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Treatment of Femoroacetabular Impingement: Labrum, Cartilage, Osseous Deformity, and Capsule
Take-Home Points
- Repair the labrum when tissue quality is good.
- Avoid overcorrection of acetabulum by measuring center edge angle.
- Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
- Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
- Routine capsular closure to prevent postoperative instability.
The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.
Management of Acetabular Labrum
The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.1 The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.1
In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.2 After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle3 is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,4 though biomechanically piercing sutures help restore the labrum seal better.1 When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.
The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.5 We prefer the ITB autograft technique.6 The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
Osseous Deformity
On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.9
The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.2 A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.2Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty2 with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.
The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
Treatment of Cartilage Lesions
The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.8 We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.
As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,13 the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.14 Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.
Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.
Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
Capsule Management
The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.17 Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),18 which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,19 which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.
Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.20 Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.
Recent evidence suggests that capsule repair restores near native hip joint stability.17 In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues21 reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.
In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,22 which can lead to labral and chondral injury.17 Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft23 (Figure 5).
Biologics
At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.
Rehabilitation
Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).
Conclusion
Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.
Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.
Take-Home Points
- Repair the labrum when tissue quality is good.
- Avoid overcorrection of acetabulum by measuring center edge angle.
- Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
- Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
- Routine capsular closure to prevent postoperative instability.
The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.
Management of Acetabular Labrum
The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.1 The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.1
In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.2 After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle3 is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,4 though biomechanically piercing sutures help restore the labrum seal better.1 When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.
The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.5 We prefer the ITB autograft technique.6 The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
Osseous Deformity
On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.9
The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.2 A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.2Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty2 with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.
The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
Treatment of Cartilage Lesions
The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.8 We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.
As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,13 the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.14 Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.
Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.
Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
Capsule Management
The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.17 Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),18 which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,19 which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.
Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.20 Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.
Recent evidence suggests that capsule repair restores near native hip joint stability.17 In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues21 reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.
In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,22 which can lead to labral and chondral injury.17 Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft23 (Figure 5).
Biologics
At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.
Rehabilitation
Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).
Conclusion
Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.
Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Repair the labrum when tissue quality is good.
- Avoid overcorrection of acetabulum by measuring center edge angle.
- Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
- Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
- Routine capsular closure to prevent postoperative instability.
The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.
Management of Acetabular Labrum
The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.1 The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.1
In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.2 After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle3 is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,4 though biomechanically piercing sutures help restore the labrum seal better.1 When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.
The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.5 We prefer the ITB autograft technique.6 The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
Osseous Deformity
On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.9
The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.2 A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.2Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty2 with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.
The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
Treatment of Cartilage Lesions
The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.8 We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.
As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,13 the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.14 Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.
Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.
Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
Capsule Management
The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.17 Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),18 which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,19 which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.
Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.20 Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.
Recent evidence suggests that capsule repair restores near native hip joint stability.17 In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues21 reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.
In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,22 which can lead to labral and chondral injury.17 Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft23 (Figure 5).
Biologics
At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.
Rehabilitation
Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).
Conclusion
Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.
Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.
Evolution of Femoroacetabular Impingement Treatment: The ANCHOR Experience
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am. 2013;95(5):417-423.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res. 2003;(407):241-248.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. 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(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am. 2013;95(5):417-423.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res. 2003;(407):241-248.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. 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(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
1. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am. 2013;95(5):417-423.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res. 2003;(407):241-248.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. 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(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
Multicenter Outcomes After Hip Arthroscopy: Epidemiology (MASH Study Group). What Are We Seeing in the Office, and Who Are We Choosing to Treat?
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med. 2011;39(2):296-303.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med. 2011;39(2):296-303.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med. 2011;39(2):296-303.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.
Current Concepts in Labral Repair and Refixation: Anatomical Approach to Labral Management
Take-Home Points
- Labral preservation is recommended when possible to ensure restoration of suction seal, stability, and contact pressure of the hip joint.
- Over 95% of labral tears can be addressed with primary repair.
- Consider using an accessory portal (ie, DALA) to allow for more anatomic placement of suture anchor.
- Mattress stitch when labrum >3 mm and looped stitch when labrum <3 mm.
- 10Control labral repair to avoid excessive inversion or eversion.
Arthroscopic labral repair and refixation have garnered much attention over the past several years. Restoration of suction seal and native labral function has been an evolving focus for achieving excellent results in hip preservation surgery.1-6 Given the superior results of labral repair, including level I evidence, repair or refixation should be pursued whenever possible.7 Authors have reported using several labral management techniques: débridement, labralization, looped suture fixation, base stitch fixation, inversion-eversion, and reconstruction.7-13 The optimal technique is yet to be determined. When possible, steps should be taken to repair the labrum to an anatomical position. Absolute indications for labral repair are a confirmed intra-articular diagnosis with symptomatic pain, joint space >2 mm with or without femoroacetabular impingement (FAI), labral tear or instability, and failed conservative management.9,11,12,14,15 More important, the surgeon must have a clear etiology of the pathologic cause of the tear and be aware of the limitations of the procedure. Labral repair is relatively contraindicated in end-stage arthritis and has failed when used alone in undiagnosed dysplasia or hip instability.16 In this article, we discuss indications for labral repair; describe Dr. Mather’s preoperative planning, labral repair technique, and postoperative care; and review published outcomes and future trends in labral repair.
Indications
At our institution, anatomical labral repair is the preferred procedure for most primary and revision hip arthroscopy procedures. We aim to restore the suction seal, re-create the contact of the labrum and the femoral head to facilitate proprioception, and restore normal stability of the labrum. Indications for primary repair are labrum width >3 mm, no more than 2 repairs, and ability to hold a suture. Our indications for reconstruction or débridement are stage 3 irreparable labral tear, calcified/cystic labrum, and multiple failed labral repairs or reconstructions. The decision to perform labral débridement or reconstruction is made on a case-by-case basis but is primarily influenced by the stability of the hip joint and the activity goals of the patient. If preoperative presentation and intraoperative examination suggest labral instability as a major component of the pathology, or if the patient wants to return to high-demand activity, we more strongly favor reconstruction over débridement. In our experience, with the technique described in this article, more than 95% of all primary labral tears can be addressed with repair.
Preoperative Planning
The goals in hip preservation surgery are to identify and address the underlying cause of the labral tear, whether it be FAI syndrome, trauma, labral instability, or all 3, and to re-create the anatomy and biomechanics of the acetabular labrum. For repair, we prefer an inversion-eversion technique with independent control of the labrum. Our initial work-up includes a thorough history and physical examination with baseline patient-reported outcome scores. Standard erect anteroposterior pelvis, Dunn lateral, and false-profile radiographs are obtained. Standard measurements of lateral center edge angle, anterior center edge angle, Tönnis angle, Tönnis grade, lateral joint space, and head extrusion indices are evaluated. Selective in-office ultrasound-guided injections are used to confirm an intra-articular source of pain. At our institution, noncontrast 3.0 Tesla magnetic resonance imaging (MRI) with volumetric interpolated breath-hold examination (VIBE) sequencing and 3-dimensional rendering is obtained for evaluation of labral and FAI morphology.17 All advanced imaging is performed without arthrogram or radiation exposure (Figures 1A-1C).
With use of the radiographs and the MRI scans, we engage the patient in an informed discussion about the labral tear, FAI, and concomitant pathology. We discuss expected outcomes of conservative or operative management given the patient’s expected functional activities, and inform the patient that primary repair is indicated for many others in similar situations. The potential for possible labral reconstruction is discussed if the patient had prior intra-articular hip surgery, has a large calcified labrum or a cystic labrum, is an athlete with failed prior surgery, or is younger than 40 years.
Labral Repair Technique
The patient is taken to the surgical suite, and a general anesthetic is administered. A peripheral nerve block is not routinely used. The patient’s feet are padded, and boots for the traction table are applied. The patient is carefully placed on a Hana table in modified supine position. Balanced traction is used to achieve proper joint distraction. The C-arm is used to verify proper distraction, assess hip stability, and achieve standard anterolateral (AL) portal placement. A midanterior portal (MAP) is created and an interportal capsulotomy is performed. Capsular suspension is performed with the InJector II Capsule Restoration System (Stryker Sports Medicine) and typically 4 or 5 high-strength No. 2 sutures (Zipline; Stryker Sports Medicine).19 Diagnostic arthroscopy is performed to identify the tear type, measure the labral width, determine the impingement area, and identify the intra-articular pathology. After the intra-articular pathology is addressed, a radiofrequency Ambient HIPVAC 50 Coblation Wand (Smith & Nephew) is used to expose the acetabular rim and subspine as indicated. Acetabuloplasty or subspine decompression is performed, and then a primary repair or refixation of the labrum is performed. We do not routinely detach the labrum for acetabular rim trimming. A crucial step here is to expose a bleeding surface to which the labrum can be repaired. If the rim is sclerotic, or the rim cannot be removed because of underlying low acetabular coverage, we prefer to obtain the bleeding surface with a microdrilling device (Stryker) that is routinely used for acetabular microfracture.
Labrum quality is used to determine which repair method to use. A hypertrophic labrum is debulked. The acetabular rim is seldom resected >3 mm, but, when it is, the newly exposed cartilage is removed. We have found that >3 mm of residual cartilage prevents refixation of the labrum directly to the bone and may interfere with anatomical positioning. When a labrum is <3 mm in width or will not hold a base technique, repair stability is the priority, and a looped method is used. A knotless anchor with No. 1 permanent suture designed for hip labral repair (CinchLock; Stryker) is our first-line anchor choice. A distal anterolateral accessory (DALA) portal is created with an outside-in technique, and anchors are drilled through this portal into zones 2 to 4 (Figures 2A-2E).
