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Editorial Commentary: Caveat Flexor—To Release or Not to Release the Iliopsoas, That Is the Question
Editorial Commentary: Caveat FlexordTo Release or Not to Release the Iliopsoas, That Is the Question Joshua D. Harris, M.D., Associate Editor
Abstract: In nonarthritic patients with femoroacetabular impingement syndrome, borderline dysplasia, and symptomatic iliopsoas snapping, arthroscopic iliopsoas fractional lengthening carries a significant risk of postarthroscopic instability. The iliopsoas is a dynamic stabilizer of the anterior hip. Thus, although statistically significant and clinically important improvements in hip function have the potential to be achieved with iliopsoas fractional lengthening, surgeons must be supremely confident in their ability to perform a secure capsular plication, labral preservation (not debridement), comprehensive cam correction, avoidance of intra-abdominal fluid extravasation, release of all iliopsoas tendon bands (if bifid or trifid), and ensure that femoral version is normal or low, neck-shaft angle is not excessively valgus, the dysplasia magnitude is no more than mild, and that there is no excessive soft tissue hypermobility. If these goals can be met, then excellent outcomes can be achieved. If not, then an iliopsoas fractional lengthening should not be performed.
See related article on page 1841
A
rthroscopic hip preservation surgery continues to be one of the most rapidly growing and evolving techniques within arthroscopic and related surgery. Patient selection continues to be critical in optimizing outcomes and reducing the risk of complications, reoperations, and conversions to hip arthroplasty. The spectrum of postoperative hip instability is one of the most controversial elements in outcome determination, influenced by both osseous (acetabular dysplasia, increased femoral anteversion, coxa valga) and soft tissue (capsular disruption, iliopsoas release, labral deficient, ligamentum teres pathology) causes.1 Hartigan, Perets, Close, Walsh, Chaharbakhshi, Mohr, and Domb, in their study “Arthroscopic Treatment of Iliopsoas Snapping in Patients With Radiographic Acetabular Dysplasia Utilizing Fractional Lengthening and Capsular Plication,”2 were able to show that excellent outcomes can be achieved in nonarthritic
The author reports the following potential conflicts of interest or sources of funding: J.D.H. is a board/committee member of AAOS, AOSSM, and AANA; is on the editorial board of American Journal of Orthopedics and Frontiers in Surgery; receives personal fees from Arthroscopy: The Journal of Arthroscopic and Related Surgery as Associate Editor, NIA Magellan, Ossur, Smith & Nephew, and SLACK; and receives grants from DePuy and Smith & Nephew. Full ICMJE author disclosure forms are available for this article online, as supplementary material. Ó 2018 by the Arthroscopy Association of North America 0749-8063/18427/$36.00 https://doi.org/10.1016/j.arthro.2018.04.010
borderline dysplastic patients with iliopsoas snapping via arthroscopic treatment of femoroacetabular impingement (FAI) syndrome, labral preservation, capsular plication, and iliopsoas fractional lengthening. To sufficiently and completely understand the kinematic role of iliopsoas fractional lengthening in the evaluation of hip stability, spinopelvic and hip anatomy must be unequivocally understood.3 Twenty-one muscles cross the hip joint, as part of the contractile layer within the Layer Concept of the hip.3,4 These muscles all, to some degree, in conjunction with the other layers (osteochondral, inert, and neuromuscular), contribute to hip stability.1 A deficiency in any component of any layer may lead to hip instability (or microinstability). The exact magnitude of “stability” provided by the iliopsoas (and “instability” after its release) is controversial. The conjoint tendon of the iliopsoas crosses anterior to the femoral head, coursing distally and posteriorly to its insertion on the lesser trochanter, affected by femoral version, lesser trochanteric version, and acetabular version.5-7 At the level of labrum, the iliopsoas is easily accessible arthroscopically and is approximately 45% tendon and 55% muscle, potentially making it an attractive location for release, if indicated due to iliopsoas impingement or iliopsoas snapping.8 The seminal publication on iliopsoas impingement, written by Domb et al.,9 reported on the observation of a distinct pattern of hip pain associated with a labral
Arthroscopy: The Journal of Arthroscopic and Related Surgery, Vol 34, No 6 (June), 2018: pp 1851-1855
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injury at the direct anterior 3 o’clock position in 36 nondysplastic, non-FAI, nonarthritic hips that were successfully treated with iliopsoas tenotomy. Three theories were proposed as causes of this unique labral pathology: (1) a tight iliopsoas impinges on the labrum in hip extension; (2) iliopsoas scarring to the anterior capsulolabral complex, leading to subsequent repetitive traction injury; and (3) hyperactive iliocapsularis similarly causes repetitive traction. A greater amount of tension in the iliopsoas transmits greater pressure to the anterior capsulolabral complex, which may be increased in the situation of a larger femoral head, low neck-shaft angle, lower iliopsoas pulley angle, increased lesser trochanteric retroversion, and high femoral version.7,10 Using 3 groups of femoral version (<5 , 5 to 15 , >15 ), although the “need” for iliopsoas release has been significantly associated with increased femoral version, short-term postarthroscopic patient-reported outcomes have not shown a difference between different version groups.11,12 However, using a 25 threshold, high version (>25 ) has been associated with worse pre- and postarthroscopic iliopsoas tenotomy hip-specific patient-reported outcome scores (vs low/ normal, defined as 25 ).13 The latter concluded that the iliopsoas is an important passive and dynamic stabilizer of the hip and release may significantly alter kinematics, particularly terminal extension. Importantly, in the paper by Hartigan et al.,2 femoral version was 7.1 8.1 and only 1 subject had femoral version >20 . This may be one reason why their outcomes showed success. Although iliopsoas