modes of medial and lateral UKA should be reported separately.
Am J Orthop. 2016;45(7):432-438, 462. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Skolnick MD, Bryan RS, Peterson LFA. Unicompartmental polycentric knee arthroplasty. Description and preliminary results. Clin Orthop Relat Res. 1975;(112):208-214.
2. Riddle DL, Jiranek WA, McGlynn FJ. Yearly Incidence of Unicompartmental Knee Arthroplasty in the United States. J Arthroplasty. 2008;23(3):408-412.
3. Australian Orthopaedic Association. Hip and Knee Arthroplasty 2014 Annual Report. https://aoanjrr.sahmri.com/documents/10180/172286/Annual%20Report%202014. Accessed June 3, 2015.
4. Swedish Knee Arthroplasty Register. 2013 Annual Report.http://myknee.se/pdf/SKAR2013_Eng.pdf. Accessed June 3, 2015.
5. The New Zealand Joint Registry. Fourteen Year Report. January 1999 to December 2012. 2013. http://nzoa.org.nz/system/files/NJR 14 Year Report.pdf. Accessed June 3, 2015.
6. Baker PN, Jameson SS, Deehan DJ, Gregg PJ, Porter M, Tucker K. Mid-term equivalent survival of medial and lateral unicondylar knee replacement: an analysis of data from a National Joint Registry. J Bone Joint Surg Br. 2012;94(12):1641-1648.
7. Lewold S, Robertsson O, Knutson K, Lidgren L. Revision of unicompartmental knee arthroplasty: outcome in 1,135 cases from the Swedish Knee Arthroplasty study. Acta Orthop Scand. 1998;69(5):469-474.
8. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
9. Hill PF, Vedi V, Williams A, Iwaki H, 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.
10. 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.
11. Ashraf T, Newman JH, Evans RL, Ackroyd CE. Lateral unicompartmental knee replacement survivorship and clinical experience over 21 years. J Bone Joint Surg Br. 2002;84(8):1126-1130.
12. Scott RD. Lateral unicompartmental replacement: a road less traveled. Orthopedics. 2005;28(9):983-984.
13. Sah AP, Scott RD. Lateral unicompartmental knee arthroplasty through a medial approach. Study with an average five-year follow-up. J Bone Joint Surg Am. 2007;89(9):1948-1954.
14. Argenson JN, Parratte S, Bertani A, Flecher X, Aubaniac JM. Long-term results with a lateral unicondylar replacement. Clin Orthop Relat Res. 2008;466(11):2686-2693.
15. Weidow J, Pak J, Karrholm J. Different patterns of cartilage wear in medial and lateral gonarthrosis. Acta Orthop Scand. 2002;73(3):326-329.
16. Ollivier M, Abdel MP, Parratte S, Argenson JN. Lateral unicondylar knee arthroplasty (UKA): contemporary indications, surgical technique, and results. Int Orthop. 2014;38(2):449-455.
17. Demange MK, Von Keudell A, Probst C, Yoshioka H, Gomoll AH. Patient-specific implants for lateral unicompartmental knee arthroplasty. Int Orthop. 2015;39(8):1519-1526.
18. Khan Z, Nawaz SZ, Kahane S, Esler C, Chatterji U. Conversion of unicompartmental knee arthroplasty to total knee arthroplasty: the challenges and need for augments. Acta Orthop Belg. 2013;79(6):699-705.
19. Epinette JA, Brunschweiler B, Mertl P, et al. Unicompartmental knee arthroplasty modes of failure: wear is not the main reason for failure: a multicentre study of 418 failed knees. Orthop Traumatol Surg Res. 2012;98(6 Suppl):S124-S130.
20. Bordini B, Stea S, Falcioni S, Ancarani C, Toni A. Unicompartmental knee arthroplasty: 11-year experience from 3929 implants in RIPO register. Knee. 2014;21(6):1275-1279.
21. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
22. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
23. van der List JP, Chawla H, Pearle AD. Robotic-assisted knee arthroplasty: an overview. Am J Orthop. 2016;45(4):202-211.
24. van der List JP, Chawla H, Joskowicz L, Pearle AD. Current state of computer navigation and robotics in unicompartmental and total knee arthroplasty: a systematic review with meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2016 Sep 6. [Epub ahead of print]
25. Zuiderbaan HA, van der List JP, Kleeblad LJ, et al. Modern indications, results and global trends in the use of unicompartmental knee arthroplasty and high tibial osteotomy for the treatment of medial unicondylar knee osteoarthritis. Am J Orthop. 2016;45(6):E355-E361.
26. Smith JR, Robinson JR, Porteous AJ, et al. Fixed bearing lateral unicompartmental knee arthroplasty--short to midterm survivorship and knee scores for 101 prostheses. Knee. 2014;21(4):843-847.
27. Berend KR, Kolczun MC 2nd, George JW Jr, Lombardi AV Jr. Lateral unicompartmental knee arthroplasty through a lateral parapatellar approach has high early survivorship. Clin Orthop Relat Res. 2012;470(1):77-83.
28. Keblish PA, Briard JL. Mobile-bearing unicompartmental knee arthroplasty: a 2-center study with an 11-year (mean) follow-up. J Arthroplasty. 2004;19(7 Suppl 2):87-94.
29. Bertani A, Flecher X, Parratte S, Aubaniac JM, Argenson JN. Unicompartmental-knee arthroplasty for treatment of lateral gonarthrosis: about 30 cases. Midterm results. Rev Chir Orthop Reparatrice Appar Mot. 2008;94(8):763-770.
30. Sebilo A, Casin C, Lebel B, et al. Clinical and technical factors influencing outcomes of unicompartmental knee arthroplasty: Retrospective multicentre study of 944 knees. Orthop Traumatol Surg Res. 2013;99(4 Suppl):S227-S234.
31. Cartier P, Khefacha A, Sanouiller JL, Frederick K. Unicondylar knee arthroplasty in middle-aged patients: A minimum 5-year follow-up. Orthopedics. 2007;30(8 Suppl):62-65.
32. Lustig S, Paillot JL, Servien E, Henry J, Ait Si Selmi T, Neyret P. Cemented all polyethylene tibial insert unicompartimental knee arthroplasty: a long term follow-up study. Orthop Traumatol Surg Res. 2009;95(1):12-21.
33. van der List JP, McDonald LS, Pearle AD. Systematic review of medial versus lateral survivorship in unicompartmental knee arthroplasty. Knee. 2015;22(6):454-460.
34. van der List JP, Zuiderbaan HA, Pearle AD. Why do medial unicompartmental knee arthroplasties fail today? J Arthroplasty. 2016;31(5):1016-1021.
35. Siddiqui NA, Ahmad ZM. Revision of unicondylar to total knee arthroplasty: a systematic review. Open Orthop J. 2012;6:268-275.
36. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
37. Kalra S, Smith TO, Berko B, Walton NP. Assessment of radiolucent lines around the Oxford unicompartmental knee replacement: sensitivity and specificity for loosening. J Bone Joint Surg Br. 2011;93(6):777-781.
38. Wynn Jones H, Chan W, Harrison T, Smith TO, Masonda P, Walton NP. Revision of medial Oxford unicompartmental knee replacement to a total knee replacement: similar to a primary? Knee. 2012;19(4):339-343.
39. Sierra RJ, Kassel CA, Wetters NG, Berend KR, Della Valle CJ, Lombardi AV. Revision of unicompartmental arthroplasty to total knee arthroplasty: not always a slam dunk! J Arthroplasty. 2013;28(8 Suppl):128-132.
40. Citak M, Dersch K, Kamath AF, Haasper C, Gehrke T, Kendoff D. Common causes of failed unicompartmental knee arthroplasty: a single-centre analysis of four hundred and seventy one cases. Int Orthop. 2014;38(5):961-965.
41. Hunter DJ, Wilson DR. Role of alignment and biomechanics in osteoarthritis and implications for imaging. Radiol Clin North Am. 2009;47(4):553-566.
42. Hunter DJ, Sharma L, Skaife T. Alignment and osteoarthritis of the knee. J Bone Joint Surg Am. 2009;91 Suppl 1:85-89.
43. Roemhildt ML, Beynnon BD, Gauthier AE, Gardner-Morse M, Ertem F, Badger GJ. Chronic in vivo load alteration induces degenerative changes in the rat tibiofemoral joint. Osteoarthritis Cartilage. 2013;21(2):346-357.
44. Hernigou P, Deschamps G. Alignment influences wear in the knee after medial unicompartmental arthroplasty. Clin Orthop Relat Res. 2004;(423):161-165.
45. Chatellard R, Sauleau V, Colmar M, et al. Medial unicompartmental knee arthroplasty: does tibial component position influence clinical outcomes and arthroplasty survival? Orthop Traumatol Surg Res. 2013;99(4 Suppl):S219-S225.
46. Harrington IJ. Static and dynamic loading patterns in knee joints with deformities. J Bone Joint Surg Am. 1983;65(2):247-259.
47. Ohdera T, Tokunaga J, Kobayashi A. Unicompartmental knee arthroplasty for lateral gonarthrosis: midterm results. J Arthroplasty. 2001;16(2):196-200.
48. van der List JP, Chawla H, Villa JC, Zuiderbaan HA, Pearle AD. Early functional outcome after lateral UKA is sensitive to postoperative lower limb alignment. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 26. [Epub ahead of print]
49. Khamaisy S, Gladnick BP, Nam D, Reinhardt KR, Heyse TJ, Pearle AD. Lower limb alignment control: Is it more challenging in lateral compared to medial unicondylar knee arthroplasty? Knee. 2015;22(4):347-350.
50. Pandit H, Jenkins C, Beard DJ, et al. Mobile bearing dislocation in lateral unicompartmental knee replacement. Knee. 2010;17(6):392-397.
51. Gunther TV, Murray DW, Miller R, et al. Lateral unicompartmental arthroplasty with the Oxford meniscal knee. Knee. 1996;3(1):33-39.
52. Pabinger C, Lumenta DB, Cupak D, Berghold A, Boehler N, Labek G. Quality of outcome data in knee arthroplasty: Comparison of registry data and worldwide non-registry studies from 4 decades. Acta Orthopaedica. 2015;86(1):58-62.
53. Lustig S, Elguindy A, Servien E, et al. 5- to 16-year follow-up of 54 consecutive lateral unicondylar knee arthroplasties with a fixed-all polyethylene bearing. J Arthroplasty. 2011;26(8):1318-1325.
54. Walton MJ, Weale AE, Newman JH. The progression of arthritis following lateral unicompartmental knee replacement. Knee. 2006;13(5):374-377.
55. Lustig S, Lording T, Frank F, Debette C, Servien E, Neyret P. Progression of medial osteoarthritis and long term results of lateral unicompartmental arthroplasty: 10 to 18 year follow-up of 54 consecutive implants. Knee. 2014;21(S1):S26-S32.
56. O’Rourke MR, Gardner JJ, Callaghan JJ, et al. Unicompartmental knee replacement: a minimum twenty-one-year followup, end-result study. Clin Orthop Relat Res. 2005;440:27-37.
57. Citak M, Cross MB, Gehrke T, Dersch K, Kendoff D. Modes of failure and revision of failed lateral unicompartmental knee arthroplasties. Knee. 2015;22(4):338-340.
58. Liebs TR, Herzberg W. Better quality of life after medial versus lateral unicondylar knee arthroplasty knee. Clin Orthop Relat Res. 2013;471(8):2629-2640.
59. Weston-Simons JS, Pandit H, Kendrick BJ, et al. The mid-term outcomes of the Oxford Domed Lateral unicompartmental knee replacement. Bone Joint J. 2014;96-B(1):59-64.
60. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
61. Saxler G, Temmen D, Bontemps G. Medium-term results of the AMC-unicompartmental knee arthroplasty. Knee. 2004;11(5):349-355.
62. Forster MC, Bauze AJ, Keene GCR. Lateral unicompartmental knee replacement: Fixed or mobile bearing? Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1107-1111.
63. Streit MR, Walker T, Bruckner T, et al. Mobile-bearing lateral unicompartmental knee replacement with the Oxford domed tibial component: an independent series. J Bone Joint Surg Br. 2012;94(10):1356-1361.
64. Altuntas AO, Alsop H, Cobb JP. Early results of a domed tibia, mobile bearing lateral unicompartmental knee arthroplasty from an independent centre. Knee. 2013;20(6):466-470.
65. Ashraf T, Newman JH, Desai VV, Beard D, Nevelos JE. Polyethylene wear in a non-congruous unicompartmental knee replacement: a retrieval analysis. Knee. 2004;11(3):177-181.
66. Schelfaut S, Beckers L, Verdonk P, Bellemans J, Victor J. The risk of bearing dislocation in lateral unicompartmental knee arthroplasty using a mobile biconcave design. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2487-2494.
67. Marson B, Prasad N, Jenkins R, Lewis M. Lateral unicompartmental knee replacements: Early results from a District General Hospital. Eur J Orthop Surg Traumatol. 2014;24(6):987-991.
68. Walker T, Gotterbarm T, Bruckner T, Merle C, Streit MR. Total versus unicompartmental knee replacement for isolated lateral osteoarthritis: a matched-pairs study. Int Orthop. 2014;38(11):2259-2264.
In 1975, Skolnick and colleagues1 introduced unicompartmental knee arthroplasty (UKA) for patients with isolated unicompartmental osteoarthritis (OA). They reported a study of 14 UKA procedures, of which 12 were at the medial and 2 at the lateral side. Forty years since this procedure was introduced, UKA is used in 8% to 12% of all knee arthroplasties.2-6 A minority of these procedures are performed at the lateral side (5%-10%).6-8
The considerable anatomical and kinematical differences between compartments9-14 make it impossible to directly compare outcomes of medial and lateral UKA. For example, a greater degree of femoral roll and more posterior translation at the lateral side in flexion9,10,13 can contribute to different pattern and volume differences of cartilage wear.15 Because of these differences, and because of implant design factors and lower surgical volume, lateral UKA is considered a technically more challenging surgery compared to medial UKA.12,16,17
Since isolated lateral compartment OA is relatively scarce, current literature on lateral UKA is limited, and most studies combine medial and lateral outcomes to report UKA outcomes and failure modes.3,4,18-20 However, as the UKA has grown in popularity over the last decade,2,21-25 the number of reports about the lateral UKA also has increased. Recent studies reported excellent short-term survivorship results of the lateral UKA (96%-99%)26,27 and smaller lateral UKA studies reported the 10-year survivorship with varying outcomes from good (84%)14,28-30 to excellent (94%-100%).8,31,32 Indeed, a recent systematic review showed survivorship of lateral UKA at 5, 10, and 15 years of 93%, 91%, and 89%, respectively.33Because of the differences between the medial and lateral compartment, it is important to know the failure modes of lateral UKA in order to improve clinical outcomes and revision rates. We performed a systematic review of cohort studies and registry-based studies that reported lateral UKA failure to assess the causes of lateral UKA failure. In addition, we compared the failure modes in cohort studies with those found in registry-based studies.
Patients and Methods
Search Strategy and Criteria
Databases of PubMed, Embase, and Cochrane (Cochrane Central Register of Clinical Trials) were searched with the terms “knee, arthroplasty, replacement,” “unicompartmental,” “unicondylar,” “partial,” “UKA,” “UKR,” “UCA,” “UCR,” “PKA,” “PKR,” “PCA,” “prosthesis failure,” “reoperation,” “survivorship,” and “treatment failure.” After removal of duplicates, 2 authors (JPvdL and HAZ) scanned the articles for their title and abstract to assess eligibility for the study.
Inclusion criteria were: (I) English language articles describing studies in humans published in the last 25 years, (II) retrospective and prospective studies, (III) featured lateral UKA, (IV) OA was indication for surgery, and (V) included failure modes data. The exclusion criteria were studies that featured: (I) only a specific group of failure (eg, bearing dislocations only), (II) previous surgery in ipsilateral knee (high tibial osteotomy, medial UKA), (III) acute concurrent knee diagnoses (acute anterior cruciate ligament rupture, acute meniscal tear), (IV) combined reporting of medial and lateral UKA, or (V) multiple studies with the same patient database.
Data Collection
All studies that reported modes of failure were used in this study and these failure modes were noted in a datasheet in Microsoft Excel 2011 (Microsoft).
Statistical Analysis
For this systematic review, statistical analysis was performed with IBM SPSS Statistics 22 (SPSS Inc.). We performed chi square tests and Fisher’s exact tests to assess a difference between cohort studies and registry-based studies with the null hypothesis of no difference between both groups. A difference was considered significant when P < .05.
Results
Through the search of the databases, 1294 studies were identified and 26 handpicked studies were added. Initially, based on the title and abstract, 184 of these studies were found eligible.
A total of 366 lateral UKA failures were included. The most common failure modes were progression of OA (29%), aseptic loosening (23%), and bearing dislocation (10%). Infection (6%), instability (6%), unexplained pain (6%), and fractures (4%) were less common causes of failure of lateral UKA (Table 2).
One hundred fifty-five of these failures were reported in the cohort studies. The most common modes of failure were OA progression (36%), bearing dislocation (17%) and aseptic loosening (16%). Less common were infection (10%), fractures (5%), pain (5%), and other causes (6%). In registry-based studies, with 211 lateral UKA failures, the most common modes of failure were aseptic loosening (28%), OA progression (24%), other causes (12%), instability (10%), pain (7%), bearing dislocation (5%), and polyethylene wear (4%) (Table 2).
When pooling cohort and registry-based studies, progression of OA was significantly more common than aseptic loosening (29% vs 23%, respectively; P < .01). It was also significantly more common in the cohort studies (36% vs 16%, respectively; P < .01) but no significant difference was found between progression of OA and aseptic loosening in registry-based studies (24% and 28%, respectively; P = .16) (Table 2).
When comparing cohort with registry-based studies, progression of OA was higher in cohort studies (36% vs. 24%; P < .01). Other failures modes that were more common in cohort studies compared with registry-based studies were bearing dislocation (17% vs 5%, respectively; P < .01) and infections (10% vs 3%, P < .01). Failure modes that were more common in registry-based studies than cohort studies were aseptic loosening (28% vs 16%, respectively; P < .01), other causes (12% vs 6%, respectively, P = .02), and instability (10% vs 1%, respectively, P < .01) (Table 2).
Discussion
In this systematic review, the most common failure modes in lateral UKA review were OA progression (29%), aseptic loosening (23%), and bearing dislocation (10%). Progression of OA and bearing dislocation were the most common modes of failure in cohort studies (36% and 17%, respectively), while aseptic loosening and OA progression were the most common failure modes in registry-based studies (28% and 24%, respectively).
As mentioned above, there are differences in anatomy and kinematics between the medial and lateral compartment. When the lateral UKA failure modes are compared with studies reporting medial UKA failure modes, differences in failure modes are seen.34 Siddiqui and Ahmad35 performed a systematic review of outcomes after UKA revision and presented a table with the failure modes of included studies. Unfortunately they did not report the ratio of medial and lateral UKA. However, when assuming an average percentage of 90% to 95% of medial UKA,6,7,36 the main failure mode in their review in 17 out of 21 studies was aseptic loosening. Indeed, a recent systematic review on medial UKA failure modes showed that aseptic loosening is the most common cause of failure following this procedure.34 Similarly, a search through registry-based studies6,7 and large cohort studies37-40 that only reported medial UKA failures showed that the majority of these studies7,37-39 also reported aseptic loosening as the main cause of failure in medial UKA. When comparing the results of our systematic review of lateral UKA failures with the results of these studies of medial UKA failures, it seems that OA progression seems to play a more dominant role in failures of lateral UKA, while aseptic loosening seems to be more common in medial UKA.
Differences in anatomy and kinematics of the medial and lateral compartment can explain this. Malalignment of the joint is an important factor in the etiology of OA41,42 and biomechanical studies showed that this malalignment can cause decreased viability and further degenerative changes of cartilage of the knee.43 Hernigou and Deschamps44 showed that the alignment of the knee after medial UKA is an important factor in postoperative joint changes. They found that overcorrection of varus deformity during medial UKA surgery, measured by the hip-knee-ankle (HKA) angle, was associated with increased OA at the lateral condyle and less tibial wear of the medial UKA. Undercorrection of the varus caused an increase in tibial wear of polyethylene. Chatellard and colleagues45 found the same results in the correction of varus, measured by HKA. In addition, they found that when the prosthetic (medial) joint space was smaller than healthy (lateral) joint space, this was correlated with lower prosthesis survival. A smaller joint space at the healthy side was correlated with OA progression at the lateral compartment and tibial component wear.
These studies explain the mechanism of progression of OA and aseptic loosening. Harrington46 assessed the load in patients with valgus and varus deformity. Patients with a valgus deformity have high mechanical load on the lateral condyle during the static phase, but during the dynamic phase, a major part of this load shifts to the medial condyle. In the patients with varus deformity, the mechanical load was noted on the medial condyle during both the static and dynamic phase. Ohdera and colleagues47 advised, based on this biomechanical study and their own experiences, to correct the knee during lateral UKA to a slight valgus angle (5°-7°) to prevent OA progression at the medial side. van der List and colleagues48 similarly showed that undercorrection of 3° to 7° was correlated with better functional outcomes when compared to more neutral alignment. Moreover, Khamaisy and colleagues49 recently showed that overcorrection during UKA surgery is more common in lateral than medial UKA.
These studies are important to understanding why OA progression is more common as a failure mode in lateral UKA. The shift of mechanical load from the lateral to medial epicondyle during the dynamic phase also could explain why aseptic loosening is less common in lateral UKA. As Hernigou and Deschamps44 and Chatellard and colleagues45 stated, undercorrection of varus deformity in medial UKA is associated with higher mechanical load on the medial prosthesis side and smaller joint space width. These factors are correlated with mechanical failure of medial UKA. We think this process can be applied to lateral UKA, with the addition that the mechanical load is higher on the healthy medial compartment during the dynamic phase. This causes more forces on the healthy (medial) side in lateral UKA, and in medial UKA more forces on the prosthesis (medial) side, which results in more OA progression in lateral UKA and more aseptic loosening in medial UKA. This finding is consistent with the results of our review of more OA progression and less aseptic loosening in lateral UKA. This study also suggests that medial and lateral UKA should not be reported together in studies that present survivorship, failure modes, or clinical outcomes.
A large discrepancy was seen in bearing dislocation between cohort studies (17%) and registry-based studies (5%). When we take a closer look to the bearing dislocation failures in the cohort studies, most of the failures were reported in only 2 cohort studies.50,51 In a study by Pandit and colleagues,50 3 different prosthesis designs were used in 3 different time periods. In the first series of lateral UKA (1983-1991), 6 out of 51 (12%) bearings dislocated. In the second series (1998-2004), a modified technique was used and 3 out of 65 (5%) bearings dislocated. In the third series (2004-2008), a modified technique and a domed tibial component was used and only 1 out of 68 bearings dislocated (1%). In a study published in 1996, Gunther and colleagues51 also used surgical techniques and implants that were modified over the course of the study period. Because of these modified techniques, different implant designs, and year of publication, bearing dislocation most likely plays a smaller role than the 17% reported in the cohort studies. This discrepancy is a good example of the important role for the registries and registry-based studies in reporting failure modes and survivorship, especially in lateral UKA due to the low surgical frequency. Pabinger and colleagues52 recently performed a systematic review of cohort studies and registry-based studies in which they stated that the reliability in non-registry-based studies should be questioned and they considered registry-based studies superior in reporting UKA outcomes and revision rates. Furthermore, given the differences in anatomic and kinematic differences between the medial and lateral compartment and different failure modes between medial and lateral UKA, it would be better if future studies presented the medial and lateral failures separately. As stated above, most large cohort studies and especially annual registries currently do not report modes of failure of medial and lateral UKA separately.3,4,18-20
There are limitations in this study. First, this systematic review is not a full meta-analysis but a pooled analysis of collected study series and retrospective studies. Therefore, we cannot exclude sampling bias, confounders, and selection bias from the literature. We included all studies reporting failure modes of lateral UKA and excluded all case reports. We made a conscious choice about including all lateral UKA failures because this is the first systematic review of lateral UKA failure modes. Another limitation is that the follow-up period of the studies differed (Table 1) and we did not correct for the follow-up period. As stated in the example of bearing dislocations, some of these studies reported old or different techniques, while other, more recently published studies used more modified techniques11,29,53-56 Unfortunately, most studies did not report the time of arthroplasty survival and therefore we could not correct for the follow-up period.
In conclusion, progression of OA is the most common failure mode in lateral UKA, followed by aseptic loosening. Anatomic and kinematic factors such as alignment, mechanical forces during dynamic phase, and correction of valgus seem to play important roles in failure modes of lateral UKA. In the future, failure modes of medial and lateral UKA should be reported separately.
Am J Orthop. 2016;45(7):432-438, 462. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
In 1975, Skolnick and colleagues1 introduced unicompartmental knee arthroplasty (UKA) for patients with isolated unicompartmental osteoarthritis (OA). They reported a study of 14 UKA procedures, of which 12 were at the medial and 2 at the lateral side. Forty years since this procedure was introduced, UKA is used in 8% to 12% of all knee arthroplasties.2-6 A minority of these procedures are performed at the lateral side (5%-10%).6-8
The considerable anatomical and kinematical differences between compartments9-14 make it impossible to directly compare outcomes of medial and lateral UKA. For example, a greater degree of femoral roll and more posterior translation at the lateral side in flexion9,10,13 can contribute to different pattern and volume differences of cartilage wear.15 Because of these differences, and because of implant design factors and lower surgical volume, lateral UKA is considered a technically more challenging surgery compared to medial UKA.12,16,17
Since isolated lateral compartment OA is relatively scarce, current literature on lateral UKA is limited, and most studies combine medial and lateral outcomes to report UKA outcomes and failure modes.3,4,18-20 However, as the UKA has grown in popularity over the last decade,2,21-25 the number of reports about the lateral UKA also has increased. Recent studies reported excellent short-term survivorship results of the lateral UKA (96%-99%)26,27 and smaller lateral UKA studies reported the 10-year survivorship with varying outcomes from good (84%)14,28-30 to excellent (94%-100%).8,31,32 Indeed, a recent systematic review showed survivorship of lateral UKA at 5, 10, and 15 years of 93%, 91%, and 89%, respectively.33Because of the differences between the medial and lateral compartment, it is important to know the failure modes of lateral UKA in order to improve clinical outcomes and revision rates. We performed a systematic review of cohort studies and registry-based studies that reported lateral UKA failure to assess the causes of lateral UKA failure. In addition, we compared the failure modes in cohort studies with those found in registry-based studies.
Patients and Methods
Search Strategy and Criteria
Databases of PubMed, Embase, and Cochrane (Cochrane Central Register of Clinical Trials) were searched with the terms “knee, arthroplasty, replacement,” “unicompartmental,” “unicondylar,” “partial,” “UKA,” “UKR,” “UCA,” “UCR,” “PKA,” “PKR,” “PCA,” “prosthesis failure,” “reoperation,” “survivorship,” and “treatment failure.” After removal of duplicates, 2 authors (JPvdL and HAZ) scanned the articles for their title and abstract to assess eligibility for the study.
Inclusion criteria were: (I) English language articles describing studies in humans published in the last 25 years, (II) retrospective and prospective studies, (III) featured lateral UKA, (IV) OA was indication for surgery, and (V) included failure modes data. The exclusion criteria were studies that featured: (I) only a specific group of failure (eg, bearing dislocations only), (II) previous surgery in ipsilateral knee (high tibial osteotomy, medial UKA), (III) acute concurrent knee diagnoses (acute anterior cruciate ligament rupture, acute meniscal tear), (IV) combined reporting of medial and lateral UKA, or (V) multiple studies with the same patient database.
Data Collection
All studies that reported modes of failure were used in this study and these failure modes were noted in a datasheet in Microsoft Excel 2011 (Microsoft).
Statistical Analysis
For this systematic review, statistical analysis was performed with IBM SPSS Statistics 22 (SPSS Inc.). We performed chi square tests and Fisher’s exact tests to assess a difference between cohort studies and registry-based studies with the null hypothesis of no difference between both groups. A difference was considered significant when P < .05.
Results
Through the search of the databases, 1294 studies were identified and 26 handpicked studies were added. Initially, based on the title and abstract, 184 of these studies were found eligible.
A total of 366 lateral UKA failures were included. The most common failure modes were progression of OA (29%), aseptic loosening (23%), and bearing dislocation (10%). Infection (6%), instability (6%), unexplained pain (6%), and fractures (4%) were less common causes of failure of lateral UKA (Table 2).
One hundred fifty-five of these failures were reported in the cohort studies. The most common modes of failure were OA progression (36%), bearing dislocation (17%) and aseptic loosening (16%). Less common were infection (10%), fractures (5%), pain (5%), and other causes (6%). In registry-based studies, with 211 lateral UKA failures, the most common modes of failure were aseptic loosening (28%), OA progression (24%), other causes (12%), instability (10%), pain (7%), bearing dislocation (5%), and polyethylene wear (4%) (Table 2).
When pooling cohort and registry-based studies, progression of OA was significantly more common than aseptic loosening (29% vs 23%, respectively; P < .01). It was also significantly more common in the cohort studies (36% vs 16%, respectively; P < .01) but no significant difference was found between progression of OA and aseptic loosening in registry-based studies (24% and 28%, respectively; P = .16) (Table 2).
When comparing cohort with registry-based studies, progression of OA was higher in cohort studies (36% vs. 24%; P < .01). Other failures modes that were more common in cohort studies compared with registry-based studies were bearing dislocation (17% vs 5%, respectively; P < .01) and infections (10% vs 3%, P < .01). Failure modes that were more common in registry-based studies than cohort studies were aseptic loosening (28% vs 16%, respectively; P < .01), other causes (12% vs 6%, respectively, P = .02), and instability (10% vs 1%, respectively, P < .01) (Table 2).
Discussion
In this systematic review, the most common failure modes in lateral UKA review were OA progression (29%), aseptic loosening (23%), and bearing dislocation (10%). Progression of OA and bearing dislocation were the most common modes of failure in cohort studies (36% and 17%, respectively), while aseptic loosening and OA progression were the most common failure modes in registry-based studies (28% and 24%, respectively).