A 2.4-mm drill guide is advanced through the DALA portal and placed in the appropriate position for drilling. We aim for 1 mm to 2 mm from the chondrolabral junction. Next, the probe is placed intra-articular and medial to the anchor insertion site, and the anchor is loaded and then inserted around the probe (Figures 3A-3E).
The hip is then reduced. If indicated, a T-capsulotomy is performed for femoral osteochondroplasty.
Postoperative Care
Patients are placed in a postoperative hip brace and use a continuous passive motion machine 6 hours a day for 2 weeks, and an ice machine. They maintain 30 lb of foot-flat weight-bearing for 3 weeks, and begin a standard labral repair protocol on postoperative days 3 to 7.
Discussion
Hip labral preservation has evolved over the past 10 years, and current options for labral management include excision, débridement, labralization, repair, and reconstruction.1-13 Labral excision was studied by Miozzari and colleagues,8 who postulated on the basis of animal models that the labrum may regenerate. In their series of 9 patients treated with surgical hip dislocation and labral excision at average 4-year follow-up, repeat magnetic resonance angiography revealed no regeneration of tissue—modified Harris Hip Score was 83. The hip scores were less than those of patients treated with the same procedure with repair, and the authors concluded that defining labral débridement versus excision in the literature, and treating patients with primary repair or reconstruction techniques, may lead to better results. Their study used a small sample and was limited to an open procedure. Arthroscopic labral débridement in isolation was also a poor option for treatment of a labral tear. In a 2-year follow-up of 59 isolated labral débridement procedures, Krych and colleagues9 found 47% combined poor results.
There is level I evidence of the importance of labral repair. In 2013, Krych and colleagues7 conducted a randomized control trial of 38 female patients who underwent hip arthroscopy for FAI. At time of surgery, patients were randomly assigned to either débridement or repair. At 1-year follow-up, activities of daily living and Sports specific Hip Outcome Scores were statistically significantly superior in the repair group. On a subjective scale, 94% vs 78% of patients reported normal or near normal hips in the repair versus débridement groups respectively. Ayeni and colleagues20 performed a systematic review of 6 studies in an attempt to develop labral management recommendations. Five of the studies (N = 490 patients total) had improved results with labral repair over reconstruction. Although the studies had a low level of evidence, they found a trend toward improved results with labral repair. These studies highlight the importance of labral preservation and proper FAI management.
Techniques for labrum repair have advanced as well—from a looped suture technique to a base stitch and knotless independent tensioning.11-13 Restoration of the hip labrum function as a suction seal, fluid circulator and anatomic capsular repair is paramount to excellent results and stresses the importance of performing an anatomic labral repair.1-6 Knotless anchor repair is not novel and has been previously described. Fry and Domb12 reported on a knotless labral repair technique that uses push-lock devices (Arthrex) that do not allow for independent tensioning. Inversion-eversion was introduced to the literature by Moreira and colleagues,13 who described an independent tensioning technique that uses speed-lock anchors (Smith & Nephew). Our technique differs in that it involves a DALA portal; labral reduction and tensioning with a probe assist to ensure the second pass of the base stitch is at the apex of the labrum; and use of No. 1 instead of No. 2 suture. Although seemingly subtle, these differences allow for proper anchor placement nearer the rim, additional support in achieving precise suture placement, and less disruption of small labra. These differences are particularly relevant for smaller labra.
Evaluating repair techniques on the basis of high-evidence literature is challenging. In a matched-cohort study of 220 patients, Jackson and colleagues21 compared 2 techniques: looped and base stitch. At 2-year follow-up, patients in both groups showed improvement, and there was no statistically significant difference in patient-reported outcome measures between the groups. Sawyer and colleagues22 studied the outcomes of 326 consecutive patients who underwent looped, pierced, or combined labral repair at an average 32-month follow-up. The groups’ revision rates were comparable, each group improved in postoperative patient-reported outcomes, and the pierced group had significantly higher preoperative scores on the Western Ontario and McMaster Universities Osteoarthritis Index. These studies described a base or pierce repair that did not differ from a looped repair, though the techniques did not allow for independent tensioning to re-create an anatomical inversion-eversion repair and may have altered the reported outcomes.
Our current technique uses independent tensioning of the repair to allow control of labrum inversion-eversion to give an anatomical repair with restoration of the suction seal. Preoperative planning, addressing the FAI appropriately, proper suture-passing technique, controlling the labrum in inversion-eversion fashion, and anatomical labral repair are the elements of Dr. Mather’s preferred method for preserving the native labrum and allowing it to assume its native function.
Future Directions
As our understanding of FAI and labral function evolves, labral preservation surgery continues to advance. With surgeons continually developing new techniques and following up on previous techniques, the ability to preserve the native hip with lasting procedures evolves as well. Proper identification of the underlying cause of the labral tear and proper anatomical repair are paramount to the success of FAI surgery.
Am J Orthop. 2017;46(1):42-48. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
3. Dwyer MK, Jones HL, Hogan MG, Field RE, McCarthy JC, Noble PC. The acetabular labrum regulates fluid circulation of the hip joint during functional activities. Am J Sports Med. 2014;42(4):812-819.
4. Greaves LL, Gilbart MK, Yung AC, Kozlowski, Wilson DR. Effect of acetabular labral tears, repair and resection on hip cartilage strain: a 7T MR study. J Biomech. 2010;43(5):858-863.
5. Freehill MT, Safran MR. The labrum of the hip: diagnosis and rationale for surgical correction. Clin Sports Med. 2011;30(2):293-315.
6. Myers CA, Register BC, Lertwanich P, et al. Role of the acetabular labrum and the iliofemoral ligament in hip stability: an in vitro biplane fluoroscopy study. Am J Sports Med. 2011;39(suppl):85S-91S.
7. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
8. Miozzari HH, Celia M, Clark JM, Werlen S, Naal FD, Nötzli HP. No regeneration of the human acetabular labrum after excision to bone. Clin Orthop Relat Res. 2015;473(4):1349-1357.
9. Krych AJ, Kuzma SA, Kovachevich R, Hudgens JL, Stuart MJ, Levy BA. Modest mid-term outcomes after isolated arthroscopic debridement of acetabular labral tears. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):763-767.
10. Matsuda DK. Arthroscopic labralization of the hip: an alternative to labral reconstruction. Arthrosc Tech. 2014;3(1):e131-e133.
11. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
12. Fry D, Domb B. Labral base refixation in the hip: rationale and technique for an anatomic approach to labral repair. Arthroscopy. 2010;26(9 suppl):S81-S89.
13. Moreira B, Pascual-Garrido C, Chadayamurri V, Mei-Dan O. Eversion-inversion labral repair and reconstruction technique for optimal suction seal. Arthrosc Tech. 2015;4(6):e697-e700.
14. Mook WR, Briggs KK, Philippon MJ. Evidence and approach for management of labral deficiency: the role for labral reconstruction. Sports Med Arthrosc. 2015;23(4):205-212.
15. Gupta A, Suarez-Ahedo C, Redmond JM, et al. Best practices during hip arthroscopy: aggregate recommendations of high-volume surgeons. Arthroscopy. 2015;31(9):1722-1727.
16. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
17. Hash TW. Magnetic resonance imaging of the hip. In: Nho SJ, Leunig M, Larson CM, Bedi A, Kelly BT, eds. Hip Arthroscopy and Hip Joint Preservation Surgery, Vol. 1. New York, NY: Springer; 2015:65-113.
18. Sutter R, Zubler V, Hoffmann A, et al. Hip MRI: how useful is intraarticular contrast material for evaluating surgically proven lesions of the labrum and articular cartilage? AJR Am J Roentgenol. 2014;202(1):160-169.
19. Federer AE, Karas V, Nho S, Coleman SH, Mather RC 3rd. Capsular suspension technique for hip arthroscopy. Arthrosc Tech. 2015;4(4):e317-e322.
20. Ayeni OR, Adamich J, Farrokhyar F, et al. Surgical management of labral tears during femoroacetabular impingement surgery: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):756-762.
21. Jackson TJ, Hammarstedt JE, Vemula SP, Domb BG. Acetabular labral base repair versus circumferential suture repair: a matched-paired comparison of clinical outcomes. Arthroscopy. 2015;31(9):1716-1721.
22. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
Take-Home Points
- Labral preservation is recommended when possible to ensure restoration of suction seal, stability, and contact pressure of the hip joint.
- Over 95% of labral tears can be addressed with primary repair.
- Consider using an accessory portal (ie, DALA) to allow for more anatomic placement of suture anchor.
- Mattress stitch when labrum >3 mm and looped stitch when labrum <3 mm.
- 10Control labral repair to avoid excessive inversion or eversion.
Arthroscopic labral repair and refixation have garnered much attention over the past several years. Restoration of suction seal and native labral function has been an evolving focus for achieving excellent results in hip preservation surgery.1-6 Given the superior results of labral repair, including level I evidence, repair or refixation should be pursued whenever possible.7 Authors have reported using several labral management techniques: débridement, labralization, looped suture fixation, base stitch fixation, inversion-eversion, and reconstruction.7-13 The optimal technique is yet to be determined. When possible, steps should be taken to repair the labrum to an anatomical position. Absolute indications for labral repair are a confirmed intra-articular diagnosis with symptomatic pain, joint space >2 mm with or without femoroacetabular impingement (FAI), labral tear or instability, and failed conservative management.9,11,12,14,15 More important, the surgeon must have a clear etiology of the pathologic cause of the tear and be aware of the limitations of the procedure. Labral repair is relatively contraindicated in end-stage arthritis and has failed when used alone in undiagnosed dysplasia or hip instability.16 In this article, we discuss indications for labral repair; describe Dr. Mather’s preoperative planning, labral repair technique, and postoperative care; and review published outcomes and future trends in labral repair.