impingement has a “characteristic” 3 o’clock anterior location of labral injury, its cause was in nondysplastic, non-FAI hips without investigation of the role of instability.9 Interestingly and comparatively, a separate investigation of nondysplastic, non-FAI hips revealed that 42% of straight anterior 3 o’clock labral tears were in an “instability-only” group, significantly higher than instability due to borderline dysplasia (8%), cam (7%), pincer (0%), or combined cam/pincer (0%).14 Combining these 2 studies, perhaps this means that the “characteristic” 3 o’clock labral tear originally described by Domb et al.,9 without mention of instability, was actually not due, in isolation, to just a tight iliopsoas, but rather instability prompted the anterior buttressing iliopsoas to dynamically stabilize the femoral head.10,15-22 This is analogous to the long head biceps brachii tendon stabilizing the humeral head in the glenohumeral joint.23 The same biomechanics between the hip and shoulder are inferred: inside-out anterior translation shear stress causing a unique chondrolabral injury. Although both Shibata et al.14 and Domb et al.9 excluded most causes of osseous
instability, analysis of femoral version was not performed in either. Similarly, soft tissue causes (joint hypermobility syndrome) were not analyzed in either. However, in the study by Hartigan et al.,2 only 1 patient had physical examination evidence of anterior instability, because patients with elevated Beighton scores were excluded and referred for periacetabular osteotomy. This is yet another reason why their outcomes showed success. The clear strengths of the study by Hartigan et al., with demonstration of statistically significant and clinically relevant improvements at 3.2-year follow-up (range, 2-6 years) in the modified Harris Hip Score (68.7-83.5, D14.8; minimal clinically important difference [MCID] 12 points; patient acceptable symptom state [PASS] 74), Hip Outcome Score-Activities of Daily Living (71.6-86.7, D15.1; MCID 9; PASS 87), Hip Outcome Score-Sports Specific Subscale (52.6-75.8, D23.2; MCID 6; PASS 75), and Non-Arthritic Hip Score (64.9-86.8, D21.9; MCID 10), must be interpreted with a considerable amount of cautiondcaveat flexor!24 These excellent outcomes are reported by a welltrained experienced high-volume hip arthroscopist. Pertinent to arthroscopic iliopsoas fractional lengthening, the senior author is well versed with 2 recent publications showing clinically important and statistically significant improvements in symptoms, satisfaction, return to sport, and resolution of internal snapping.25,26 Nonetheless, it is well documented that the learning curve of hip arthroscopy is steep. Recent publications even suggest a 519-case threshold to significantly lower the risk of revision hip surgery.27 Two recent systematic reviews have illustrated concordant findings of the risk of postarthroscopic hip macroinstability (dislocation, subluxation), which is increased with iliopsoas release, based on its role as an anterior hip stabilizer.28,29 The cumulative effect of an unrepaired (or torn) capsule with an iliopsoas release could be catastrophic.30,31 The senior author of the paper by Hartigan et al. is experienced in capsular management, with several publications illustrating the importance of capsular plication and shift in patients at risk for instability.32,33 Furthermore, unrecognized and iatrogenic dysplasia are also significant postarthroscopic instability (and failure) risk factors.28,29,34 The actual technical considerations of the joint-level tenotomy require either larger degrees of interportal capsulotomy (making subsequent repair/plication more important) or an enlarged capsular window, with complete visualization of the iliopsoas muscle-tendon complex. The latter has, surprisingly, only recently been discovered to be essential, as Philippon et al.35 reported that the prevalence of a single-, double-, or triple-banded
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iliopsoas tendon was 28.3%, 64.2%, and 7.5%, respectively. Thus, it is imperative to be cognizant of the risk of more than 1 tendon being present to ensure complete release. This was not evaluated in the paper by Hartigan et al.2 The effect of arthroscopic iliopsoas release on hip flexion strength and iliopsoas muscle volume has been recently investigated. Brandenburg et al.36 showed that the iliopsoas muscle is smaller (25% volume loss) and weaker (19% reduction in seated hip flexion strength) than the contralateral limb. Walczak et al.,37 in a study of 28 hips that underwent arthroscopic labral level iliopsoas release, showed that although most patients (89%) developed some degree of fatty infiltration (which they defined as “atrophy”), only 7% was grade IV (>75% fatty infiltration), in comparison with 90% infiltration and 55% grade IV in lesser trochanteric iliopsoas release. On the osseous side, dysplasia is a complex threedimensional entity frequently represented with 2dimensional imaging (plain radiographs). Although Hartigan et al.2 defined “dysplasia” singly and simply via a lateral center edge angle of 19 to 24 , these values are more frequently referred to as “borderline” or “mild dysplasia.” Although not used in the latter to form their definition of dysplasia, plain radiographic measures of anterior center edge angle (preop 25.5 to postop 24.4 ) and Tonnis angle (preop 7 to postop 7.4 ) were nonetheless collected. Other plain radiographic measures of femoral head extrusion index, Sharp’s index, and Shenton’s line continuity were not assessed. Although computed tomography has been shown to be the best imaging modality to measure acetabular coverage, it was not routinely obtained either.38,39 Increased appreciation of the role of athletic groin pain etiologies outside of the hip joint led to creation of the Doha Agreement, where iliopsoas-related groin pain is 1 of 4 defined clinical entities for groin (also adductor-, pubic-, and inguinal-related).40 This was omitted from the paper by Hartigan et al.2 The risk of intra-abdominal fluid extravasation and abdominal compartment syndrome with arthroscopic iliopsoas release is real and can be catastrophic.41 Hence, it should be performed as late as possible in the surgery, as Hartigan et al.2 did at the conclusion of central compartment work. Also, if one of the main reasons why iliopsoas release should not be routinely or casually performed in the setting of hip dysplasia is the risk of commencement or exacerbation of hip instability (with possible resultant articular cartilage damage), then only longer term follow-up (mean follow-up of only 38 months) with a more generalizable sex distribution (30 of 32 subjects were female) will yield the true outcome. Finally, as arthroscopic hip preservation surgeons, we cannot forget that the