As mentioned above, there are differences in anatomy and kinematics between the medial and lateral compartment. When the lateral UKA failure modes are compared with studies reporting medial UKA failure modes, differences in failure modes are seen.34 Siddiqui and Ahmad35 performed a systematic review of outcomes after UKA revision and presented a table with the failure modes of included studies. Unfortunately they did not report the ratio of medial and lateral UKA. However, when assuming an average percentage of 90% to 95% of medial UKA,6,7,36 the main failure mode in their review in 17 out of 21 studies was aseptic loosening. Indeed, a recent systematic review on medial UKA failure modes showed that aseptic loosening is the most common cause of failure following this procedure.34 Similarly, a search through registry-based studies6,7 and large cohort studies37-40 that only reported medial UKA failures showed that the majority of these studies7,37-39 also reported aseptic loosening as the main cause of failure in medial UKA. When comparing the results of our systematic review of lateral UKA failures with the results of these studies of medial UKA failures, it seems that OA progression seems to play a more dominant role in failures of lateral UKA, while aseptic loosening seems to be more common in medial UKA.
Differences in anatomy and kinematics of the medial and lateral compartment can explain this. Malalignment of the joint is an important factor in the etiology of OA41,42 and biomechanical studies showed that this malalignment can cause decreased viability and further degenerative changes of cartilage of the knee.43 Hernigou and Deschamps44 showed that the alignment of the knee after medial UKA is an important factor in postoperative joint changes. They found that overcorrection of varus deformity during medial UKA surgery, measured by the hip-knee-ankle (HKA) angle, was associated with increased OA at the lateral condyle and less tibial wear of the medial UKA. Undercorrection of the varus caused an increase in tibial wear of polyethylene. Chatellard and colleagues45 found the same results in the correction of varus, measured by HKA. In addition, they found that when the prosthetic (medial) joint space was smaller than healthy (lateral) joint space, this was correlated with lower prosthesis survival. A smaller joint space at the healthy side was correlated with OA progression at the lateral compartment and tibial component wear.
These studies explain the mechanism of progression of OA and aseptic loosening. Harrington46 assessed the load in patients with valgus and varus deformity. Patients with a valgus deformity have high mechanical load on the lateral condyle during the static phase, but during the dynamic phase, a major part of this load shifts to the medial condyle. In the patients with varus deformity, the mechanical load was noted on the medial condyle during both the static and dynamic phase. Ohdera and colleagues47 advised, based on this biomechanical study and their own experiences, to correct the knee during lateral UKA to a slight valgus angle (5°-7°) to prevent OA progression at the medial side. van der List and colleagues48 similarly showed that undercorrection of 3° to 7° was correlated with better functional outcomes when compared to more neutral alignment. Moreover, Khamaisy and colleagues49 recently showed that overcorrection during UKA surgery is more common in lateral than medial UKA.
These studies are important to understanding why OA progression is more common as a failure mode in lateral UKA. The shift of mechanical load from the lateral to medial epicondyle during the dynamic phase also could explain why aseptic loosening is less common in lateral UKA. As Hernigou and Deschamps44 and Chatellard and colleagues45 stated, undercorrection of varus deformity in medial UKA is associated with higher mechanical load on the medial prosthesis side and smaller joint space width. These factors are correlated with mechanical failure of medial UKA. We think this process can be applied to lateral UKA, with the addition that the mechanical load is higher on the healthy medial compartment during the dynamic phase. This causes more forces on the healthy (medial) side in lateral UKA, and in medial UKA more forces on the prosthesis (medial) side, which results in more OA progression in lateral UKA and more aseptic loosening in medial UKA. This finding is consistent with the results of our review of more OA progression and less aseptic loosening in lateral UKA. This study also suggests that medial and lateral UKA should not be reported together in studies that present survivorship, failure modes, or clinical outcomes.
A large discrepancy was seen in bearing dislocation between cohort studies (17%) and registry-based studies (5%). When we take a closer look to the bearing dislocation failures in the cohort studies, most of the failures were reported in only 2 cohort studies.50,51 In a study by Pandit and colleagues,50 3 different prosthesis designs were used in 3 different time periods. In the first series of lateral UKA (1983-1991), 6 out of 51 (12%) bearings dislocated. In the second series (1998-2004), a modified technique was used and 3 out of 65 (5%) bearings dislocated. In the third series (2004-2008), a modified technique and a domed tibial component was used and only 1 out of 68 bearings dislocated (1%). In a study published in 1996, Gunther and colleagues51 also used surgical techniques and implants that were modified over the course of the study period. Because of these modified techniques, different implant designs, and year of publication, bearing dislocation most likely plays a smaller role than the 17% reported in the cohort studies. This discrepancy is a good example of the important role for the registries and registry-based studies in reporting failure modes and survivorship, especially in lateral UKA due to the low surgical frequency. Pabinger and colleagues52 recently performed a systematic review of cohort studies and registry-based studies in which they stated that the reliability in non-registry-based studies should be questioned and they considered registry-based studies superior in reporting UKA outcomes and revision rates. Furthermore, given the differences in anatomic and kinematic differences between the medial and lateral compartment and different failure modes between medial and lateral UKA, it would be better if future studies presented the medial and lateral failures separately. As stated above, most large cohort studies and especially annual registries currently do not report modes of failure of medial and lateral UKA separately.3,4,18-20
There are limitations in this study. First, this systematic review is not a full meta-analysis but a pooled analysis of collected study series and retrospective studies. Therefore, we cannot exclude sampling bias, confounders, and selection bias from the literature. We included all studies reporting failure modes of lateral UKA and excluded all case reports. We made a conscious choice about including all lateral UKA failures because this is the first systematic review of lateral UKA failure modes. Another limitation is that the follow-up period of the studies differed (Table 1) and we did not correct for the follow-up period. As stated in the example of bearing dislocations, some of these studies reported old or different techniques, while other, more recently published studies used more modified techniques11,29,53-56 Unfortunately, most studies did not report the time of arthroplasty survival and therefore we could not correct for the follow-up period.
In conclusion, progression of OA is the most common failure mode in lateral UKA, followed by aseptic loosening. Anatomic and kinematic factors such as alignment, mechanical forces during dynamic phase, and correction of valgus seem to play important roles in failure modes of lateral UKA. In the future, failure modes of medial and lateral UKA should be reported separately.
Am J Orthop. 2016;45(7):432-438, 462. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Skolnick MD, Bryan RS, Peterson LFA. Unicompartmental polycentric knee arthroplasty. Description and preliminary results. Clin Orthop Relat Res. 1975;(112):208-214.
2. Riddle DL, Jiranek WA, McGlynn FJ. Yearly Incidence of Unicompartmental Knee Arthroplasty in the United States. J Arthroplasty. 2008;23(3):408-412.
3. Australian Orthopaedic Association. Hip and Knee Arthroplasty 2014 Annual Report. https://aoanjrr.sahmri.com/documents/10180/172286/Annual%20Report%202014. Accessed June 3, 2015.
4. Swedish Knee Arthroplasty Register. 2013 Annual Report.http://myknee.se/pdf/SKAR2013_Eng.pdf. Accessed June 3, 2015.
5. The New Zealand Joint Registry. Fourteen Year Report. January 1999 to December 2012. 2013. http://nzoa.org.nz/system/files/NJR 14 Year Report.pdf. Accessed June 3, 2015.
6. Baker PN, Jameson SS, Deehan DJ, Gregg PJ, Porter M, Tucker K. Mid-term equivalent survival of medial and lateral unicondylar knee replacement: an analysis of data from a National Joint Registry. J Bone Joint Surg Br. 2012;94(12):1641-1648.
7. Lewold S, Robertsson O, Knutson K, Lidgren L. Revision of unicompartmental knee arthroplasty: outcome in 1,135 cases from the Swedish Knee Arthroplasty study. Acta Orthop Scand. 1998;69(5):469-474.
8. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
9. Hill PF, Vedi V, Williams A, Iwaki H, 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.
10. 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.
11. Ashraf T, Newman JH, Evans RL, Ackroyd CE. Lateral unicompartmental knee replacement survivorship and clinical experience over 21 years. J Bone Joint Surg Br. 2002;84(8):1126-1130.
12. Scott RD. Lateral unicompartmental replacement: a road less traveled. Orthopedics. 2005;28(9):983-984.
13. Sah AP, Scott RD. Lateral unicompartmental knee arthroplasty through a medial approach. Study with an average five-year follow-up. J Bone Joint Surg Am. 2007;89(9):1948-1954.
14. Argenson JN, Parratte S, Bertani A, Flecher X, Aubaniac JM. Long-term results with a lateral unicondylar replacement. Clin Orthop Relat Res. 2008;466(11):2686-2693.
15. Weidow J, Pak J, Karrholm J. Different patterns of cartilage wear in medial and lateral gonarthrosis. Acta Orthop Scand. 2002;73(3):326-329.
16. Ollivier M, Abdel MP, Parratte S, Argenson JN. Lateral unicondylar knee arthroplasty (UKA): contemporary indications, surgical technique, and results. Int Orthop. 2014;38(2):449-455.
17. Demange MK, Von Keudell A, Probst C, Yoshioka H, Gomoll AH. Patient-specific implants for lateral unicompartmental knee arthroplasty. Int Orthop. 2015;39(8):1519-1526.
18. Khan Z, Nawaz SZ, Kahane S, Esler C, Chatterji U. Conversion of unicompartmental knee arthroplasty to total knee arthroplasty: the challenges and need for augments. Acta Orthop Belg. 2013;79(6):699-705.
19. Epinette JA, Brunschweiler B, Mertl P, et al. Unicompartmental knee arthroplasty modes of failure: wear is not the main reason for failure: a multicentre study of 418 failed knees. Orthop Traumatol Surg Res. 2012;98(6 Suppl):S124-S130.
20. Bordini B, Stea S, Falcioni S, Ancarani C, Toni A. Unicompartmental knee arthroplasty: 11-year experience from 3929 implants in RIPO register. Knee. 2014;21(6):1275-1279.
21. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
22. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
23. van der List JP, Chawla H, Pearle AD. Robotic-assisted knee arthroplasty: an overview. Am J Orthop. 2016;45(4):202-211.
24. van der List JP, Chawla H, Joskowicz L, Pearle AD. Current state of computer navigation and robotics in unicompartmental and total knee arthroplasty: a systematic review with meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2016 Sep 6. [Epub ahead of print]
25. Zuiderbaan HA, van der List JP, Kleeblad LJ, et al. Modern indications, results and global trends in the use of unicompartmental knee arthroplasty and high tibial osteotomy for the treatment of medial unicondylar knee osteoarthritis. Am J Orthop. 2016;45(6):E355-E361.
26. Smith JR, Robinson JR, Porteous AJ, et al. Fixed bearing lateral unicompartmental knee arthroplasty--short to midterm survivorship and knee scores for 101 prostheses. Knee. 2014;21(4):843-847.
27. Berend KR, Kolczun MC 2nd, George JW Jr, Lombardi AV Jr. Lateral unicompartmental knee arthroplasty through a lateral parapatellar approach has high early survivorship. Clin Orthop Relat Res. 2012;470(1):77-83.
28. Keblish PA, Briard JL. Mobile-bearing unicompartmental knee arthroplasty: a 2-center study with an 11-year (mean) follow-up. J Arthroplasty. 2004;19(7 Suppl 2):87-94.
29. Bertani A, Flecher X, Parratte S, Aubaniac JM, Argenson JN. Unicompartmental-knee arthroplasty for treatment of lateral gonarthrosis: about 30 cases. Midterm results. Rev Chir Orthop Reparatrice Appar Mot. 2008;94(8):763-770.
30. Sebilo A, Casin C, Lebel B, et al. Clinical and technical factors influencing outcomes of unicompartmental knee arthroplasty: Retrospective multicentre study of 944 knees. Orthop Traumatol Surg Res. 2013;99(4 Suppl):S227-S234.
31. Cartier P, Khefacha A, Sanouiller JL, Frederick K. Unicondylar knee arthroplasty in middle-aged patients: A minimum 5-year follow-up. Orthopedics. 2007;30(8 Suppl):62-65.
32. Lustig S, Paillot JL, Servien E, Henry J, Ait Si Selmi T, Neyret P. Cemented all polyethylene tibial insert unicompartimental knee arthroplasty: a long term follow-up study. Orthop Traumatol Surg Res. 2009;95(1):12-21.
33. van der List JP, McDonald LS, Pearle AD. Systematic review of medial versus lateral survivorship in unicompartmental knee arthroplasty. Knee. 2015;22(6):454-460.
34. van der List JP, Zuiderbaan HA, Pearle AD. Why do medial unicompartmental knee arthroplasties fail today? J Arthroplasty. 2016;31(5):1016-1021.
35. Siddiqui NA, Ahmad ZM. Revision of unicondylar to total knee arthroplasty: a systematic review. Open Orthop J. 2012;6:268-275.
36. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
37. Kalra S, Smith TO, Berko B, Walton NP. Assessment of radiolucent lines around the Oxford unicompartmental knee replacement: sensitivity and specificity for loosening. J Bone Joint Surg Br. 2011;93(6):777-781.
38. Wynn Jones H, Chan W, Harrison T, Smith TO, Masonda P, Walton NP. Revision of medial Oxford unicompartmental knee replacement to a total knee replacement: similar to a primary? Knee. 2012;19(4):339-343.
39. Sierra RJ, Kassel CA, Wetters NG, Berend KR, Della Valle CJ, Lombardi AV. Revision of unicompartmental arthroplasty to total knee arthroplasty: not always a slam dunk! J Arthroplasty. 2013;28(8 Suppl):128-132.
40. Citak M, Dersch K, Kamath AF, Haasper C, Gehrke T, Kendoff D. Common causes of failed unicompartmental knee arthroplasty: a single-centre analysis of four hundred and seventy one cases. Int Orthop. 2014;38(5):961-965.
41. Hunter DJ, Wilson DR. Role of alignment and biomechanics in osteoarthritis and implications for imaging. Radiol Clin North Am. 2009;47(4):553-566.
42. Hunter DJ, Sharma L, Skaife T. Alignment and osteoarthritis of the knee. J Bone Joint Surg Am. 2009;91 Suppl 1:85-89.
43. Roemhildt ML, Beynnon BD, Gauthier AE, Gardner-Morse M, Ertem F, Badger GJ. Chronic in vivo load alteration induces degenerative changes in the rat tibiofemoral joint. Osteoarthritis Cartilage. 2013;21(2):346-357.
44. Hernigou P, Deschamps G. Alignment influences wear in the knee after medial unicompartmental arthroplasty. Clin Orthop Relat Res. 2004;(423):161-165.
45. Chatellard R, Sauleau V, Colmar M, et al. Medial unicompartmental knee arthroplasty: does tibial component position influence clinical outcomes and arthroplasty survival? Orthop Traumatol Surg Res. 2013;99(4 Suppl):S219-S225.
46. Harrington IJ. Static and dynamic loading patterns in knee joints with deformities. J Bone Joint Surg Am. 1983;65(2):247-259.
47. Ohdera T, Tokunaga J, Kobayashi A. Unicompartmental knee arthroplasty for lateral gonarthrosis: midterm results. J Arthroplasty. 2001;16(2):196-200.
48. van der List JP, Chawla H, Villa JC, Zuiderbaan HA, Pearle AD. Early functional outcome after lateral UKA is sensitive to postoperative lower limb alignment. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 26. [Epub ahead of print]
49. Khamaisy S, Gladnick BP, Nam D, Reinhardt KR, Heyse TJ, Pearle AD. Lower limb alignment control: Is it more challenging in lateral compared to medial unicondylar knee arthroplasty? Knee. 2015;22(4):347-350.
50. Pandit H, Jenkins C, Beard DJ, et al. Mobile bearing dislocation in lateral unicompartmental knee replacement. Knee. 2010;17(6):392-397.
51. Gunther TV, Murray DW, Miller R, et al. Lateral unicompartmental arthroplasty with the Oxford meniscal knee. Knee. 1996;3(1):33-39.
52. Pabinger C, Lumenta DB, Cupak D, Berghold A, Boehler N, Labek G. Quality of outcome data in knee arthroplasty: Comparison of registry data and worldwide non-registry studies from 4 decades. Acta Orthopaedica. 2015;86(1):58-62.
53. Lustig S, Elguindy A, Servien E, et al. 5- to 16-year follow-up of 54 consecutive lateral unicondylar knee arthroplasties with a fixed-all polyethylene bearing. J Arthroplasty. 2011;26(8):1318-1325.
54. Walton MJ, Weale AE, Newman JH. The progression of arthritis following lateral unicompartmental knee replacement. Knee. 2006;13(5):374-377.
55. Lustig S, Lording T, Frank F, Debette C, Servien E, Neyret P. Progression of medial osteoarthritis and long term results of lateral unicompartmental arthroplasty: 10 to 18 year follow-up of 54 consecutive implants. Knee. 2014;21(S1):S26-S32.
56. O’Rourke MR, Gardner JJ, Callaghan JJ, et al. Unicompartmental knee replacement: a minimum twenty-one-year followup, end-result study. Clin Orthop Relat Res. 2005;440:27-37.
57. Citak M, Cross MB, Gehrke T, Dersch K, Kendoff D. Modes of failure and revision of failed lateral unicompartmental knee arthroplasties. Knee. 2015;22(4):338-340.
58. Liebs TR, Herzberg W. Better quality of life after medial versus lateral unicondylar knee arthroplasty knee. Clin Orthop Relat Res. 2013;471(8):2629-2640.
59. Weston-Simons JS, Pandit H, Kendrick BJ, et al. The mid-term outcomes of the Oxford Domed Lateral unicompartmental knee replacement. Bone Joint J. 2014;96-B(1):59-64.
60. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
61. Saxler G, Temmen D, Bontemps G. Medium-term results of the AMC-unicompartmental knee arthroplasty. Knee. 2004;11(5):349-355.
62. Forster MC, Bauze AJ, Keene GCR. Lateral unicompartmental knee replacement: Fixed or mobile bearing? Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1107-1111.
63. Streit MR, Walker T, Bruckner T, et al. Mobile-bearing lateral unicompartmental knee replacement with the Oxford domed tibial component: an independent series. J Bone Joint Surg Br. 2012;94(10):1356-1361.
64. Altuntas AO, Alsop H, Cobb JP. Early results of a domed tibia, mobile bearing lateral unicompartmental knee arthroplasty from an independent centre. Knee. 2013;20(6):466-470.
65. Ashraf T, Newman JH, Desai VV, Beard D, Nevelos JE. Polyethylene wear in a non-congruous unicompartmental knee replacement: a retrieval analysis. Knee. 2004;11(3):177-181.
66. Schelfaut S, Beckers L, Verdonk P, Bellemans J, Victor J. The risk of bearing dislocation in lateral unicompartmental knee arthroplasty using a mobile biconcave design. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2487-2494.
67. Marson B, Prasad N, Jenkins R, Lewis M. Lateral unicompartmental knee replacements: Early results from a District General Hospital. Eur J Orthop Surg Traumatol. 2014;24(6):987-991.
68. Walker T, Gotterbarm T, Bruckner T, Merle C, Streit MR. Total versus unicompartmental knee replacement for isolated lateral osteoarthritis: a matched-pairs study. Int Orthop. 2014;38(11):2259-2264.
1. Skolnick MD, Bryan RS, Peterson LFA. Unicompartmental polycentric knee arthroplasty. Description and preliminary results. Clin Orthop Relat Res. 1975;(112):208-214.
2. Riddle DL, Jiranek WA, McGlynn FJ. Yearly Incidence of Unicompartmental Knee Arthroplasty in the United States. J Arthroplasty. 2008;23(3):408-412.
3. Australian Orthopaedic Association. Hip and Knee Arthroplasty 2014 Annual Report. https://aoanjrr.sahmri.com/documents/10180/172286/Annual%20Report%202014. Accessed June 3, 2015.
4. Swedish Knee Arthroplasty Register. 2013 Annual Report.http://myknee.se/pdf/SKAR2013_Eng.pdf. Accessed June 3, 2015.
5. The New Zealand Joint Registry. Fourteen Year Report. January 1999 to December 2012. 2013. http://nzoa.org.nz/system/files/NJR 14 Year Report.pdf. Accessed June 3, 2015.
6. Baker PN, Jameson SS, Deehan DJ, Gregg PJ, Porter M, Tucker K. Mid-term equivalent survival of medial and lateral unicondylar knee replacement: an analysis of data from a National Joint Registry. J Bone Joint Surg Br. 2012;94(12):1641-1648.
7. Lewold S, Robertsson O, Knutson K, Lidgren L. Revision of unicompartmental knee arthroplasty: outcome in 1,135 cases from the Swedish Knee Arthroplasty study. Acta Orthop Scand. 1998;69(5):469-474.
8. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
9. Hill PF, Vedi V, Williams A, Iwaki H, 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.
10. 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.
11. Ashraf T, Newman JH, Evans RL, Ackroyd CE. Lateral unicompartmental knee replacement survivorship and clinical experience over 21 years. J Bone Joint Surg Br. 2002;84(8):1126-1130.
12. Scott RD. Lateral unicompartmental replacement: a road less traveled. Orthopedics. 2005;28(9):983-984.
13. Sah AP, Scott RD. Lateral unicompartmental knee arthroplasty through a medial approach. Study with an average five-year follow-up. J Bone Joint Surg Am. 2007;89(9):1948-1954.
14. Argenson JN, Parratte S, Bertani A, Flecher X, Aubaniac JM. Long-term results with a lateral unicondylar replacement. Clin Orthop Relat Res. 2008;466(11):2686-2693.
15. Weidow J, Pak J, Karrholm J. Different patterns of cartilage wear in medial and lateral gonarthrosis. Acta Orthop Scand. 2002;73(3):326-329.
16. Ollivier M, Abdel MP, Parratte S, Argenson JN. Lateral unicondylar knee arthroplasty (UKA): contemporary indications, surgical technique, and results. Int Orthop. 2014;38(2):449-455.
17. Demange MK, Von Keudell A, Probst C, Yoshioka H, Gomoll AH. Patient-specific implants for lateral unicompartmental knee arthroplasty. Int Orthop. 2015;39(8):1519-1526.
18. Khan Z, Nawaz SZ, Kahane S, Esler C, Chatterji U. Conversion of unicompartmental knee arthroplasty to total knee arthroplasty: the challenges and need for augments. Acta Orthop Belg. 2013;79(6):699-705.
19. Epinette JA, Brunschweiler B, Mertl P, et al. Unicompartmental knee arthroplasty modes of failure: wear is not the main reason for failure: a multicentre study of 418 failed knees. Orthop Traumatol Surg Res. 2012;98(6 Suppl):S124-S130.
20. Bordini B, Stea S, Falcioni S, Ancarani C, Toni A. Unicompartmental knee arthroplasty: 11-year experience from 3929 implants in RIPO register. Knee. 2014;21(6):1275-1279.
21. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
22. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
23. van der List JP, Chawla H, Pearle AD. Robotic-assisted knee arthroplasty: an overview. Am J Orthop. 2016;45(4):202-211.
24. van der List JP, Chawla H, Joskowicz L, Pearle AD. Current state of computer navigation and robotics in unicompartmental and total knee arthroplasty: a systematic review with meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2016 Sep 6. [Epub ahead of print]
25. Zuiderbaan HA, van der List JP, Kleeblad LJ, et al. Modern indications, results and global trends in the use of unicompartmental knee arthroplasty and high tibial osteotomy for the treatment of medial unicondylar knee osteoarthritis. Am J Orthop. 2016;45(6):E355-E361.
26. Smith JR, Robinson JR, Porteous AJ, et al. Fixed bearing lateral unicompartmental knee arthroplasty--short to midterm survivorship and knee scores for 101 prostheses. Knee. 2014;21(4):843-847.
27. Berend KR, Kolczun MC 2nd, George JW Jr, Lombardi AV Jr. Lateral unicompartmental knee arthroplasty through a lateral parapatellar approach has high early survivorship. Clin Orthop Relat Res. 2012;470(1):77-83.
28. Keblish PA, Briard JL. Mobile-bearing unicompartmental knee arthroplasty: a 2-center study with an 11-year (mean) follow-up. J Arthroplasty. 2004;19(7 Suppl 2):87-94.
29. Bertani A, Flecher X, Parratte S, Aubaniac JM, Argenson JN. Unicompartmental-knee arthroplasty for treatment of lateral gonarthrosis: about 30 cases. Midterm results. Rev Chir Orthop Reparatrice Appar Mot. 2008;94(8):763-770.
30. Sebilo A, Casin C, Lebel B, et al. Clinical and technical factors influencing outcomes of unicompartmental knee arthroplasty: Retrospective multicentre study of 944 knees. Orthop Traumatol Surg Res. 2013;99(4 Suppl):S227-S234.
31. Cartier P, Khefacha A, Sanouiller JL, Frederick K. Unicondylar knee arthroplasty in middle-aged patients: A minimum 5-year follow-up. Orthopedics. 2007;30(8 Suppl):62-65.
32. Lustig S, Paillot JL, Servien E, Henry J, Ait Si Selmi T, Neyret P. Cemented all polyethylene tibial insert unicompartimental knee arthroplasty: a long term follow-up study. Orthop Traumatol Surg Res. 2009;95(1):12-21.
33. van der List JP, McDonald LS, Pearle AD. Systematic review of medial versus lateral survivorship in unicompartmental knee arthroplasty. Knee. 2015;22(6):454-460.
34. van der List JP, Zuiderbaan HA, Pearle AD. Why do medial unicompartmental knee arthroplasties fail today? J Arthroplasty. 2016;31(5):1016-1021.
35. Siddiqui NA, Ahmad ZM. Revision of unicondylar to total knee arthroplasty: a systematic review. Open Orthop J. 2012;6:268-275.
36. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Lateral unicompartmental knee arthroplasty: survivorship and technical considerations at an average follow-up of 12.4 years. J Arthroplasty. 2006;21(1):13-17.
37. Kalra S, Smith TO, Berko B, Walton NP. Assessment of radiolucent lines around the Oxford unicompartmental knee replacement: sensitivity and specificity for loosening. J Bone Joint Surg Br. 2011;93(6):777-781.
38. Wynn Jones H, Chan W, Harrison T, Smith TO, Masonda P, Walton NP. Revision of medial Oxford unicompartmental knee replacement to a total knee replacement: similar to a primary? Knee. 2012;19(4):339-343.
39. Sierra RJ, Kassel CA, Wetters NG, Berend KR, Della Valle CJ, Lombardi AV. Revision of unicompartmental arthroplasty to total knee arthroplasty: not always a slam dunk! J Arthroplasty. 2013;28(8 Suppl):128-132.
40. Citak M, Dersch K, Kamath AF, Haasper C, Gehrke T, Kendoff D. Common causes of failed unicompartmental knee arthroplasty: a single-centre analysis of four hundred and seventy one cases. Int Orthop. 2014;38(5):961-965.
41. Hunter DJ, Wilson DR. Role of alignment and biomechanics in osteoarthritis and implications for imaging. Radiol Clin North Am. 2009;47(4):553-566.
42. Hunter DJ, Sharma L, Skaife T. Alignment and osteoarthritis of the knee. J Bone Joint Surg Am. 2009;91 Suppl 1:85-89.
43. Roemhildt ML, Beynnon BD, Gauthier AE, Gardner-Morse M, Ertem F, Badger GJ. Chronic in vivo load alteration induces degenerative changes in the rat tibiofemoral joint. Osteoarthritis Cartilage. 2013;21(2):346-357.
44. Hernigou P, Deschamps G. Alignment influences wear in the knee after medial unicompartmental arthroplasty. Clin Orthop Relat Res. 2004;(423):161-165.
45. Chatellard R, Sauleau V, Colmar M, et al. Medial unicompartmental knee arthroplasty: does tibial component position influence clinical outcomes and arthroplasty survival? Orthop Traumatol Surg Res. 2013;99(4 Suppl):S219-S225.
46. Harrington IJ. Static and dynamic loading patterns in knee joints with deformities. J Bone Joint Surg Am. 1983;65(2):247-259.
47. Ohdera T, Tokunaga J, Kobayashi A. Unicompartmental knee arthroplasty for lateral gonarthrosis: midterm results. J Arthroplasty. 2001;16(2):196-200.
48. van der List JP, Chawla H, Villa JC, Zuiderbaan HA, Pearle AD. Early functional outcome after lateral UKA is sensitive to postoperative lower limb alignment. Knee Surg Sports Traumatol Arthrosc. 2015 Nov 26. [Epub ahead of print]
49. Khamaisy S, Gladnick BP, Nam D, Reinhardt KR, Heyse TJ, Pearle AD. Lower limb alignment control: Is it more challenging in lateral compared to medial unicondylar knee arthroplasty? Knee. 2015;22(4):347-350.
50. Pandit H, Jenkins C, Beard DJ, et al. Mobile bearing dislocation in lateral unicompartmental knee replacement. Knee. 2010;17(6):392-397.
51. Gunther TV, Murray DW, Miller R, et al. Lateral unicompartmental arthroplasty with the Oxford meniscal knee. Knee. 1996;3(1):33-39.
52. Pabinger C, Lumenta DB, Cupak D, Berghold A, Boehler N, Labek G. Quality of outcome data in knee arthroplasty: Comparison of registry data and worldwide non-registry studies from 4 decades. Acta Orthopaedica. 2015;86(1):58-62.
53. Lustig S, Elguindy A, Servien E, et al. 5- to 16-year follow-up of 54 consecutive lateral unicondylar knee arthroplasties with a fixed-all polyethylene bearing. J Arthroplasty. 2011;26(8):1318-1325.
54. Walton MJ, Weale AE, Newman JH. The progression of arthritis following lateral unicompartmental knee replacement. Knee. 2006;13(5):374-377.
55. Lustig S, Lording T, Frank F, Debette C, Servien E, Neyret P. Progression of medial osteoarthritis and long term results of lateral unicompartmental arthroplasty: 10 to 18 year follow-up of 54 consecutive implants. Knee. 2014;21(S1):S26-S32.
56. O’Rourke MR, Gardner JJ, Callaghan JJ, et al. Unicompartmental knee replacement: a minimum twenty-one-year followup, end-result study. Clin Orthop Relat Res. 2005;440:27-37.
57. Citak M, Cross MB, Gehrke T, Dersch K, Kendoff D. Modes of failure and revision of failed lateral unicompartmental knee arthroplasties. Knee. 2015;22(4):338-340.
58. Liebs TR, Herzberg W. Better quality of life after medial versus lateral unicondylar knee arthroplasty knee. Clin Orthop Relat Res. 2013;471(8):2629-2640.
59. Weston-Simons JS, Pandit H, Kendrick BJ, et al. The mid-term outcomes of the Oxford Domed Lateral unicompartmental knee replacement. Bone Joint J. 2014;96-B(1):59-64.
60. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
61. Saxler G, Temmen D, Bontemps G. Medium-term results of the AMC-unicompartmental knee arthroplasty. Knee. 2004;11(5):349-355.