Indications
At our institution, anatomical labral repair is the preferred procedure for most primary and revision hip arthroscopy procedures. We aim to restore the suction seal, re-create the contact of the labrum and the femoral head to facilitate proprioception, and restore normal stability of the labrum. Indications for primary repair are labrum width >3 mm, no more than 2 repairs, and ability to hold a suture. Our indications for reconstruction or débridement are stage 3 irreparable labral tear, calcified/cystic labrum, and multiple failed labral repairs or reconstructions. The decision to perform labral débridement or reconstruction is made on a case-by-case basis but is primarily influenced by the stability of the hip joint and the activity goals of the patient. If preoperative presentation and intraoperative examination suggest labral instability as a major component of the pathology, or if the patient wants to return to high-demand activity, we more strongly favor reconstruction over débridement. In our experience, with the technique described in this article, more than 95% of all primary labral tears can be addressed with repair.
Preoperative Planning
The goals in hip preservation surgery are to identify and address the underlying cause of the labral tear, whether it be FAI syndrome, trauma, labral instability, or all 3, and to re-create the anatomy and biomechanics of the acetabular labrum. For repair, we prefer an inversion-eversion technique with independent control of the labrum. Our initial work-up includes a thorough history and physical examination with baseline patient-reported outcome scores. Standard erect anteroposterior pelvis, Dunn lateral, and false-profile radiographs are obtained. Standard measurements of lateral center edge angle, anterior center edge angle, Tönnis angle, Tönnis grade, lateral joint space, and head extrusion indices are evaluated. Selective in-office ultrasound-guided injections are used to confirm an intra-articular source of pain. At our institution, noncontrast 3.0 Tesla magnetic resonance imaging (MRI) with volumetric interpolated breath-hold examination (VIBE) sequencing and 3-dimensional rendering is obtained for evaluation of labral and FAI morphology.17 All advanced imaging is performed without arthrogram or radiation exposure (Figures 1A-1C).
With use of the radiographs and the MRI scans, we engage the patient in an informed discussion about the labral tear, FAI, and concomitant pathology. We discuss expected outcomes of conservative or operative management given the patient’s expected functional activities, and inform the patient that primary repair is indicated for many others in similar situations. The potential for possible labral reconstruction is discussed if the patient had prior intra-articular hip surgery, has a large calcified labrum or a cystic labrum, is an athlete with failed prior surgery, or is younger than 40 years.
Labral Repair Technique
The patient is taken to the surgical suite, and a general anesthetic is administered. A peripheral nerve block is not routinely used. The patient’s feet are padded, and boots for the traction table are applied. The patient is carefully placed on a Hana table in modified supine position. Balanced traction is used to achieve proper joint distraction. The C-arm is used to verify proper distraction, assess hip stability, and achieve standard anterolateral (AL) portal placement. A midanterior portal (MAP) is created and an interportal capsulotomy is performed. Capsular suspension is performed with the InJector II Capsule Restoration System (Stryker Sports Medicine) and typically 4 or 5 high-strength No. 2 sutures (Zipline; Stryker Sports Medicine).19 Diagnostic arthroscopy is performed to identify the tear type, measure the labral width, determine the impingement area, and identify the intra-articular pathology. After the intra-articular pathology is addressed, a radiofrequency Ambient HIPVAC 50 Coblation Wand (Smith & Nephew) is used to expose the acetabular rim and subspine as indicated. Acetabuloplasty or subspine decompression is performed, and then a primary repair or refixation of the labrum is performed. We do not routinely detach the labrum for acetabular rim trimming. A crucial step here is to expose a bleeding surface to which the labrum can be repaired. If the rim is sclerotic, or the rim cannot be removed because of underlying low acetabular coverage, we prefer to obtain the bleeding surface with a microdrilling device (Stryker) that is routinely used for acetabular microfracture.
Labrum quality is used to determine which repair method to use. A hypertrophic labrum is debulked. The acetabular rim is seldom resected >3 mm, but, when it is, the newly exposed cartilage is removed. We have found that >3 mm of residual cartilage prevents refixation of the labrum directly to the bone and may interfere with anatomical positioning. When a labrum is <3 mm in width or will not hold a base technique, repair stability is the priority, and a looped method is used. A knotless anchor with No. 1 permanent suture designed for hip labral repair (CinchLock; Stryker) is our first-line anchor choice. A distal anterolateral accessory (DALA) portal is created with an outside-in technique, and anchors are drilled through this portal into zones 2 to 4 (Figures 2A-2E).
A 2.4-mm drill guide is advanced through the DALA portal and placed in the appropriate position for drilling. We aim for 1 mm to 2 mm from the chondrolabral junction. Next, the probe is placed intra-articular and medial to the anchor insertion site, and the anchor is loaded and then inserted around the probe (Figures 3A-3E).
The hip is then reduced. If indicated, a T-capsulotomy is performed for femoral osteochondroplasty.
Postoperative Care
Patients are placed in a postoperative hip brace and use a continuous passive motion machine 6 hours a day for 2 weeks, and an ice machine. They maintain 30 lb of foot-flat weight-bearing for 3 weeks, and begin a standard labral repair protocol on postoperative days 3 to 7.
Discussion
Hip labral preservation has evolved over the past 10 years, and current options for labral management include excision, débridement, labralization, repair, and reconstruction.1-13 Labral excision was studied by Miozzari and colleagues,8 who postulated on the basis of animal models that the labrum may regenerate. In their series of 9 patients treated with surgical hip dislocation and labral excision at average 4-year follow-up, repeat magnetic resonance angiography revealed no regeneration of tissue—modified Harris Hip Score was 83. The hip scores were less than those of patients treated with the same procedure with repair, and the authors concluded that defining labral débridement versus excision in the literature, and treating patients with primary repair or reconstruction techniques, may lead to better results. Their study used a small sample and was limited to an open procedure. Arthroscopic labral débridement in isolation was also a poor option for treatment of a labral tear. In a 2-year follow-up of 59 isolated labral débridement procedures, Krych and colleagues9 found 47% combined poor results.
There is level I evidence of the importance of labral repair. In 2013, Krych and colleagues7 conducted a randomized control trial of 38 female patients who underwent hip arthroscopy for FAI. At time of surgery, patients were randomly assigned to either débridement or repair. At 1-year follow-up, activities of daily living and Sports specific Hip Outcome Scores were statistically significantly superior in the repair group. On a subjective scale, 94% vs 78% of patients reported normal or near normal hips in the repair versus débridement groups respectively. Ayeni and colleagues20 performed a systematic review of 6 studies in an attempt to develop labral management recommendations. Five of the studies (N = 490 patients total) had improved results with labral repair over reconstruction. Although the studies had a low level of evidence, they found a trend toward improved results with labral repair. These studies highlight the importance of labral preservation and proper FAI management.
Techniques for labrum repair have advanced as well—from a looped suture technique to a base stitch and knotless independent tensioning.11-13 Restoration of the hip labrum function as a suction seal, fluid circulator and anatomic capsular repair is paramount to excellent results and stresses the importance of performing an anatomic labral repair.1-6 Knotless anchor repair is not novel and has been previously described. Fry and Domb12 reported on a knotless labral repair technique that uses push-lock devices (Arthrex) that do not allow for independent tensioning. Inversion-eversion was introduced to the literature by Moreira and colleagues,13 who described an independent tensioning technique that uses speed-lock anchors (Smith & Nephew). Our technique differs in that it involves a DALA portal; labral reduction and tensioning with a probe assist to ensure the second pass of the base stitch is at the apex of the labrum; and use of No. 1 instead of No. 2 suture. Although seemingly subtle, these differences allow for proper anchor placement nearer the rim, additional support in achieving precise suture placement, and less disruption of small labra. These differences are particularly relevant for smaller labra.
Evaluating repair techniques on the basis of high-evidence literature is challenging. In a matched-cohort study of 220 patients, Jackson and colleagues21 compared 2 techniques: looped and base stitch. At 2-year follow-up, patients in both groups showed improvement, and there was no statistically significant difference in patient-reported outcome measures between the groups. Sawyer and colleagues22 studied the outcomes of 326 consecutive patients who underwent looped, pierced, or combined labral repair at an average 32-month follow-up. The groups’ revision rates were comparable, each group improved in postoperative patient-reported outcomes, and the pierced group had significantly higher preoperative scores on the Western Ontario and McMaster Universities Osteoarthritis Index. These studies described a base or pierce repair that did not differ from a looped repair, though the techniques did not allow for independent tensioning to re-create an anatomical inversion-eversion repair and may have altered the reported outcomes.
Our current technique uses independent tensioning of the repair to allow control of labrum inversion-eversion to give an anatomical repair with restoration of the suction seal. Preoperative planning, addressing the FAI appropriately, proper suture-passing technique, controlling the labrum in inversion-eversion fashion, and anatomical labral repair are the elements of Dr. Mather’s preferred method for preserving the native labrum and allowing it to assume its native function.