iliopsoas has a profound effect on the lumbar spine (origin from T12 spanning to L5 vertebral bodies and iliac fossa) and any alteration of its muscle-tendon unit may have an effect on low back symptoms as well.42,43 This was not investigated in the study by Hartigan et al.2 Thus, caveat flexor! If you are going to perform an arthroscopic iliopsoas release for symptomatic internal snapping in patients with borderline dysplasia, in conjunction with management of FAI/labrum, then you must be absolutely sure that it is only mild dysplasia, with normal or low femoral version, without excessive soft tissue hypermobility, and that you can plicate/shift the iliofemoral ligament capsular closure, preserve the labrum, comprehensively correct cam morphology, release all iliopsoas tendon bands (if bifid or trifid), and avoid fluid extravasation (low arthroscopic pump pressures, release at near case conclusion). If you can do all of the above, then the Level IV evidence study published by Hartigan et al. has shown that excellent outcomes can be achieved. If you cannot do all of the above, then “to release or not to release the iliopsoas” should be answered in favor of the latter, as the results could lead to a high risk of failure.
References 1. Harris JD, Gerrie BJ, Lintner DM, Varner KE, McCulloch PC. Microinstability of the hip and the splits radiograph. Orthopedics 2016;39:e169-e175. 2. Hartigan DE, Perets I, Close MR, et al. Arthroscopic treatment of iliopsoas snapping in patients with radiographic acetabular dysplasia utilizing fractional lengthening and capsular plication. Arthroscopy 2018;34:1841-1850. 3. Neumann DA. Kinesiology of the hip: A focus on muscular actions. J Orthop Sports Phys Ther 2010;40:82-94. 4. Draovitch P, Edelstein J, Kelly BT. The layer concept: Utilization in determining the pain generators, pathology and how structure determines treatment. Curr Rev Musculoskelet Med 2012;5:1-8. 5. Schroder RG, Reddy M, Hatem MA, et al. A MRI study of the lesser trochanteric version and its relationship to proximal femoral osseous anatomy. J Hip Preserv Surg 2015;2:410-416. 6. Gomez-Hoyos J, Schroder R, Reddy M, Palmer IJ, Martin HD. Femoral neck anteversion and lesser trochanteric retroversion in patients with ischiofemoral impingement: A case-control magnetic resonance imaging study. Arthroscopy 2016;32:13-18. 7. Gomez-Hoyos J, Schroder R, Reddy M, Palmer IJ, Khoury A, Martin HD. Is there a relationship between psoas impingement and increased trochanteric retroversion? J Hip Preserv Surg 2015;2:164-169. 8. Alpert JM, Kozanek M, Li G, Kelly BT, Asnis PD. Crosssectional analysis of the iliopsoas tendon and its relationship to the acetabular labrum: An anatomic study. Am J Sports Med 2009;37:1594-1598.
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9. Domb BG, Shindle MK, McArthur B, Voos JE, Magennis EM, Kelly BT. Iliopsoas impingement: A newly identified cause of labral pathology in the hip. HSS J 2011;7:145-150. 10. Yoshio M, Murakami G, Sato T, Sato S, Noriyasu S. The function of the psoas major muscle: Passive kinetics and morphological studies using donated cadavers. J Orthop Sci 2002;7:199-207. 11. Ejnisman L, Philippon MJ, Lertwanich P, et al. Relationship between femoral anteversion and findings in hips with femoroacetabular impingement. Orthopedics 2013;36: e293-e300. 12. Ferro FP, Ho CP, Briggs KK, Philippon MJ. Patientcentered outcomes after hip arthroscopy for femoroacetabular impingement and labral tears are not different in patients with normal, high, or low femoral version. Arthroscopy 2015;31:454-459. 13. Fabricant PD, Bedi A, De La Torre K, Kelly BT. Clinical outcomes after arthroscopic psoas lengthening: The effect of femoral version. Arthroscopy 2012;28:965-971. 14. Shibata KR, Matsuda S, Safran MR. Is there a distinct pattern to the acetabular labrum and articular cartilage damage in the non-dysplastic hip with instability? Knee Surg Sports Traumatol Arthrosc 2017;25:84-93. 15. Sajko S, Stuber K. Psoas Major: A case report and review of its anatomy, biomechanics, and clinical implications. J Can Chiropr Assoc 2009;53:311-318. 16. Glauber A, Vizkelety T. The influence of the iliopsoas muscle on femoral antetorsion. Arch Orthop Unfallchir 1966;60:71-79. 17. Lewis CL, Sahrmann SA, Moran DW. Anterior hip joint force increases with hip extension, decreased gluteal force, or decreased iliopsoas force. J Biomech 2007;40:3725-3731. 18. Guanche CA, Sikka RS. Acetabular labral tears with underlying chondromalacia: A possible association with high-level running. Arthroscopy 2005;21:580-585. 19. Lewis CL, Sahrmann SA, Moran DW. Effect of hip angle on anterior hip joint force during gait. Gait Posture 2010;32:603-607. 20. Philippon MJ. The role of arthroscopic thermal capsulorrhaphy in the hip. Clin Sports Med 2001;20:817-829. 21. Andersson E, Oddsson L, Grundstrom H, Thorstensson A. The role of the psoas and iliacus muscles for stability and movement of the lumbar spine, pelvis and hip. Scand J Med Sci Sports 1995;5:10-16. 22. Sahrmann S. Diagnosis and treatment of movement impairment syndromes. In: Sahrmann S, ed. Diagnosis and treatment of movement impairment syndromes. Ed 1. St Louis: Mosby, 2002;121-190. 23. Malicky DM, Soslowsky LJ, Blasier RB, Shyr Y. Anterior glenohumeral stabilization factors: Progressive effects in a biomechanical model. J Orthop Res 1996;14:282-288. 24. Harris JD, Brand JC, Cote MP, Faucett SC, Dhawan A. Research pearls: The significance of statistics and perils of pooling. Part 1: Clinical versus statistical significance. Arthroscopy 2017;33:1102-1112. 25. El Bitar YF, Stake CE, Dunne KF, Botser IB, Domb BG. Arthroscopic iliopsoas fractional lengthening for internal snapping of the hip: Clinical outcomes with a minimum 2-year follow-up. Am J Sports Med 2014;42: 1696-1703.