62. Forster MC, Bauze AJ, Keene GCR. Lateral unicompartmental knee replacement: Fixed or mobile bearing? Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1107-1111.
63. Streit MR, Walker T, Bruckner T, et al. Mobile-bearing lateral unicompartmental knee replacement with the Oxford domed tibial component: an independent series. J Bone Joint Surg Br. 2012;94(10):1356-1361.
64. Altuntas AO, Alsop H, Cobb JP. Early results of a domed tibia, mobile bearing lateral unicompartmental knee arthroplasty from an independent centre. Knee. 2013;20(6):466-470.
65. Ashraf T, Newman JH, Desai VV, Beard D, Nevelos JE. Polyethylene wear in a non-congruous unicompartmental knee replacement: a retrieval analysis. Knee. 2004;11(3):177-181.
66. Schelfaut S, Beckers L, Verdonk P, Bellemans J, Victor J. The risk of bearing dislocation in lateral unicompartmental knee arthroplasty using a mobile biconcave design. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2487-2494.
67. Marson B, Prasad N, Jenkins R, Lewis M. Lateral unicompartmental knee replacements: Early results from a District General Hospital. Eur J Orthop Surg Traumatol. 2014;24(6):987-991.
68. Walker T, Gotterbarm T, Bruckner T, Merle C, Streit MR. Total versus unicompartmental knee replacement for isolated lateral osteoarthritis: a matched-pairs study. Int Orthop. 2014;38(11):2259-2264.
Ultrasound-Guided Percutaneous Reconstruction of the Anterolateral Ligament: Surgical Technique and Case Report
Restoring native kinematics of the knee has been a primary goal of anterior cruciate ligament (ACL) procedures. Double-bundle ACL reconstruction, compared to single-bundle, has been hypothesized to more effectively re-establish rotational stability by re-creating the anatomic ACL, but has not yet proven to result in better clinical outcomes.1
In 1879, Dr. Paul Segond described a “fibrous, pearly band” at the lateral aspect of the knee that avulsed off the anterolateral proximal tibia during many ACL injuries.2 The role of the lateral tissues in knee stability and their relationship with ACL pathology has attracted noteworthy attention in recent time. There have been multiple studies presenting an anatomical description of a structure at the anterolateral portion of the knee with definitive femoral, meniscal, and tibial attachments, which helps control internal rotational forces.3-7 Claes and colleagues4 later found that band of tissue to be the anterolateral ligament (ALL) and determined its injury to be pathognomonic with ACL ruptures.
The ALL is a vital static stabilizer of the tibio-femoral joint, especially during internal tibial rotation.8-10 In their report on ALL and ACL reconstruction, Helito and colleagues11 acknowledge the necessity of accurate assessment of the lateral structures through imaging to determine the presence of extra-articular injury. Musculoskeletal diagnostic ultrasound has been established as an appropriate means to identify the ALL.12
Ultrasound can accurately determine the exact anatomic location of the origin and insertion of the ALL. Reconstruction of the ALL could yield better patient outcomes for those who experience concurrent ACL/ALL injury. Here we present an innovative technique for an ultrasound-guided percutaneous method for reconstruction of the ALL and report on a patient who had underwent ALL reconstruction.
Surgical Indications
All patients undergo an ultrasound evaluation preoperatively to determine if the ALL is intact or injured. Our experience has shown that when ultrasound evaluation reveals an intact ALL, the pivot shift has never been a grade III.
Surgical Technique
For a demonstration of this technique, see the video that accompanies this article.
The pivot shift test is conducted under anesthesia to determine whether an ALL reconstruction is required. The patient is placed in a supine position with the knee flexed at 30o, at neutral rotation, and without any varus or valgus stress.
A No. 15 blade is used to make a small incision centered on each spinal needle. The spinal needle is replaced with a 2.4-mm drill pin (Figure 2).
The graft and FiberTape are then passed under the IT band to the distal incision. Using the length of the BioComposite SwiveLock anchor as a guide, a mark is made on the graft after tensioning the construct in line with the leg, distal to the tibial drill pin (Table 2, Figure 4).
Rehabilitation
Rehabilitation following an ALL procedure is similar to traditional ACL rehabilitation with an added emphasis on minimizing rotational torque of the tibia in the early stages.
Case Report
In January 2013, a 17-year-old male soccer player suffered an ACL rupture of his right knee. Later that spring, he had an ACL reconstruction with an allograft. Twelve months postoperatively, the patient returned, saying that he felt much better; however, anytime he tried to plant his foot and rotate over that fixed foot, his knee felt unstable. The physical examination revealed both negative Lachman and anterior drawer tests but a I+ pivot shift test. A magnetic resonance imaging (MRI) examination revealed an intact ACL graft. A diagnostic ultrasound evaluation revealed a distal ALL injury. After discussing the risks, benefits, and goals with the patient, we opted for a diagnostic arthroscopy and a percutaneous, ultrasound-guided reconstruction of the ALL.
Postoperatively, the patient did very well. One week after surgery, he returned, saying he felt completely stable and demonstrated by repeating the rotation of his knee. The patient continued to have no issues until he returned 13 months post-ALL surgery, complaining of a recent injury that had caused the return of his feelings of instability. An MRI evaluation showed an intact ACL graft and the possibility of a ruptured ALL. Fifteen months after the initial ALL reconstruction, we proceeded with surgery. At arthroscopy, the patient was found to have a pivot shift of I+ and an intact ACL graft. The ALL was reconstructed again using an allograft, internal brace, and bone marrow concentrate. At 13 months post-ALL reconstruction revision, the patient had no complaints.
Discussion
Reconstruction of the ALL is aimed to restore anatomic rotational kinematics. Sonnery-Cottet and colleagues14 have reported promising initial results in their 2-year follow-up study of combined ACL and ALL reconstruction outcomes. This surgical technique includes use of an internal brace, which negates the necessity for external support devices and allows for earlier mobilization of the joint. A reconstruction of the ALL, performed concurrently with the ACL, does not add recovery time, but could prevent postsurgical complications and improve rehabilitation by eliminating rotational instability that presents in some ACL-reconstructed patients.
Sonnery-Cottet and colleagues15 state that their arthroscopic identification of the ALL can help to cultivate a “less invasive and more anatomic” reconstruction. The use of musculoskeletal ultrasound allows our technique to utilize a completely noninvasive imaging tool that allows proper establishment of ALL anatomy prior to the procedure. The entirety of the ALL is easily identifiable,4,12 which has proven to be shortcoming of MRI evaluation.15-17 Accurate preoperative assessment of the lateral structures is necessary in ACL-deficient individuals.11,15 Sonography also provides a means of accurate guidance and socket creation, without generating large incisions.
If the ALL is responsible for internal rotatory stability as asserted, the structure should exhibit biomechanical properties during movement. In their study on the function of the ligament, Parsons and colleagues9 established the inverse relationship between the ALL and ACL during internal rotation. As their cadaveric knees were subjected to an internal rotatory force through increasing angles of flexion, the contribution of the ALL towards stability significantly increased while the ACL declined. Helito and colleagues8 and Zens and colleagues10 have demonstrated length changes of the ligament through varying degrees of flexion and internal rotation. Their reports indicate greater tension during knee movements, coinciding with the description of increasing ALL stability contribution by Parsons and colleagues.9 Kennedy and colleagues7 conducted a pull-to-failure test on the ALL. The average failure load was 175 N with a stiffness of 20 N/mm, illustrating the structure is a candidate for most traditional soft tissue grafts. The biomechanical evidence of the structural properties of the ALL confirms its importance in knee function and the necessity for its reconstruction.
With the understanding that ACL contributes to rotatory stability to some extent, the notion begs the question of how a centrally located ligament is able to prevent excessive rotation in a structure with a large relative radius. Biomechanically, with such a small moment arm, the ACL would experience tremendous stress when a rotatory force is applied. The same torque applied to a more superficial structure, with a greater moment, would sustain a large reduction in the applied force. The concept of a wheel and an axle should be considered. The equation is F1 × R1 = F2 × R2. We measured on a cadaveric knee the distance from the center of rotation to the ACL and the ALL, finding the radii were 5 mm and 30 mm, respectively. Taking these measurements, we would then expect the force experienced on the axle (ACL) to be 6 times greater than what would be experienced on the periphery of the wheel (ALL). The ALL (wheel) has a significant biomechanical advantage over the ACL (axle) in controlling and enduring internal rotatory forces of the knee. This would imply that if the ALL were damaged and not re-established, the ACL would experience a 6 times greater force trying to control internal rotation, which would result in a significantly increased chance of failure and rupture.
While there is a degree of dissent on the presence of the ALL, a number of studies have classified the tissue as an independent ligamentous structure.3-7 While there is disagreement on the precise location of the femoral attachment, there is a consensus on the location of the tibial and meniscal attachments. Claes and colleagues4 originally outlined the femoral attachment as anterior and distal to the origin of the fibular collateral ligament (FCL), which is the description this technique follows. Since Claes and colleagues’4 report, many have investigated the ligament’s femoral origin with delineations ranging from posterior and proximal3,5,7 to anterior and distal.6,16-18
The accurate, noninvasive nature of the musculoskeletal ultrasound prior to any incisions being made makes this technique innovative and superior to other open surgical techniques or those that require fluoroscopy.
Conclusion
The ALL has been determined to play an integral role in the rotational stability of the knee. In the setting of instability and insufficiency, reconstruction will lead to better patient outcomes for concurrent ACL/ALL injuries and postsurgical rotatory instability following ACL procedures. This innovative technique utilizes ultrasound to ascertain the precise anatomical attachments of the ALL prior to the operation. The novel nature of this ultrasound-guided reconstruction has the potential to be applicable in many other surgical procedures.
1. Suomalainen P, Järvelä T, Paakkala A, Kannus P, Järvinen M. Double-bundle versus single-bundle anterior cruciate ligament reconstruction: A prospective randomized study with 5-year results. Am J Sports Med. 2012;40(7):1511-1518.
2. Segond P. Recherches cliniques et expérimentales sur les épanchements sanguins du genou par entorse. Progrés Médical. 1879;6(6):1-85. French.
3. Caterine S, Litchfield R, Johnson M, Chronik B, Getgood A. A cadaveric study of the anterolateral ligament: re-introducing the lateral capsular ligament. Knee Surg Sports Traumatol Athrosc. 2015;23(11):3186-3195.
4. Claes S, Vereecke E, Maes M, Victor J, Verdonk P, Bellemans J. Anatomy of the anterolateral ligament of the knee. J Anat. 2013;223(4):321-328.
5. Dodds AL, Halewood C, Gupte CM, Williams A, Amis AA. The anterolateral ligament: Anatomy, length changes and association with the segond fracture. Bone Joint J. 2014;96-B(3):325-331.
6. Helito CP, Demange MK, Bonadio MB, et al. Anatomy and histology of the knee anterolateral ligament. Orthop J Sports Med. 2013;1(7):2325967113513546.
7. Kennedy MI, Claes S, Fuso FA, et al. The anterolateral ligament: An anatomic, radiographic, and biomechanical analysis. Am J Sports Med. 2015;43(7):1606-1615.
8. Helito CP, Helito PV, Bonadio MB, et al. Evaluation of the length and isometric pattern of the anterolateral ligament with serial computer tomography. Orthop J Sports Med. 2014;2(12):2325967114562205.
9. Parsons EM, Gee AO, Spiekerman C, Cavanagh PR. The biomechanical function of the anterolateral ligament of the knee. Am J Sports Med. 2015;43(3):669-674.
10. Zens M, Niemeyer P, Ruhhamer J, et al. Length changes of the anterolateral ligament during passive knee motion: A human cadaveric study. Am J Sports Med. 2015;43(10):2545-2552.
11. Helito CP, Bonadio MB, Gobbi RG, et al. Combined intra- and extra-articular reconstruction of the anterior cruciate ligament: the reconstruction of the knee anterolateral ligament. Arthrosc Tech. 2015;4(3):e239-e244.
12. Cianca J, John J, Pandit S, Chiou-Tan FY. Musculoskeletal ultrasound imaging of the recently described anterolateral ligament of the knee. Am J Phys Med Rehabil. 2014;93(2):186
13. Adams JE, Zobitz ME, Reach JS, et al. Rotator cuff repair using an acellular dermal matrix graft: An in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
14. Sonnery-Cottet B, Thaunat M, Freychet B, Pupim BHB, Murphy CG, Claes S. Outcome of a combined anterior cruciate ligament and anterolateral ligament reconstruction technique with a minimum 2-year follow-up. Am J Sports Med. 2015;43(7):1598-1605.
15. Sonnery-Cottet B, Archbold P, Rezende FC, Neto AM, Fayard JM, Thaunat M. Arthroscopic identification of the anterolateral ligament of the knee. Arthrosc Tech. 2014;3(3):e389-e392.
16. Helito CP, Helito PV, Costa HP, et al. MRI evaluation of the anterolateral ligament of the knee: assessment in routine 1.5-T scans. Skeletal Radiol. 2014;43(10):1421-1427.
17. Helito CP, Demange MK, Helito PV, et al. Evaluation of the anterolateral ligament of the knee by means of magnetic resonance examination. Rev Bras Orthop. 2015;50(2):214-219.
18. Helito CP, Demange MK, Bonadio MB, et al. Radiographic landmarks for locating the femoral origin and tibial insertion of the knee anterolateral ligament. Am J Sports Med. 2014;42(10):2356-2362.
Restoring native kinematics of the knee has been a primary goal of anterior cruciate ligament (ACL) procedures. Double-bundle ACL reconstruction, compared to single-bundle, has been hypothesized to more effectively re-establish rotational stability by re-creating the anatomic ACL, but has not yet proven to result in better clinical outcomes.1
In 1879, Dr. Paul Segond described a “fibrous, pearly band” at the lateral aspect of the knee that avulsed off the anterolateral proximal tibia during many ACL injuries.2 The role of the lateral tissues in knee stability and their relationship with ACL pathology has attracted noteworthy attention in recent time. There have been multiple studies presenting an anatomical description of a structure at the anterolateral portion of the knee with definitive femoral, meniscal, and tibial attachments, which helps control internal rotational forces.3-7 Claes and colleagues4 later found that band of tissue to be the anterolateral ligament (ALL) and determined its injury to be pathognomonic with ACL ruptures.
The ALL is a vital static stabilizer of the tibio-femoral joint, especially during internal tibial rotation.8-10 In their report on ALL and ACL reconstruction, Helito and colleagues11 acknowledge the necessity of accurate assessment of the lateral structures through imaging to determine the presence of extra-articular injury. Musculoskeletal diagnostic ultrasound has been established as an appropriate means to identify the ALL.12
Ultrasound can accurately determine the exact anatomic location of the origin and insertion of the ALL. Reconstruction of the ALL could yield better patient outcomes for those who experience concurrent ACL/ALL injury. Here we present an innovative technique for an ultrasound-guided percutaneous method for reconstruction of the ALL and report on a patient who had underwent ALL reconstruction.
Surgical Indications
All patients undergo an ultrasound evaluation preoperatively to determine if the ALL is intact or injured. Our experience has shown that when ultrasound evaluation reveals an intact ALL, the pivot shift has never been a grade III.
Surgical Technique
For a demonstration of this technique, see the video that accompanies this article.
The pivot shift test is conducted under anesthesia to determine whether an ALL reconstruction is required. The patient is placed in a supine position with the knee flexed at 30o, at neutral rotation, and without any varus or valgus stress.
A No. 15 blade is used to make a small incision centered on each spinal needle. The spinal needle is replaced with a 2.4-mm drill pin (Figure 2).
The graft and FiberTape are then passed under the IT band to the distal incision. Using the length of the BioComposite SwiveLock anchor as a guide, a mark is made on the graft after tensioning the construct in line with the leg, distal to the tibial drill pin (Table 2, Figure 4).
Rehabilitation
Rehabilitation following an ALL procedure is similar to traditional ACL rehabilitation with an added emphasis on minimizing rotational torque of the tibia in the early stages.
Case Report
In January 2013, a 17-year-old male soccer player suffered an ACL rupture of his right knee. Later that spring, he had an ACL reconstruction with an allograft. Twelve months postoperatively, the patient returned, saying that he felt much better; however, anytime he tried to plant his foot and rotate over that fixed foot, his knee felt unstable. The physical examination revealed both negative Lachman and anterior drawer tests but a I+ pivot shift test. A magnetic resonance imaging (MRI) examination revealed an intact ACL graft. A diagnostic ultrasound evaluation revealed a distal ALL injury. After discussing the risks, benefits, and goals with the patient, we opted for a diagnostic arthroscopy and a percutaneous, ultrasound-guided reconstruction of the ALL.
Postoperatively, the patient did very well. One week after surgery, he returned, saying he felt completely stable and demonstrated by repeating the rotation of his knee. The patient continued to have no issues until he returned 13 months post-ALL surgery, complaining of a recent injury that had caused the return of his feelings of instability. An MRI evaluation showed an intact ACL graft and the possibility of a ruptured ALL. Fifteen months after the initial ALL reconstruction, we proceeded with surgery. At arthroscopy, the patient was found to have a pivot shift of I+ and an intact ACL graft. The ALL was reconstructed again using an allograft, internal brace, and bone marrow concentrate. At 13 months post-ALL reconstruction revision, the patient had no complaints.
Discussion
Reconstruction of the ALL is aimed to restore anatomic rotational kinematics. Sonnery-Cottet and colleagues14 have reported promising initial results in their 2-year follow-up study of combined ACL and ALL reconstruction outcomes. This surgical technique includes use of an internal brace, which negates the necessity for external support devices and allows for earlier mobilization of the joint. A reconstruction of the ALL, performed concurrently with the ACL, does not add recovery time, but could prevent postsurgical complications and improve rehabilitation by eliminating rotational instability that presents in some ACL-reconstructed patients.
Sonnery-Cottet and colleagues15 state that their arthroscopic identification of the ALL can help to cultivate a “less invasive and more anatomic” reconstruction. The use of musculoskeletal ultrasound allows our technique to utilize a completely noninvasive imaging tool that allows proper establishment of ALL anatomy prior to the procedure. The entirety of the ALL is easily identifiable,4,12 which has proven to be shortcoming of MRI evaluation.15-17 Accurate preoperative assessment of the lateral structures is necessary in ACL-deficient individuals.11,15 Sonography also provides a means of accurate guidance and socket creation, without generating large incisions.
If the ALL is responsible for internal rotatory stability as asserted, the structure should exhibit biomechanical properties during movement. In their study on the function of the ligament, Parsons and colleagues9 established the inverse relationship between the ALL and ACL during internal rotation. As their cadaveric knees were subjected to an internal rotatory force through increasing angles of flexion, the contribution of the ALL towards stability significantly increased while the ACL declined. Helito and colleagues8 and Zens and colleagues10 have demonstrated length changes of the ligament through varying degrees of flexion and internal rotation. Their reports indicate greater tension during knee movements, coinciding with the description of increasing ALL stability contribution by Parsons and colleagues.9 Kennedy and colleagues7 conducted a pull-to-failure test on the ALL. The average failure load was 175 N with a stiffness of 20 N/mm, illustrating the structure is a candidate for most traditional soft tissue grafts. The biomechanical evidence of the structural properties of the ALL confirms its importance in knee function and the necessity for its reconstruction.
With the understanding that ACL contributes to rotatory stability to some extent, the notion begs the question of how a centrally located ligament is able to prevent excessive rotation in a structure with a large relative radius. Biomechanically, with such a small moment arm, the ACL would experience tremendous stress when a rotatory force is applied. The same torque applied to a more superficial structure, with a greater moment, would sustain a large reduction in the applied force. The concept of a wheel and an axle should be considered. The equation is F1 × R1 = F2 × R2. We measured on a cadaveric knee the distance from the center of rotation to the ACL and the ALL, finding the radii were 5 mm and 30 mm, respectively. Taking these measurements, we would then expect the force experienced on the axle (ACL) to be 6 times greater than what would be experienced on the periphery of the wheel (ALL). The ALL (wheel) has a significant biomechanical advantage over the ACL (axle) in controlling and enduring internal rotatory forces of the knee. This would imply that if the ALL were damaged and not re-established, the ACL would experience a 6 times greater force trying to control internal rotation, which would result in a significantly increased chance of failure and rupture.
While there is a degree of dissent on the presence of the ALL, a number of studies have classified the tissue as an independent ligamentous structure.3-7 While there is disagreement on the precise location of the femoral attachment, there is a consensus on the location of the tibial and meniscal attachments. Claes and colleagues4 originally outlined the femoral attachment as anterior and distal to the origin of the fibular collateral ligament (FCL), which is the description this technique follows. Since Claes and colleagues’4 report, many have investigated the ligament’s femoral origin with delineations ranging from posterior and proximal3,5,7 to anterior and distal.6,16-18
The accurate, noninvasive nature of the musculoskeletal ultrasound prior to any incisions being made makes this technique innovative and superior to other open surgical techniques or those that require fluoroscopy.
Conclusion
The ALL has been determined to play an integral role in the rotational stability of the knee. In the setting of instability and insufficiency, reconstruction will lead to better patient outcomes for concurrent ACL/ALL injuries and postsurgical rotatory instability following ACL procedures. This innovative technique utilizes ultrasound to ascertain the precise anatomical attachments of the ALL prior to the operation. The novel nature of this ultrasound-guided reconstruction has the potential to be applicable in many other surgical procedures.
Restoring native kinematics of the knee has been a primary goal of anterior cruciate ligament (ACL) procedures. Double-bundle ACL reconstruction, compared to single-bundle, has been hypothesized to more effectively re-establish rotational stability by re-creating the anatomic ACL, but has not yet proven to result in better clinical outcomes.1
In 1879, Dr. Paul Segond described a “fibrous, pearly band” at the lateral aspect of the knee that avulsed off the anterolateral proximal tibia during many ACL injuries.2 The role of the lateral tissues in knee stability and their relationship with ACL pathology has attracted noteworthy attention in recent time. There have been multiple studies presenting an anatomical description of a structure at the anterolateral portion of the knee with definitive femoral, meniscal, and tibial attachments, which helps control internal rotational forces.3-7 Claes and colleagues4 later found that band of tissue to be the anterolateral ligament (ALL) and determined its injury to be pathognomonic with ACL ruptures.
The ALL is a vital static stabilizer of the tibio-femoral joint, especially during internal tibial rotation.8-10 In their report on ALL and ACL reconstruction, Helito and colleagues11 acknowledge the necessity of accurate assessment of the lateral structures through imaging to determine the presence of extra-articular injury. Musculoskeletal diagnostic ultrasound has been established as an appropriate means to identify the ALL.12
Ultrasound can accurately determine the exact anatomic location of the origin and insertion of the ALL. Reconstruction of the ALL could yield better patient outcomes for those who experience concurrent ACL/ALL injury. Here we present an innovative technique for an ultrasound-guided percutaneous method for reconstruction of the ALL and report on a patient who had underwent ALL reconstruction.
Surgical Indications
All patients undergo an ultrasound evaluation preoperatively to determine if the ALL is intact or injured. Our experience has shown that when ultrasound evaluation reveals an intact ALL, the pivot shift has never been a grade III.
Surgical Technique
For a demonstration of this technique, see the video that accompanies this article.
The pivot shift test is conducted under anesthesia to determine whether an ALL reconstruction is required. The patient is placed in a supine position with the knee flexed at 30o, at neutral rotation, and without any varus or valgus stress.
A No. 15 blade is used to make a small incision centered on each spinal needle. The spinal needle is replaced with a 2.4-mm drill pin (Figure 2).
The graft and FiberTape are then passed under the IT band to the distal incision. Using the length of the BioComposite SwiveLock anchor as a guide, a mark is made on the graft after tensioning the construct in line with the leg, distal to the tibial drill pin (Table 2, Figure 4).
Rehabilitation
Rehabilitation following an ALL procedure is similar to traditional ACL rehabilitation with an added emphasis on minimizing rotational torque of the tibia in the early stages.
Case Report
In January 2013, a 17-year-old male soccer player suffered an ACL rupture of his right knee. Later that spring, he had an ACL reconstruction with an allograft. Twelve months postoperatively, the patient returned, saying that he felt much better; however, anytime he tried to plant his foot and rotate over that fixed foot, his knee felt unstable. The physical examination revealed both negative Lachman and anterior drawer tests but a I+ pivot shift test. A magnetic resonance imaging (MRI) examination revealed an intact ACL graft. A diagnostic ultrasound evaluation revealed a distal ALL injury. After discussing the risks, benefits, and goals with the patient, we opted for a diagnostic arthroscopy and a percutaneous, ultrasound-guided reconstruction of the ALL.
Postoperatively, the patient did very well. One week after surgery, he returned, saying he felt completely stable and demonstrated by repeating the rotation of his knee. The patient continued to have no issues until he returned 13 months post-ALL surgery, complaining of a recent injury that had caused the return of his feelings of instability. An MRI evaluation showed an intact ACL graft and the possibility of a ruptured ALL. Fifteen months after the initial ALL reconstruction, we proceeded with surgery. At arthroscopy, the patient was found to have a pivot shift of I+ and an intact ACL graft. The ALL was reconstructed again using an allograft, internal brace, and bone marrow concentrate. At 13 months post-ALL reconstruction revision, the patient had no complaints.
Discussion
Reconstruction of the ALL is aimed to restore anatomic rotational kinematics. Sonnery-Cottet and colleagues14 have reported promising initial results in their 2-year follow-up study of combined ACL and ALL reconstruction outcomes. This surgical technique includes use of an internal brace, which negates the necessity for external support devices and allows for earlier mobilization of the joint. A reconstruction of the ALL, performed concurrently with the ACL, does not add recovery time, but could prevent postsurgical complications and improve rehabilitation by eliminating rotational instability that presents in some ACL-reconstructed patients.
Sonnery-Cottet and colleagues15 state that their arthroscopic identification of the ALL can help to cultivate a “less invasive and more anatomic” reconstruction. The use of musculoskeletal ultrasound allows our technique to utilize a completely noninvasive imaging tool that allows proper establishment of ALL anatomy prior to the procedure. The entirety of the ALL is easily identifiable,4,12 which has proven to be shortcoming of MRI evaluation.15-17 Accurate preoperative assessment of the lateral structures is necessary in ACL-deficient individuals.11,15 Sonography also provides a means of accurate guidance and socket creation, without generating large incisions.
If the ALL is responsible for internal rotatory stability as asserted, the structure should exhibit biomechanical properties during movement. In their study on the function of the ligament, Parsons and colleagues9 established the inverse relationship between the ALL and ACL during internal rotation. As their cadaveric knees were subjected to an internal rotatory force through increasing angles of flexion, the contribution of the ALL towards stability significantly increased while the ACL declined. Helito and colleagues8 and Zens and colleagues10 have demonstrated length changes of the ligament through varying degrees of flexion and internal rotation. Their reports indicate greater tension during knee movements, coinciding with the description of increasing ALL stability contribution by Parsons and colleagues.9 Kennedy and colleagues7 conducted a pull-to-failure test on the ALL. The average failure load was 175 N with a stiffness of 20 N/mm, illustrating the structure is a candidate for most traditional soft tissue grafts. The biomechanical evidence of the structural properties of the ALL confirms its importance in knee function and the necessity for its reconstruction.
With the understanding that ACL contributes to rotatory stability to some extent, the notion begs the question of how a centrally located ligament is able to prevent excessive rotation in a structure with a large relative radius. Biomechanically, with such a small moment arm, the ACL would experience tremendous stress when a rotatory force is applied. The same torque applied to a more superficial structure, with a greater moment, would sustain a large reduction in the applied force. The concept of a wheel and an axle should be considered. The equation is F1 × R1 = F2 × R2. We measured on a cadaveric knee the distance from the center of rotation to the ACL and the ALL, finding the radii were 5 mm and 30 mm, respectively. Taking these measurements, we would then expect the force experienced on the axle (ACL) to be 6 times greater than what would be experienced on the periphery of the wheel (ALL). The ALL (wheel) has a significant biomechanical advantage over the ACL (axle) in controlling and enduring internal rotatory forces of the knee. This would imply that if the ALL were damaged and not re-established, the ACL would experience a 6 times greater force trying to control internal rotation, which would result in a significantly increased chance of failure and rupture.
While there is a degree of dissent on the presence of the ALL, a number of studies have classified the tissue as an independent ligamentous structure.3-7 While there is disagreement on the precise location of the femoral attachment, there is a consensus on the location of the tibial and meniscal attachments. Claes and colleagues4 originally outlined the femoral attachment as anterior and distal to the origin of the fibular collateral ligament (FCL), which is the description this technique follows. Since Claes and colleagues’4 report, many have investigated the ligament’s femoral origin with delineations ranging from posterior and proximal3,5,7 to anterior and distal.6,16-18
The accurate, noninvasive nature of the musculoskeletal ultrasound prior to any incisions being made makes this technique innovative and superior to other open surgical techniques or those that require fluoroscopy.
Conclusion
The ALL has been determined to play an integral role in the rotational stability of the knee. In the setting of instability and insufficiency, reconstruction will lead to better patient outcomes for concurrent ACL/ALL injuries and postsurgical rotatory instability following ACL procedures. This innovative technique utilizes ultrasound to ascertain the precise anatomical attachments of the ALL prior to the operation. The novel nature of this ultrasound-guided reconstruction has the potential to be applicable in many other surgical procedures.
1. Suomalainen P, Järvelä T, Paakkala A, Kannus P, Järvinen M. Double-bundle versus single-bundle anterior cruciate ligament reconstruction: A prospective randomized study with 5-year results. Am J Sports Med. 2012;40(7):1511-1518.
2. Segond P. Recherches cliniques et expérimentales sur les épanchements sanguins du genou par entorse. Progrés Médical. 1879;6(6):1-85. French.
3. Caterine S, Litchfield R, Johnson M, Chronik B, Getgood A. A cadaveric study of the anterolateral ligament: re-introducing the lateral capsular ligament. Knee Surg Sports Traumatol Athrosc. 2015;23(11):3186-3195.
4. Claes S, Vereecke E, Maes M, Victor J, Verdonk P, Bellemans J. Anatomy of the anterolateral ligament of the knee. J Anat. 2013;223(4):321-328.
5. Dodds AL, Halewood C, Gupte CM, Williams A, Amis AA. The anterolateral ligament: Anatomy, length changes and association with the segond fracture. Bone Joint J. 2014;96-B(3):325-331.
6. Helito CP, Demange MK, Bonadio MB, et al. Anatomy and histology of the knee anterolateral ligament. Orthop J Sports Med. 2013;1(7):2325967113513546.