Future Directions
As our understanding of FAI and labral function evolves, labral preservation surgery continues to advance. With surgeons continually developing new techniques and following up on previous techniques, the ability to preserve the native hip with lasting procedures evolves as well. Proper identification of the underlying cause of the labral tear and proper anatomical repair are paramount to the success of FAI surgery.
Am J Orthop. 2017;46(1):42-48. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Labral preservation is recommended when possible to ensure restoration of suction seal, stability, and contact pressure of the hip joint.
- Over 95% of labral tears can be addressed with primary repair.
- Consider using an accessory portal (ie, DALA) to allow for more anatomic placement of suture anchor.
- Mattress stitch when labrum >3 mm and looped stitch when labrum <3 mm.
- 10Control labral repair to avoid excessive inversion or eversion.
Arthroscopic labral repair and refixation have garnered much attention over the past several years. Restoration of suction seal and native labral function has been an evolving focus for achieving excellent results in hip preservation surgery.1-6 Given the superior results of labral repair, including level I evidence, repair or refixation should be pursued whenever possible.7 Authors have reported using several labral management techniques: débridement, labralization, looped suture fixation, base stitch fixation, inversion-eversion, and reconstruction.7-13 The optimal technique is yet to be determined. When possible, steps should be taken to repair the labrum to an anatomical position. Absolute indications for labral repair are a confirmed intra-articular diagnosis with symptomatic pain, joint space >2 mm with or without femoroacetabular impingement (FAI), labral tear or instability, and failed conservative management.9,11,12,14,15 More important, the surgeon must have a clear etiology of the pathologic cause of the tear and be aware of the limitations of the procedure. Labral repair is relatively contraindicated in end-stage arthritis and has failed when used alone in undiagnosed dysplasia or hip instability.16 In this article, we discuss indications for labral repair; describe Dr. Mather’s preoperative planning, labral repair technique, and postoperative care; and review published outcomes and future trends in labral repair.
Indications
At our institution, anatomical labral repair is the preferred procedure for most primary and revision hip arthroscopy procedures. We aim to restore the suction seal, re-create the contact of the labrum and the femoral head to facilitate proprioception, and restore normal stability of the labrum. Indications for primary repair are labrum width >3 mm, no more than 2 repairs, and ability to hold a suture. Our indications for reconstruction or débridement are stage 3 irreparable labral tear, calcified/cystic labrum, and multiple failed labral repairs or reconstructions. The decision to perform labral débridement or reconstruction is made on a case-by-case basis but is primarily influenced by the stability of the hip joint and the activity goals of the patient. If preoperative presentation and intraoperative examination suggest labral instability as a major component of the pathology, or if the patient wants to return to high-demand activity, we more strongly favor reconstruction over débridement. In our experience, with the technique described in this article, more than 95% of all primary labral tears can be addressed with repair.
Preoperative Planning
The goals in hip preservation surgery are to identify and address the underlying cause of the labral tear, whether it be FAI syndrome, trauma, labral instability, or all 3, and to re-create the anatomy and biomechanics of the acetabular labrum. For repair, we prefer an inversion-eversion technique with independent control of the labrum. Our initial work-up includes a thorough history and physical examination with baseline patient-reported outcome scores. Standard erect anteroposterior pelvis, Dunn lateral, and false-profile radiographs are obtained. Standard measurements of lateral center edge angle, anterior center edge angle, Tönnis angle, Tönnis grade, lateral joint space, and head extrusion indices are evaluated. Selective in-office ultrasound-guided injections are used to confirm an intra-articular source of pain. At our institution, noncontrast 3.0 Tesla magnetic resonance imaging (MRI) with volumetric interpolated breath-hold examination (VIBE) sequencing and 3-dimensional rendering is obtained for evaluation of labral and FAI morphology.17 All advanced imaging is performed without arthrogram or radiation exposure (Figures 1A-1C).
With use of the radiographs and the MRI scans, we engage the patient in an informed discussion about the labral tear, FAI, and concomitant pathology. We discuss expected outcomes of conservative or operative management given the patient’s expected functional activities, and inform the patient that primary repair is indicated for many others in similar situations. The potential for possible labral reconstruction is discussed if the patient had prior intra-articular hip surgery, has a large calcified labrum or a cystic labrum, is an athlete with failed prior surgery, or is younger than 40 years.
Labral Repair Technique
The patient is taken to the surgical suite, and a general anesthetic is administered. A peripheral nerve block is not routinely used. The patient’s feet are padded, and boots for the traction table are applied. The patient is carefully placed on a Hana table in modified supine position. Balanced traction is used to achieve proper joint distraction. The C-arm is used to verify proper distraction, assess hip stability, and achieve standard anterolateral (AL) portal placement. A midanterior portal (MAP) is created and an interportal capsulotomy is performed. Capsular suspension is performed with the InJector II Capsule Restoration System (Stryker Sports Medicine) and typically 4 or 5 high-strength No. 2 sutures (Zipline; Stryker Sports Medicine).19 Diagnostic arthroscopy is performed to identify the tear type, measure the labral width, determine the impingement area, and identify the intra-articular pathology. After the intra-articular pathology is addressed, a radiofrequency Ambient HIPVAC 50 Coblation Wand (Smith & Nephew) is used to expose the acetabular rim and subspine as indicated. Acetabuloplasty or subspine decompression is performed, and then a primary repair or refixation of the labrum is performed. We do not routinely detach the labrum for acetabular rim trimming. A crucial step here is to expose a bleeding surface to which the labrum can be repaired. If the rim is sclerotic, or the rim cannot be removed because of underlying low acetabular coverage, we prefer to obtain the bleeding surface with a microdrilling device (Stryker) that is routinely used for acetabular microfracture.
Labrum quality is used to determine which repair method to use. A hypertrophic labrum is debulked. The acetabular rim is seldom resected >3 mm, but, when it is, the newly exposed cartilage is removed. We have found that >3 mm of residual cartilage prevents refixation of the labrum directly to the bone and may interfere with anatomical positioning. When a labrum is <3 mm in width or will not hold a base technique, repair stability is the priority, and a looped method is used. A knotless anchor with No. 1 permanent suture designed for hip labral repair (CinchLock; Stryker) is our first-line anchor choice. A distal anterolateral accessory (DALA) portal is created with an outside-in technique, and anchors are drilled through this portal into zones 2 to 4 (Figures 2A-2E).
A 2.4-mm drill guide is advanced through the DALA portal and placed in the appropriate position for drilling. We aim for 1 mm to 2 mm from the chondrolabral junction. Next, the probe is placed intra-articular and medial to the anchor insertion site, and the anchor is loaded and then inserted around the probe (Figures 3A-3E).
The hip is then reduced. If indicated, a T-capsulotomy is performed for femoral osteochondroplasty.
Postoperative Care
Patients are placed in a postoperative hip brace and use a continuous passive motion machine 6 hours a day for 2 weeks, and an ice machine. They maintain 30 lb of foot-flat weight-bearing for 3 weeks, and begin a standard labral repair protocol on postoperative days 3 to 7.
Discussion
Hip labral preservation has evolved over the past 10 years, and current options for labral management include excision, débridement, labralization, repair, and reconstruction.1-13 Labral excision was studied by Miozzari and colleagues,8 who postulated on the basis of animal models that the labrum may regenerate. In their series of 9 patients treated with surgical hip dislocation and labral excision at average 4-year follow-up, repeat magnetic resonance angiography revealed no regeneration of tissue—modified Harris Hip Score was 83. The hip scores were less than those of patients treated with the same procedure with repair, and the authors concluded that defining labral débridement versus excision in the literature, and treating patients with primary repair or reconstruction techniques, may lead to better results. Their study used a small sample and was limited to an open procedure. Arthroscopic labral débridement in isolation was also a poor option for treatment of a labral tear. In a 2-year follow-up of 59 isolated labral débridement procedures, Krych and colleagues9 found 47% combined poor results.
There is level I evidence of the importance of labral repair. In 2013, Krych and colleagues7 conducted a randomized control trial of 38 female patients who underwent hip arthroscopy for FAI. At time of surgery, patients were randomly assigned to either débridement or repair. At 1-year follow-up, activities of daily living and Sports specific Hip Outcome Scores were statistically significantly superior in the repair group. On a subjective scale, 94% vs 78% of patients reported normal or near normal hips in the repair versus débridement groups respectively. Ayeni and colleagues20 performed a systematic review of 6 studies in an attempt to develop labral management recommendations. Five of the studies (N = 490 patients total) had improved results with labral repair over reconstruction. Although the studies had a low level of evidence, they found a trend toward improved results with labral repair. These studies highlight the importance of labral preservation and proper FAI management.
Techniques for labrum repair have advanced as well—from a looped suture technique to a base stitch and knotless independent tensioning.11-13 Restoration of the hip labrum function as a suction seal, fluid circulator and anatomic capsular repair is paramount to excellent results and stresses the importance of performing an anatomic labral repair.1-6 Knotless anchor repair is not novel and has been previously described. Fry and Domb12 reported on a knotless labral repair technique that uses push-lock devices (Arthrex) that do not allow for independent tensioning. Inversion-eversion was introduced to the literature by Moreira and colleagues,13 who described an independent tensioning technique that uses speed-lock anchors (Smith & Nephew). Our technique differs in that it involves a DALA portal; labral reduction and tensioning with a probe assist to ensure the second pass of the base stitch is at the apex of the labrum; and use of No. 1 instead of No. 2 suture. Although seemingly subtle, these differences allow for proper anchor placement nearer the rim, additional support in achieving precise suture placement, and less disruption of small labra. These differences are particularly relevant for smaller labra.