26. Perets I, Hartigan DE, Chaharbakhshi EO, Ashberg L, Mu B, Domb BG. Clinical outcomes and return to sport in competitive athletes undergoing arthroscopic iliopsoas fractional lengthening compared with a matched control group without iliopsoas fractional lengthening. Arthroscopy 2018;34:456-463. 27. Mehta N, Chamberlin P, Marx RG, et al. Defining the learning curve for hip arthroscopy: A threshold analysis of the volume-outcomes relationship. Am J Sports Med 2018;46:1284-1293. 28. Duplantier NL, McCulloch PC, Nho SJ, Mather RC III, Lewis BD, Harris JD. Hip dislocation or subluxation after hip arthroscopy: A systematic review. Arthroscopy 2016;32: 1428-1434. 29. Yeung M, Memon M, Simunovic N, Belzile E, Philippon MJ, Ayeni OR. Gross instability after hip arthroscopy: An analysis of case reports evaluating surgical and patient factors. Arthroscopy 2016;32: 1196-1204.e1. 30. Sansone M, Ahlden M, Jonasson P, Sward L, Eriksson T, Karlsson J. Total dislocation of the hip joint after arthroscopy and iliopsoas tenotomy. Knee Surg Sports Traumatol Arthrosc 2013;21:420-423. 31. Austin DC, Horneff JG III, Kelly JDT. Anterior hip dislocation 5 months after hip arthroscopy. Arthroscopy 2014;30:1380-1382. 32. Domb BG, Chaharbakhshi EO, Perets I, Walsh JP, Yuen LC, Ashberg LJ. Patient-reported outcomes of capsular repair versus capsulotomy in patients undergoing hip arthroscopy: Minimum 5-year follow-up-a matched comparison study. Arthroscopy 2018;34: 853-863.e1. 33. Domb BG, Chaharbakhshi EO, Perets I, Yuen LC, Walsh JP, Ashberg L. Hip arthroscopic surgery with labral preservation and capsular plication in patients with borderline hip dysplasia: Minimum 5-year patientreported outcomes. Am J Sports Med 2018;46:305-313. 34. Larson CM, Ross JR, Stone RM, et al. Arthroscopic management of dysplastic hip deformities: Predictors of success and failures with comparison to an arthroscopic FAI cohort. Am J Sports Med 2016;44:447-453. 35. Philippon MJ, Devitt BM, Campbell KJ, et al. Anatomic variance of the iliopsoas tendon. Am J Sports Med 2014;42: 807-811. 36. Brandenburg JB, Kapron AL, Wylie JD, et al. The functional and structural outcomes of arthroscopic iliopsoas release. Am J Sports Med 2016;44:1286-1291. 37. Walczak BE, Blankenbaker DG, Tuite MR, Keene JS. Magnetic resonance imaging appearance of the hip musculature after arthroscopic labral-level iliopsoas tenotomies. Orthop J Sports Med 2017;5: 2325967117707498. 38. Nepple JJ, Wells J, Ross JR, Bedi A, Schoenecker PL, Clohisy JC. Three patterns of acetabular deficiency are common in young adult patients with acetabular dysplasia. Clin Orthop Relat Res 2017;475:1037-1044. 39. Larson CM, Moreau-Gaudry A, Kelly BT, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res 2015;473:1247-1254.
EDITORIAL COMMENTARY 40. Weir A, Brukner P, Delahunt E, et al. Doha agreement meeting on terminology and definitions in groin pain in athletes. Br J Sports Med 2015;49:768-774. 41. Ekhtiari S, Haldane CE, de Sa D, Simunovic N, Ayeni OR. Fluid extravasation in hip arthroscopy: A systematic review. Arthroscopy 2017;33:873-880.
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42. Bogduk N, Pearcy M, Hadfield G. Anatomy and biomechanics of psoas major. Clin Biomech (Bristol, Avon) 1992;7: 109-119. 43. Harris JD. Editorial Commentary: The hip bone’s connected to the spine bone-but correlation does not equal causation. Arthroscopy 2016;32:2249-2250.