7. Kennedy MI, Claes S, Fuso FA, et al. The anterolateral ligament: An anatomic, radiographic, and biomechanical analysis. Am J Sports Med. 2015;43(7):1606-1615.
8. Helito CP, Helito PV, Bonadio MB, et al. Evaluation of the length and isometric pattern of the anterolateral ligament with serial computer tomography. Orthop J Sports Med. 2014;2(12):2325967114562205.
9. Parsons EM, Gee AO, Spiekerman C, Cavanagh PR. The biomechanical function of the anterolateral ligament of the knee. Am J Sports Med. 2015;43(3):669-674.
10. Zens M, Niemeyer P, Ruhhamer J, et al. Length changes of the anterolateral ligament during passive knee motion: A human cadaveric study. Am J Sports Med. 2015;43(10):2545-2552.
11. Helito CP, Bonadio MB, Gobbi RG, et al. Combined intra- and extra-articular reconstruction of the anterior cruciate ligament: the reconstruction of the knee anterolateral ligament. Arthrosc Tech. 2015;4(3):e239-e244.
12. Cianca J, John J, Pandit S, Chiou-Tan FY. Musculoskeletal ultrasound imaging of the recently described anterolateral ligament of the knee. Am J Phys Med Rehabil. 2014;93(2):186
13. Adams JE, Zobitz ME, Reach JS, et al. Rotator cuff repair using an acellular dermal matrix graft: An in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
14. Sonnery-Cottet B, Thaunat M, Freychet B, Pupim BHB, Murphy CG, Claes S. Outcome of a combined anterior cruciate ligament and anterolateral ligament reconstruction technique with a minimum 2-year follow-up. Am J Sports Med. 2015;43(7):1598-1605.
15. Sonnery-Cottet B, Archbold P, Rezende FC, Neto AM, Fayard JM, Thaunat M. Arthroscopic identification of the anterolateral ligament of the knee. Arthrosc Tech. 2014;3(3):e389-e392.
16. Helito CP, Helito PV, Costa HP, et al. MRI evaluation of the anterolateral ligament of the knee: assessment in routine 1.5-T scans. Skeletal Radiol. 2014;43(10):1421-1427.
17. Helito CP, Demange MK, Helito PV, et al. Evaluation of the anterolateral ligament of the knee by means of magnetic resonance examination. Rev Bras Orthop. 2015;50(2):214-219.
18. Helito CP, Demange MK, Bonadio MB, et al. Radiographic landmarks for locating the femoral origin and tibial insertion of the knee anterolateral ligament. Am J Sports Med. 2014;42(10):2356-2362.
1. Suomalainen P, Järvelä T, Paakkala A, Kannus P, Järvinen M. Double-bundle versus single-bundle anterior cruciate ligament reconstruction: A prospective randomized study with 5-year results. Am J Sports Med. 2012;40(7):1511-1518.
2. Segond P. Recherches cliniques et expérimentales sur les épanchements sanguins du genou par entorse. Progrés Médical. 1879;6(6):1-85. French.
3. Caterine S, Litchfield R, Johnson M, Chronik B, Getgood A. A cadaveric study of the anterolateral ligament: re-introducing the lateral capsular ligament. Knee Surg Sports Traumatol Athrosc. 2015;23(11):3186-3195.
4. Claes S, Vereecke E, Maes M, Victor J, Verdonk P, Bellemans J. Anatomy of the anterolateral ligament of the knee. J Anat. 2013;223(4):321-328.
5. Dodds AL, Halewood C, Gupte CM, Williams A, Amis AA. The anterolateral ligament: Anatomy, length changes and association with the segond fracture. Bone Joint J. 2014;96-B(3):325-331.
6. Helito CP, Demange MK, Bonadio MB, et al. Anatomy and histology of the knee anterolateral ligament. Orthop J Sports Med. 2013;1(7):2325967113513546.
7. Kennedy MI, Claes S, Fuso FA, et al. The anterolateral ligament: An anatomic, radiographic, and biomechanical analysis. Am J Sports Med. 2015;43(7):1606-1615.
8. Helito CP, Helito PV, Bonadio MB, et al. Evaluation of the length and isometric pattern of the anterolateral ligament with serial computer tomography. Orthop J Sports Med. 2014;2(12):2325967114562205.
9. Parsons EM, Gee AO, Spiekerman C, Cavanagh PR. The biomechanical function of the anterolateral ligament of the knee. Am J Sports Med. 2015;43(3):669-674.
10. Zens M, Niemeyer P, Ruhhamer J, et al. Length changes of the anterolateral ligament during passive knee motion: A human cadaveric study. Am J Sports Med. 2015;43(10):2545-2552.
11. Helito CP, Bonadio MB, Gobbi RG, et al. Combined intra- and extra-articular reconstruction of the anterior cruciate ligament: the reconstruction of the knee anterolateral ligament. Arthrosc Tech. 2015;4(3):e239-e244.
12. Cianca J, John J, Pandit S, Chiou-Tan FY. Musculoskeletal ultrasound imaging of the recently described anterolateral ligament of the knee. Am J Phys Med Rehabil. 2014;93(2):186
13. Adams JE, Zobitz ME, Reach JS, et al. Rotator cuff repair using an acellular dermal matrix graft: An in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
14. Sonnery-Cottet B, Thaunat M, Freychet B, Pupim BHB, Murphy CG, Claes S. Outcome of a combined anterior cruciate ligament and anterolateral ligament reconstruction technique with a minimum 2-year follow-up. Am J Sports Med. 2015;43(7):1598-1605.
15. Sonnery-Cottet B, Archbold P, Rezende FC, Neto AM, Fayard JM, Thaunat M. Arthroscopic identification of the anterolateral ligament of the knee. Arthrosc Tech. 2014;3(3):e389-e392.
16. Helito CP, Helito PV, Costa HP, et al. MRI evaluation of the anterolateral ligament of the knee: assessment in routine 1.5-T scans. Skeletal Radiol. 2014;43(10):1421-1427.
17. Helito CP, Demange MK, Helito PV, et al. Evaluation of the anterolateral ligament of the knee by means of magnetic resonance examination. Rev Bras Orthop. 2015;50(2):214-219.
18. Helito CP, Demange MK, Bonadio MB, et al. Radiographic landmarks for locating the femoral origin and tibial insertion of the knee anterolateral ligament. Am J Sports Med. 2014;42(10):2356-2362.
Back to the Future
Those who cannot remember the past are condemned to repeat it.
—George Santayana (Life of Reason, 1905)
Zero. That’s the number I put on the screen when I start the lecture I give to residents about the future of orthopedics. It represents the number of cases I still do exactly the same way now as I did when I graduated from my residency program. It represents the commitment to lifelong learning that we’ve made as orthopedists. Surgical techniques innovate so rapidly that they often outpace our research, leaving us performing new techniques based solely on industry and key opinion leader recommendation, and not on randomized controlled studies. Sometimes we’re led down the wrong path (remember when the meniscus was thought to be vestigial?) and other times new techniques lead to disappoint
So it seems “everything old is new again.” That’s why this issue of AJO is called The Throwback Issue. In this issue, we revisit ideas whose time has come and gone and now come again.
Our lead article this month focuses on ACL repair. Once abandoned after a landmark paper by Feagin and Curl1 showed poor mid-term results, new and innovative techniques and instrumentation for knee surgery have made this possible. Investigators such as Murray2 and DiFelice3 have done outstanding work showing the feasibility of ACL repair. In this issue we offer a comprehensive review and surgical technique for adding ACL repair to your portfolio of surgical offerings (see pages 408 and 454). Expanded versions of both of these articles are available at amjorthopedics.com.
Our second feature article discusses the reemergence of the ALL, an idea so hot in the public domain that it has been featured as a Jeopardy question. Described originally by Müller4 as the missing link in persistent rotational instability, the ALL might offer the key to improved long-term outcomes for patients undergoing ACL surgery. Read the article on page 418 and learn how to identify which patients are candidates for ALL reconstruction, and a simple surgical technique you can apply to your practice. Scan the provided QR code to watch the accompanying surgical technique video.
The Throwback Issue marks the fifth edition of the “new AJO.” It’s time to let us know how we are doing. Please email us at ajo@frontlinemedcom.com to suggest future themes, articles you’d like to read, or suggestions for improvement.
Recently, based on the work of the authors mentioned above, I’ve begun offering ACL repair to select patients in my practice. I wouldn’t be able to do this if we as orthopedists weren’t constantly looking to improve, and weren’t willing to revisit old ideas to do it. Our goal at AJO is to present something in every article that can be immediately applied to your practice. Take a look at the articles presented this month, as we go “Back to the Future” to see what discarded ideas from our recent past can be applied to improve outcomes for your patients in the future.
1. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
2. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. Müller W. The Knee: Form, Function, and Ligament Reconstruction. Berlin: Springer-Verlag, 1983.
Those who cannot remember the past are condemned to repeat it.
—George Santayana (Life of Reason, 1905)
Zero. That’s the number I put on the screen when I start the lecture I give to residents about the future of orthopedics. It represents the number of cases I still do exactly the same way now as I did when I graduated from my residency program. It represents the commitment to lifelong learning that we’ve made as orthopedists. Surgical techniques innovate so rapidly that they often outpace our research, leaving us performing new techniques based solely on industry and key opinion leader recommendation, and not on randomized controlled studies. Sometimes we’re led down the wrong path (remember when the meniscus was thought to be vestigial?) and other times new techniques lead to disappoint
So it seems “everything old is new again.” That’s why this issue of AJO is called The Throwback Issue. In this issue, we revisit ideas whose time has come and gone and now come again.
Our lead article this month focuses on ACL repair. Once abandoned after a landmark paper by Feagin and Curl1 showed poor mid-term results, new and innovative techniques and instrumentation for knee surgery have made this possible. Investigators such as Murray2 and DiFelice3 have done outstanding work showing the feasibility of ACL repair. In this issue we offer a comprehensive review and surgical technique for adding ACL repair to your portfolio of surgical offerings (see pages 408 and 454). Expanded versions of both of these articles are available at amjorthopedics.com.
Our second feature article discusses the reemergence of the ALL, an idea so hot in the public domain that it has been featured as a Jeopardy question. Described originally by Müller4 as the missing link in persistent rotational instability, the ALL might offer the key to improved long-term outcomes for patients undergoing ACL surgery. Read the article on page 418 and learn how to identify which patients are candidates for ALL reconstruction, and a simple surgical technique you can apply to your practice. Scan the provided QR code to watch the accompanying surgical technique video.
The Throwback Issue marks the fifth edition of the “new AJO.” It’s time to let us know how we are doing. Please email us at ajo@frontlinemedcom.com to suggest future themes, articles you’d like to read, or suggestions for improvement.
Recently, based on the work of the authors mentioned above, I’ve begun offering ACL repair to select patients in my practice. I wouldn’t be able to do this if we as orthopedists weren’t constantly looking to improve, and weren’t willing to revisit old ideas to do it. Our goal at AJO is to present something in every article that can be immediately applied to your practice. Take a look at the articles presented this month, as we go “Back to the Future” to see what discarded ideas from our recent past can be applied to improve outcomes for your patients in the future.
Those who cannot remember the past are condemned to repeat it.
—George Santayana (Life of Reason, 1905)
Zero. That’s the number I put on the screen when I start the lecture I give to residents about the future of orthopedics. It represents the number of cases I still do exactly the same way now as I did when I graduated from my residency program. It represents the commitment to lifelong learning that we’ve made as orthopedists. Surgical techniques innovate so rapidly that they often outpace our research, leaving us performing new techniques based solely on industry and key opinion leader recommendation, and not on randomized controlled studies. Sometimes we’re led down the wrong path (remember when the meniscus was thought to be vestigial?) and other times new techniques lead to disappoint
So it seems “everything old is new again.” That’s why this issue of AJO is called The Throwback Issue. In this issue, we revisit ideas whose time has come and gone and now come again.
Our lead article this month focuses on ACL repair. Once abandoned after a landmark paper by Feagin and Curl1 showed poor mid-term results, new and innovative techniques and instrumentation for knee surgery have made this possible. Investigators such as Murray2 and DiFelice3 have done outstanding work showing the feasibility of ACL repair. In this issue we offer a comprehensive review and surgical technique for adding ACL repair to your portfolio of surgical offerings (see pages 408 and 454). Expanded versions of both of these articles are available at amjorthopedics.com.
Our second feature article discusses the reemergence of the ALL, an idea so hot in the public domain that it has been featured as a Jeopardy question. Described originally by Müller4 as the missing link in persistent rotational instability, the ALL might offer the key to improved long-term outcomes for patients undergoing ACL surgery. Read the article on page 418 and learn how to identify which patients are candidates for ALL reconstruction, and a simple surgical technique you can apply to your practice. Scan the provided QR code to watch the accompanying surgical technique video.
The Throwback Issue marks the fifth edition of the “new AJO.” It’s time to let us know how we are doing. Please email us at ajo@frontlinemedcom.com to suggest future themes, articles you’d like to read, or suggestions for improvement.
Recently, based on the work of the authors mentioned above, I’ve begun offering ACL repair to select patients in my practice. I wouldn’t be able to do this if we as orthopedists weren’t constantly looking to improve, and weren’t willing to revisit old ideas to do it. Our goal at AJO is to present something in every article that can be immediately applied to your practice. Take a look at the articles presented this month, as we go “Back to the Future” to see what discarded ideas from our recent past can be applied to improve outcomes for your patients in the future.
1. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
2. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. Müller W. The Knee: Form, Function, and Ligament Reconstruction. Berlin: Springer-Verlag, 1983.
1. Feagin JA Jr, Curl WW. Isolated tear of the anterior cruciate ligament: 5-year follow-up study. Am J Sports Med. 1976;4(3):95-100.
2. Murray MM, Fleming BC. Use of a bioactive scaffold to stimulate anterior cruciate ligament healing also minimizes posttraumatic osteoarthritis after surgery. Am J Sports Med. 2013;41(8):1762-1770.
3. DiFelice GS, Villegas C, Taylor SA. Anterior cruciate ligament preservation: early results of a novel arthroscopic technique for suture anchor primary anterior cruciate ligament repair. Arthroscopy. 2015;31(11):2162-2171.
4. Müller W. The Knee: Form, Function, and Ligament Reconstruction. Berlin: Springer-Verlag, 1983.
Anti–nerve growth factor drug has long-term OA pain benefit, but unclear safety
Treatment for a year with the human anti–nerve growth factor monoclonal antibody fulranumab provided pain relief and functional benefits to patients with moderate to severe chronic osteoarthritis knee or hip pain but continued to show signs that the biologic may contribute to rapid progression of disease in a proportion of patients who came to need joint replacement, especially when used concurrently with nonsteroidal anti-inflammatory drugs.
The findings come from the double-blind extension phase of a 12-week, phase II, placebo-controlled, double-blind, randomized study that found significant reduction in the average pain intensity score (P less than or equal to .030) for patients who took fulranumab (Pain. 2013 Oct;154[10]:1910-9). The investigators wanted to determine the long-term safety of the biologic in light of the Food and Drug Administration’s 2010 “clinical hold” on studies of anti–nerve growth factor (anti-NGF) drugs such as fulranumab after concerns emerged that the class of anti-NGF antibodies may be associated with potential treatment-emergent adverse events (TEAEs) leading to joint destruction.
The long-term safety and efficacy results in the extension phase of the study when fulranumab was given as an adjunctive therapy to standard pain therapy revealed higher rates of serious TEAEs, including joint replacement, that were associated with fulranumab. While most of those TEAEs were independently adjudicated to stem from normal progression of OA, one-fifth of the patients on fulranumab who needed joint replacement had rapid progression of OA (RPOA).
Investigators led by Panna Sanga, MD, director of clinical research at Janssen, sought to determine the effects of the anti-NGF biologic as an adjunctive therapy to standard pain therapy over a 92-week period in 401 patients who had completed the 12-week efficacy study, as well as over a 26-week posttreatment follow-up. In the current extension phase of the trial, patients continued on their randomized dose in the original trial of placebo or subcutaneous fulranumab 1 mg or 3 mg every 4 weeks or fulranumab 3 mg, 6 mg, or 10 mg every 8 weeks, but they were permitted to change their concurrent pain medications as clinically needed.
Although the study intended for patients to receive 2 years of treatment (104 weeks), the FDA’s clinical hold meant that the median duration of exposure to fulranumab in the extension study was only 365-393 days across the dosing regimens, the authors explained (Arthritis Rheumatol. 2016 Oct 16 doi: 10.1002/art.39943).
Overall, 421 (90%) of 466 intent-to-treat patients experienced at least one TEAE during both study phases, with similar incidence between those randomized to placebo (n = 69, 88%) and the fulranumab groups (n = 352, 91%).
TEAEs that occurred with a frequency of 10% or more among all fulranumab-treated patients were arthralgia (21%), OA (18%), paresthesia, and upper respiratory tract infection (13% each), while these were arthralgia (15%), OA (14%), and sinusitis (12%) among patients randomized to placebo.
A total of 109 patients (23%) reported serious TEAEs, including 13 (17%) taking placebo and 96 (25%) taking fulranumab. Serious TEAEs that were reported in 5% or more of patients in the fulranumab groups were knee arthroplasty (n = 38, 10%) and hip arthroplasty (n = 26, 7%). Overall, 81 joint replacements occurred in 71 patients (placebo: n = , 11%; fulranumab: n = 63, 89%).
An independent adjudication committee that the study sponsor, Janssen, established after the study was put on hold ruled that the majority of these joint replacements resulted from the normal progression of OA (n = 56, 79%). However, the adjudication committee determined that 15 (21%) patients in the fulranumab treatment groups had RPOA.
The study authors pointed out that the patients with RPOA regularly used NSAIDs and had a prior history of OA in the affected joint. Nevertheless, because of the small number of RPOA cases per treatment group, a drug or dose effect for RPOA could not be evaluated, they said.
“Future studies are warranted to demonstrate whether limiting the use of concomitant chronic NSAIDs and using only lower doses of fulranumab may reduce the risk of RPOA,” they wrote.
The extension study also looked at the longer-term efficacy of fulranumab. Efficacy endpoints on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales and the Patient Global Assessment (PGA) scores that looked at changes from baseline showed that in comparison with placebo, dosing regimens of fulranumab 3 mg every 4 weeks and 10 mg every 8 weeks gave “continued effective relief of the pain associated with knee and hip OA as early as week 4 and was maintained up to week 53,” the researchers reported.
These results were further corroborated by improvements in physical function on the WOMAC physical function subscale and PGA scale scores, which suggested “sustained efficacy of long-term fulranumab treatment,” they said.
All authors except one were employees of Janssen.
Treatment for a year with the human anti–nerve growth factor monoclonal antibody fulranumab provided pain relief and functional benefits to patients with moderate to severe chronic osteoarthritis knee or hip pain but continued to show signs that the biologic may contribute to rapid progression of disease in a proportion of patients who came to need joint replacement, especially when used concurrently with nonsteroidal anti-inflammatory drugs.
The findings come from the double-blind extension phase of a 12-week, phase II, placebo-controlled, double-blind, randomized study that found significant reduction in the average pain intensity score (P less than or equal to .030) for patients who took fulranumab (Pain. 2013 Oct;154[10]:1910-9). The investigators wanted to determine the long-term safety of the biologic in light of the Food and Drug Administration’s 2010 “clinical hold” on studies of anti–nerve growth factor (anti-NGF) drugs such as fulranumab after concerns emerged that the class of anti-NGF antibodies may be associated with potential treatment-emergent adverse events (TEAEs) leading to joint destruction.
The long-term safety and efficacy results in the extension phase of the study when fulranumab was given as an adjunctive therapy to standard pain therapy revealed higher rates of serious TEAEs, including joint replacement, that were associated with fulranumab. While most of those TEAEs were independently adjudicated to stem from normal progression of OA, one-fifth of the patients on fulranumab who needed joint replacement had rapid progression of OA (RPOA).
Investigators led by Panna Sanga, MD, director of clinical research at Janssen, sought to determine the effects of the anti-NGF biologic as an adjunctive therapy to standard pain therapy over a 92-week period in 401 patients who had completed the 12-week efficacy study, as well as over a 26-week posttreatment follow-up. In the current extension phase of the trial, patients continued on their randomized dose in the original trial of placebo or subcutaneous fulranumab 1 mg or 3 mg every 4 weeks or fulranumab 3 mg, 6 mg, or 10 mg every 8 weeks, but they were permitted to change their concurrent pain medications as clinically needed.
Although the study intended for patients to receive 2 years of treatment (104 weeks), the FDA’s clinical hold meant that the median duration of exposure to fulranumab in the extension study was only 365-393 days across the dosing regimens, the authors explained (Arthritis Rheumatol. 2016 Oct 16 doi: 10.1002/art.39943).
Overall, 421 (90%) of 466 intent-to-treat patients experienced at least one TEAE during both study phases, with similar incidence between those randomized to placebo (n = 69, 88%) and the fulranumab groups (n = 352, 91%).
TEAEs that occurred with a frequency of 10% or more among all fulranumab-treated patients were arthralgia (21%), OA (18%), paresthesia, and upper respiratory tract infection (13% each), while these were arthralgia (15%), OA (14%), and sinusitis (12%) among patients randomized to placebo.
A total of 109 patients (23%) reported serious TEAEs, including 13 (17%) taking placebo and 96 (25%) taking fulranumab. Serious TEAEs that were reported in 5% or more of patients in the fulranumab groups were knee arthroplasty (n = 38, 10%) and hip arthroplasty (n = 26, 7%). Overall, 81 joint replacements occurred in 71 patients (placebo: n = , 11%; fulranumab: n = 63, 89%).
An independent adjudication committee that the study sponsor, Janssen, established after the study was put on hold ruled that the majority of these joint replacements resulted from the normal progression of OA (n = 56, 79%). However, the adjudication committee determined that 15 (21%) patients in the fulranumab treatment groups had RPOA.
The study authors pointed out that the patients with RPOA regularly used NSAIDs and had a prior history of OA in the affected joint. Nevertheless, because of the small number of RPOA cases per treatment group, a drug or dose effect for RPOA could not be evaluated, they said.
“Future studies are warranted to demonstrate whether limiting the use of concomitant chronic NSAIDs and using only lower doses of fulranumab may reduce the risk of RPOA,” they wrote.
The extension study also looked at the longer-term efficacy of fulranumab. Efficacy endpoints on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales and the Patient Global Assessment (PGA) scores that looked at changes from baseline showed that in comparison with placebo, dosing regimens of fulranumab 3 mg every 4 weeks and 10 mg every 8 weeks gave “continued effective relief of the pain associated with knee and hip OA as early as week 4 and was maintained up to week 53,” the researchers reported.
These results were further corroborated by improvements in physical function on the WOMAC physical function subscale and PGA scale scores, which suggested “sustained efficacy of long-term fulranumab treatment,” they said.
All authors except one were employees of Janssen.
Treatment for a year with the human anti–nerve growth factor monoclonal antibody fulranumab provided pain relief and functional benefits to patients with moderate to severe chronic osteoarthritis knee or hip pain but continued to show signs that the biologic may contribute to rapid progression of disease in a proportion of patients who came to need joint replacement, especially when used concurrently with nonsteroidal anti-inflammatory drugs.
The findings come from the double-blind extension phase of a 12-week, phase II, placebo-controlled, double-blind, randomized study that found significant reduction in the average pain intensity score (P less than or equal to .030) for patients who took fulranumab (Pain. 2013 Oct;154[10]:1910-9). The investigators wanted to determine the long-term safety of the biologic in light of the Food and Drug Administration’s 2010 “clinical hold” on studies of anti–nerve growth factor (anti-NGF) drugs such as fulranumab after concerns emerged that the class of anti-NGF antibodies may be associated with potential treatment-emergent adverse events (TEAEs) leading to joint destruction.
The long-term safety and efficacy results in the extension phase of the study when fulranumab was given as an adjunctive therapy to standard pain therapy revealed higher rates of serious TEAEs, including joint replacement, that were associated with fulranumab. While most of those TEAEs were independently adjudicated to stem from normal progression of OA, one-fifth of the patients on fulranumab who needed joint replacement had rapid progression of OA (RPOA).
Investigators led by Panna Sanga, MD, director of clinical research at Janssen, sought to determine the effects of the anti-NGF biologic as an adjunctive therapy to standard pain therapy over a 92-week period in 401 patients who had completed the 12-week efficacy study, as well as over a 26-week posttreatment follow-up. In the current extension phase of the trial, patients continued on their randomized dose in the original trial of placebo or subcutaneous fulranumab 1 mg or 3 mg every 4 weeks or fulranumab 3 mg, 6 mg, or 10 mg every 8 weeks, but they were permitted to change their concurrent pain medications as clinically needed.
Although the study intended for patients to receive 2 years of treatment (104 weeks), the FDA’s clinical hold meant that the median duration of exposure to fulranumab in the extension study was only 365-393 days across the dosing regimens, the authors explained (Arthritis Rheumatol. 2016 Oct 16 doi: 10.1002/art.39943).
Overall, 421 (90%) of 466 intent-to-treat patients experienced at least one TEAE during both study phases, with similar incidence between those randomized to placebo (n = 69, 88%) and the fulranumab groups (n = 352, 91%).
TEAEs that occurred with a frequency of 10% or more among all fulranumab-treated patients were arthralgia (21%), OA (18%), paresthesia, and upper respiratory tract infection (13% each), while these were arthralgia (15%), OA (14%), and sinusitis (12%) among patients randomized to placebo.
A total of 109 patients (23%) reported serious TEAEs, including 13 (17%) taking placebo and 96 (25%) taking fulranumab. Serious TEAEs that were reported in 5% or more of patients in the fulranumab groups were knee arthroplasty (n = 38, 10%) and hip arthroplasty (n = 26, 7%). Overall, 81 joint replacements occurred in 71 patients (placebo: n = , 11%; fulranumab: n = 63, 89%).
An independent adjudication committee that the study sponsor, Janssen, established after the study was put on hold ruled that the majority of these joint replacements resulted from the normal progression of OA (n = 56, 79%). However, the adjudication committee determined that 15 (21%) patients in the fulranumab treatment groups had RPOA.
The study authors pointed out that the patients with RPOA regularly used NSAIDs and had a prior history of OA in the affected joint. Nevertheless, because of the small number of RPOA cases per treatment group, a drug or dose effect for RPOA could not be evaluated, they said.
“Future studies are warranted to demonstrate whether limiting the use of concomitant chronic NSAIDs and using only lower doses of fulranumab may reduce the risk of RPOA,” they wrote.
The extension study also looked at the longer-term efficacy of fulranumab. Efficacy endpoints on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales and the Patient Global Assessment (PGA) scores that looked at changes from baseline showed that in comparison with placebo, dosing regimens of fulranumab 3 mg every 4 weeks and 10 mg every 8 weeks gave “continued effective relief of the pain associated with knee and hip OA as early as week 4 and was maintained up to week 53,” the researchers reported.
These results were further corroborated by improvements in physical function on the WOMAC physical function subscale and PGA scale scores, which suggested “sustained efficacy of long-term fulranumab treatment,” they said.
All authors except one were employees of Janssen.
FROM ARTHRITIS & RHEUMATOLOGY
Key clinical point:
Major finding: A total of 81 joint replacements occurred in 71 patients (placebo: n = 8, 11%; fulranumab: n = 63, 89%).
Data source: Phase II randomized double-blind extension study of 401 patients with moderate to severe chronic OA knee or hip pain.
Disclosures: All authors except one were employees of Janssen, which funded the study.
Ultrasound-Guided Percutaneous Reconstruction of the Anterolateral Ligament: Surgical Technique
Modern Indications, Results, and Global Trends in the Use of Unicompartmental Knee Arthroplasty and High Tibial Osteotomy in the Treatment of Isolated Medial Compartment Osteoarthritis
An increasingly number of patients with symptomatic isolated medial unicompartmental knee osteoarthritis (OA) are too young and too functionally active to be ideal candidates for total knee arthroplasty (TKA). Isolated medial compartment OA occurs in 10% to 29.5% of all cases, whereas the isolated lateral variant is less common, with a reported incidence of 1% to 7%.1,2 In 1961, Jackson and Waugh3 introduced the high tibial osteotomy (HTO) as a surgical treatment for single-compartment OA. This procedure is designed to increase the life span of articular cartilage by unloading and redistributing the mechanical forces over the nonaffected compartment. Unicompartmental knee arthroplasty (UKA) was introduced in the 1970s as an alternative to TKA or HTO for single-compartment OA.
Since the introduction of these methods, there has been debate about which patients are appropriate candidates for each procedure. Improved surgical techniques and implant designs have led surgeons to reexamine the selection criteria and contraindications for these procedures. Furthermore, given the increasing popularity and use of UKA, the question arises as to whether HTO still has a role in clinical practice in the surgical treatment of medial OA of the knee.
To clarify current ambiguities, we review the modern indications, subjective outcome scores, and survivorship results of UKA and HTO in the treatment of isolated medial compartment degeneration of the knee. In addition, in a thorough review of the literature, we evaluate global trends in the use of both methods.
High Tibial Osteotomy for Medial Compartment OA
Indications
Before the introduction of TKA and UKA for single-compartment OA, surgical management consisted of HTO. When the mechanical axis is slightly overcorrected, the medial compartment is decompressed, ensuring tissue viability and delaying progressive compartment degeneration.
Traditionally, HTO is indicated for young (age <60 years), normal-weight, active patients with radiographic single-compartment OA.6 The knee should be stable and have good range of motion (ROM; flexion >120°), and pain should be localized to the tibiofemoral joint line.
Over the past few decades, numerous authors have reported similar inclusion criteria, clarifying their definition. This definition should be further refined in order to optimize survivorship and clinical outcomes.
Confirming age as an inclusion criterion for HTO, Trieb and colleagues7 found that the risk of failure was significantly (P = .046) higher for HTO patients older than 65 years than for those younger than 65 years (relative risk, 1.5). This finding agrees with findings of other studies, which suggests that, in particular, young patients benefit from HTO.8-11
Moreover, there is a clear relation between HTO survival and obesity. In a study of 159 CWHTOs, Akizuki and colleagues12 reported that preoperative body mass index (BMI) higher than 27.5 kg/m2 was a significant risk factor for early failure. Using BMI higher than 30 kg/m2 as a threshold, Howells and colleagues9 found significantly inferior Knee Society Score (KSS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) results for the obese group 5 years after HTO.