Evaluating repair techniques on the basis of high-evidence literature is challenging. In a matched-cohort study of 220 patients, Jackson and colleagues21 compared 2 techniques: looped and base stitch. At 2-year follow-up, patients in both groups showed improvement, and there was no statistically significant difference in patient-reported outcome measures between the groups. Sawyer and colleagues22 studied the outcomes of 326 consecutive patients who underwent looped, pierced, or combined labral repair at an average 32-month follow-up. The groups’ revision rates were comparable, each group improved in postoperative patient-reported outcomes, and the pierced group had significantly higher preoperative scores on the Western Ontario and McMaster Universities Osteoarthritis Index. These studies described a base or pierce repair that did not differ from a looped repair, though the techniques did not allow for independent tensioning to re-create an anatomical inversion-eversion repair and may have altered the reported outcomes.
Our current technique uses independent tensioning of the repair to allow control of labrum inversion-eversion to give an anatomical repair with restoration of the suction seal. Preoperative planning, addressing the FAI appropriately, proper suture-passing technique, controlling the labrum in inversion-eversion fashion, and anatomical labral repair are the elements of Dr. Mather’s preferred method for preserving the native labrum and allowing it to assume its native function.
Future Directions
As our understanding of FAI and labral function evolves, labral preservation surgery continues to advance. With surgeons continually developing new techniques and following up on previous techniques, the ability to preserve the native hip with lasting procedures evolves as well. Proper identification of the underlying cause of the labral tear and proper anatomical repair are paramount to the success of FAI surgery.
Am J Orthop. 2017;46(1):42-48. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
3. Dwyer MK, Jones HL, Hogan MG, Field RE, McCarthy JC, Noble PC. The acetabular labrum regulates fluid circulation of the hip joint during functional activities. Am J Sports Med. 2014;42(4):812-819.
4. Greaves LL, Gilbart MK, Yung AC, Kozlowski, Wilson DR. Effect of acetabular labral tears, repair and resection on hip cartilage strain: a 7T MR study. J Biomech. 2010;43(5):858-863.
5. Freehill MT, Safran MR. The labrum of the hip: diagnosis and rationale for surgical correction. Clin Sports Med. 2011;30(2):293-315.
6. Myers CA, Register BC, Lertwanich P, et al. Role of the acetabular labrum and the iliofemoral ligament in hip stability: an in vitro biplane fluoroscopy study. Am J Sports Med. 2011;39(suppl):85S-91S.
7. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
8. Miozzari HH, Celia M, Clark JM, Werlen S, Naal FD, Nötzli HP. No regeneration of the human acetabular labrum after excision to bone. Clin Orthop Relat Res. 2015;473(4):1349-1357.
9. Krych AJ, Kuzma SA, Kovachevich R, Hudgens JL, Stuart MJ, Levy BA. Modest mid-term outcomes after isolated arthroscopic debridement of acetabular labral tears. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):763-767.
10. Matsuda DK. Arthroscopic labralization of the hip: an alternative to labral reconstruction. Arthrosc Tech. 2014;3(1):e131-e133.
11. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
12. Fry D, Domb B. Labral base refixation in the hip: rationale and technique for an anatomic approach to labral repair. Arthroscopy. 2010;26(9 suppl):S81-S89.
13. Moreira B, Pascual-Garrido C, Chadayamurri V, Mei-Dan O. Eversion-inversion labral repair and reconstruction technique for optimal suction seal. Arthrosc Tech. 2015;4(6):e697-e700.
14. Mook WR, Briggs KK, Philippon MJ. Evidence and approach for management of labral deficiency: the role for labral reconstruction. Sports Med Arthrosc. 2015;23(4):205-212.
15. Gupta A, Suarez-Ahedo C, Redmond JM, et al. Best practices during hip arthroscopy: aggregate recommendations of high-volume surgeons. Arthroscopy. 2015;31(9):1722-1727.
16. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
17. Hash TW. Magnetic resonance imaging of the hip. In: Nho SJ, Leunig M, Larson CM, Bedi A, Kelly BT, eds. Hip Arthroscopy and Hip Joint Preservation Surgery, Vol. 1. New York, NY: Springer; 2015:65-113.
18. Sutter R, Zubler V, Hoffmann A, et al. Hip MRI: how useful is intraarticular contrast material for evaluating surgically proven lesions of the labrum and articular cartilage? AJR Am J Roentgenol. 2014;202(1):160-169.
19. Federer AE, Karas V, Nho S, Coleman SH, Mather RC 3rd. Capsular suspension technique for hip arthroscopy. Arthrosc Tech. 2015;4(4):e317-e322.
20. Ayeni OR, Adamich J, Farrokhyar F, et al. Surgical management of labral tears during femoroacetabular impingement surgery: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):756-762.
21. Jackson TJ, Hammarstedt JE, Vemula SP, Domb BG. Acetabular labral base repair versus circumferential suture repair: a matched-paired comparison of clinical outcomes. Arthroscopy. 2015;31(9):1716-1721.
22. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
3. Dwyer MK, Jones HL, Hogan MG, Field RE, McCarthy JC, Noble PC. The acetabular labrum regulates fluid circulation of the hip joint during functional activities. Am J Sports Med. 2014;42(4):812-819.
4. Greaves LL, Gilbart MK, Yung AC, Kozlowski, Wilson DR. Effect of acetabular labral tears, repair and resection on hip cartilage strain: a 7T MR study. J Biomech. 2010;43(5):858-863.
5. Freehill MT, Safran MR. The labrum of the hip: diagnosis and rationale for surgical correction. Clin Sports Med. 2011;30(2):293-315.
6. Myers CA, Register BC, Lertwanich P, et al. Role of the acetabular labrum and the iliofemoral ligament in hip stability: an in vitro biplane fluoroscopy study. Am J Sports Med. 2011;39(suppl):85S-91S.
7. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
8. Miozzari HH, Celia M, Clark JM, Werlen S, Naal FD, Nötzli HP. No regeneration of the human acetabular labrum after excision to bone. Clin Orthop Relat Res. 2015;473(4):1349-1357.
9. Krych AJ, Kuzma SA, Kovachevich R, Hudgens JL, Stuart MJ, Levy BA. Modest mid-term outcomes after isolated arthroscopic debridement of acetabular labral tears. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):763-767.
10. Matsuda DK. Arthroscopic labralization of the hip: an alternative to labral reconstruction. Arthrosc Tech. 2014;3(1):e131-e133.
11. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
12. Fry D, Domb B. Labral base refixation in the hip: rationale and technique for an anatomic approach to labral repair. Arthroscopy. 2010;26(9 suppl):S81-S89.
13. Moreira B, Pascual-Garrido C, Chadayamurri V, Mei-Dan O. Eversion-inversion labral repair and reconstruction technique for optimal suction seal. Arthrosc Tech. 2015;4(6):e697-e700.
14. Mook WR, Briggs KK, Philippon MJ. Evidence and approach for management of labral deficiency: the role for labral reconstruction. Sports Med Arthrosc. 2015;23(4):205-212.
15. Gupta A, Suarez-Ahedo C, Redmond JM, et al. Best practices during hip arthroscopy: aggregate recommendations of high-volume surgeons. Arthroscopy. 2015;31(9):1722-1727.
16. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
17. Hash TW. Magnetic resonance imaging of the hip. In: Nho SJ, Leunig M, Larson CM, Bedi A, Kelly BT, eds. Hip Arthroscopy and Hip Joint Preservation Surgery, Vol. 1. New York, NY: Springer; 2015:65-113.
18. Sutter R, Zubler V, Hoffmann A, et al. Hip MRI: how useful is intraarticular contrast material for evaluating surgically proven lesions of the labrum and articular cartilage? AJR Am J Roentgenol. 2014;202(1):160-169.
19. Federer AE, Karas V, Nho S, Coleman SH, Mather RC 3rd. Capsular suspension technique for hip arthroscopy. Arthrosc Tech. 2015;4(4):e317-e322.
20. Ayeni OR, Adamich J, Farrokhyar F, et al. Surgical management of labral tears during femoroacetabular impingement surgery: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):756-762.
21. Jackson TJ, Hammarstedt JE, Vemula SP, Domb BG. Acetabular labral base repair versus circumferential suture repair: a matched-paired comparison of clinical outcomes. Arthroscopy. 2015;31(9):1716-1721.
22. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
New and Noteworthy Information—January 2017
Students who played varsity high school football between 1956 and 1970 do not have an increased risk of neurodegenerative diseases, compared with athletes engaged in other varsity sports, according to a study published online ahead of print December 12, 2016, in Mayo Clinic Proceedings. Researchers identified 296 male varsity football players in public high schools in Rochester, Minnesota, and 190 male varsity swimmers, wrestlers, and basketball players. Using records from the Rochester Epidemiology Project, investigators ascertained the incidence of late-life neurodegenerative diseases. Football players had an increased risk of medically documented head trauma, especially if they played football for more than one year. Compared with other athletes, football players did not have an increased risk of neurodegenerative disease overall, nor an increased risk of dementia, parkinsonism, or amyotrophic lateral sclerosis.