Abstract: In nonarthritic patients with femoroacetabular impingement syndrome, borderline dysplasia, and symptomatic iliopsoas snapping, arthroscopic iliopsoas fractional lengthening carries a significant risk of postarthroscopic instability. The iliopsoas is a dynamic stabilizer of the anterior hip. Thus, although statistically significant and clinically important improvements in hip function have the potential to be achieved with iliopsoas fractional lengthening, surgeons must be supremely confident in their ability to perform a secure capsular plication, labral preservation (not debridement), comprehensive cam correction, avoidance of intra-abdominal fluid extravasation, release of all iliopsoas tendon bands (if bifid or trifid), and ensure that femoral version is normal or low, neck-shaft angle is not excessively valgus, the dysplasia magnitude is no more than mild, and that there is no excessive soft tissue hypermobility. If these goals can be met, then excellent outcomes can be achieved. If not, then an iliopsoas fractional lengthening should not be performed.
See related article on page 1841
A
rthroscopic hip preservation surgery continues to be one of the most rapidly growing and evolving techniques within arthroscopic and related surgery. Patient selection continues to be critical in optimizing outcomes and reducing the risk of complications, reoperations, and conversions to hip arthroplasty. The spectrum of postoperative hip instability is one of the most controversial elements in outcome determination, influenced by both osseous (acetabular dysplasia, increased femoral anteversion, coxa valga) and soft tissue (capsular disruption, iliopsoas release, labral deficient, ligamentum teres pathology) causes.1 Hartigan, Perets, Close, Walsh, Chaharbakhshi, Mohr, and Domb, in their study “Arthroscopic Treatment of Iliopsoas Snapping in Patients With Radiographic Acetabular Dysplasia Utilizing Fractional Lengthening and Capsular Plication,”2 were able to show that excellent outcomes can be achieved in nonarthritic
The author reports the following potential conflicts of interest or sources of funding: J.D.H. is a board/committee member of AAOS, AOSSM, and AANA; is on the editorial board of American Journal of Orthopedics and Frontiers in Surgery; receives personal fees from Arthroscopy: The Journal of Arthroscopic and Related Surgery as Associate Editor, NIA Magellan, Ossur, Smith & Nephew, and SLACK; and receives grants from DePuy and Smith & Nephew. Full ICMJE author disclosure forms are available for this article online, as supplementary material. Ó 2018 by the Arthroscopy Association of North America 0749-8063/18427/$36.00 https://doi.org/10.1016/j.arthro.2018.04.010
borderline dysplastic patients with iliopsoas snapping via arthroscopic treatment of femoroacetabular impingement (FAI) syndrome, labral preservation, capsular plication, and iliopsoas fractional lengthening. To sufficiently and completely understand the kinematic role of iliopsoas fractional lengthening in the evaluation of hip stability, spinopelvic and hip anatomy must be unequivocally understood.3 Twenty-one muscles cross the hip joint, as part of the contractile layer within the Layer Concept of the hip.3,4 These muscles all, to some degree, in conjunction with the other layers (osteochondral, inert, and neuromuscular), contribute to hip stability.1 A deficiency in any component of any layer may lead to hip instability (or microinstability). The exact magnitude of “stability” provided by the iliopsoas (and “instability” after its release) is controversial. The conjoint tendon of the iliopsoas crosses anterior to the femoral head, coursing distally and posteriorly to its insertion on the lesser trochanter, affected by femoral version, lesser trochanteric version, and acetabular version.5-7 At the level of labrum, the iliopsoas is easily accessible arthroscopically and is approximately 45% tendon and 55% muscle, potentially making it an attractive location for release, if indicated due to iliopsoas impingement or iliopsoas snapping.8 The seminal publication on iliopsoas impingement, written by Domb et al.,9 reported on the observation of a distinct pattern of hip pain associated with a labral
Arthroscopy: The Journal of Arthroscopic and Related Surgery, Vol 34, No 6 (June), 2018: pp 1851-1855
1851
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injury at the direct anterior 3 o’clock position in 36 nondysplastic, non-FAI, nonarthritic hips that were successfully treated with iliopsoas tenotomy. Three theories were proposed as causes of this unique labral pathology: (1) a tight iliopsoas impinges on the labrum in hip extension; (2) iliopsoas scarring to the anterior capsulolabral complex, leading to subsequent repetitive traction injury; and (3) hyperactive iliocapsularis similarly causes repetitive traction. A greater amount of tension in the iliopsoas transmits greater pressure to the anterior capsulolabral complex, which may be increased in the situation of a larger femoral head, low neck-shaft angle, lower iliopsoas pulley angle, increased lesser trochanteric retroversion, and high femoral version.7,10 Using 3 groups of femoral version (<5 , 5 to 15 , >15 ), although the “need” for iliopsoas release has been significantly associated with increased femoral version, short-term postarthroscopic patient-reported outcomes have not shown a difference between different version groups.11,12 However, using a 25 threshold, high version (>25 ) has been associated with worse pre- and postarthroscopic iliopsoas tenotomy hip-specific patient-reported outcome scores (vs low/ normal, defined as 25 ).13 The latter concluded that the iliopsoas is an important passive and dynamic stabilizer of the hip and release may significantly alter kinematics, particularly terminal extension. Importantly, in the paper by Hartigan et al.,2 femoral version was 7.1 8.1 and only 1 subject had femoral version >20 . This may be one reason why their outcomes showed success. Although iliopsoas impingement has a “characteristic” 3 o’clock anterior location of labral injury, its cause was in nondysplastic, non-FAI hips without investigation of the role of instability.9 Interestingly and