Radiographic evidence of severe preoperative compartment degeneration has been associated with early conversion to TKA. Flecher and colleagues11 and van Raaij and colleagues13 both concluded the best long-term survival grades are achieved in HTO patients with mild compartment OA (Ahlbäck14 grade I). The question then becomes whether these patients should be treated nonoperatively instead.15,16The literature supports strict adherence to inclusion criteria in the selection of a potential HTO candidate. Age, BMI, and the preoperative state of OA should be taken into account in order to optimize clinical outcome and survivorship results in patients about to undergo HTO.
Outcomes
Multiple authors have described or compared the midterm or long-term results of the various surgical HTO techniques. Howells and colleagues9 noted overall survival rates of 87% (5 years after CWHTO) and 79% (10 years after CWHTO). Over the 10-year postoperative period, there was significant deterioration in clinical outcome scores and survivorship. Others authors have had similar findings.17-19 van Raaij and colleagues13 found that the 10-year probability of survival after CWHTO was 75%. In 455 patients who underwent lateral CWHTO, Hui and colleagues8 found that 5-year probability of survival was 95%, 10-year probability was 79%, and 15-year probability was 56%. Niinimäki and colleagues10 used the Finnish Arthroplasty Register to report HTO survivorship at a national level. Using conversion to TKA as a cutoff, they noted 5-year survivorship of 89% and 10-year survivorship of 73%. To our knowledge, 2 groups, both in Japan, have reported substantially higher 15-year survival rates: 90%12 and 93%.20 The authors acknowledged that their results were significantly better than in other countries and that Japanese lifestyle, culture, and body habitus therefore require further investigation. At this time, it is not possible to compare their results with Western results.
In an attempt to compare the different survival rates of the various HTO techniques, Schallberger and colleagues21 conducted a retrospective study of OWHTOs and CWHTOs. At median follow-up of 16.5 years, comparative survival rates showed a trend of deterioration. Although data were limited, there were no significant differences in survival or functional outcome between the 2 techniques. In a recent randomized clinical trial, Duivenvoorden and colleagues5 compared these techniques’ midterm results (mean follow-up, 6 years). Clinical outcomes were not significantly different. There were more complications in the OWHTO group and more conversions to TKA in the CWHTO group. Considering these results, the authors suggested OWHTO without autologous bone graft is the best HTO treatment strategy for medial gonarthritis with varus malalignment of <12°.
The HTO results noted in these studies show a similar deteriorating trend; expected 10-year survivorship is 75%. Although modern implants and surgical techniques are being used, evidence supporting use of one surgical HTO method over another is lacking.
UKA for Medial Compartment OA
Indications
Since it was first introduced in the 1970s, use of UKA for single-compartment OA has been a subject of debate. The high failure rates reported at the time raised skepticism about the new treatment.22 Kozinn and Scott23 defined classic indications and contraindications. Indications included isolated medial or lateral compartment OA or osteonecrosis of the knee, age over 60 years, and weight under 82 kg. In addition, the angular deformity of the affected lower extremity had to be <15° and passively correctable to neutral at time of surgery. Last, the flexion contracture had to be <5°, and ideal ROM was 90°. Contraindications included high activity, age under 60 years, and inflammatory arthritis. Strict adherence led to improved implant survival and lower revision rates. Because of improved surgical techniques, modern implant designs, and accumulating experience with the procedure, the surgical indications for UKA have expanded. Exact thresholds for UKA inclusion, however, remain unclear.
The modern literature is overturning the traditional idea that UKA is not indicated for patients under age 60 years.23 Using KSS, Thompson and colleagues24 found that younger patients did better than older patients 2 years after UKA using various types of implants. Analyzing survivorship results, Heyse and colleagues25 concluded that UKA can be successful in patients under age 60 years and reported a 15-year survivorship rate of 85.6% and excellent outcome scores. Other authors have had similar findings.26-28
Evaluating the influence of weight, Thompson and colleagues24 found obese patients did not have a higher revision rate but did have slower progression of improvement 2 years after UKA. Cavaignac and colleagues29 concluded that, at minimum follow-up of 7 years (range, 7-22 years), weight did not influence UKA survivorship. Other authors30-33 have found no significant influence of BMI on survival.
Reports on preoperative radiographic parameters that can potentially influence UKA results are limited. In 113 medial UKAs studied by Niinimäki and colleagues,34 mild medial compartment degeneration, seen on preoperative radiographs, was associated with significantly higher failure rates. The authors concluded that other treatment options should be favored in the absence of severe isolated compartment OA.
Although the classic indications defined by Kozinn and Scott23 have yielded good to excellent UKA results, improvements in implants and surgical techniques35-38 have extended the criteria. The modern literature demonstrates that age and BMI should not be used as criteria for excluding UKA candidates. Radiographically, there should be significant isolated compartment degeneration in order to optimize patient-reported outcome and survivorship.
Outcomes
Improved implant designs and modern minimally invasive techniques have effected a change in outcome results and a renewed interest in implants. Over the past decade, multiple authors have described the various modern UKA implants and their survivorship. Reports published since UKA was introduced in the 1970s show a continual increase in implant survival. Koskinen and colleagues,39 using Finnish Arthroplasty Register data on 1819 UKAs performed between 1985 and 2003, found 10-year survival rates of 81% for Oxford implants (Zimmer Biomet), 79% for Miller-Galante II (Zimmer Biomet), 78% for Duracon (Howmedica), and 53% for PCA unicompartmental knee (Howmedica). Heyse and colleagues25 reported 10- and 15-year survivorship data (93.5% and 86.3%, respectively) for 223 patients under age 60 years at the time of their index surgery (Genesis Unicondylar implant, Smith & Nephew), performed between 1993 and 2005. KSS was good to excellent. Similar numbers in cohorts under age 60 years were reported by Schai and colleagues26 using the PFC system (Johnson & Johnson) and by Price and colleagues27 using the medial Oxford UKA. Both groups reported excellent survivorship rates: 93% at 2- to 6-year follow-up and 91% at 10-year follow-up. The outcome in older patients seems satisfactory as well. In another multicenter report, by Price and colleagues,40 medial Oxford UKAs had a 15-year survival rate of 93%. Berger and colleagues41 reported similar numbers for the Miller-Galante prosthesis. Survival rates were 98% (10 years) and 95.7% (13 years), and 92% of patients had good to excellent Hospital for Special Surgery knee scores.
Although various modern implants have had good to excellent results, the historical question of what type of UKA to use (mobile or fixed-bearing) remains unanswered. To try to address it, Peersman and colleagues42 performed a systematic review of 44 papers (9463 knees). The 2 implant types had comparable revision rates. Another recent retrospective study tried to determine what is crucial for implant survival: implant design or surgeon experience.43 The authors concluded that prosthetic component positioning is key. Other authors have reported high-volume centers are crucial for satisfactory UKA results and lower revision rates.44-46
Results of these studies indicate that, where UKAs are being performed in volume, 10-year survivorship rates higher than 90% and good to excellent outcomes can be expected.
UKA vs HTO
Cohort studies that have directly compared the 2 treatment modalities are scarce, and most have been retrospective. In a prospective study, Stukenborg-Colsman and colleagues47 randomized patients with medial compartment OA to undergo either CWHTO (32 patients) with a technique reported by Coventry48 or UKA (28 patients) with the unicondylar knee sliding prosthesis, Tübingen pattern (Aesculap), between 1988 and 1991. Patients were assessed 2.5, 4.5, and 7.5 years after surgery. More postoperative complications were noted in the HTO group. At 7- to 10-year follow-up, 71% of the HTO group and 65% of the UKA group had excellent KSS. Mean ROM was 103° after UKA (range, 35°-140°) and 117° after HTO (range, 85°-135°) during the same assessment. Although differences were not significant, Kaplan-Meier survival analysis was 60% for HTO and 77% for UKA at 10 years. Results were not promising for the implants used, compared with other implants, but the authors concluded that, because of improvements in implant designs and image-guided techniques, better long-term success can be expected with UKA than with HTO.
In another prospective study, Börjesson and colleagues49 evaluated pain during walking, ROM, British Orthopaedic Association (BOA) scores, and gait variables at 1- and 5-year follow-up. Patients with moderate medial OA (Ahlbäck14 grade I-III) were randomly selected to undergo CWHTO or UKA (Brigham, DePuy). There were no significant differences in BOA scores, ROM, or pain during walking between the 2 groups at 3 months, 1 year, and 5 years after surgery. Gait analysis showed a significant difference in favor of UKA only at 3 months after surgery. At 1- and 5-year follow-up, no significant differences were noted.
To clarify current ambiguities, Fu and colleagues50 performed a systematic review of all (11) comparative studies. These studies had a total of 5840 (5081 UKA, 759 HTO) patients. Although ROM was significantly better for the HTO group than the UKA group, the UKA group had significantly better functional results. Walking after surgery was significantly faster for the UKA group. The authors suggested the difference might be attributed to the different postoperative regimens—HTO patients wore a whole-leg plaster cast for 6 weeks, and UKA patients were allowed immediate postoperative weight-bearing. Regarding rates of survival and complications, pooled data showed no significant differences. Despite these results, the authors acknowledged the limitation of available randomized clinical trials and the multiple techniques and implants used. We share their assertion that larger prospective controlled trials are needed. These are crucial to getting a definitive answer regarding which of the 2 treatment strategies should be used for isolated compartment OA.
Current Trends in Use of UKA and HTO
Evaluation of national registries and recent reports showed a global shift in use of both HTO and UKA. Despite the lack of national HTO registries, a few reports have described use of TKA, UKA, and HTO in Western populations over the past 2 decades. Using 1998-2007 data from the Swedish Knee Arthroplasty Register, W-Dahl and colleagues51 found a 3-fold increase in UKA use, whereas HTO use was halved over the same period. Niinimäki and colleagues52 reported similar findings with the Finnish National Hospital Discharge Register. They noted a steady 6.8% annual decrease in osteotomies, whereas UKA use increased sharply after the Oxford UKA was introduced (Phase 3; Biomet). These findings are consistent with several reports from North America. In their epidemiologic analysis covering the period 1985-1990, Wright and colleagues53 found an 11% to 14% annual decrease in osteotomies among the elderly, compared with an annual decrease of only 3% to 4% among patients younger than 65 years. Nwachukwu and colleagues54 recently compared UKA and HTO practice patterns between 2007 and 2011, using data from a large US private payer insurance database. They noted an annual growth rate of 4.7% in UKA use, compared with an annual 3.9% decrease in HTO use. Furthermore, based on their subgroup analysis, they speculated there was a demographic shift toward UKA, as opposed to TKA, particularly in older women. Bolognesi and colleagues55 investigated further. Evaluating all Medicare beneficiaries who underwent knee arthroplasty in the United States between 2000 and 2009, they noted a 1.7-fold increase in TKA use and a 6.2-fold increase in UKA use. As there were no substantial changes in patient characteristics over that period, the authors hypothesized that a possible broadening of inclusion criteria may have led to the increased use of UKA.
There is a possible multifactorial explanation for the current global shift in favor of UKA. First, UKA was once a technically demanding procedure, but improved surgical techniques, image guidance, and robot assistance56 have made it relatively less difficult. Second, UKA surgery is associated with lower reported perioperative morbidities.57 We think these factors have contributed to the global trend of less HTO use and more UKA use in the treatment of unicompartmental OA.
Conclusion
The modern literature suggests the inclusion criteria for HTO have been well investigated and defined; the UKA criteria remain a matter of debate but seem to be expanding. Long-term survival results seem to favor UKA, though patient satisfaction with both procedures is good to excellent. The broadening range of inclusion criteria and consistent reports of durable outcomes, coupled with excellent patient satisfaction, likely explain the shift toward UKA in the treatment of isolated compartment degeneration.
Am J Orthop. 2016;45(6):E355-E361. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Ledingham J, Regan M, Jones A, Doherty M. Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital. Ann Rheum Dis. 1993;52(7): 520-526.
2. Wise BL, Niu J, Yang M, et al; Multicenter Osteoarthritis (MOST) Group. Patterns of compartment involvement in tibiofemoral osteoarthritis in men and women and in whites and African Americans. Arthritis Care Res. 2012;64(6): 847-852.
3. Jackson JP, Waugh W. Tibial osteotomy for osteoarthritis of the knee. J Bone Joint Surg Br. 1961;43:746-751.
4. Brouwer RW, Bierma-Zeinstra SM, van Raaij TM, Verhaar JA. Osteotomy for medial compartment arthritis of the knee using a closing wedge or an opening wedge controlled by a Puddu plate. A one-year randomised, controlled study. J Bone Joint Surg Br. 2006;88(11):1454-1459.
5. Duivenvoorden T, Brouwer RW, Baan A, et al. Comparison of closing-wedge and opening-wedge high tibial osteotomy for medial compartment osteoarthritis of the knee: a randomized controlled trial with a six-year follow-up. J Bone Joint Surg Am. 2014;96(17):1425-1432.
6. Hutchison CR, Cho B, Wong N, Agnidis Z, Gross AE. Proximal valgus tibial osteotomy for osteoarthritis of the knee. Instr Course Lect. 1999;48:131-134.
7. Trieb K, Grohs J, Hanslik-Schnabel B, Stulnig T, Panotopoulos J, Wanivenhaus A. Age predicts outcome of high-tibial osteotomy. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):149-152.
8. Hui C, Salmon LJ, Kok A, et al. Long-term survival of high tibial osteotomy for medial compartment osteoarthritis of the knee. Am J Sports Med. 2011;39(1):64-70.
9. Howells NR, Salmon L, Waller A, Scanelli J, Pinczewski LA. The outcome at ten years of lateral closing-wedge high tibial osteotomy: determinants of survival and functional outcome. Bone Joint J Br. 2014;96(11):1491-1497.
10. Niinimäki TT, Eskelinen A, Mann BS, Junnila M, Ohtonen P, Leppilahti J. Survivorship of high tibial osteotomy in the treatment of osteoarthritis of the knee: Finnish registry-based study of 3195 knees. J Bone Joint Surg Br. 2012;94(11):1517-1521.
11. Flecher X, Parratte S, Aubaniac JM, Argenson JN. A 12-28-year followup study of closing wedge high tibial osteotomy. Clin Orthop Relat Res. 2006;(452):91-96.
12. Akizuki S, Shibakawa A, Takizawa T, Yamazaki I, Horiuchi H. The long-term outcome of high tibial osteotomy: a ten- to 20-year follow-up. J Bone Joint Surg Br. 2008;90(5):592-596.
13. van Raaij T, Reijman M, Brouwer RW, Jakma TS, Verhaar JN. Survival of closing-wedge high tibial osteotomy: good outcome in men with low-grade osteoarthritis after 10-16 years. Acta Orthop. 2008;79:230-234.
14. Ahlbäck S. Osteoarthrosis of the knee. A radiographic investigation. Acta Radiol Diagn. 1968;(suppl 277):7-72.
15. Bannuru RR, Natov NS, Obadan IE, Price LL, Schmid CH, McAlindon TE. Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and meta-analysis. Arthritis Rheum. 2009;61(12):1704-1711.
16. Evanich JD, Evanich CJ, Wright MB, Rydlewicz JA. Efficacy of intraarticular hyaluronic acid injections in knee osteoarthritis. Clin Orthop Relat Res. 2001;(390):173-181.
17. Naudie D, Bourne RB, Rorabeck CH, Bourne TJ. The Install Award. Survivorship of the high tibial valgus osteotomy. A 10- to -22-year followup study. Clin Orthop Relat Res. 1999;(367):18-27.
18. Sprenger TR, Doerzbacher JF. Tibial osteotomy for the treatment of varus gonarthrosis. Survival and failure analysis to twenty-two years. J Bone Joint Surg Br. 2003;85(3):469-474.
19. Billings A, Scott DF, Camargo MP, Hofmann AA. High tibial osteotomy with a calibrated osteotomy guide, rigid internal fixation, and early motion. Long-term follow-up. J Bone Joint Surg Am. 2000;82(1):70-79.
20. Koshino T, Yoshida T, Ara Y, Saito I, Saito T. Fifteen to twenty-eight years’ follow-up results of high tibial valgus osteotomy for osteoarthritic knee. Knee. 2004;11(6):439-444.
21. Schallberger A, Jacobi M, Wahl P, Maestretti G, Jakob RP. High tibial valgus osteotomy in unicompartmental medial osteoarthritis of the knee: a retrospective follow-up study over 13-21 years. Knee Surg Sports Traumatol Arthrosc. 2011;19(1):122-127.
22. Insall J, Aglietti P. A five to seven-year follow-up of unicondylar arthroplasty. J Bone Joint Surg Am. 1980;62(8):1329-1337.
23. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg Am. 1989;71(1):145-150.
24. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
25. Heyse TJ, Khefacha A, Peersman G, Cartier P. Survivorship of UKA in the middle-aged. Knee. 2012;19(5):585-591.
26. Schai PA, Suh JT, Thornhill TS, Scott RD. Unicompartmental knee arthroplasty in middle-aged patients: a 2- to 6-year follow-up evaluation. J Arthroplasty. 1998;13(4):365-372.
27. Price AJ, Dodd CA, Svard UG, Murray DW. Oxford medial unicompartmental knee arthroplasty in patients younger and older than 60 years of age. J Bone Joint Surg Br. 2005;87(11):1488-1492.
28. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg Am. 2003;85(10):1968-1973.
29. Cavaignac E, Lafontan V, Reina N, et al. Obesity has no adverse effect on the outcome of unicompartmental knee replacement at a minimum follow-up of seven years. Bone Joint J Br. 2013;95(8):1064-1068.
30. Tabor OB Jr, Tabor OB, Bernard M, Wan JY. Unicompartmental knee arthroplasty: long-term success in middle-age and obese patients. J Surg Orthop Adv. 2005;14(2):59-63.
31. Berend KR, Lombardi AV Jr, Adams JB. Obesity, young age, patellofemoral disease, and anterior knee pain: identifying the unicondylar arthroplasty patient in the United States. Orthopedics. 2007;30(5 suppl):19-23.
32. Xing Z, Katz J, Jiranek W. Unicompartmental knee arthroplasty: factors influencing the outcome. J Knee Surg. 2012;25(5):369-373.
33. Plate JF, Augart MA, Seyler TM, et al. Obesity has no effect on outcomes following unicompartmental knee arthroplasty [published online April 12, 2015]. Knee Surg Sports Traumatol Arthrosc. doi:10.1007/s00167-015-3597-5.
34. Niinimäki TT, Murray DW, Partanen J, Pajala A, Leppilahti JI. Unicompartmental knee arthroplasties implanted for osteoarthritis with partial loss of joint space have high re-operation rates. Knee. 2011;18(6):432-435.
35. Carlsson LV, Albrektsson BE, Regnér LR. Minimally invasive surgery vs conventional exposure using the Miller-Galante unicompartmental knee arthroplasty: a randomized radiostereometric study. J Arthroplasty. 2006;21(2):151-156.
36. Repicci JA. Mini-invasive knee unicompartmental arthroplasty: bone-sparing technique. Surg Technol Int. 2003;11:282-286.
37. Pandit H, Jenkins C, Barker K, Dodd CA, Murray DW. The Oxford medial unicompartmental knee replacement using a minimally-invasive approach. J Bone Joint Surg Br. 2006;88(1):54-60.
38. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
39. Koskinen E, Paavolainen P, Eskelinen A, Pulkkinen P, Remes V. Unicondylar knee replacement for primary osteoarthritis: a prospective follow-up study of 1,819 patients from the Finnish Arthroplasty Register. Acta Orthop. 2007;78(1):128-135.
40. Price AJ, Waite JC, Svard U. Long-term clinical results of the medial Oxford unicompartmental knee arthroplasty. Clin Orthop Relat Res. 2005;(435):171-180.
41. Berger RA, Meneghini RM, Jacobs JJ, et al. Results of unicompartmental knee arthroplasty at a minimum of ten years of follow-up. J Bone Joint Surg Am. 2005;87(5):999-1006.
42. Peersman G, Stuyts B, Vandenlangenbergh T, Cartier P, Fennema P. Fixed- versus mobile-bearing UKA: a systematic review and meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2015;23(11):3296-3305.
43. Zambianchi F, Digennaro V, Giorgini A, et al. Surgeon’s experience influences UKA survivorship: a comparative study between all-poly and metal back designs. Knee Surg Sports Traumatol Arthrosc. 2015;23(7):2074-2080.
44. Robertsson O, Knutson K, Lewold S, Lidgren L. The routine of surgical management reduces failure after unicompartmental knee arthroplasty. J Bone Joint Surg Br. 2001;83(1):45-49.
45. Furnes O, Espehaug B, Lie SA, Vollset SE, Engesaeter LB, Havelin LI. Failure mechanisms after unicompartmental and tricompartmental primary knee replacement with cement. J Bone Joint Surg Am. 2007;89(3):519-525.
46. Robertsson O, Lidgren L. The short-term results of 3 common UKA implants during different periods in Sweden. J Arthroplasty. 2008;23(6):801-807.
47. Stukenborg-Colsman C, Wirth CJ, Lazovic D, Wefer A. High tibial osteotomy versus unicompartmental joint replacement in unicompartmental knee joint osteoarthritis: 7-10-year follow-up prospective randomised study. Knee. 2001;8(3):187-194.
48. Coventry MB. Osteotomy about the knee for degenerative and rheumatoid arthritis. J Bone Joint Surg Am. 1973;55(1):23-48.
49. Börjesson M, Weidenhielm L, Mattsson E, Olsson E. Gait and clinical measurements in patients with knee osteoarthritis after surgery: a prospective 5-year follow-up study. Knee. 2005;12(2):121-127.
50. Fu D, Li G, Chen K, Zhao Y, Hua Y, Cai Z. Comparison of high tibial osteotomy and unicompartmental knee arthroplasty in the treatment of unicompartmental osteoarthritis: a meta-analysis. J Arthroplasty. 2013;28(5):759-765.
51. W-Dahl A, Robertsson O, Lidgren L. Surgery for knee osteoarthritis in younger patients. Acta Orthop. 2010;81(2):161-164.
52. Niinimäki TT, Eskelinen A, Ohtonen P, Junnila M, Leppilahti J. Incidence of osteotomies around the knee for the treatment of knee osteoarthritis: a 22-year population-based study. Int Orthop. 2012;36(7):1399-1402.
53. Wright J, Heck D, Hawker G, et al. Rates of tibial osteotomies in Canada and the United States. Clin Orthop Relat Res. 1995;(319):266-275.
54. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
55. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
56. Pearle AD, O’Loughlin PF, Kendoff DO. Robot-assisted unicompartmental knee arthroplasty. J Arthroplasty. 2010;25(2):230-237.
57. Brown NM, Sheth NP, Davis K, et al. Total knee arthroplasty has higher postoperative morbidity than unicompartmental knee arthroplasty: a multicenter analysis. J Arthroplasty. 2012;27(8 suppl):86-90.
An increasingly number of patients with symptomatic isolated medial unicompartmental knee osteoarthritis (OA) are too young and too functionally active to be ideal candidates for total knee arthroplasty (TKA). Isolated medial compartment OA occurs in 10% to 29.5% of all cases, whereas the isolated lateral variant is less common, with a reported incidence of 1% to 7%.1,2 In 1961, Jackson and Waugh3 introduced the high tibial osteotomy (HTO) as a surgical treatment for single-compartment OA. This procedure is designed to increase the life span of articular cartilage by unloading and redistributing the mechanical forces over the nonaffected compartment. Unicompartmental knee arthroplasty (UKA) was introduced in the 1970s as an alternative to TKA or HTO for single-compartment OA.
Since the introduction of these methods, there has been debate about which patients are appropriate candidates for each procedure. Improved surgical techniques and implant designs have led surgeons to reexamine the selection criteria and contraindications for these procedures. Furthermore, given the increasing popularity and use of UKA, the question arises as to whether HTO still has a role in clinical practice in the surgical treatment of medial OA of the knee.
To clarify current ambiguities, we review the modern indications, subjective outcome scores, and survivorship results of UKA and HTO in the treatment of isolated medial compartment degeneration of the knee. In addition, in a thorough review of the literature, we evaluate global trends in the use of both methods.
High Tibial Osteotomy for Medial Compartment OA
Indications
Before the introduction of TKA and UKA for single-compartment OA, surgical management consisted of HTO. When the mechanical axis is slightly overcorrected, the medial compartment is decompressed, ensuring tissue viability and delaying progressive compartment degeneration.
Traditionally, HTO is indicated for young (age <60 years), normal-weight, active patients with radiographic single-compartment OA.6 The knee should be stable and have good range of motion (ROM; flexion >120°), and pain should be localized to the tibiofemoral joint line.
Over the past few decades, numerous authors have reported similar inclusion criteria, clarifying their definition. This definition should be further refined in order to optimize survivorship and clinical outcomes.
Confirming age as an inclusion criterion for HTO, Trieb and colleagues7 found that the risk of failure was significantly (P = .046) higher for HTO patients older than 65 years than for those younger than 65 years (relative risk, 1.5). This finding agrees with findings of other studies, which suggests that, in particular, young patients benefit from HTO.8-11
Moreover, there is a clear relation between HTO survival and obesity. In a study of 159 CWHTOs, Akizuki and colleagues12 reported that preoperative body mass index (BMI) higher than 27.5 kg/m2 was a significant risk factor for early failure. Using BMI higher than 30 kg/m2 as a threshold, Howells and colleagues9 found significantly inferior Knee Society Score (KSS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) results for the obese group 5 years after HTO.
Radiographic evidence of severe preoperative compartment degeneration has been associated with early conversion to TKA. Flecher and colleagues11 and van Raaij and colleagues13 both concluded the best long-term survival grades are achieved in HTO patients with mild compartment OA (Ahlbäck14 grade I). The question then becomes whether these patients should be treated nonoperatively instead.15,16The literature supports strict adherence to inclusion criteria in the selection of a potential HTO candidate. Age, BMI, and the preoperative state of OA should be taken into account in order to optimize clinical outcome and survivorship results in patients about to undergo HTO.
Outcomes
Multiple authors have described or compared the midterm or long-term results of the various surgical HTO techniques. Howells and colleagues9 noted overall survival rates of 87% (5 years after CWHTO) and 79% (10 years after CWHTO). Over the 10-year postoperative period, there was significant deterioration in clinical outcome scores and survivorship. Others authors have had similar findings.17-19 van Raaij and colleagues13 found that the 10-year probability of survival after CWHTO was 75%. In 455 patients who underwent lateral CWHTO, Hui and colleagues8 found that 5-year probability of survival was 95%, 10-year probability was 79%, and 15-year probability was 56%. Niinimäki and colleagues10 used the Finnish Arthroplasty Register to report HTO survivorship at a national level. Using conversion to TKA as a cutoff, they noted 5-year survivorship of 89% and 10-year survivorship of 73%. To our knowledge, 2 groups, both in Japan, have reported substantially higher 15-year survival rates: 90%12 and 93%.20 The authors acknowledged that their results were significantly better than in other countries and that Japanese lifestyle, culture, and body habitus therefore require further investigation. At this time, it is not possible to compare their results with Western results.
In an attempt to compare the different survival rates of the various HTO techniques, Schallberger and colleagues21 conducted a retrospective study of OWHTOs and CWHTOs. At median follow-up of 16.5 years, comparative survival rates showed a trend of deterioration. Although data were limited, there were no significant differences in survival or functional outcome between the 2 techniques. In a recent randomized clinical trial, Duivenvoorden and colleagues5 compared these techniques’ midterm results (mean follow-up, 6 years). Clinical outcomes were not significantly different. There were more complications in the OWHTO group and more conversions to TKA in the CWHTO group. Considering these results, the authors suggested OWHTO without autologous bone graft is the best HTO treatment strategy for medial gonarthritis with varus malalignment of <12°.
The HTO results noted in these studies show a similar deteriorating trend; expected 10-year survivorship is 75%. Although modern implants and surgical techniques are being used, evidence supporting use of one surgical HTO method over another is lacking.
UKA for Medial Compartment OA
Indications
Since it was first introduced in the 1970s, use of UKA for single-compartment OA has been a subject of debate. The high failure rates reported at the time raised skepticism about the new treatment.22 Kozinn and Scott23 defined classic indications and contraindications. Indications included isolated medial or lateral compartment OA or osteonecrosis of the knee, age over 60 years, and weight under 82 kg. In addition, the angular deformity of the affected lower extremity had to be <15° and passively correctable to neutral at time of surgery. Last, the flexion contracture had to be <5°, and ideal ROM was 90°. Contraindications included high activity, age under 60 years, and inflammatory arthritis. Strict adherence led to improved implant survival and lower revision rates. Because of improved surgical techniques, modern implant designs, and accumulating experience with the procedure, the surgical indications for UKA have expanded. Exact thresholds for UKA inclusion, however, remain unclear.
The modern literature is overturning the traditional idea that UKA is not indicated for patients under age 60 years.23 Using KSS, Thompson and colleagues24 found that younger patients did better than older patients 2 years after UKA using various types of implants. Analyzing survivorship results, Heyse and colleagues25 concluded that UKA can be successful in patients under age 60 years and reported a 15-year survivorship rate of 85.6% and excellent outcome scores. Other authors have had similar findings.26-28
Evaluating the influence of weight, Thompson and colleagues24 found obese patients did not have a higher revision rate but did have slower progression of improvement 2 years after UKA. Cavaignac and colleagues29 concluded that, at minimum follow-up of 7 years (range, 7-22 years), weight did not influence UKA survivorship. Other authors30-33 have found no significant influence of BMI on survival.
Reports on preoperative radiographic parameters that can potentially influence UKA results are limited. In 113 medial UKAs studied by Niinimäki and colleagues,34 mild medial compartment degeneration, seen on preoperative radiographs, was associated with significantly higher failure rates. The authors concluded that other treatment options should be favored in the absence of severe isolated compartment OA.
Although the classic indications defined by Kozinn and Scott23 have yielded good to excellent UKA results, improvements in implants and surgical techniques35-38 have extended the criteria. The modern literature demonstrates that age and BMI should not be used as criteria for excluding UKA candidates. Radiographically, there should be significant isolated compartment degeneration in order to optimize patient-reported outcome and survivorship.