Antipsychotic drug use is associated with a 60% increased risk of mortality among persons with Alzheimer's disease, according to a study published online ahead of print December 5, 2016, in the Journal of Alzheimer's Disease. Researchers examined data from the MEDALZ study for 70,718 people who were newly diagnosed with Alzheimer's disease in Finland from 2005 to 2011. Death, excluding death from cancer, was extracted from the Causes of Death Register. Incident antipsychotic use was compared with time without antipsychotics using Cox proportional hazard models. The absolute difference in mortality rate was 4.58 deaths per 100 person-years. The risk of mortality was increased from the first days of antipsychotic use and attenuated gradually. Antipsychotic polypharmacy was associated with an almost doubled risk of mortality, compared with monotherapy.
A disruption of structural connections in a brain network contributes to cognitive deficits in patients with Parkinson's disease, according to a study published online ahead of print December 7, 2016, in Radiology. The structural brain connectomes of 170 patients with Parkinson's disease and 41 healthy controls were obtained with deterministic diffusion-tensor tractography. Patients with Parkinson's disease and mild cognitive impairment (MCI) had global network alterations, compared with controls and patients with Parkinson's disease without MCI. Relative to controls, patients with Parkinson's disease and MCI had a large basal ganglia and frontoparietal network with decreased fractional anisotropy in the right hemisphere and a subnetwork with increased mean diffusivity involving similar regions bilaterally. Compared with patients with Parkinson's disease without MCI, people with Parkinson's disease and MCI had networks with decreased fractional anisotropy.
A proposed diagnostic algorithm for sporadic Creutzfeldt-Jakob disease combines CSF and olfactory mucosa real-time quaking-induced conversion testing to provide approximately 100% sensitivity and specificity in the clinical phase of the disease, according to a study published online ahead of print December 12, 2016, in JAMA Neurology. Among the 86 patients included in this analysis, 61 patients with sporadic Creutzfeldt-Jakob disease had positive real-time quaking-induced conversion findings using olfactory mucosa, CSF samples, or both, for an overall real-time quaking-induced conversion sensitivity of 100%. All patients with a final diagnosis of nonprion disease had negative real-time quaking-induced conversion findings, for 100% specificity. Of eight symptomatic patients with various mutations causing Creutzfeldt-Jakob disease or Gerstmann-Sträussler-Scheinker syndrome, six had positive and two had negative real-time quaking-induced conversion findings, for a sensitivity of 75%.
CSF autotaxin may be a useful biomarker of dysmetabolism for examining risk for and outcomes of Alzheimer's disease, according to research published December 1, 2016, in the Journal of Alzheimer's Disease. Investigators studied 287 participants in the Alzheimer's Disease Neuroimaging Initiative, including 86 cognitively normal participants, 135 participants with mild cognitive impairment (MCI), and 66 participants with Alzheimer's disease. Autotaxin levels were significantly higher in patients with MCI and those with Alzheimer's disease. Each point increase in log-based autotaxin corresponded to a 3.5- to 5-times higher likelihood of having MCI and Alzheimer's disease, respectively. Higher autotaxin in Alzheimer's disease predicted hypometabolism in the medial temporal lobe and prefrontal cortex, and worse performance on executive function and memory factors. Autotaxin was associated with decreased cortical thickness in prefrontal cortex areas.
Marital history is significantly associated with survival after stroke, according to a study published December 14, 2016, in the Journal of the American Heart Association. Data from a nationally representative sample of 2,351 older adults who experienced a stroke were used to examine whether and to what extent current marital status and past marital losses were associated with risks of dying after the onset of disease. Results showed that the risks of dying following a stroke were significantly higher among people who were never married, remarried, divorced, and widowed, relative to those who remained continuously married. Researchers also found that having multiple marital losses was especially detrimental to survival, regardless of current marital status and accounting for multiple socioeconomic, psychosocial, behavioral, and physiologic risk factors.
Prefrontal brain activity levels during a cognitively demanding walking condition predict falls in high-functioning senior citizens, according to a study published online ahead of print December 7, 2016, in Neurology. Researchers examined 166 people with a mean age of 75 with functional near-infrared spectroscopy during motor, cognitive, and combined motor and cognitive tasks. Incident falls were prospectively assessed during a 50-month study period. During a mean follow-up of 33.9 months, 116 falls occurred. Higher levels of prefrontal cortical activation during the dual-task walking condition predicted falls. Neither behavioral outcomes on the dual task nor brain activation patterns on the single tasks predicted falls in this high-functioning sample. The results remained robust after accounting for multiple confounders, cognitive status, slow gait, previous falls, and frailty.
Localized brain injury and repair, indicated by higher translocator protein 18 kDa signal and white matter changes, may be associated with National Football League (NFL) play, according to a study published online ahead of print November 28, 2016, in JAMA Neurology. This cross-sectional, case-control study included young active or former NFL players recruited from across the United States and 16 age-, sex-, highest educational level-, and BMI-matched control participants. Researchers used [11C]DPA-713 PET data and other imaging data from 12 active or former NFL players and 11 matched control participants. The NFL players showed higher total distribution volume in eight of 12 brain regions examined. Investigators also observed limited change in white matter fractional anisotropy and mean diffusivity in 13 players, compared with 15 control participants.
Exposure to maternal rheumatoid arthritis is associated with an increased risk of childhood epilepsy, while exposure to paternal rheumatoid arthritis is not, according to a study published December 13, 2016, in Neurology. Researchers performed a nationwide cohort study of 1,917,723 people that were born between 1977 and 2008. Compared with unexposed children, children exposed to maternal rheumatoid arthritis had an increased risk of early and late childhood epilepsy, while children exposed to maternal rheumatoid arthritis had no increased risk of epilepsy in adolescence and adulthood. Paternal rheumatoid arthritis was not associated with an overall risk of epilepsy in the offspring or at any age. Children exposed to maternal rheumatoid arthritis in utero had a more pronounced increased risk of early childhood epilepsy than children of mothers who were diagnosed with rheumatoid arthritis after childbirth.
Having surgery may be linked to developing Guillain-Barré syndrome for people with cancer or autoimmune disorders, according to a study published online ahead of print November 23, 2016, in Neurology Clinical Practice. Researchers retrospectively reviewed consecutive patients diagnosed with Guillain-Barré syndrome within eight weeks of a surgical procedure between January 1995 and June 2014. Of the 208 people treated for Guillain-Barré syndrome, 31 people developed the syndrome within eight weeks of having a surgical procedure. People who had had cancer within the previous six months were seven times more likely to develop Guillain-Barré syndrome after surgery than people who had not had cancer. People who had pre-existing autoimmune disorders were five times more likely to develop Guillain-Barré syndrome after surgery than those without autoimmune disorders.
Patients with Parkinson's disease and orthostatic hypotension have transient, posture-mediated changes in cognition, according to a study published online ahead of print November 30, 2016, in Neurology. To investigate the relation between orthostatic hypotension and posture-mediated cognitive impairment in Parkinson disease, researchers used a cross-sectional and within-group design. Participants included 18 patients with Parkinson's disease and orthostatic hypotension, 19 patients with Parkinson's disease but without orthostatic hypotension, and 18 healthy controls. Participants underwent neuropsychologic tests in the supine and upright-tilted positions. When relative performances were compared with each other, postural changes had no significant impact on participants with Parkinson's disease but without orthostatic hypotension, compared with the control group. Participants with Parkinson's disease and orthostatic hypotension, however, were more susceptible to posture-related impairment on several tests.
Low concentrations of neonatal vitamin D are associated with an increased risk of multiple sclerosis (MS), according to a study published online ahead of print November 30, 2016, in Neurology. Researchers conducted a matched case-control study. Dried blood spots samples from 521 patients with MS were identified in the Danish Newborn Screening Biobank. For every patient with MS, one to two controls with the same sex and birth date were retrieved from the Biobank. Lower levels of 25-hydroxyvitamin D in neonates were associated with an increased risk of MS. In the analysis by quintiles, MS risk was highest among individuals in the bottom quintile and lowest among those in the top quintile of 25-hydroxyvitamin D, with an odds ratio for top versus bottom of 0.53.
Children exposed to valproate in the womb are at an increased risk of having a malformation at birth, and the dose of valproate that the child is exposed to determines the level of risk, according to a study published November 7, 2016, in the Cochrane Database of Systematic Reviews. Researchers analyzed 50 studies, with 31 contributing to a meta-analysis. Children exposed to valproate were at a higher risk of malformation, compared with children born to women without epilepsy and to women with untreated epilepsy. Investigators found significantly higher rates of specific malformations associating phenobarbital exposure with cardiac malformations and valproate exposure with neural tube, cardiac, orofacial, craniofacial, skeletal, and limb malformations, compared with other antiepileptic drugs. Dose of exposure mediated the risk of malformation following valproate exposure.
—Kimberly Williams
Students who played varsity high school football between 1956 and 1970 do not have an increased risk of neurodegenerative diseases, compared with athletes engaged in other varsity sports, according to a study published online ahead of print December 12, 2016, in Mayo Clinic Proceedings. Researchers identified 296 male varsity football players in public high schools in Rochester, Minnesota, and 190 male varsity swimmers, wrestlers, and basketball players. Using records from the Rochester Epidemiology Project, investigators ascertained the incidence of late-life neurodegenerative diseases. Football players had an increased risk of medically documented head trauma, especially if they played football for more than one year. Compared with other athletes, football players did not have an increased risk of neurodegenerative disease overall, nor an increased risk of dementia, parkinsonism, or amyotrophic lateral sclerosis.