comparatively, a separate investigation of nondysplastic, non-FAI hips revealed that 42% of straight anterior 3 o’clock labral tears were in an “instability-only” group, significantly higher than instability due to borderline dysplasia (8%), cam (7%), pincer (0%), or combined cam/pincer (0%).14 Combining these 2 studies, perhaps this means that the “characteristic” 3 o’clock labral tear originally described by Domb et al.,9 without mention of instability, was actually not due, in isolation, to just a tight iliopsoas, but rather instability prompted the anterior buttressing iliopsoas to dynamically stabilize the femoral head.10,15-22 This is analogous to the long head biceps brachii tendon stabilizing the humeral head in the glenohumeral joint.23 The same biomechanics between the hip and shoulder are inferred: inside-out anterior translation shear stress causing a unique chondrolabral injury. Although both Shibata et al.14 and Domb et al.9 excluded most causes of osseous
instability, analysis of femoral version was not performed in either. Similarly, soft tissue causes (joint hypermobility syndrome) were not analyzed in either. However, in the study by Hartigan et al.,2 only 1 patient had physical examination evidence of anterior instability, because patients with elevated Beighton scores were excluded and referred for periacetabular osteotomy. This is yet another reason why their outcomes showed success. The clear strengths of the study by Hartigan et al., with demonstration of statistically significant and clinically relevant improvements at 3.2-year follow-up (range, 2-6 years) in the modified Harris Hip Score (68.7-83.5, D14.8; minimal clinically important difference [MCID] 12 points; patient acceptable symptom state [PASS] 74), Hip Outcome Score-Activities of Daily Living (71.6-86.7, D15.1; MCID 9; PASS 87), Hip Outcome Score-Sports Specific Subscale (52.6-75.8, D23.2; MCID 6; PASS 75), and Non-Arthritic Hip Score (64.9-86.8, D21.9; MCID 10), must be interpreted with a considerable amount of cautiondcaveat flexor!24 These excellent outcomes are reported by a welltrained experienced high-volume hip arthroscopist. Pertinent to arthroscopic iliopsoas fractional lengthening, the senior author is well versed with 2 recent publications showing clinically important and statistically significant improvements in symptoms, satisfaction, return to sport, and resolution of internal snapping.25,26 Nonetheless, it is well documented that the learning curve of hip arthroscopy is steep. Recent publications even suggest a 519-case threshold to significantly lower the risk of revision hip surgery.27 Two recent systematic reviews have illustrated concordant findings of the risk of postarthroscopic hip macroinstability (dislocation, subluxation), which is increased with iliopsoas release, based on its role as an anterior hip stabilizer.28,29 The cumulative effect of an unrepaired (or torn) capsule with an iliopsoas release could be catastrophic.30,31 The senior author of the paper by Hartigan et al. is experienced in capsular management, with several publications illustrating the importance of capsular plication and shift in patients at risk for instability.32,33 Furthermore, unrecognized and iatrogenic dysplasia are also significant postarthroscopic instability (and failure) risk factors.28,29,34 The actual technical considerations of the joint-level tenotomy require either larger degrees of interportal capsulotomy (making subsequent repair/plication more important) or an enlarged capsular window, with complete visualization of the iliopsoas muscle-tendon complex. The latter has, surprisingly, only recently been discovered to be essential, as Philippon et al.35 reported that the prevalence of a single-, double-, or triple-banded
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iliopsoas tendon was 28.3%, 64.2%, and 7.5%, respectively. Thus, it is imperative to be cognizant of the risk of more than 1 tendon being present to ensure complete release. This was not evaluated in the paper by Hartigan et al.2 The effect of arthroscopic iliopsoas release on hip flexion strength and iliopsoas muscle volume has been recently investigated. Brandenburg et al.36 showed that the iliopsoas muscle is smaller (25% volume loss) and weaker (19% reduction in seated hip flexion strength) than the contralateral limb. Walczak et al.,37 in a study of 28 hips that underwent arthroscopic labral level iliopsoas release, showed that although most patients (89%) developed some degree of fatty infiltration (which they defined as “atrophy”), only 7% was grade IV (>75% fatty infiltration), in comparison with 90% infiltration and 55% grade IV in lesser trochanteric iliopsoas release. On the osseous side, dysplasia is a complex threedimensional entity frequently represented with 2dimensional imaging (plain radiographs). Although Hartigan et al.2 defined “dysplasia” singly and simply via a lateral center edge angle of 19 to 24 , these values are more frequently referred to as “borderline” or “mild dysplasia.” Although not used in the latter to form their definition of dysplasia, plain radiographic measures of anterior center edge angle (preop 25.5 to postop 24.4 ) and Tonnis angle (preop 7 to postop 7.4 ) were nonetheless collected. Other plain radiographic measures of femoral head extrusion index, Sharp’s index, and Shenton’s line continuity were not assessed. Although computed tomography has been shown to be the best imaging modality to measure acetabular coverage, it was not routinely obtained either.38,39 Increased appreciation of the role of athletic groin pain etiologies outside of the hip joint led to creation of the Doha Agreement, where iliopsoas-related groin pain is 1 of 4 defined clinical entities for groin (also adductor-, pubic-, and inguinal-related).40 This was omitted from the paper by Hartigan et al.2 The risk of intra-abdominal fluid extravasation and abdominal compartment syndrome with arthroscopic iliopsoas release is real and can be catastrophic.41 Hence, it should be performed as late as possible in the surgery, as Hartigan et al.2 did at the conclusion of central compartment work. Also, if one of the main reasons why iliopsoas release should not be routinely or casually performed in the setting of hip dysplasia is the risk of commencement or exacerbation of hip instability (with possible resultant articular cartilage damage), then only longer term follow-up (mean follow-up of only 38 months) with a more generalizable sex distribution (30 of 32 subjects were female) will yield the true outcome. Finally, as arthroscopic hip preservation surgeons, we cannot forget that the