Outcomes
Improved implant designs and modern minimally invasive techniques have effected a change in outcome results and a renewed interest in implants. Over the past decade, multiple authors have described the various modern UKA implants and their survivorship. Reports published since UKA was introduced in the 1970s show a continual increase in implant survival. Koskinen and colleagues,39 using Finnish Arthroplasty Register data on 1819 UKAs performed between 1985 and 2003, found 10-year survival rates of 81% for Oxford implants (Zimmer Biomet), 79% for Miller-Galante II (Zimmer Biomet), 78% for Duracon (Howmedica), and 53% for PCA unicompartmental knee (Howmedica). Heyse and colleagues25 reported 10- and 15-year survivorship data (93.5% and 86.3%, respectively) for 223 patients under age 60 years at the time of their index surgery (Genesis Unicondylar implant, Smith & Nephew), performed between 1993 and 2005. KSS was good to excellent. Similar numbers in cohorts under age 60 years were reported by Schai and colleagues26 using the PFC system (Johnson & Johnson) and by Price and colleagues27 using the medial Oxford UKA. Both groups reported excellent survivorship rates: 93% at 2- to 6-year follow-up and 91% at 10-year follow-up. The outcome in older patients seems satisfactory as well. In another multicenter report, by Price and colleagues,40 medial Oxford UKAs had a 15-year survival rate of 93%. Berger and colleagues41 reported similar numbers for the Miller-Galante prosthesis. Survival rates were 98% (10 years) and 95.7% (13 years), and 92% of patients had good to excellent Hospital for Special Surgery knee scores.
Although various modern implants have had good to excellent results, the historical question of what type of UKA to use (mobile or fixed-bearing) remains unanswered. To try to address it, Peersman and colleagues42 performed a systematic review of 44 papers (9463 knees). The 2 implant types had comparable revision rates. Another recent retrospective study tried to determine what is crucial for implant survival: implant design or surgeon experience.43 The authors concluded that prosthetic component positioning is key. Other authors have reported high-volume centers are crucial for satisfactory UKA results and lower revision rates.44-46
Results of these studies indicate that, where UKAs are being performed in volume, 10-year survivorship rates higher than 90% and good to excellent outcomes can be expected.
UKA vs HTO
Cohort studies that have directly compared the 2 treatment modalities are scarce, and most have been retrospective. In a prospective study, Stukenborg-Colsman and colleagues47 randomized patients with medial compartment OA to undergo either CWHTO (32 patients) with a technique reported by Coventry48 or UKA (28 patients) with the unicondylar knee sliding prosthesis, Tübingen pattern (Aesculap), between 1988 and 1991. Patients were assessed 2.5, 4.5, and 7.5 years after surgery. More postoperative complications were noted in the HTO group. At 7- to 10-year follow-up, 71% of the HTO group and 65% of the UKA group had excellent KSS. Mean ROM was 103° after UKA (range, 35°-140°) and 117° after HTO (range, 85°-135°) during the same assessment. Although differences were not significant, Kaplan-Meier survival analysis was 60% for HTO and 77% for UKA at 10 years. Results were not promising for the implants used, compared with other implants, but the authors concluded that, because of improvements in implant designs and image-guided techniques, better long-term success can be expected with UKA than with HTO.
In another prospective study, Börjesson and colleagues49 evaluated pain during walking, ROM, British Orthopaedic Association (BOA) scores, and gait variables at 1- and 5-year follow-up. Patients with moderate medial OA (Ahlbäck14 grade I-III) were randomly selected to undergo CWHTO or UKA (Brigham, DePuy). There were no significant differences in BOA scores, ROM, or pain during walking between the 2 groups at 3 months, 1 year, and 5 years after surgery. Gait analysis showed a significant difference in favor of UKA only at 3 months after surgery. At 1- and 5-year follow-up, no significant differences were noted.
To clarify current ambiguities, Fu and colleagues50 performed a systematic review of all (11) comparative studies. These studies had a total of 5840 (5081 UKA, 759 HTO) patients. Although ROM was significantly better for the HTO group than the UKA group, the UKA group had significantly better functional results. Walking after surgery was significantly faster for the UKA group. The authors suggested the difference might be attributed to the different postoperative regimens—HTO patients wore a whole-leg plaster cast for 6 weeks, and UKA patients were allowed immediate postoperative weight-bearing. Regarding rates of survival and complications, pooled data showed no significant differences. Despite these results, the authors acknowledged the limitation of available randomized clinical trials and the multiple techniques and implants used. We share their assertion that larger prospective controlled trials are needed. These are crucial to getting a definitive answer regarding which of the 2 treatment strategies should be used for isolated compartment OA.
Current Trends in Use of UKA and HTO
Evaluation of national registries and recent reports showed a global shift in use of both HTO and UKA. Despite the lack of national HTO registries, a few reports have described use of TKA, UKA, and HTO in Western populations over the past 2 decades. Using 1998-2007 data from the Swedish Knee Arthroplasty Register, W-Dahl and colleagues51 found a 3-fold increase in UKA use, whereas HTO use was halved over the same period. Niinimäki and colleagues52 reported similar findings with the Finnish National Hospital Discharge Register. They noted a steady 6.8% annual decrease in osteotomies, whereas UKA use increased sharply after the Oxford UKA was introduced (Phase 3; Biomet). These findings are consistent with several reports from North America. In their epidemiologic analysis covering the period 1985-1990, Wright and colleagues53 found an 11% to 14% annual decrease in osteotomies among the elderly, compared with an annual decrease of only 3% to 4% among patients younger than 65 years. Nwachukwu and colleagues54 recently compared UKA and HTO practice patterns between 2007 and 2011, using data from a large US private payer insurance database. They noted an annual growth rate of 4.7% in UKA use, compared with an annual 3.9% decrease in HTO use. Furthermore, based on their subgroup analysis, they speculated there was a demographic shift toward UKA, as opposed to TKA, particularly in older women. Bolognesi and colleagues55 investigated further. Evaluating all Medicare beneficiaries who underwent knee arthroplasty in the United States between 2000 and 2009, they noted a 1.7-fold increase in TKA use and a 6.2-fold increase in UKA use. As there were no substantial changes in patient characteristics over that period, the authors hypothesized that a possible broadening of inclusion criteria may have led to the increased use of UKA.
There is a possible multifactorial explanation for the current global shift in favor of UKA. First, UKA was once a technically demanding procedure, but improved surgical techniques, image guidance, and robot assistance56 have made it relatively less difficult. Second, UKA surgery is associated with lower reported perioperative morbidities.57 We think these factors have contributed to the global trend of less HTO use and more UKA use in the treatment of unicompartmental OA.
Conclusion
The modern literature suggests the inclusion criteria for HTO have been well investigated and defined; the UKA criteria remain a matter of debate but seem to be expanding. Long-term survival results seem to favor UKA, though patient satisfaction with both procedures is good to excellent. The broadening range of inclusion criteria and consistent reports of durable outcomes, coupled with excellent patient satisfaction, likely explain the shift toward UKA in the treatment of isolated compartment degeneration.
Am J Orthop. 2016;45(6):E355-E361. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
An increasingly number of patients with symptomatic isolated medial unicompartmental knee osteoarthritis (OA) are too young and too functionally active to be ideal candidates for total knee arthroplasty (TKA). Isolated medial compartment OA occurs in 10% to 29.5% of all cases, whereas the isolated lateral variant is less common, with a reported incidence of 1% to 7%.1,2 In 1961, Jackson and Waugh3 introduced the high tibial osteotomy (HTO) as a surgical treatment for single-compartment OA. This procedure is designed to increase the life span of articular cartilage by unloading and redistributing the mechanical forces over the nonaffected compartment. Unicompartmental knee arthroplasty (UKA) was introduced in the 1970s as an alternative to TKA or HTO for single-compartment OA.
Since the introduction of these methods, there has been debate about which patients are appropriate candidates for each procedure. Improved surgical techniques and implant designs have led surgeons to reexamine the selection criteria and contraindications for these procedures. Furthermore, given the increasing popularity and use of UKA, the question arises as to whether HTO still has a role in clinical practice in the surgical treatment of medial OA of the knee.
To clarify current ambiguities, we review the modern indications, subjective outcome scores, and survivorship results of UKA and HTO in the treatment of isolated medial compartment degeneration of the knee. In addition, in a thorough review of the literature, we evaluate global trends in the use of both methods.
High Tibial Osteotomy for Medial Compartment OA
Indications
Before the introduction of TKA and UKA for single-compartment OA, surgical management consisted of HTO. When the mechanical axis is slightly overcorrected, the medial compartment is decompressed, ensuring tissue viability and delaying progressive compartment degeneration.
Traditionally, HTO is indicated for young (age <60 years), normal-weight, active patients with radiographic single-compartment OA.6 The knee should be stable and have good range of motion (ROM; flexion >120°), and pain should be localized to the tibiofemoral joint line.
Over the past few decades, numerous authors have reported similar inclusion criteria, clarifying their definition. This definition should be further refined in order to optimize survivorship and clinical outcomes.
Confirming age as an inclusion criterion for HTO, Trieb and colleagues7 found that the risk of failure was significantly (P = .046) higher for HTO patients older than 65 years than for those younger than 65 years (relative risk, 1.5). This finding agrees with findings of other studies, which suggests that, in particular, young patients benefit from HTO.8-11
Moreover, there is a clear relation between HTO survival and obesity. In a study of 159 CWHTOs, Akizuki and colleagues12 reported that preoperative body mass index (BMI) higher than 27.5 kg/m2 was a significant risk factor for early failure. Using BMI higher than 30 kg/m2 as a threshold, Howells and colleagues9 found significantly inferior Knee Society Score (KSS) and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) results for the obese group 5 years after HTO.
Radiographic evidence of severe preoperative compartment degeneration has been associated with early conversion to TKA. Flecher and colleagues11 and van Raaij and colleagues13 both concluded the best long-term survival grades are achieved in HTO patients with mild compartment OA (Ahlbäck14 grade I). The question then becomes whether these patients should be treated nonoperatively instead.15,16The literature supports strict adherence to inclusion criteria in the selection of a potential HTO candidate. Age, BMI, and the preoperative state of OA should be taken into account in order to optimize clinical outcome and survivorship results in patients about to undergo HTO.
Outcomes
Multiple authors have described or compared the midterm or long-term results of the various surgical HTO techniques. Howells and colleagues9 noted overall survival rates of 87% (5 years after CWHTO) and 79% (10 years after CWHTO). Over the 10-year postoperative period, there was significant deterioration in clinical outcome scores and survivorship. Others authors have had similar findings.17-19 van Raaij and colleagues13 found that the 10-year probability of survival after CWHTO was 75%. In 455 patients who underwent lateral CWHTO, Hui and colleagues8 found that 5-year probability of survival was 95%, 10-year probability was 79%, and 15-year probability was 56%. Niinimäki and colleagues10 used the Finnish Arthroplasty Register to report HTO survivorship at a national level. Using conversion to TKA as a cutoff, they noted 5-year survivorship of 89% and 10-year survivorship of 73%. To our knowledge, 2 groups, both in Japan, have reported substantially higher 15-year survival rates: 90%12 and 93%.20 The authors acknowledged that their results were significantly better than in other countries and that Japanese lifestyle, culture, and body habitus therefore require further investigation. At this time, it is not possible to compare their results with Western results.
In an attempt to compare the different survival rates of the various HTO techniques, Schallberger and colleagues21 conducted a retrospective study of OWHTOs and CWHTOs. At median follow-up of 16.5 years, comparative survival rates showed a trend of deterioration. Although data were limited, there were no significant differences in survival or functional outcome between the 2 techniques. In a recent randomized clinical trial, Duivenvoorden and colleagues5 compared these techniques’ midterm results (mean follow-up, 6 years). Clinical outcomes were not significantly different. There were more complications in the OWHTO group and more conversions to TKA in the CWHTO group. Considering these results, the authors suggested OWHTO without autologous bone graft is the best HTO treatment strategy for medial gonarthritis with varus malalignment of <12°.
The HTO results noted in these studies show a similar deteriorating trend; expected 10-year survivorship is 75%. Although modern implants and surgical techniques are being used, evidence supporting use of one surgical HTO method over another is lacking.
UKA for Medial Compartment OA
Indications
Since it was first introduced in the 1970s, use of UKA for single-compartment OA has been a subject of debate. The high failure rates reported at the time raised skepticism about the new treatment.22 Kozinn and Scott23 defined classic indications and contraindications. Indications included isolated medial or lateral compartment OA or osteonecrosis of the knee, age over 60 years, and weight under 82 kg. In addition, the angular deformity of the affected lower extremity had to be <15° and passively correctable to neutral at time of surgery. Last, the flexion contracture had to be <5°, and ideal ROM was 90°. Contraindications included high activity, age under 60 years, and inflammatory arthritis. Strict adherence led to improved implant survival and lower revision rates. Because of improved surgical techniques, modern implant designs, and accumulating experience with the procedure, the surgical indications for UKA have expanded. Exact thresholds for UKA inclusion, however, remain unclear.
The modern literature is overturning the traditional idea that UKA is not indicated for patients under age 60 years.23 Using KSS, Thompson and colleagues24 found that younger patients did better than older patients 2 years after UKA using various types of implants. Analyzing survivorship results, Heyse and colleagues25 concluded that UKA can be successful in patients under age 60 years and reported a 15-year survivorship rate of 85.6% and excellent outcome scores. Other authors have had similar findings.26-28
Evaluating the influence of weight, Thompson and colleagues24 found obese patients did not have a higher revision rate but did have slower progression of improvement 2 years after UKA. Cavaignac and colleagues29 concluded that, at minimum follow-up of 7 years (range, 7-22 years), weight did not influence UKA survivorship. Other authors30-33 have found no significant influence of BMI on survival.
Reports on preoperative radiographic parameters that can potentially influence UKA results are limited. In 113 medial UKAs studied by Niinimäki and colleagues,34 mild medial compartment degeneration, seen on preoperative radiographs, was associated with significantly higher failure rates. The authors concluded that other treatment options should be favored in the absence of severe isolated compartment OA.
Although the classic indications defined by Kozinn and Scott23 have yielded good to excellent UKA results, improvements in implants and surgical techniques35-38 have extended the criteria. The modern literature demonstrates that age and BMI should not be used as criteria for excluding UKA candidates. Radiographically, there should be significant isolated compartment degeneration in order to optimize patient-reported outcome and survivorship.
Outcomes
Improved implant designs and modern minimally invasive techniques have effected a change in outcome results and a renewed interest in implants. Over the past decade, multiple authors have described the various modern UKA implants and their survivorship. Reports published since UKA was introduced in the 1970s show a continual increase in implant survival. Koskinen and colleagues,39 using Finnish Arthroplasty Register data on 1819 UKAs performed between 1985 and 2003, found 10-year survival rates of 81% for Oxford implants (Zimmer Biomet), 79% for Miller-Galante II (Zimmer Biomet), 78% for Duracon (Howmedica), and 53% for PCA unicompartmental knee (Howmedica). Heyse and colleagues25 reported 10- and 15-year survivorship data (93.5% and 86.3%, respectively) for 223 patients under age 60 years at the time of their index surgery (Genesis Unicondylar implant, Smith & Nephew), performed between 1993 and 2005. KSS was good to excellent. Similar numbers in cohorts under age 60 years were reported by Schai and colleagues26 using the PFC system (Johnson & Johnson) and by Price and colleagues27 using the medial Oxford UKA. Both groups reported excellent survivorship rates: 93% at 2- to 6-year follow-up and 91% at 10-year follow-up. The outcome in older patients seems satisfactory as well. In another multicenter report, by Price and colleagues,40 medial Oxford UKAs had a 15-year survival rate of 93%. Berger and colleagues41 reported similar numbers for the Miller-Galante prosthesis. Survival rates were 98% (10 years) and 95.7% (13 years), and 92% of patients had good to excellent Hospital for Special Surgery knee scores.
Although various modern implants have had good to excellent results, the historical question of what type of UKA to use (mobile or fixed-bearing) remains unanswered. To try to address it, Peersman and colleagues42 performed a systematic review of 44 papers (9463 knees). The 2 implant types had comparable revision rates. Another recent retrospective study tried to determine what is crucial for implant survival: implant design or surgeon experience.43 The authors concluded that prosthetic component positioning is key. Other authors have reported high-volume centers are crucial for satisfactory UKA results and lower revision rates.44-46
Results of these studies indicate that, where UKAs are being performed in volume, 10-year survivorship rates higher than 90% and good to excellent outcomes can be expected.
UKA vs HTO
Cohort studies that have directly compared the 2 treatment modalities are scarce, and most have been retrospective. In a prospective study, Stukenborg-Colsman and colleagues47 randomized patients with medial compartment OA to undergo either CWHTO (32 patients) with a technique reported by Coventry48 or UKA (28 patients) with the unicondylar knee sliding prosthesis, Tübingen pattern (Aesculap), between 1988 and 1991. Patients were assessed 2.5, 4.5, and 7.5 years after surgery. More postoperative complications were noted in the HTO group. At 7- to 10-year follow-up, 71% of the HTO group and 65% of the UKA group had excellent KSS. Mean ROM was 103° after UKA (range, 35°-140°) and 117° after HTO (range, 85°-135°) during the same assessment. Although differences were not significant, Kaplan-Meier survival analysis was 60% for HTO and 77% for UKA at 10 years. Results were not promising for the implants used, compared with other implants, but the authors concluded that, because of improvements in implant designs and image-guided techniques, better long-term success can be expected with UKA than with HTO.
In another prospective study, Börjesson and colleagues49 evaluated pain during walking, ROM, British Orthopaedic Association (BOA) scores, and gait variables at 1- and 5-year follow-up. Patients with moderate medial OA (Ahlbäck14 grade I-III) were randomly selected to undergo CWHTO or UKA (Brigham, DePuy). There were no significant differences in BOA scores, ROM, or pain during walking between the 2 groups at 3 months, 1 year, and 5 years after surgery. Gait analysis showed a significant difference in favor of UKA only at 3 months after surgery. At 1- and 5-year follow-up, no significant differences were noted.
To clarify current ambiguities, Fu and colleagues50 performed a systematic review of all (11) comparative studies. These studies had a total of 5840 (5081 UKA, 759 HTO) patients. Although ROM was significantly better for the HTO group than the UKA group, the UKA group had significantly better functional results. Walking after surgery was significantly faster for the UKA group. The authors suggested the difference might be attributed to the different postoperative regimens—HTO patients wore a whole-leg plaster cast for 6 weeks, and UKA patients were allowed immediate postoperative weight-bearing. Regarding rates of survival and complications, pooled data showed no significant differences. Despite these results, the authors acknowledged the limitation of available randomized clinical trials and the multiple techniques and implants used. We share their assertion that larger prospective controlled trials are needed. These are crucial to getting a definitive answer regarding which of the 2 treatment strategies should be used for isolated compartment OA.
Current Trends in Use of UKA and HTO
Evaluation of national registries and recent reports showed a global shift in use of both HTO and UKA. Despite the lack of national HTO registries, a few reports have described use of TKA, UKA, and HTO in Western populations over the past 2 decades. Using 1998-2007 data from the Swedish Knee Arthroplasty Register, W-Dahl and colleagues51 found a 3-fold increase in UKA use, whereas HTO use was halved over the same period. Niinimäki and colleagues52 reported similar findings with the Finnish National Hospital Discharge Register. They noted a steady 6.8% annual decrease in osteotomies, whereas UKA use increased sharply after the Oxford UKA was introduced (Phase 3; Biomet). These findings are consistent with several reports from North America. In their epidemiologic analysis covering the period 1985-1990, Wright and colleagues53 found an 11% to 14% annual decrease in osteotomies among the elderly, compared with an annual decrease of only 3% to 4% among patients younger than 65 years. Nwachukwu and colleagues54 recently compared UKA and HTO practice patterns between 2007 and 2011, using data from a large US private payer insurance database. They noted an annual growth rate of 4.7% in UKA use, compared with an annual 3.9% decrease in HTO use. Furthermore, based on their subgroup analysis, they speculated there was a demographic shift toward UKA, as opposed to TKA, particularly in older women. Bolognesi and colleagues55 investigated further. Evaluating all Medicare beneficiaries who underwent knee arthroplasty in the United States between 2000 and 2009, they noted a 1.7-fold increase in TKA use and a 6.2-fold increase in UKA use. As there were no substantial changes in patient characteristics over that period, the authors hypothesized that a possible broadening of inclusion criteria may have led to the increased use of UKA.
There is a possible multifactorial explanation for the current global shift in favor of UKA. First, UKA was once a technically demanding procedure, but improved surgical techniques, image guidance, and robot assistance56 have made it relatively less difficult. Second, UKA surgery is associated with lower reported perioperative morbidities.57 We think these factors have contributed to the global trend of less HTO use and more UKA use in the treatment of unicompartmental OA.
Conclusion
The modern literature suggests the inclusion criteria for HTO have been well investigated and defined; the UKA criteria remain a matter of debate but seem to be expanding. Long-term survival results seem to favor UKA, though patient satisfaction with both procedures is good to excellent. The broadening range of inclusion criteria and consistent reports of durable outcomes, coupled with excellent patient satisfaction, likely explain the shift toward UKA in the treatment of isolated compartment degeneration.
Am J Orthop. 2016;45(6):E355-E361. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Ledingham J, Regan M, Jones A, Doherty M. Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital. Ann Rheum Dis. 1993;52(7): 520-526.
2. Wise BL, Niu J, Yang M, et al; Multicenter Osteoarthritis (MOST) Group. Patterns of compartment involvement in tibiofemoral osteoarthritis in men and women and in whites and African Americans. Arthritis Care Res. 2012;64(6): 847-852.
3. Jackson JP, Waugh W. Tibial osteotomy for osteoarthritis of the knee. J Bone Joint Surg Br. 1961;43:746-751.
4. Brouwer RW, Bierma-Zeinstra SM, van Raaij TM, Verhaar JA. Osteotomy for medial compartment arthritis of the knee using a closing wedge or an opening wedge controlled by a Puddu plate. A one-year randomised, controlled study. J Bone Joint Surg Br. 2006;88(11):1454-1459.
5. Duivenvoorden T, Brouwer RW, Baan A, et al. Comparison of closing-wedge and opening-wedge high tibial osteotomy for medial compartment osteoarthritis of the knee: a randomized controlled trial with a six-year follow-up. J Bone Joint Surg Am. 2014;96(17):1425-1432.
6. Hutchison CR, Cho B, Wong N, Agnidis Z, Gross AE. Proximal valgus tibial osteotomy for osteoarthritis of the knee. Instr Course Lect. 1999;48:131-134.
7. Trieb K, Grohs J, Hanslik-Schnabel B, Stulnig T, Panotopoulos J, Wanivenhaus A. Age predicts outcome of high-tibial osteotomy. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):149-152.
8. Hui C, Salmon LJ, Kok A, et al. Long-term survival of high tibial osteotomy for medial compartment osteoarthritis of the knee. Am J Sports Med. 2011;39(1):64-70.
9. Howells NR, Salmon L, Waller A, Scanelli J, Pinczewski LA. The outcome at ten years of lateral closing-wedge high tibial osteotomy: determinants of survival and functional outcome. Bone Joint J Br. 2014;96(11):1491-1497.
10. Niinimäki TT, Eskelinen A, Mann BS, Junnila M, Ohtonen P, Leppilahti J. Survivorship of high tibial osteotomy in the treatment of osteoarthritis of the knee: Finnish registry-based study of 3195 knees. J Bone Joint Surg Br. 2012;94(11):1517-1521.
11. Flecher X, Parratte S, Aubaniac JM, Argenson JN. A 12-28-year followup study of closing wedge high tibial osteotomy. Clin Orthop Relat Res. 2006;(452):91-96.
12. Akizuki S, Shibakawa A, Takizawa T, Yamazaki I, Horiuchi H. The long-term outcome of high tibial osteotomy: a ten- to 20-year follow-up. J Bone Joint Surg Br. 2008;90(5):592-596.
13. van Raaij T, Reijman M, Brouwer RW, Jakma TS, Verhaar JN. Survival of closing-wedge high tibial osteotomy: good outcome in men with low-grade osteoarthritis after 10-16 years. Acta Orthop. 2008;79:230-234.
14. Ahlbäck S. Osteoarthrosis of the knee. A radiographic investigation. Acta Radiol Diagn. 1968;(suppl 277):7-72.
15. Bannuru RR, Natov NS, Obadan IE, Price LL, Schmid CH, McAlindon TE. Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and meta-analysis. Arthritis Rheum. 2009;61(12):1704-1711.
16. Evanich JD, Evanich CJ, Wright MB, Rydlewicz JA. Efficacy of intraarticular hyaluronic acid injections in knee osteoarthritis. Clin Orthop Relat Res. 2001;(390):173-181.
17. Naudie D, Bourne RB, Rorabeck CH, Bourne TJ. The Install Award. Survivorship of the high tibial valgus osteotomy. A 10- to -22-year followup study. Clin Orthop Relat Res. 1999;(367):18-27.
18. Sprenger TR, Doerzbacher JF. Tibial osteotomy for the treatment of varus gonarthrosis. Survival and failure analysis to twenty-two years. J Bone Joint Surg Br. 2003;85(3):469-474.
19. Billings A, Scott DF, Camargo MP, Hofmann AA. High tibial osteotomy with a calibrated osteotomy guide, rigid internal fixation, and early motion. Long-term follow-up. J Bone Joint Surg Am. 2000;82(1):70-79.
20. Koshino T, Yoshida T, Ara Y, Saito I, Saito T. Fifteen to twenty-eight years’ follow-up results of high tibial valgus osteotomy for osteoarthritic knee. Knee. 2004;11(6):439-444.
21. Schallberger A, Jacobi M, Wahl P, Maestretti G, Jakob RP. High tibial valgus osteotomy in unicompartmental medial osteoarthritis of the knee: a retrospective follow-up study over 13-21 years. Knee Surg Sports Traumatol Arthrosc. 2011;19(1):122-127.
22. Insall J, Aglietti P. A five to seven-year follow-up of unicondylar arthroplasty. J Bone Joint Surg Am. 1980;62(8):1329-1337.
23. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg Am. 1989;71(1):145-150.
24. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
25. Heyse TJ, Khefacha A, Peersman G, Cartier P. Survivorship of UKA in the middle-aged. Knee. 2012;19(5):585-591.
26. Schai PA, Suh JT, Thornhill TS, Scott RD. Unicompartmental knee arthroplasty in middle-aged patients: a 2- to 6-year follow-up evaluation. J Arthroplasty. 1998;13(4):365-372.
27. Price AJ, Dodd CA, Svard UG, Murray DW. Oxford medial unicompartmental knee arthroplasty in patients younger and older than 60 years of age. J Bone Joint Surg Br. 2005;87(11):1488-1492.
28. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg Am. 2003;85(10):1968-1973.
29. Cavaignac E, Lafontan V, Reina N, et al. Obesity has no adverse effect on the outcome of unicompartmental knee replacement at a minimum follow-up of seven years. Bone Joint J Br. 2013;95(8):1064-1068.
30. Tabor OB Jr, Tabor OB, Bernard M, Wan JY. Unicompartmental knee arthroplasty: long-term success in middle-age and obese patients. J Surg Orthop Adv. 2005;14(2):59-63.
31. Berend KR, Lombardi AV Jr, Adams JB. Obesity, young age, patellofemoral disease, and anterior knee pain: identifying the unicondylar arthroplasty patient in the United States. Orthopedics. 2007;30(5 suppl):19-23.
32. Xing Z, Katz J, Jiranek W. Unicompartmental knee arthroplasty: factors influencing the outcome. J Knee Surg. 2012;25(5):369-373.
33. Plate JF, Augart MA, Seyler TM, et al. Obesity has no effect on outcomes following unicompartmental knee arthroplasty [published online April 12, 2015]. Knee Surg Sports Traumatol Arthrosc. doi:10.1007/s00167-015-3597-5.
34. Niinimäki TT, Murray DW, Partanen J, Pajala A, Leppilahti JI. Unicompartmental knee arthroplasties implanted for osteoarthritis with partial loss of joint space have high re-operation rates. Knee. 2011;18(6):432-435.
35. Carlsson LV, Albrektsson BE, Regnér LR. Minimally invasive surgery vs conventional exposure using the Miller-Galante unicompartmental knee arthroplasty: a randomized radiostereometric study. J Arthroplasty. 2006;21(2):151-156.
36. Repicci JA. Mini-invasive knee unicompartmental arthroplasty: bone-sparing technique. Surg Technol Int. 2003;11:282-286.
37. Pandit H, Jenkins C, Barker K, Dodd CA, Murray DW. The Oxford medial unicompartmental knee replacement using a minimally-invasive approach. J Bone Joint Surg Br. 2006;88(1):54-60.
38. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
39. Koskinen E, Paavolainen P, Eskelinen A, Pulkkinen P, Remes V. Unicondylar knee replacement for primary osteoarthritis: a prospective follow-up study of 1,819 patients from the Finnish Arthroplasty Register. Acta Orthop. 2007;78(1):128-135.
40. Price AJ, Waite JC, Svard U. Long-term clinical results of the medial Oxford unicompartmental knee arthroplasty. Clin Orthop Relat Res. 2005;(435):171-180.
41. Berger RA, Meneghini RM, Jacobs JJ, et al. Results of unicompartmental knee arthroplasty at a minimum of ten years of follow-up. J Bone Joint Surg Am. 2005;87(5):999-1006.
42. Peersman G, Stuyts B, Vandenlangenbergh T, Cartier P, Fennema P. Fixed- versus mobile-bearing UKA: a systematic review and meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2015;23(11):3296-3305.
43. Zambianchi F, Digennaro V, Giorgini A, et al. Surgeon’s experience influences UKA survivorship: a comparative study between all-poly and metal back designs. Knee Surg Sports Traumatol Arthrosc. 2015;23(7):2074-2080.
44. Robertsson O, Knutson K, Lewold S, Lidgren L. The routine of surgical management reduces failure after unicompartmental knee arthroplasty. J Bone Joint Surg Br. 2001;83(1):45-49.
45. Furnes O, Espehaug B, Lie SA, Vollset SE, Engesaeter LB, Havelin LI. Failure mechanisms after unicompartmental and tricompartmental primary knee replacement with cement. J Bone Joint Surg Am. 2007;89(3):519-525.
46. Robertsson O, Lidgren L. The short-term results of 3 common UKA implants during different periods in Sweden. J Arthroplasty. 2008;23(6):801-807.
47. Stukenborg-Colsman C, Wirth CJ, Lazovic D, Wefer A. High tibial osteotomy versus unicompartmental joint replacement in unicompartmental knee joint osteoarthritis: 7-10-year follow-up prospective randomised study. Knee. 2001;8(3):187-194.
48. Coventry MB. Osteotomy about the knee for degenerative and rheumatoid arthritis. J Bone Joint Surg Am. 1973;55(1):23-48.