Antipsychotic drug use is associated with a 60% increased risk of mortality among persons with Alzheimer's disease, according to a study published online ahead of print December 5, 2016, in the Journal of Alzheimer's Disease. Researchers examined data from the MEDALZ study for 70,718 people who were newly diagnosed with Alzheimer's disease in Finland from 2005 to 2011. Death, excluding death from cancer, was extracted from the Causes of Death Register. Incident antipsychotic use was compared with time without antipsychotics using Cox proportional hazard models. The absolute difference in mortality rate was 4.58 deaths per 100 person-years. The risk of mortality was increased from the first days of antipsychotic use and attenuated gradually. Antipsychotic polypharmacy was associated with an almost doubled risk of mortality, compared with monotherapy.
A disruption of structural connections in a brain network contributes to cognitive deficits in patients with Parkinson's disease, according to a study published online ahead of print December 7, 2016, in Radiology. The structural brain connectomes of 170 patients with Parkinson's disease and 41 healthy controls were obtained with deterministic diffusion-tensor tractography. Patients with Parkinson's disease and mild cognitive impairment (MCI) had global network alterations, compared with controls and patients with Parkinson's disease without MCI. Relative to controls, patients with Parkinson's disease and MCI had a large basal ganglia and frontoparietal network with decreased fractional anisotropy in the right hemisphere and a subnetwork with increased mean diffusivity involving similar regions bilaterally. Compared with patients with Parkinson's disease without MCI, people with Parkinson's disease and MCI had networks with decreased fractional anisotropy.
A proposed diagnostic algorithm for sporadic Creutzfeldt-Jakob disease combines CSF and olfactory mucosa real-time quaking-induced conversion testing to provide approximately 100% sensitivity and specificity in the clinical phase of the disease, according to a study published online ahead of print December 12, 2016, in JAMA Neurology. Among the 86 patients included in this analysis, 61 patients with sporadic Creutzfeldt-Jakob disease had positive real-time quaking-induced conversion findings using olfactory mucosa, CSF samples, or both, for an overall real-time quaking-induced conversion sensitivity of 100%. All patients with a final diagnosis of nonprion disease had negative real-time quaking-induced conversion findings, for 100% specificity. Of eight symptomatic patients with various mutations causing Creutzfeldt-Jakob disease or Gerstmann-Sträussler-Scheinker syndrome, six had positive and two had negative real-time quaking-induced conversion findings, for a sensitivity of 75%.
CSF autotaxin may be a useful biomarker of dysmetabolism for examining risk for and outcomes of Alzheimer's disease, according to research published December 1, 2016, in the Journal of Alzheimer's Disease. Investigators studied 287 participants in the Alzheimer's Disease Neuroimaging Initiative, including 86 cognitively normal participants, 135 participants with mild cognitive impairment (MCI), and 66 participants with Alzheimer's disease. Autotaxin levels were significantly higher in patients with MCI and those with Alzheimer's disease. Each point increase in log-based autotaxin corresponded to a 3.5- to 5-times higher likelihood of having MCI and Alzheimer's disease, respectively. Higher autotaxin in Alzheimer's disease predicted hypometabolism in the medial temporal lobe and prefrontal cortex, and worse performance on executive function and memory factors. Autotaxin was associated with decreased cortical thickness in prefrontal cortex areas.
Marital history is significantly associated with survival after stroke, according to a study published December 14, 2016, in the Journal of the American Heart Association. Data from a nationally representative sample of 2,351 older adults who experienced a stroke were used to examine whether and to what extent current marital status and past marital losses were associated with risks of dying after the onset of disease. Results showed that the risks of dying following a stroke were significantly higher among people who were never married, remarried, divorced, and widowed, relative to those who remained continuously married. Researchers also found that having multiple marital losses was especially detrimental to survival, regardless of current marital status and accounting for multiple socioeconomic, psychosocial, behavioral, and physiologic risk factors.
Prefrontal brain activity levels during a cognitively demanding walking condition predict falls in high-functioning senior citizens, according to a study published online ahead of print December 7, 2016, in Neurology. Researchers examined 166 people with a mean age of 75 with functional near-infrared spectroscopy during motor, cognitive, and combined motor and cognitive tasks. Incident falls were prospectively assessed during a 50-month study period. During a mean follow-up of 33.9 months, 116 falls occurred. Higher levels of prefrontal cortical activation during the dual-task walking condition predicted falls. Neither behavioral outcomes on the dual task nor brain activation patterns on the single tasks predicted falls in this high-functioning sample. The results remained robust after accounting for multiple confounders, cognitive status, slow gait, previous falls, and frailty.
Localized brain injury and repair, indicated by higher translocator protein 18 kDa signal and white matter changes, may be associated with National Football League (NFL) play, according to a study published online ahead of print November 28, 2016, in JAMA Neurology. This cross-sectional, case-control study included young active or former NFL players recruited from across the United States and 16 age-, sex-, highest educational level-, and BMI-matched control participants. Researchers used [11C]DPA-713 PET data and other imaging data from 12 active or former NFL players and 11 matched control participants. The NFL players showed higher total distribution volume in eight of 12 brain regions examined. Investigators also observed limited change in white matter fractional anisotropy and mean diffusivity in 13 players, compared with 15 control participants.
Exposure to maternal rheumatoid arthritis is associated with an increased risk of childhood epilepsy, while exposure to paternal rheumatoid arthritis is not, according to a study published December 13, 2016, in Neurology. Researchers performed a nationwide cohort study of 1,917,723 people that were born between 1977 and 2008. Compared with unexposed children, children exposed to maternal rheumatoid arthritis had an increased risk of early and late childhood epilepsy, while children exposed to maternal rheumatoid arthritis had no increased risk of epilepsy in adolescence and adulthood. Paternal rheumatoid arthritis was not associated with an overall risk of epilepsy in the offspring or at any age. Children exposed to maternal rheumatoid arthritis in utero had a more pronounced increased risk of early childhood epilepsy than children of mothers who were diagnosed with rheumatoid arthritis after childbirth.
Having surgery may be linked to developing Guillain-Barré syndrome for people with cancer or autoimmune disorders, according to a study published online ahead of print November 23, 2016, in Neurology Clinical Practice. Researchers retrospectively reviewed consecutive patients diagnosed with Guillain-Barré syndrome within eight weeks of a surgical procedure between January 1995 and June 2014. Of the 208 people treated for Guillain-Barré syndrome, 31 people developed the syndrome within eight weeks of having a surgical procedure. People who had had cancer within the previous six months were seven times more likely to develop Guillain-Barré syndrome after surgery than people who had not had cancer. People who had pre-existing autoimmune disorders were five times more likely to develop Guillain-Barré syndrome after surgery than those without autoimmune disorders.
Patients with Parkinson's disease and orthostatic hypotension have transient, posture-mediated changes in cognition, according to a study published online ahead of print November 30, 2016, in Neurology. To investigate the relation between orthostatic hypotension and posture-mediated cognitive impairment in Parkinson disease, researchers used a cross-sectional and within-group design. Participants included 18 patients with Parkinson's disease and orthostatic hypotension, 19 patients with Parkinson's disease but without orthostatic hypotension, and 18 healthy controls. Participants underwent neuropsychologic tests in the supine and upright-tilted positions. When relative performances were compared with each other, postural changes had no significant impact on participants with Parkinson's disease but without orthostatic hypotension, compared with the control group. Participants with Parkinson's disease and orthostatic hypotension, however, were more susceptible to posture-related impairment on several tests.
Low concentrations of neonatal vitamin D are associated with an increased risk of multiple sclerosis (MS), according to a study published online ahead of print November 30, 2016, in Neurology. Researchers conducted a matched case-control study. Dried blood spots samples from 521 patients with MS were identified in the Danish Newborn Screening Biobank. For every patient with MS, one to two controls with the same sex and birth date were retrieved from the Biobank. Lower levels of 25-hydroxyvitamin D in neonates were associated with an increased risk of MS. In the analysis by quintiles, MS risk was highest among individuals in the bottom quintile and lowest among those in the top quintile of 25-hydroxyvitamin D, with an odds ratio for top versus bottom of 0.53.
Children exposed to valproate in the womb are at an increased risk of having a malformation at birth, and the dose of valproate that the child is exposed to determines the level of risk, according to a study published November 7, 2016, in the Cochrane Database of Systematic Reviews. Researchers analyzed 50 studies, with 31 contributing to a meta-analysis. Children exposed to valproate were at a higher risk of malformation, compared with children born to women without epilepsy and to women with untreated epilepsy. Investigators found significantly higher rates of specific malformations associating phenobarbital exposure with cardiac malformations and valproate exposure with neural tube, cardiac, orofacial, craniofacial, skeletal, and limb malformations, compared with other antiepileptic drugs. Dose of exposure mediated the risk of malformation following valproate exposure.
—Kimberly Williams
Students who played varsity high school football between 1956 and 1970 do not have an increased risk of neurodegenerative diseases, compared with athletes engaged in other varsity sports, according to a study published online ahead of print December 12, 2016, in Mayo Clinic Proceedings. Researchers identified 296 male varsity football players in public high schools in Rochester, Minnesota, and 190 male varsity swimmers, wrestlers, and basketball players. Using records from the Rochester Epidemiology Project, investigators ascertained the incidence of late-life neurodegenerative diseases. Football players had an increased risk of medically documented head trauma, especially if they played football for more than one year. Compared with other athletes, football players did not have an increased risk of neurodegenerative disease overall, nor an increased risk of dementia, parkinsonism, or amyotrophic lateral sclerosis.