iliopsoas has a profound effect on the lumbar spine (origin from T12 spanning to L5 vertebral bodies and iliac fossa) and any alteration of its muscle-tendon unit may have an effect on low back symptoms as well.42,43 This was not investigated in the study by Hartigan et al.2 Thus, caveat flexor! If you are going to perform an arthroscopic iliopsoas release for symptomatic internal snapping in patients with borderline dysplasia, in conjunction with management of FAI/labrum, then you must be absolutely sure that it is only mild dysplasia, with normal or low femoral version, without excessive soft tissue hypermobility, and that you can plicate/shift the iliofemoral ligament capsular closure, preserve the labrum, comprehensively correct cam morphology, release all iliopsoas tendon bands (if bifid or trifid), and avoid fluid extravasation (low arthroscopic pump pressures, release at near case conclusion). If you can do all of the above, then the Level IV evidence study published by Hartigan et al. has shown that excellent outcomes can be achieved. If you cannot do all of the above, then “to release or not to release the iliopsoas” should be answered in favor of the latter, as the results could lead to a high risk of failure.
References 1. Harris JD, Gerrie BJ, Lintner DM, Varner KE, McCulloch PC. Microinstability of the hip and the splits radiograph. Orthopedics 2016;39:e169-e175. 2. Hartigan DE, Perets I, Close MR, et al. Arthroscopic treatment of iliopsoas snapping in patients with radiographic acetabular dysplasia utilizing fractional lengthening and capsular plication. Arthroscopy 2018;34:1841-1850. 3. Neumann DA. Kinesiology of the hip: A focus on muscular actions. J Orthop Sports Phys Ther 2010;40:82-94. 4. Draovitch P, Edelstein J, Kelly BT. The layer concept: Utilization in determining the pain generators, pathology and how structure determines treatment. Curr Rev Musculoskelet Med 2012;5:1-8. 5. Schroder RG, Reddy M, Hatem MA, et al. A MRI study of the lesser trochanteric version and its relationship to proximal femoral osseous anatomy. J Hip Preserv Surg 2015;2:410-416. 6. Gomez-Hoyos J, Schroder R, Reddy M, Palmer IJ, Martin HD. Femoral neck anteversion and lesser trochanteric retroversion in patients with ischiofemoral impingement: A case-control magnetic resonance imaging study. Arthroscopy 2016;32:13-18. 7. Gomez-Hoyos J, Schroder R, Reddy M, Palmer IJ, Khoury A, Martin HD. Is there a relationship between psoas impingement and increased trochanteric retroversion? J Hip Preserv Surg 2015;2:164-169. 8. Alpert JM, Kozanek M, Li G, Kelly BT, Asnis PD. Crosssectional analysis of the iliopsoas tendon and its relationship to the acetabular labrum: An anatomic study. Am J Sports Med 2009;37:1594-1598.
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9. Domb BG, Shindle MK, McArthur B, Voos JE, Magennis EM, Kelly BT. Iliopsoas impingement: A newly identified cause of labral pathology in the hip. HSS J 2011;7:145-150. 10. Yoshio M, Murakami G, Sato T, Sato S, Noriyasu S. The function of the psoas major muscle: Passive kinetics and morphological studies using donated cadavers. J Orthop Sci 2002;7:199-207. 11. Ejnisman L, Philippon MJ, Lertwanich P, et al. Relationship between femoral anteversion and findings in hips with femoroacetabular impingement. Orthopedics 2013;36: e293-e300. 12. Ferro FP, Ho CP, Briggs KK, Philippon MJ. Patientcentered outcomes after hip arthroscopy for femoroacetabular impingement and labral tears are not different in patients with normal, high, or low femoral version. Arthroscopy 2015;31:454-459. 13. Fabricant PD, Bedi A, De La Torre K, Kelly BT. Clinical outcomes after arthroscopic psoas lengthening: The effect of femoral version. Arthroscopy 2012;28:965-971. 14. Shibata KR, Matsuda S, Safran MR. Is there a distinct pattern to the acetabular labrum and articular cartilage damage in the non-dysplastic hip with instability? Knee Surg Sports Traumatol Arthrosc 2017;25:84-93. 15. Sajko S, Stuber K. Psoas Major: A case report and review of its anatomy, biomechanics, and clinical implications. J Can Chiropr Assoc 2009;53:311-318. 16. Glauber A, Vizkelety T. The influence of the iliopsoas muscle on femoral antetorsion. Arch Orthop Unfallchir 1966;60:71-79. 17. Lewis CL, Sahrmann SA, Moran DW. Anterior hip joint force increases with hip extension, decreased gluteal force, or decreased iliopsoas force. J Biomech 2007;40:3725-3731. 18. Guanche CA, Sikka RS. Acetabular labral tears with underlying chondromalacia: A possible association with high-level running. Arthroscopy 2005;21:580-585. 19. Lewis CL, Sahrmann SA, Moran DW. Effect of hip angle on anterior hip joint force during gait. Gait Posture 2010;32:603-607. 20. Philippon MJ. The role of arthroscopic thermal capsulorrhaphy in the hip. Clin Sports Med 2001;20:817-829. 21. Andersson E, Oddsson L, Grundstrom H, Thorstensson A. The role of the psoas and iliacus muscles for stability and movement of the lumbar spine, pelvis and hip. Scand J Med Sci Sports 1995;5:10-16. 22. Sahrmann S. Diagnosis and treatment of movement impairment syndromes. In: Sahrmann S, ed. Diagnosis and treatment of movement impairment syndromes. Ed 1. St Louis: Mosby, 2002;121-190. 23. Malicky DM, Soslowsky LJ, Blasier RB, Shyr Y. Anterior glenohumeral stabilization factors: Progressive effects in a biomechanical model. J Orthop Res 1996;14:282-288. 24. Harris JD, Brand JC, Cote MP, Faucett SC, Dhawan A. Research pearls: The significance of statistics and perils of pooling. Part 1: Clinical versus statistical significance. Arthroscopy 2017;33:1102-1112. 25. El Bitar YF, Stake CE, Dunne KF, Botser IB, Domb BG. Arthroscopic iliopsoas fractional lengthening for internal snapping of the hip: Clinical outcomes with a minimum 2-year follow-up. Am J Sports Med 2014;42: 1696-1703.