49. Börjesson M, Weidenhielm L, Mattsson E, Olsson E. Gait and clinical measurements in patients with knee osteoarthritis after surgery: a prospective 5-year follow-up study. Knee. 2005;12(2):121-127.
50. Fu D, Li G, Chen K, Zhao Y, Hua Y, Cai Z. Comparison of high tibial osteotomy and unicompartmental knee arthroplasty in the treatment of unicompartmental osteoarthritis: a meta-analysis. J Arthroplasty. 2013;28(5):759-765.
51. W-Dahl A, Robertsson O, Lidgren L. Surgery for knee osteoarthritis in younger patients. Acta Orthop. 2010;81(2):161-164.
52. Niinimäki TT, Eskelinen A, Ohtonen P, Junnila M, Leppilahti J. Incidence of osteotomies around the knee for the treatment of knee osteoarthritis: a 22-year population-based study. Int Orthop. 2012;36(7):1399-1402.
53. Wright J, Heck D, Hawker G, et al. Rates of tibial osteotomies in Canada and the United States. Clin Orthop Relat Res. 1995;(319):266-275.
54. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
55. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
56. Pearle AD, O’Loughlin PF, Kendoff DO. Robot-assisted unicompartmental knee arthroplasty. J Arthroplasty. 2010;25(2):230-237.
57. Brown NM, Sheth NP, Davis K, et al. Total knee arthroplasty has higher postoperative morbidity than unicompartmental knee arthroplasty: a multicenter analysis. J Arthroplasty. 2012;27(8 suppl):86-90.
1. Ledingham J, Regan M, Jones A, Doherty M. Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital. Ann Rheum Dis. 1993;52(7): 520-526.
2. Wise BL, Niu J, Yang M, et al; Multicenter Osteoarthritis (MOST) Group. Patterns of compartment involvement in tibiofemoral osteoarthritis in men and women and in whites and African Americans. Arthritis Care Res. 2012;64(6): 847-852.
3. Jackson JP, Waugh W. Tibial osteotomy for osteoarthritis of the knee. J Bone Joint Surg Br. 1961;43:746-751.
4. Brouwer RW, Bierma-Zeinstra SM, van Raaij TM, Verhaar JA. Osteotomy for medial compartment arthritis of the knee using a closing wedge or an opening wedge controlled by a Puddu plate. A one-year randomised, controlled study. J Bone Joint Surg Br. 2006;88(11):1454-1459.
5. Duivenvoorden T, Brouwer RW, Baan A, et al. Comparison of closing-wedge and opening-wedge high tibial osteotomy for medial compartment osteoarthritis of the knee: a randomized controlled trial with a six-year follow-up. J Bone Joint Surg Am. 2014;96(17):1425-1432.
6. Hutchison CR, Cho B, Wong N, Agnidis Z, Gross AE. Proximal valgus tibial osteotomy for osteoarthritis of the knee. Instr Course Lect. 1999;48:131-134.
7. Trieb K, Grohs J, Hanslik-Schnabel B, Stulnig T, Panotopoulos J, Wanivenhaus A. Age predicts outcome of high-tibial osteotomy. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):149-152.
8. Hui C, Salmon LJ, Kok A, et al. Long-term survival of high tibial osteotomy for medial compartment osteoarthritis of the knee. Am J Sports Med. 2011;39(1):64-70.
9. Howells NR, Salmon L, Waller A, Scanelli J, Pinczewski LA. The outcome at ten years of lateral closing-wedge high tibial osteotomy: determinants of survival and functional outcome. Bone Joint J Br. 2014;96(11):1491-1497.
10. Niinimäki TT, Eskelinen A, Mann BS, Junnila M, Ohtonen P, Leppilahti J. Survivorship of high tibial osteotomy in the treatment of osteoarthritis of the knee: Finnish registry-based study of 3195 knees. J Bone Joint Surg Br. 2012;94(11):1517-1521.
11. Flecher X, Parratte S, Aubaniac JM, Argenson JN. A 12-28-year followup study of closing wedge high tibial osteotomy. Clin Orthop Relat Res. 2006;(452):91-96.
12. Akizuki S, Shibakawa A, Takizawa T, Yamazaki I, Horiuchi H. The long-term outcome of high tibial osteotomy: a ten- to 20-year follow-up. J Bone Joint Surg Br. 2008;90(5):592-596.
13. van Raaij T, Reijman M, Brouwer RW, Jakma TS, Verhaar JN. Survival of closing-wedge high tibial osteotomy: good outcome in men with low-grade osteoarthritis after 10-16 years. Acta Orthop. 2008;79:230-234.
14. Ahlbäck S. Osteoarthrosis of the knee. A radiographic investigation. Acta Radiol Diagn. 1968;(suppl 277):7-72.
15. Bannuru RR, Natov NS, Obadan IE, Price LL, Schmid CH, McAlindon TE. Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and meta-analysis. Arthritis Rheum. 2009;61(12):1704-1711.
16. Evanich JD, Evanich CJ, Wright MB, Rydlewicz JA. Efficacy of intraarticular hyaluronic acid injections in knee osteoarthritis. Clin Orthop Relat Res. 2001;(390):173-181.
17. Naudie D, Bourne RB, Rorabeck CH, Bourne TJ. The Install Award. Survivorship of the high tibial valgus osteotomy. A 10- to -22-year followup study. Clin Orthop Relat Res. 1999;(367):18-27.
18. Sprenger TR, Doerzbacher JF. Tibial osteotomy for the treatment of varus gonarthrosis. Survival and failure analysis to twenty-two years. J Bone Joint Surg Br. 2003;85(3):469-474.
19. Billings A, Scott DF, Camargo MP, Hofmann AA. High tibial osteotomy with a calibrated osteotomy guide, rigid internal fixation, and early motion. Long-term follow-up. J Bone Joint Surg Am. 2000;82(1):70-79.
20. Koshino T, Yoshida T, Ara Y, Saito I, Saito T. Fifteen to twenty-eight years’ follow-up results of high tibial valgus osteotomy for osteoarthritic knee. Knee. 2004;11(6):439-444.
21. Schallberger A, Jacobi M, Wahl P, Maestretti G, Jakob RP. High tibial valgus osteotomy in unicompartmental medial osteoarthritis of the knee: a retrospective follow-up study over 13-21 years. Knee Surg Sports Traumatol Arthrosc. 2011;19(1):122-127.
22. Insall J, Aglietti P. A five to seven-year follow-up of unicondylar arthroplasty. J Bone Joint Surg Am. 1980;62(8):1329-1337.
23. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg Am. 1989;71(1):145-150.
24. Thompson SA, Liabaud B, Nellans KW, Geller JA. Factors associated with poor outcomes following unicompartmental knee arthroplasty: redefining the “classic” indications for surgery. J Arthroplasty. 2013;28(9):1561-1564.
25. Heyse TJ, Khefacha A, Peersman G, Cartier P. Survivorship of UKA in the middle-aged. Knee. 2012;19(5):585-591.
26. Schai PA, Suh JT, Thornhill TS, Scott RD. Unicompartmental knee arthroplasty in middle-aged patients: a 2- to 6-year follow-up evaluation. J Arthroplasty. 1998;13(4):365-372.
27. Price AJ, Dodd CA, Svard UG, Murray DW. Oxford medial unicompartmental knee arthroplasty in patients younger and older than 60 years of age. J Bone Joint Surg Br. 2005;87(11):1488-1492.
28. Pennington DW, Swienckowski JJ, Lutes WB, Drake GN. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg Am. 2003;85(10):1968-1973.
29. Cavaignac E, Lafontan V, Reina N, et al. Obesity has no adverse effect on the outcome of unicompartmental knee replacement at a minimum follow-up of seven years. Bone Joint J Br. 2013;95(8):1064-1068.
30. Tabor OB Jr, Tabor OB, Bernard M, Wan JY. Unicompartmental knee arthroplasty: long-term success in middle-age and obese patients. J Surg Orthop Adv. 2005;14(2):59-63.
31. Berend KR, Lombardi AV Jr, Adams JB. Obesity, young age, patellofemoral disease, and anterior knee pain: identifying the unicondylar arthroplasty patient in the United States. Orthopedics. 2007;30(5 suppl):19-23.
32. Xing Z, Katz J, Jiranek W. Unicompartmental knee arthroplasty: factors influencing the outcome. J Knee Surg. 2012;25(5):369-373.
33. Plate JF, Augart MA, Seyler TM, et al. Obesity has no effect on outcomes following unicompartmental knee arthroplasty [published online April 12, 2015]. Knee Surg Sports Traumatol Arthrosc. doi:10.1007/s00167-015-3597-5.
34. Niinimäki TT, Murray DW, Partanen J, Pajala A, Leppilahti JI. Unicompartmental knee arthroplasties implanted for osteoarthritis with partial loss of joint space have high re-operation rates. Knee. 2011;18(6):432-435.
35. Carlsson LV, Albrektsson BE, Regnér LR. Minimally invasive surgery vs conventional exposure using the Miller-Galante unicompartmental knee arthroplasty: a randomized radiostereometric study. J Arthroplasty. 2006;21(2):151-156.
36. Repicci JA. Mini-invasive knee unicompartmental arthroplasty: bone-sparing technique. Surg Technol Int. 2003;11:282-286.
37. Pandit H, Jenkins C, Barker K, Dodd CA, Murray DW. The Oxford medial unicompartmental knee replacement using a minimally-invasive approach. J Bone Joint Surg Br. 2006;88(1):54-60.
38. Romanowski MR, Repicci JA. Minimally invasive unicondylar arthroplasty: eight-year follow-up. J Knee Surg. 2002;15(1):17-22.
39. Koskinen E, Paavolainen P, Eskelinen A, Pulkkinen P, Remes V. Unicondylar knee replacement for primary osteoarthritis: a prospective follow-up study of 1,819 patients from the Finnish Arthroplasty Register. Acta Orthop. 2007;78(1):128-135.
40. Price AJ, Waite JC, Svard U. Long-term clinical results of the medial Oxford unicompartmental knee arthroplasty. Clin Orthop Relat Res. 2005;(435):171-180.
41. Berger RA, Meneghini RM, Jacobs JJ, et al. Results of unicompartmental knee arthroplasty at a minimum of ten years of follow-up. J Bone Joint Surg Am. 2005;87(5):999-1006.
42. Peersman G, Stuyts B, Vandenlangenbergh T, Cartier P, Fennema P. Fixed- versus mobile-bearing UKA: a systematic review and meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2015;23(11):3296-3305.
43. Zambianchi F, Digennaro V, Giorgini A, et al. Surgeon’s experience influences UKA survivorship: a comparative study between all-poly and metal back designs. Knee Surg Sports Traumatol Arthrosc. 2015;23(7):2074-2080.
44. Robertsson O, Knutson K, Lewold S, Lidgren L. The routine of surgical management reduces failure after unicompartmental knee arthroplasty. J Bone Joint Surg Br. 2001;83(1):45-49.
45. Furnes O, Espehaug B, Lie SA, Vollset SE, Engesaeter LB, Havelin LI. Failure mechanisms after unicompartmental and tricompartmental primary knee replacement with cement. J Bone Joint Surg Am. 2007;89(3):519-525.
46. Robertsson O, Lidgren L. The short-term results of 3 common UKA implants during different periods in Sweden. J Arthroplasty. 2008;23(6):801-807.
47. Stukenborg-Colsman C, Wirth CJ, Lazovic D, Wefer A. High tibial osteotomy versus unicompartmental joint replacement in unicompartmental knee joint osteoarthritis: 7-10-year follow-up prospective randomised study. Knee. 2001;8(3):187-194.
48. Coventry MB. Osteotomy about the knee for degenerative and rheumatoid arthritis. J Bone Joint Surg Am. 1973;55(1):23-48.
49. Börjesson M, Weidenhielm L, Mattsson E, Olsson E. Gait and clinical measurements in patients with knee osteoarthritis after surgery: a prospective 5-year follow-up study. Knee. 2005;12(2):121-127.
50. Fu D, Li G, Chen K, Zhao Y, Hua Y, Cai Z. Comparison of high tibial osteotomy and unicompartmental knee arthroplasty in the treatment of unicompartmental osteoarthritis: a meta-analysis. J Arthroplasty. 2013;28(5):759-765.
51. W-Dahl A, Robertsson O, Lidgren L. Surgery for knee osteoarthritis in younger patients. Acta Orthop. 2010;81(2):161-164.
52. Niinimäki TT, Eskelinen A, Ohtonen P, Junnila M, Leppilahti J. Incidence of osteotomies around the knee for the treatment of knee osteoarthritis: a 22-year population-based study. Int Orthop. 2012;36(7):1399-1402.
53. Wright J, Heck D, Hawker G, et al. Rates of tibial osteotomies in Canada and the United States. Clin Orthop Relat Res. 1995;(319):266-275.
54. Nwachukwu BU, McCormick FM, Schairer WW, Frank RM, Provencher MT, Roche MW. Unicompartmental knee arthroplasty versus high tibial osteotomy: United States practice patterns for the surgical treatment of unicompartmental arthritis. J Arthroplasty. 2014;29(8):1586-1589.
55. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg Am. 2013;95(22):e174.
56. Pearle AD, O’Loughlin PF, Kendoff DO. Robot-assisted unicompartmental knee arthroplasty. J Arthroplasty. 2010;25(2):230-237.
57. Brown NM, Sheth NP, Davis K, et al. Total knee arthroplasty has higher postoperative morbidity than unicompartmental knee arthroplasty: a multicenter analysis. J Arthroplasty. 2012;27(8 suppl):86-90.
Does Accelerated Physical Therapy After Elective Primary Hip and Knee Arthroplasty Facilitate Early Discharge?
Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are among the most effective surgical procedures in modern medicine. Use of primary THA in the United States is projected to increase by 174% by 2030, to 532,000 cases annually, and the estimate for TKA is even greater.1 Hospital length of stay (LOS) accounts for a significant portion of the overall cost of these procedures. Reducing LOS to limit costs without compromising patient safety, satisfaction, and outcomes remains the goal at all joint arthroplasty centers. Rapid-recovery or fast-track clinical pathways limiting opioid use and emphasizing patient education and early (day-of-surgery) mobilization have been shown to reduce LOS without compromising patient outcomes.2-5 Factors correlated with LOS after THA include surgical approach, use of multimodal analgesia, obesity, age, and social situations or living conditions.4,6-10
Our institution recently implemented a protocol in which certified physical therapists provide accelerated (day-of-surgery) physical therapy (PT) for all total joint arthroplasty patients. For the study reported here, we hypothesized that, compared with PT started on postoperative day 1 (POD-1), PT started day of surgery (Day 0) would result in shorter LOS for unilateral primary THA and TKA patients. In addition, we wanted to evaluate any predischarge differences in function, as measured by gait distance, between the groups.
Methods
After obtaining Institutional Review Board approval, we retrospectively evaluated use of the new postoperative protocol (Day 0 PT) for primary THA and TKA patients. We reviewed all cases of primary unilateral THA or TKA performed by a single surgeon over the 12-month period immediately following initiation of the protocol. There were 116 THA cases and 126 TKA cases. Charts were reviewed for patient demographics, intraoperative data, in-hospital course, and PT session notes. Patients who had a PT session at any point on day of surgery were designated the Day 0 group, and patients who had PT starting the next day (POD-1) were designated the Non-Day 0 group. Although the medical records showed that Day 0 PT had been ordered in all cases, not all patients received PT on the day of their surgery; the most common reason was that they returned from postanesthesia care after the physical therapists’ work shift had ended. Another reason was patient noncompliance or unwillingness stemming from the prolonged effects of general anesthesia, diminished mental orientation, excess fatigue, or inadequate pain control. PT sessions after THA and TKA remained consistent over the study period, with twice daily sessions directed at patient mobility, range of motion, and gentle strengthening exercise. PT was performed only with patient consent.
Surgery
A combination of general and spinal anesthesia was used in almost all THA and TKA cases. In <5% of cases, either the patient refused spinal anesthesia, or it was unsuccessful. In addition, tranexamic acid was administered to limit blood loss in all THA and TKA cases. Of the 116 THAs performed over the study period, 3 were excluded (see below). Of the 113 patients included in the study, 88 (77.9%) used a minimally invasive posterolateral approach, 18 (15.9%) a direct anterior approach, and 7 (6.2%) an anterolateral approach. All THAs were performed with conventional instruments and uncemented components. All TKAs were performed with a standard medial parapatellar approach, conventional instruments, and a tourniquet; in each case, the patella was resurfaced, and cemented fixation was used. Drains were not used in any THA or TKA cases. A local anesthetic cocktail (100 mL of 0.25% ropivacaine, 15 mL of 0.5% ropivacaine, and 1 mL of 1:1000 epinephrine) was injected for postoperative analgesia in all THA and TKA cases.
There were 3 important intraoperative findings in the THA Day 0 group: 2 cases of incidental gluteus medius tendon tears requiring repair and 1 case of nondisplaced calcar fracture treated with a cerclage cable. The THA Non-Day 0 group and both TKA groups had no major intraoperative findings.
Physical Therapy
Day-of-surgery PT was ordered for all patients. Patients did not receive formal PT before surgery. The PT protocol consisted of subjective assessment of patient condition, expectations, and goals; lower limb strengthening exercises; and maximum gait training with use of an assistive device as tolerated. Standard hip movement restrictions were ordered for posterolateral approach patients to protect the soft-tissue repair. Continuous passive motion (CPM) was not used during this study period.
Discharge Criteria
Patients were cleared for discharge by a multidisciplinary team using several criteria: no medical condition that would require readmission, intact surgical incision without discharge or concerning erythema, adequate analgesia (oral medications), intact neurovascular examination, and PT goals achieved (independence with bed mobility, transfers, standing balance, and minimum gait distance of 150 feet). Patients who could not be discharged home because of family or occupation issues or because of problems with gait or transfer were referred to skilled nursing or home healthcare. Follow-up for wound assessment and for examination of radiographs and functional range of motion was planned for 2 to 3 weeks after surgery (all patients followed up). Two patients, 1 in the THA Non-Day 0 group and 1 in the TKA Day 0 group, had a mechanical fall 1 day before discharge, but there were no complication-related discharge delays. In addition, there were no readmissions during the first 4 weeks after surgery.
Excluded Patients
Of the 116 THA cases, 113 (63 Day 0, 50 Non-Day 0) were analyzed. To establish homogeneity between groups and remove potential confounding factors, we excluded 4 THA patients (all Non-Day 0) from analysis because of medical complications prolonging LOS. In 1 of these cases, the patient developed respiratory insufficiency and myocardial infarction on POD-3, and critical care support was required (LOS, 16 days). In another case, anticoagulation treatment led to the development of a hip hematoma on POD-9 and to treatment (evacuation) in the operating room (LOS, 14 days). The other 2 cases involved exacerbation of dysphagia from preexisting myasthenia gravis (LOS, 5 days) and Ogilvie syndrome, managed conservatively (LOS, 9 days).
Of the 126 TKA cases, 123 (97 Day 0, 26 Non-Day 0) were analyzed. Three TKA patients were excluded because of prolonged hospitalization for medical reasons: One developed a deep vein thrombosis, 1 acquired Clostridium difficile colitis (history of lung transplantation, multiple immunosuppressive drugs), and 1 developed respiratory insufficiency from asthma exacerbation.
Statistical Analysis
Power analysis (G*Power) was used to determine an appropriate sample size for comparison.11 Given a previously published mean LOS after THA of 4 days, the hypothesized mean LOS reducing that by at least 0.5 day to 3.5 days, a significance level set at 5%, a power of test set at 0.95, and an allocation ratio of 1, a minimum of 23 subjects would be needed in each group to attain a statistically significant difference using the nonparametric Mann-Whitney test. The Shapiro-Wilk test was used to assess data normality. Regarding statistical significance, the Mann-Whitney U test was used for non-normally distributed data, the 2-sided Fisher exact test and χ2 test for qualitative data and contingency, and the 2-tailed, unpaired, independent-samples Student t test for normally distributed data. Data were analyzed with SPSS Statistics for Windows Version 20 (IBM).
Results
TKA and THA patients had similar demographic profiles, types of anesthesia, operating room and surgery times, surgical approaches, and total number of PT sessions before discharge. Estimated blood loss, however, was significantly (P < .05) higher for Non-Day 0 patients than for Non-Day 0 patients (Table 1).
Mean (SD) distance ambulated during first PT session was 2-fold farther (P = .014) for Non-Day 0 patients, 84.1 (10.4) feet, than for Day 0 patients, 42.1 (6.4) feet. On POD-1, mean (SD) gait was significantly (P = .019) longer for Day 0 patients, 162.4 (12.9) feet, than for Non-Day 0 patients, 118 (11.7) feet (Figure 2).
In TKA patients, although mean (SD) distance ambulated tended to be farther for the Day 0 group than for the Non-Day 0 group—114 (12.3) feet on POD-1 and 176 (15.2) feet on POD-2 for Day 0 vs 94 (22.2) feet on POD-1 and 148 (22.1) feet on POD-2 for Non-Day 0—the differences were not statistically significant. In addition, knee arc of motion during first PT session was statistically significantly (P = .3) higher for Day 0 patients, 69.1° (18.7°), than for Non-Day 0 patients, 61.7° (18.8°).
Statistical analysis revealed no difference in LOS based on surgical approach to the hip: 2.4 days for posterolateral (2.2 days for Day 0 and 2.6 days for Non-Day 0; P = .06); 2.1 days for direct anterior (2.1 days for Day 0 and 2.0 days for Non-Day 0; P = .7); and 2.7 days for anterolateral (3.0 days for Day 0 and 2.6 days for Non-Day 0; P = .6).
Discussion
Protocols for PT after THA and TKA remain unstandardized and largely dependent on institutions and surgeons. Factors permitting successful implementation of accelerated rehabilitation include patient motivation, adequate analgesia, and adequate support by physical therapists.12 A potential risk associated with accelerated PT after THA is dislocation, which did not occur in any patient in our Day 0 group. Other risks are increased pain and swelling leading to increased risk of falling and bleeding, which were not observed in our cohort. Although Day 0 PT was ordered in all cases in this study, only 55% of THA patients and 79% of TKA patients received PT the same day as their surgery. The delay can be addressed by making physical therapists’ work shifts more flexible for cases that finish later in the day and by providing preoperative education on the importance of day-of-surgery PT. Dr. Incavo and office staff routinely discuss discharge planning with all patients before surgery, but there was no stimulus protocol or communication to discuss or emphasize LOS with patients before surgery, and there was no questionnaire or survey given to assess patient expectations about PT and discharge.
Our finding of no statistically significant reduction in mean LOS after implementation of accelerated PT for THA or TKA differs from findings in multiple other reports.4,5,13-17 Baseline or control group mean LOS tended to be higher in previous studies3,5,18-23 (3.4-11.4 days) than in our control group (2.5 days) (Table 2).
Conclusion
These results provide useful information for providers who are managing primary THA and TKA cases and seeking continual improvement in postoperative patient care and better resource allocation. Hospitals, particularly those operating in bundled-care environments, are increasingly coming under scrutiny to control costs. Our study results showed that the costs associated with Day 0 PT are justified for THA but not for TKA.
Am J Orthop. 2016;45(6):E337-E342. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.
2. Barbieri A, Vanhaecht K, Van Herck P, et al. Effects of clinical pathways in the joint replacement: a meta-analysis. BMC Med. 2009;7:32.
3. den Hartog YM, Mathijssen NM, Vehmeijer SB. Reduced length of hospital stay after the introduction of a rapid recovery protocol for primary THA procedures. Acta Orthop. 2013;84(5):444-447.
4. Husted H, Holm G, Jacobsen S. Predictors of length of stay and patient satisfaction after hip and knee replacement surgery: fast-track experience in 712 patients. Acta Orthop. 2008;79(2):168-173.
5. Robbins CE, Casey D, Bono JV, Murphy SB, Talmo CT, Ward DM. A multidisciplinary total hip arthroplasty protocol with accelerated postoperative rehabilitation: does the patient benefit? Am J Orthop. 2014;43(4):178-181.
6. den Hartog YM, Mathijssen NM, Hannink G, Vehmeijer SB. Which patient characteristics influence length of hospital stay after primary total hip arthroplasty in a ‘fast-track’ setting? Bone Joint J. 2015;97(1):19-23.
7. Forrest G, Fuchs M, Gutierrez A, Girardy J. Factors affecting length of stay and need for rehabilitation after hip and knee arthroplasty. J Arthroplasty. 1998;13(2):186-190.
8. Foote J, Panchoo K, Blair P, Bannister G. Length of stay following primary total hip replacement. Ann R Coll Surg Engl. 2009;91(6):500-504.
9. Sharma V, Morgan PM, Cheng EY. Factors influencing early rehabilitation after THA: a systematic review. Clin Orthop Relat Res. 2009;467(6):1400-1411.
10. Dorr LD, Maheshwari AV, Long WT, Wan Z, Sirianni LE. Early pain relief and function after posterior minimally invasive and conventional total hip arthroplasty. A prospective, randomized, blinded study. J Bone Joint Surg Am. 2007;89(6):1153-1160.
11. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
12. Ranawat AS, Ranawat CS. Pain management and accelerated rehabilitation for total hip and total knee arthroplasty. J Arthroplasty. 2007;22(7 suppl 3):12-15.
13. Husted H, Otte KS, Kristensen BB, Orsnes T, Kehlet H. Readmissions after fast-track hip and knee arthroplasty. Arch Orthop Trauma Surg. 2010;130(9):1185-1191.
14. Husted H, Lunn TH, Troelsen A, Gaarn-Larsen L, Kristensen BB, Kehlet H. Why still in hospital after fast-track hip and knee arthroplasty? Acta Orthop. 2011;82(6):679-684.
15. Husted H, Jensen CM, Solgaard S, Kehlet H. Reduced length of stay following hip and knee arthroplasty in Denmark 2000-2009: from research to implementation. Arch Orthop Trauma Surg. 2012;132(1):101-104.
16. Berger RA, Sanders SA, Thill ES, Sporer SM, Della Valle C. Newer anesthesia and rehabilitation protocols enable outpatient hip replacement in selected patients. Clin Orthop Relat Res. 2009;467(6):1424-1430.
17. Peck CN, Foster A, McLauchlan GJ. Reducing incision length or intensifying rehabilitation: what makes the difference to length of stay in total hip replacement in a UK setting? Int Orthop. 2006;30(5):395-398.
18. Isaac D, Falode T, Liu P, I’Anson H, Dillow K, Gill P. Accelerated rehabilitation after total knee replacement. Knee. 2005;12(5):346-350.
19. Labraca NS, Castro-Sánchez AM, Matarán-Peñarrocha GA, Arroyo-Morales M, Sánchez-Joya Mdel M, Moreno-Lorenzo C. Benefits of starting rehabilitation within 24 hours of primary total knee arthroplasty: randomized clinical trial. Clin Rehabil. 2011;25(6):557-566.
20. Larsen K, Hansen TB, Søballe K. Hip arthroplasty patients benefit from accelerated perioperative care and rehabilitation: a quasi-experimental study of 98 patients. Acta Orthop. 2008;79(5):624-630.
21. Larsen K, Hansen TB, Thomsen PB, Christiansen T, Søballe K. Cost-effectiveness of accelerated perioperative care and rehabilitation after total hip and knee arthroplasty. J Bone Joint Surg Am. 2009;91(4):761-772.
22. Larsen K, Sørensen OG, Hansen TB, Thomsen PB, Søballe K. Accelerated perioperative care and rehabilitation intervention for hip and knee replacement is effective: a randomized clinical trial involving 87 patients with 3 months of follow-up. Acta Orthop. 2008;79(2):149-159.
23. Wellman SS, Murphy AC, Gulcynski D. Murphy SB. Implementation of an accelerated mobilization protocol following primary total hip arthroplasty: impact on length of stay and disposition. Curr Rev Musculoskelet Med. 2011;4(3):84-90.
Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are among the most effective surgical procedures in modern medicine. Use of primary THA in the United States is projected to increase by 174% by 2030, to 532,000 cases annually, and the estimate for TKA is even greater.1 Hospital length of stay (LOS) accounts for a significant portion of the overall cost of these procedures. Reducing LOS to limit costs without compromising patient safety, satisfaction, and outcomes remains the goal at all joint arthroplasty centers. Rapid-recovery or fast-track clinical pathways limiting opioid use and emphasizing patient education and early (day-of-surgery) mobilization have been shown to reduce LOS without compromising patient outcomes.2-5 Factors correlated with LOS after THA include surgical approach, use of multimodal analgesia, obesity, age, and social situations or living conditions.4,6-10
Our institution recently implemented a protocol in which certified physical therapists provide accelerated (day-of-surgery) physical therapy (PT) for all total joint arthroplasty patients. For the study reported here, we hypothesized that, compared with PT started on postoperative day 1 (POD-1), PT started day of surgery (Day 0) would result in shorter LOS for unilateral primary THA and TKA patients. In addition, we wanted to evaluate any predischarge differences in function, as measured by gait distance, between the groups.
Methods
After obtaining Institutional Review Board approval, we retrospectively evaluated use of the new postoperative protocol (Day 0 PT) for primary THA and TKA patients. We reviewed all cases of primary unilateral THA or TKA performed by a single surgeon over the 12-month period immediately following initiation of the protocol. There were 116 THA cases and 126 TKA cases. Charts were reviewed for patient demographics, intraoperative data, in-hospital course, and PT session notes. Patients who had a PT session at any point on day of surgery were designated the Day 0 group, and patients who had PT starting the next day (POD-1) were designated the Non-Day 0 group. Although the medical records showed that Day 0 PT had been ordered in all cases, not all patients received PT on the day of their surgery; the most common reason was that they returned from postanesthesia care after the physical therapists’ work shift had ended. Another reason was patient noncompliance or unwillingness stemming from the prolonged effects of general anesthesia, diminished mental orientation, excess fatigue, or inadequate pain control. PT sessions after THA and TKA remained consistent over the study period, with twice daily sessions directed at patient mobility, range of motion, and gentle strengthening exercise. PT was performed only with patient consent.
Surgery
A combination of general and spinal anesthesia was used in almost all THA and TKA cases. In <5% of cases, either the patient refused spinal anesthesia, or it was unsuccessful. In addition, tranexamic acid was administered to limit blood loss in all THA and TKA cases. Of the 116 THAs performed over the study period, 3 were excluded (see below). Of the 113 patients included in the study, 88 (77.9%) used a minimally invasive posterolateral approach, 18 (15.9%) a direct anterior approach, and 7 (6.2%) an anterolateral approach. All THAs were performed with conventional instruments and uncemented components. All TKAs were performed with a standard medial parapatellar approach, conventional instruments, and a tourniquet; in each case, the patella was resurfaced, and cemented fixation was used. Drains were not used in any THA or TKA cases. A local anesthetic cocktail (100 mL of 0.25% ropivacaine, 15 mL of 0.5% ropivacaine, and 1 mL of 1:1000 epinephrine) was injected for postoperative analgesia in all THA and TKA cases.