26. Perets I, Hartigan DE, Chaharbakhshi EO, Ashberg L, Mu B, Domb BG. Clinical outcomes and return to sport in competitive athletes undergoing arthroscopic iliopsoas fractional lengthening compared with a matched control group without iliopsoas fractional lengthening. Arthroscopy 2018;34:456-463. 27. Mehta N, Chamberlin P, Marx RG, et al. Defining the learning curve for hip arthroscopy: A threshold analysis of the volume-outcomes relationship. Am J Sports Med 2018;46:1284-1293. 28. Duplantier NL, McCulloch PC, Nho SJ, Mather RC III, Lewis BD, Harris JD. Hip dislocation or subluxation after hip arthroscopy: A systematic review. Arthroscopy 2016;32: 1428-1434. 29. Yeung M, Memon M, Simunovic N, Belzile E, Philippon MJ, Ayeni OR. Gross instability after hip arthroscopy: An analysis of case reports evaluating surgical and patient factors. Arthroscopy 2016;32: 1196-1204.e1. 30. Sansone M, Ahlden M, Jonasson P, Sward L, Eriksson T, Karlsson J. Total dislocation of the hip joint after arthroscopy and iliopsoas tenotomy. Knee Surg Sports Traumatol Arthrosc 2013;21:420-423. 31. Austin DC, Horneff JG III, Kelly JDT. Anterior hip dislocation 5 months after hip arthroscopy. Arthroscopy 2014;30:1380-1382. 32. Domb BG, Chaharbakhshi EO, Perets I, Walsh JP, Yuen LC, Ashberg LJ. Patient-reported outcomes of capsular repair versus capsulotomy in patients undergoing hip arthroscopy: Minimum 5-year follow-up-a matched comparison study. Arthroscopy 2018;34: 853-863.e1. 33. Domb BG, Chaharbakhshi EO, Perets I, Yuen LC, Walsh JP, Ashberg L. Hip arthroscopic surgery with labral preservation and capsular plication in patients with borderline hip dysplasia: Minimum 5-year patientreported outcomes. Am J Sports Med 2018;46:305-313. 34. Larson CM, Ross JR, Stone RM, et al. Arthroscopic management of dysplastic hip deformities: Predictors of success and failures with comparison to an arthroscopic FAI cohort. Am J Sports Med 2016;44:447-453. 35. Philippon MJ, Devitt BM, Campbell KJ, et al. Anatomic variance of the iliopsoas tendon. Am J Sports Med 2014;42: 807-811. 36. Brandenburg JB, Kapron AL, Wylie JD, et al. The functional and structural outcomes of arthroscopic iliopsoas release. Am J Sports Med 2016;44:1286-1291. 37. Walczak BE, Blankenbaker DG, Tuite MR, Keene JS. Magnetic resonance imaging appearance of the hip musculature after arthroscopic labral-level iliopsoas tenotomies. Orthop J Sports Med 2017;5: 2325967117707498. 38. Nepple JJ, Wells J, Ross JR, Bedi A, Schoenecker PL, Clohisy JC. Three patterns of acetabular deficiency are common in young adult patients with acetabular dysplasia. Clin Orthop Relat Res 2017;475:1037-1044. 39. Larson CM, Moreau-Gaudry A, Kelly BT, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res 2015;473:1247-1254.
EDITORIAL COMMENTARY 40. Weir A, Brukner P, Delahunt E, et al. Doha agreement meeting on terminology and definitions in groin pain in athletes. Br J Sports Med 2015;49:768-774. 41. Ekhtiari S, Haldane CE, de Sa D, Simunovic N, Ayeni OR. Fluid extravasation in hip arthroscopy: A systematic review. Arthroscopy 2017;33:873-880.
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42. Bogduk N, Pearcy M, Hadfield G. Anatomy and biomechanics of psoas major. Clin Biomech (Bristol, Avon) 1992;7: 109-119. 43. Harris JD. Editorial Commentary: The hip bone’s connected to the spine bone-but correlation does not equal causation. Arthroscopy 2016;32:2249-2250.