There were 3 important intraoperative findings in the THA Day 0 group: 2 cases of incidental gluteus medius tendon tears requiring repair and 1 case of nondisplaced calcar fracture treated with a cerclage cable. The THA Non-Day 0 group and both TKA groups had no major intraoperative findings.
Physical Therapy
Day-of-surgery PT was ordered for all patients. Patients did not receive formal PT before surgery. The PT protocol consisted of subjective assessment of patient condition, expectations, and goals; lower limb strengthening exercises; and maximum gait training with use of an assistive device as tolerated. Standard hip movement restrictions were ordered for posterolateral approach patients to protect the soft-tissue repair. Continuous passive motion (CPM) was not used during this study period.
Discharge Criteria
Patients were cleared for discharge by a multidisciplinary team using several criteria: no medical condition that would require readmission, intact surgical incision without discharge or concerning erythema, adequate analgesia (oral medications), intact neurovascular examination, and PT goals achieved (independence with bed mobility, transfers, standing balance, and minimum gait distance of 150 feet). Patients who could not be discharged home because of family or occupation issues or because of problems with gait or transfer were referred to skilled nursing or home healthcare. Follow-up for wound assessment and for examination of radiographs and functional range of motion was planned for 2 to 3 weeks after surgery (all patients followed up). Two patients, 1 in the THA Non-Day 0 group and 1 in the TKA Day 0 group, had a mechanical fall 1 day before discharge, but there were no complication-related discharge delays. In addition, there were no readmissions during the first 4 weeks after surgery.
Excluded Patients
Of the 116 THA cases, 113 (63 Day 0, 50 Non-Day 0) were analyzed. To establish homogeneity between groups and remove potential confounding factors, we excluded 4 THA patients (all Non-Day 0) from analysis because of medical complications prolonging LOS. In 1 of these cases, the patient developed respiratory insufficiency and myocardial infarction on POD-3, and critical care support was required (LOS, 16 days). In another case, anticoagulation treatment led to the development of a hip hematoma on POD-9 and to treatment (evacuation) in the operating room (LOS, 14 days). The other 2 cases involved exacerbation of dysphagia from preexisting myasthenia gravis (LOS, 5 days) and Ogilvie syndrome, managed conservatively (LOS, 9 days).
Of the 126 TKA cases, 123 (97 Day 0, 26 Non-Day 0) were analyzed. Three TKA patients were excluded because of prolonged hospitalization for medical reasons: One developed a deep vein thrombosis, 1 acquired Clostridium difficile colitis (history of lung transplantation, multiple immunosuppressive drugs), and 1 developed respiratory insufficiency from asthma exacerbation.
Statistical Analysis
Power analysis (G*Power) was used to determine an appropriate sample size for comparison.11 Given a previously published mean LOS after THA of 4 days, the hypothesized mean LOS reducing that by at least 0.5 day to 3.5 days, a significance level set at 5%, a power of test set at 0.95, and an allocation ratio of 1, a minimum of 23 subjects would be needed in each group to attain a statistically significant difference using the nonparametric Mann-Whitney test. The Shapiro-Wilk test was used to assess data normality. Regarding statistical significance, the Mann-Whitney U test was used for non-normally distributed data, the 2-sided Fisher exact test and χ2 test for qualitative data and contingency, and the 2-tailed, unpaired, independent-samples Student t test for normally distributed data. Data were analyzed with SPSS Statistics for Windows Version 20 (IBM).
Results
TKA and THA patients had similar demographic profiles, types of anesthesia, operating room and surgery times, surgical approaches, and total number of PT sessions before discharge. Estimated blood loss, however, was significantly (P < .05) higher for Non-Day 0 patients than for Non-Day 0 patients (Table 1).
Mean (SD) distance ambulated during first PT session was 2-fold farther (P = .014) for Non-Day 0 patients, 84.1 (10.4) feet, than for Day 0 patients, 42.1 (6.4) feet. On POD-1, mean (SD) gait was significantly (P = .019) longer for Day 0 patients, 162.4 (12.9) feet, than for Non-Day 0 patients, 118 (11.7) feet (Figure 2).
In TKA patients, although mean (SD) distance ambulated tended to be farther for the Day 0 group than for the Non-Day 0 group—114 (12.3) feet on POD-1 and 176 (15.2) feet on POD-2 for Day 0 vs 94 (22.2) feet on POD-1 and 148 (22.1) feet on POD-2 for Non-Day 0—the differences were not statistically significant. In addition, knee arc of motion during first PT session was statistically significantly (P = .3) higher for Day 0 patients, 69.1° (18.7°), than for Non-Day 0 patients, 61.7° (18.8°).
Statistical analysis revealed no difference in LOS based on surgical approach to the hip: 2.4 days for posterolateral (2.2 days for Day 0 and 2.6 days for Non-Day 0; P = .06); 2.1 days for direct anterior (2.1 days for Day 0 and 2.0 days for Non-Day 0; P = .7); and 2.7 days for anterolateral (3.0 days for Day 0 and 2.6 days for Non-Day 0; P = .6).
Discussion
Protocols for PT after THA and TKA remain unstandardized and largely dependent on institutions and surgeons. Factors permitting successful implementation of accelerated rehabilitation include patient motivation, adequate analgesia, and adequate support by physical therapists.12 A potential risk associated with accelerated PT after THA is dislocation, which did not occur in any patient in our Day 0 group. Other risks are increased pain and swelling leading to increased risk of falling and bleeding, which were not observed in our cohort. Although Day 0 PT was ordered in all cases in this study, only 55% of THA patients and 79% of TKA patients received PT the same day as their surgery. The delay can be addressed by making physical therapists’ work shifts more flexible for cases that finish later in the day and by providing preoperative education on the importance of day-of-surgery PT. Dr. Incavo and office staff routinely discuss discharge planning with all patients before surgery, but there was no stimulus protocol or communication to discuss or emphasize LOS with patients before surgery, and there was no questionnaire or survey given to assess patient expectations about PT and discharge.
Our finding of no statistically significant reduction in mean LOS after implementation of accelerated PT for THA or TKA differs from findings in multiple other reports.4,5,13-17 Baseline or control group mean LOS tended to be higher in previous studies3,5,18-23 (3.4-11.4 days) than in our control group (2.5 days) (Table 2).
Conclusion
These results provide useful information for providers who are managing primary THA and TKA cases and seeking continual improvement in postoperative patient care and better resource allocation. Hospitals, particularly those operating in bundled-care environments, are increasingly coming under scrutiny to control costs. Our study results showed that the costs associated with Day 0 PT are justified for THA but not for TKA.
Am J Orthop. 2016;45(6):E337-E342. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are among the most effective surgical procedures in modern medicine. Use of primary THA in the United States is projected to increase by 174% by 2030, to 532,000 cases annually, and the estimate for TKA is even greater.1 Hospital length of stay (LOS) accounts for a significant portion of the overall cost of these procedures. Reducing LOS to limit costs without compromising patient safety, satisfaction, and outcomes remains the goal at all joint arthroplasty centers. Rapid-recovery or fast-track clinical pathways limiting opioid use and emphasizing patient education and early (day-of-surgery) mobilization have been shown to reduce LOS without compromising patient outcomes.2-5 Factors correlated with LOS after THA include surgical approach, use of multimodal analgesia, obesity, age, and social situations or living conditions.4,6-10
Our institution recently implemented a protocol in which certified physical therapists provide accelerated (day-of-surgery) physical therapy (PT) for all total joint arthroplasty patients. For the study reported here, we hypothesized that, compared with PT started on postoperative day 1 (POD-1), PT started day of surgery (Day 0) would result in shorter LOS for unilateral primary THA and TKA patients. In addition, we wanted to evaluate any predischarge differences in function, as measured by gait distance, between the groups.
Methods
After obtaining Institutional Review Board approval, we retrospectively evaluated use of the new postoperative protocol (Day 0 PT) for primary THA and TKA patients. We reviewed all cases of primary unilateral THA or TKA performed by a single surgeon over the 12-month period immediately following initiation of the protocol. There were 116 THA cases and 126 TKA cases. Charts were reviewed for patient demographics, intraoperative data, in-hospital course, and PT session notes. Patients who had a PT session at any point on day of surgery were designated the Day 0 group, and patients who had PT starting the next day (POD-1) were designated the Non-Day 0 group. Although the medical records showed that Day 0 PT had been ordered in all cases, not all patients received PT on the day of their surgery; the most common reason was that they returned from postanesthesia care after the physical therapists’ work shift had ended. Another reason was patient noncompliance or unwillingness stemming from the prolonged effects of general anesthesia, diminished mental orientation, excess fatigue, or inadequate pain control. PT sessions after THA and TKA remained consistent over the study period, with twice daily sessions directed at patient mobility, range of motion, and gentle strengthening exercise. PT was performed only with patient consent.
Surgery
A combination of general and spinal anesthesia was used in almost all THA and TKA cases. In <5% of cases, either the patient refused spinal anesthesia, or it was unsuccessful. In addition, tranexamic acid was administered to limit blood loss in all THA and TKA cases. Of the 116 THAs performed over the study period, 3 were excluded (see below). Of the 113 patients included in the study, 88 (77.9%) used a minimally invasive posterolateral approach, 18 (15.9%) a direct anterior approach, and 7 (6.2%) an anterolateral approach. All THAs were performed with conventional instruments and uncemented components. All TKAs were performed with a standard medial parapatellar approach, conventional instruments, and a tourniquet; in each case, the patella was resurfaced, and cemented fixation was used. Drains were not used in any THA or TKA cases. A local anesthetic cocktail (100 mL of 0.25% ropivacaine, 15 mL of 0.5% ropivacaine, and 1 mL of 1:1000 epinephrine) was injected for postoperative analgesia in all THA and TKA cases.
There were 3 important intraoperative findings in the THA Day 0 group: 2 cases of incidental gluteus medius tendon tears requiring repair and 1 case of nondisplaced calcar fracture treated with a cerclage cable. The THA Non-Day 0 group and both TKA groups had no major intraoperative findings.
Physical Therapy
Day-of-surgery PT was ordered for all patients. Patients did not receive formal PT before surgery. The PT protocol consisted of subjective assessment of patient condition, expectations, and goals; lower limb strengthening exercises; and maximum gait training with use of an assistive device as tolerated. Standard hip movement restrictions were ordered for posterolateral approach patients to protect the soft-tissue repair. Continuous passive motion (CPM) was not used during this study period.
Discharge Criteria
Patients were cleared for discharge by a multidisciplinary team using several criteria: no medical condition that would require readmission, intact surgical incision without discharge or concerning erythema, adequate analgesia (oral medications), intact neurovascular examination, and PT goals achieved (independence with bed mobility, transfers, standing balance, and minimum gait distance of 150 feet). Patients who could not be discharged home because of family or occupation issues or because of problems with gait or transfer were referred to skilled nursing or home healthcare. Follow-up for wound assessment and for examination of radiographs and functional range of motion was planned for 2 to 3 weeks after surgery (all patients followed up). Two patients, 1 in the THA Non-Day 0 group and 1 in the TKA Day 0 group, had a mechanical fall 1 day before discharge, but there were no complication-related discharge delays. In addition, there were no readmissions during the first 4 weeks after surgery.
Excluded Patients
Of the 116 THA cases, 113 (63 Day 0, 50 Non-Day 0) were analyzed. To establish homogeneity between groups and remove potential confounding factors, we excluded 4 THA patients (all Non-Day 0) from analysis because of medical complications prolonging LOS. In 1 of these cases, the patient developed respiratory insufficiency and myocardial infarction on POD-3, and critical care support was required (LOS, 16 days). In another case, anticoagulation treatment led to the development of a hip hematoma on POD-9 and to treatment (evacuation) in the operating room (LOS, 14 days). The other 2 cases involved exacerbation of dysphagia from preexisting myasthenia gravis (LOS, 5 days) and Ogilvie syndrome, managed conservatively (LOS, 9 days).
Of the 126 TKA cases, 123 (97 Day 0, 26 Non-Day 0) were analyzed. Three TKA patients were excluded because of prolonged hospitalization for medical reasons: One developed a deep vein thrombosis, 1 acquired Clostridium difficile colitis (history of lung transplantation, multiple immunosuppressive drugs), and 1 developed respiratory insufficiency from asthma exacerbation.
Statistical Analysis
Power analysis (G*Power) was used to determine an appropriate sample size for comparison.11 Given a previously published mean LOS after THA of 4 days, the hypothesized mean LOS reducing that by at least 0.5 day to 3.5 days, a significance level set at 5%, a power of test set at 0.95, and an allocation ratio of 1, a minimum of 23 subjects would be needed in each group to attain a statistically significant difference using the nonparametric Mann-Whitney test. The Shapiro-Wilk test was used to assess data normality. Regarding statistical significance, the Mann-Whitney U test was used for non-normally distributed data, the 2-sided Fisher exact test and χ2 test for qualitative data and contingency, and the 2-tailed, unpaired, independent-samples Student t test for normally distributed data. Data were analyzed with SPSS Statistics for Windows Version 20 (IBM).
Results
TKA and THA patients had similar demographic profiles, types of anesthesia, operating room and surgery times, surgical approaches, and total number of PT sessions before discharge. Estimated blood loss, however, was significantly (P < .05) higher for Non-Day 0 patients than for Non-Day 0 patients (Table 1).
Mean (SD) distance ambulated during first PT session was 2-fold farther (P = .014) for Non-Day 0 patients, 84.1 (10.4) feet, than for Day 0 patients, 42.1 (6.4) feet. On POD-1, mean (SD) gait was significantly (P = .019) longer for Day 0 patients, 162.4 (12.9) feet, than for Non-Day 0 patients, 118 (11.7) feet (Figure 2).
In TKA patients, although mean (SD) distance ambulated tended to be farther for the Day 0 group than for the Non-Day 0 group—114 (12.3) feet on POD-1 and 176 (15.2) feet on POD-2 for Day 0 vs 94 (22.2) feet on POD-1 and 148 (22.1) feet on POD-2 for Non-Day 0—the differences were not statistically significant. In addition, knee arc of motion during first PT session was statistically significantly (P = .3) higher for Day 0 patients, 69.1° (18.7°), than for Non-Day 0 patients, 61.7° (18.8°).
Statistical analysis revealed no difference in LOS based on surgical approach to the hip: 2.4 days for posterolateral (2.2 days for Day 0 and 2.6 days for Non-Day 0; P = .06); 2.1 days for direct anterior (2.1 days for Day 0 and 2.0 days for Non-Day 0; P = .7); and 2.7 days for anterolateral (3.0 days for Day 0 and 2.6 days for Non-Day 0; P = .6).
Discussion
Protocols for PT after THA and TKA remain unstandardized and largely dependent on institutions and surgeons. Factors permitting successful implementation of accelerated rehabilitation include patient motivation, adequate analgesia, and adequate support by physical therapists.12 A potential risk associated with accelerated PT after THA is dislocation, which did not occur in any patient in our Day 0 group. Other risks are increased pain and swelling leading to increased risk of falling and bleeding, which were not observed in our cohort. Although Day 0 PT was ordered in all cases in this study, only 55% of THA patients and 79% of TKA patients received PT the same day as their surgery. The delay can be addressed by making physical therapists’ work shifts more flexible for cases that finish later in the day and by providing preoperative education on the importance of day-of-surgery PT. Dr. Incavo and office staff routinely discuss discharge planning with all patients before surgery, but there was no stimulus protocol or communication to discuss or emphasize LOS with patients before surgery, and there was no questionnaire or survey given to assess patient expectations about PT and discharge.
Our finding of no statistically significant reduction in mean LOS after implementation of accelerated PT for THA or TKA differs from findings in multiple other reports.4,5,13-17 Baseline or control group mean LOS tended to be higher in previous studies3,5,18-23 (3.4-11.4 days) than in our control group (2.5 days) (Table 2).
Conclusion
These results provide useful information for providers who are managing primary THA and TKA cases and seeking continual improvement in postoperative patient care and better resource allocation. Hospitals, particularly those operating in bundled-care environments, are increasingly coming under scrutiny to control costs. Our study results showed that the costs associated with Day 0 PT are justified for THA but not for TKA.
Am J Orthop. 2016;45(6):E337-E342. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.
2. Barbieri A, Vanhaecht K, Van Herck P, et al. Effects of clinical pathways in the joint replacement: a meta-analysis. BMC Med. 2009;7:32.
3. den Hartog YM, Mathijssen NM, Vehmeijer SB. Reduced length of hospital stay after the introduction of a rapid recovery protocol for primary THA procedures. Acta Orthop. 2013;84(5):444-447.
4. Husted H, Holm G, Jacobsen S. Predictors of length of stay and patient satisfaction after hip and knee replacement surgery: fast-track experience in 712 patients. Acta Orthop. 2008;79(2):168-173.
5. Robbins CE, Casey D, Bono JV, Murphy SB, Talmo CT, Ward DM. A multidisciplinary total hip arthroplasty protocol with accelerated postoperative rehabilitation: does the patient benefit? Am J Orthop. 2014;43(4):178-181.
6. den Hartog YM, Mathijssen NM, Hannink G, Vehmeijer SB. Which patient characteristics influence length of hospital stay after primary total hip arthroplasty in a ‘fast-track’ setting? Bone Joint J. 2015;97(1):19-23.
7. Forrest G, Fuchs M, Gutierrez A, Girardy J. Factors affecting length of stay and need for rehabilitation after hip and knee arthroplasty. J Arthroplasty. 1998;13(2):186-190.
8. Foote J, Panchoo K, Blair P, Bannister G. Length of stay following primary total hip replacement. Ann R Coll Surg Engl. 2009;91(6):500-504.
9. Sharma V, Morgan PM, Cheng EY. Factors influencing early rehabilitation after THA: a systematic review. Clin Orthop Relat Res. 2009;467(6):1400-1411.
10. Dorr LD, Maheshwari AV, Long WT, Wan Z, Sirianni LE. Early pain relief and function after posterior minimally invasive and conventional total hip arthroplasty. A prospective, randomized, blinded study. J Bone Joint Surg Am. 2007;89(6):1153-1160.
11. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
12. Ranawat AS, Ranawat CS. Pain management and accelerated rehabilitation for total hip and total knee arthroplasty. J Arthroplasty. 2007;22(7 suppl 3):12-15.
13. Husted H, Otte KS, Kristensen BB, Orsnes T, Kehlet H. Readmissions after fast-track hip and knee arthroplasty. Arch Orthop Trauma Surg. 2010;130(9):1185-1191.
14. Husted H, Lunn TH, Troelsen A, Gaarn-Larsen L, Kristensen BB, Kehlet H. Why still in hospital after fast-track hip and knee arthroplasty? Acta Orthop. 2011;82(6):679-684.
15. Husted H, Jensen CM, Solgaard S, Kehlet H. Reduced length of stay following hip and knee arthroplasty in Denmark 2000-2009: from research to implementation. Arch Orthop Trauma Surg. 2012;132(1):101-104.
16. Berger RA, Sanders SA, Thill ES, Sporer SM, Della Valle C. Newer anesthesia and rehabilitation protocols enable outpatient hip replacement in selected patients. Clin Orthop Relat Res. 2009;467(6):1424-1430.
17. Peck CN, Foster A, McLauchlan GJ. Reducing incision length or intensifying rehabilitation: what makes the difference to length of stay in total hip replacement in a UK setting? Int Orthop. 2006;30(5):395-398.
18. Isaac D, Falode T, Liu P, I’Anson H, Dillow K, Gill P. Accelerated rehabilitation after total knee replacement. Knee. 2005;12(5):346-350.
19. Labraca NS, Castro-Sánchez AM, Matarán-Peñarrocha GA, Arroyo-Morales M, Sánchez-Joya Mdel M, Moreno-Lorenzo C. Benefits of starting rehabilitation within 24 hours of primary total knee arthroplasty: randomized clinical trial. Clin Rehabil. 2011;25(6):557-566.
20. Larsen K, Hansen TB, Søballe K. Hip arthroplasty patients benefit from accelerated perioperative care and rehabilitation: a quasi-experimental study of 98 patients. Acta Orthop. 2008;79(5):624-630.
21. Larsen K, Hansen TB, Thomsen PB, Christiansen T, Søballe K. Cost-effectiveness of accelerated perioperative care and rehabilitation after total hip and knee arthroplasty. J Bone Joint Surg Am. 2009;91(4):761-772.
22. Larsen K, Sørensen OG, Hansen TB, Thomsen PB, Søballe K. Accelerated perioperative care and rehabilitation intervention for hip and knee replacement is effective: a randomized clinical trial involving 87 patients with 3 months of follow-up. Acta Orthop. 2008;79(2):149-159.
23. Wellman SS, Murphy AC, Gulcynski D. Murphy SB. Implementation of an accelerated mobilization protocol following primary total hip arthroplasty: impact on length of stay and disposition. Curr Rev Musculoskelet Med. 2011;4(3):84-90.
1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.
2. Barbieri A, Vanhaecht K, Van Herck P, et al. Effects of clinical pathways in the joint replacement: a meta-analysis. BMC Med. 2009;7:32.
3. den Hartog YM, Mathijssen NM, Vehmeijer SB. Reduced length of hospital stay after the introduction of a rapid recovery protocol for primary THA procedures. Acta Orthop. 2013;84(5):444-447.
4. Husted H, Holm G, Jacobsen S. Predictors of length of stay and patient satisfaction after hip and knee replacement surgery: fast-track experience in 712 patients. Acta Orthop. 2008;79(2):168-173.
5. Robbins CE, Casey D, Bono JV, Murphy SB, Talmo CT, Ward DM. A multidisciplinary total hip arthroplasty protocol with accelerated postoperative rehabilitation: does the patient benefit? Am J Orthop. 2014;43(4):178-181.
6. den Hartog YM, Mathijssen NM, Hannink G, Vehmeijer SB. Which patient characteristics influence length of hospital stay after primary total hip arthroplasty in a ‘fast-track’ setting? Bone Joint J. 2015;97(1):19-23.
7. Forrest G, Fuchs M, Gutierrez A, Girardy J. Factors affecting length of stay and need for rehabilitation after hip and knee arthroplasty. J Arthroplasty. 1998;13(2):186-190.
8. Foote J, Panchoo K, Blair P, Bannister G. Length of stay following primary total hip replacement. Ann R Coll Surg Engl. 2009;91(6):500-504.
9. Sharma V, Morgan PM, Cheng EY. Factors influencing early rehabilitation after THA: a systematic review. Clin Orthop Relat Res. 2009;467(6):1400-1411.
10. Dorr LD, Maheshwari AV, Long WT, Wan Z, Sirianni LE. Early pain relief and function after posterior minimally invasive and conventional total hip arthroplasty. A prospective, randomized, blinded study. J Bone Joint Surg Am. 2007;89(6):1153-1160.
11. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
12. Ranawat AS, Ranawat CS. Pain management and accelerated rehabilitation for total hip and total knee arthroplasty. J Arthroplasty. 2007;22(7 suppl 3):12-15.
13. Husted H, Otte KS, Kristensen BB, Orsnes T, Kehlet H. Readmissions after fast-track hip and knee arthroplasty. Arch Orthop Trauma Surg. 2010;130(9):1185-1191.
14. Husted H, Lunn TH, Troelsen A, Gaarn-Larsen L, Kristensen BB, Kehlet H. Why still in hospital after fast-track hip and knee arthroplasty? Acta Orthop. 2011;82(6):679-684.
15. Husted H, Jensen CM, Solgaard S, Kehlet H. Reduced length of stay following hip and knee arthroplasty in Denmark 2000-2009: from research to implementation. Arch Orthop Trauma Surg. 2012;132(1):101-104.
16. Berger RA, Sanders SA, Thill ES, Sporer SM, Della Valle C. Newer anesthesia and rehabilitation protocols enable outpatient hip replacement in selected patients. Clin Orthop Relat Res. 2009;467(6):1424-1430.
17. Peck CN, Foster A, McLauchlan GJ. Reducing incision length or intensifying rehabilitation: what makes the difference to length of stay in total hip replacement in a UK setting? Int Orthop. 2006;30(5):395-398.
18. Isaac D, Falode T, Liu P, I’Anson H, Dillow K, Gill P. Accelerated rehabilitation after total knee replacement. Knee. 2005;12(5):346-350.
19. Labraca NS, Castro-Sánchez AM, Matarán-Peñarrocha GA, Arroyo-Morales M, Sánchez-Joya Mdel M, Moreno-Lorenzo C. Benefits of starting rehabilitation within 24 hours of primary total knee arthroplasty: randomized clinical trial. Clin Rehabil. 2011;25(6):557-566.
20. Larsen K, Hansen TB, Søballe K. Hip arthroplasty patients benefit from accelerated perioperative care and rehabilitation: a quasi-experimental study of 98 patients. Acta Orthop. 2008;79(5):624-630.
21. Larsen K, Hansen TB, Thomsen PB, Christiansen T, Søballe K. Cost-effectiveness of accelerated perioperative care and rehabilitation after total hip and knee arthroplasty. J Bone Joint Surg Am. 2009;91(4):761-772.
22. Larsen K, Sørensen OG, Hansen TB, Thomsen PB, Søballe K. Accelerated perioperative care and rehabilitation intervention for hip and knee replacement is effective: a randomized clinical trial involving 87 patients with 3 months of follow-up. Acta Orthop. 2008;79(2):149-159.
23. Wellman SS, Murphy AC, Gulcynski D. Murphy SB. Implementation of an accelerated mobilization protocol following primary total hip arthroplasty: impact on length of stay and disposition. Curr Rev Musculoskelet Med. 2011;4(3):84-90.
Pain starting in knee later arises in other joints
People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.
In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.
The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).
Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.
The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).
When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.
“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.
The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”
While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”
Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”
The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.
People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.
In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.
The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).
Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.
The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).
When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.
“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.
The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”
While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”
Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”
The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.
People who develop knee pain associated with osteoarthritis often subsequently develop pain in other joints, according to a study of two observational, community-based cohorts that could not discern any pattern of new pain sites.
In the “first investigation of the association of knee pain with pain in multiple other sites,” David T. Felson, MD, of Boston University and his colleagues reported that the regions where pain developed after first appearing in the knee varied from person to person and occurred in both upper and lower extremities, which goes against the hypothesis that adjacent joints are most often affected by knee pain.
The study involved patients from the MOST (Multicenter Osteoarthritis Study) trial, including 281 with knee pain at the index visit (168 unilaterally) and 852 without, as well as patients from OAI (the Osteoarthritis Initiative), including 412 with knee pain at the index visit (241 unilaterally), and 1,941 without. The investigators assessed the patients’ data for 14 total joints outside of the knees: 2 each of feet, ankles, hips, hands, wrists, elbows, and shoulders (Arthritis Rheumatol. 2016 Sep 2. doi: 10.1002/art.39848).
Patients with new-onset knee pain at the index visit reported a mean of 2.3 painful joints outside the knee, compared with a significantly lower number of 1.3 reported by those without knee pain. The mean number of nonknee joints with pain was higher among patients with bilateral knee pain, compared with unilateral knee pain. The percentage of patients who reported pain outside the knee rose with the number of painful knees: 80% for two, 64% for one, and 50% for none.
The patients who developed new unilateral knee pain at the index visit also experienced an increase in prevalent joint pain in multiple joints in upper- and lower-extremity sites. In particular, the investigators noted that ipsilateral prevalent hip joint pain, which they characterized as pain in the groin or front of the thigh, was more than twice as likely to occur among those with new unilateral knee pain at the index visit, but the odds for contralateral hip joint pain did not reach statistical significance. The comparisons were adjusted for age, sex, body mass index, depression at the index visit, study (MOST or OAI), and count of painful upper and lower limb joints at the index visit (excluding knees).
When examining only patients with new-onset joint pain outside of the knee, the odds of patients with new knee pain to later develop new-onset joint pain outside the knee were 30% higher than for those without knee pain. Patients with new knee pain had a mean 2.6 new painful joints out of 12.1 eligible joints, compared with 2.0 new painful joints in those without knee pain out of 12.7 eligible joints. (Joint regions with prevalent symptoms at the index visit were excluded as incident painful sites.) Patients with knee pain also had a consistently higher rate of new-onset pain in nonknee joints when compared with patients without knee pain in at least half of the follow-up visits over the course of the MOST and OAI studies. Sensitivity analyses indicated that the association between knee pain and subsequent pain in other joints was not driven by the inclusion of patients with widespread pain.
“There was no clear-cut predilection for pain in any specific lower-extremity joint region,” the investigators wrote.
The investigators noted that other researchers have suggested that patients with knee pain may be at higher risk for lower-extremity joint pain because of changes to their gait that gradually cause damage to other joints, but evidence in this study doesn’t “necessarily support the argument that in persons with knee pain, aberrant loading by altered movement patterns induces pain in only nearby joints. Our findings suggest that the sites affected are more than just hip and ankle and that there is no special predilection for pain in these locations.”
While the investigators cannot differentiate underlying mechanisms for their study’s finding of multiple co-occurring sites of joint pain in people with new-onset knee pain, they suggested that it “supports either a predilection for osteoarthritic changes at multiple joint sites and/or raises the possibility that nervous system–driven pain sensitization increases the risk not only of widespread pain but even of regional pain. Since symptomatic OA is unusual in some of these painful sites (e.g., elbow, shoulder, ankle), pain sensitization would seem a more likely explanation.”
Some of the study’s limitations described by the investigators included the uncertainty surrounding whether new-onset knee pain was truly new onset or whether it was a reoccurrence, and also the fact that most of the people in the two cohorts had multiple sites of joint pain at both the baseline and the index visit and there were too few people with no sites of pain outside the knee to carry out subanalyses in that group, which “speaks to the high prevalence of multiple joint pains in older adult cohorts.”
The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.
FROM ARTHRITIS & RHEUMATOLOGY
Key clinical point:People with frequently painful knees often develop pain in joints outside the knee, and the sites vary from person to person.
Major finding: The odds of patients with new knee pain to later develop joint pain outside the knee were 30% higher than for those without knee pain.
Data source: A study of 693 persons with index visit knee pain and 2,793 without it from two community-based cohorts.
Disclosures: The research was supported by grants from the National Institutes of Health. The authors had no disclosures to report.