Antipsychotic drug use is associated with a 60% increased risk of mortality among persons with Alzheimer's disease, according to a study published online ahead of print December 5, 2016, in the Journal of Alzheimer's Disease. Researchers examined data from the MEDALZ study for 70,718 people who were newly diagnosed with Alzheimer's disease in Finland from 2005 to 2011. Death, excluding death from cancer, was extracted from the Causes of Death Register. Incident antipsychotic use was compared with time without antipsychotics using Cox proportional hazard models. The absolute difference in mortality rate was 4.58 deaths per 100 person-years. The risk of mortality was increased from the first days of antipsychotic use and attenuated gradually. Antipsychotic polypharmacy was associated with an almost doubled risk of mortality, compared with monotherapy.
A disruption of structural connections in a brain network contributes to cognitive deficits in patients with Parkinson's disease, according to a study published online ahead of print December 7, 2016, in Radiology. The structural brain connectomes of 170 patients with Parkinson's disease and 41 healthy controls were obtained with deterministic diffusion-tensor tractography. Patients with Parkinson's disease and mild cognitive impairment (MCI) had global network alterations, compared with controls and patients with Parkinson's disease without MCI. Relative to controls, patients with Parkinson's disease and MCI had a large basal ganglia and frontoparietal network with decreased fractional anisotropy in the right hemisphere and a subnetwork with increased mean diffusivity involving similar regions bilaterally. Compared with patients with Parkinson's disease without MCI, people with Parkinson's disease and MCI had networks with decreased fractional anisotropy.
A proposed diagnostic algorithm for sporadic Creutzfeldt-Jakob disease combines CSF and olfactory mucosa real-time quaking-induced conversion testing to provide approximately 100% sensitivity and specificity in the clinical phase of the disease, according to a study published online ahead of print December 12, 2016, in JAMA Neurology. Among the 86 patients included in this analysis, 61 patients with sporadic Creutzfeldt-Jakob disease had positive real-time quaking-induced conversion findings using olfactory mucosa, CSF samples, or both, for an overall real-time quaking-induced conversion sensitivity of 100%. All patients with a final diagnosis of nonprion disease had negative real-time quaking-induced conversion findings, for 100% specificity. Of eight symptomatic patients with various mutations causing Creutzfeldt-Jakob disease or Gerstmann-Sträussler-Scheinker syndrome, six had positive and two had negative real-time quaking-induced conversion findings, for a sensitivity of 75%.
CSF autotaxin may be a useful biomarker of dysmetabolism for examining risk for and outcomes of Alzheimer's disease, according to research published December 1, 2016, in the Journal of Alzheimer's Disease. Investigators studied 287 participants in the Alzheimer's Disease Neuroimaging Initiative, including 86 cognitively normal participants, 135 participants with mild cognitive impairment (MCI), and 66 participants with Alzheimer's disease. Autotaxin levels were significantly higher in patients with MCI and those with Alzheimer's disease. Each point increase in log-based autotaxin corresponded to a 3.5- to 5-times higher likelihood of having MCI and Alzheimer's disease, respectively. Higher autotaxin in Alzheimer's disease predicted hypometabolism in the medial temporal lobe and prefrontal cortex, and worse performance on executive function and memory factors. Autotaxin was associated with decreased cortical thickness in prefrontal cortex areas.
Marital history is significantly associated with survival after stroke, according to a study published December 14, 2016, in the Journal of the American Heart Association. Data from a nationally representative sample of 2,351 older adults who experienced a stroke were used to examine whether and to what extent current marital status and past marital losses were associated with risks of dying after the onset of disease. Results showed that the risks of dying following a stroke were significantly higher among people who were never married, remarried, divorced, and widowed, relative to those who remained continuously married. Researchers also found that having multiple marital losses was especially detrimental to survival, regardless of current marital status and accounting for multiple socioeconomic, psychosocial, behavioral, and physiologic risk factors.
Prefrontal brain activity levels during a cognitively demanding walking condition predict falls in high-functioning senior citizens, according to a study published online ahead of print December 7, 2016, in Neurology. Researchers examined 166 people with a mean age of 75 with functional near-infrared spectroscopy during motor, cognitive, and combined motor and cognitive tasks. Incident falls were prospectively assessed during a 50-month study period. During a mean follow-up of 33.9 months, 116 falls occurred. Higher levels of prefrontal cortical activation during the dual-task walking condition predicted falls. Neither behavioral outcomes on the dual task nor brain activation patterns on the single tasks predicted falls in this high-functioning sample. The results remained robust after accounting for multiple confounders, cognitive status, slow gait, previous falls, and frailty.
Localized brain injury and repair, indicated by higher translocator protein 18 kDa signal and white matter changes, may be associated with National Football League (NFL) play, according to a study published online ahead of print November 28, 2016, in JAMA Neurology. This cross-sectional, case-control study included young active or former NFL players recruited from across the United States and 16 age-, sex-, highest educational level-, and BMI-matched control participants. Researchers used [11C]DPA-713 PET data and other imaging data from 12 active or former NFL players and 11 matched control participants. The NFL players showed higher total distribution volume in eight of 12 brain regions examined. Investigators also observed limited change in white matter fractional anisotropy and mean diffusivity in 13 players, compared with 15 control participants.
Exposure to maternal rheumatoid arthritis is associated with an increased risk of childhood epilepsy, while exposure to paternal rheumatoid arthritis is not, according to a study published December 13, 2016, in Neurology. Researchers performed a nationwide cohort study of 1,917,723 people that were born between 1977 and 2008. Compared with unexposed children, children exposed to maternal rheumatoid arthritis had an increased risk of early and late childhood epilepsy, while children exposed to maternal rheumatoid arthritis had no increased risk of epilepsy in adolescence and adulthood. Paternal rheumatoid arthritis was not associated with an overall risk of epilepsy in the offspring or at any age. Children exposed to maternal rheumatoid arthritis in utero had a more pronounced increased risk of early childhood epilepsy than children of mothers who were diagnosed with rheumatoid arthritis after childbirth.
Having surgery may be linked to developing Guillain-Barré syndrome for people with cancer or autoimmune disorders, according to a study published online ahead of print November 23, 2016, in Neurology Clinical Practice. Researchers retrospectively reviewed consecutive patients diagnosed with Guillain-Barré syndrome within eight weeks of a surgical procedure between January 1995 and June 2014. Of the 208 people treated for Guillain-Barré syndrome, 31 people developed the syndrome within eight weeks of having a surgical procedure. People who had had cancer within the previous six months were seven times more likely to develop Guillain-Barré syndrome after surgery than people who had not had cancer. People who had pre-existing autoimmune disorders were five times more likely to develop Guillain-Barré syndrome after surgery than those without autoimmune disorders.
Patients with Parkinson's disease and orthostatic hypotension have transient, posture-mediated changes in cognition, according to a study published online ahead of print November 30, 2016, in Neurology. To investigate the relation between orthostatic hypotension and posture-mediated cognitive impairment in Parkinson disease, researchers used a cross-sectional and within-group design. Participants included 18 patients with Parkinson's disease and orthostatic hypotension, 19 patients with Parkinson's disease but without orthostatic hypotension, and 18 healthy controls. Participants underwent neuropsychologic tests in the supine and upright-tilted positions. When relative performances were compared with each other, postural changes had no significant impact on participants with Parkinson's disease but without orthostatic hypotension, compared with the control group. Participants with Parkinson's disease and orthostatic hypotension, however, were more susceptible to posture-related impairment on several tests.
Low concentrations of neonatal vitamin D are associated with an increased risk of multiple sclerosis (MS), according to a study published online ahead of print November 30, 2016, in Neurology. Researchers conducted a matched case-control study. Dried blood spots samples from 521 patients with MS were identified in the Danish Newborn Screening Biobank. For every patient with MS, one to two controls with the same sex and birth date were retrieved from the Biobank. Lower levels of 25-hydroxyvitamin D in neonates were associated with an increased risk of MS. In the analysis by quintiles, MS risk was highest among individuals in the bottom quintile and lowest among those in the top quintile of 25-hydroxyvitamin D, with an odds ratio for top versus bottom of 0.53.
Children exposed to valproate in the womb are at an increased risk of having a malformation at birth, and the dose of valproate that the child is exposed to determines the level of risk, according to a study published November 7, 2016, in the Cochrane Database of Systematic Reviews. Researchers analyzed 50 studies, with 31 contributing to a meta-analysis. Children exposed to valproate were at a higher risk of malformation, compared with children born to women without epilepsy and to women with untreated epilepsy. Investigators found significantly higher rates of specific malformations associating phenobarbital exposure with cardiac malformations and valproate exposure with neural tube, cardiac, orofacial, craniofacial, skeletal, and limb malformations, compared with other antiepileptic drugs. Dose of exposure mediated the risk of malformation following valproate exposure.
—Kimberly Williams
Current Techniques in Treating Femoroacetabular Impingement: Capsular Repair and Plication
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
Relapsing Polychondritis With Meningoencephalitis
Relapsing polychondritis (RP) is an autoimmune disease affecting cartilaginous structures such as the ears, respiratory passages, joints, and cardiovascular system.1,2 In rare cases, the systemic effects of this autoimmune process can cause central nervous system (CNS) involvement such as meningoencephalitis (ME).3 In 2011, Wang et al4 described 4 cases of RP with ME and reviewed 24 cases from the literature. We present a case of a man with RP-associated ME that was responsive to steroid treatment. We also provide an updated review of the literature.
Case Report
A 44-year-old man developed gradually worsening bilateral ear pain, headaches, and seizures. He was briefly hospitalized and discharged with levetiracetam and quetiapine. However, his mental status continued to deteriorate and he was subsequently hospitalized 3 months later with confusion, hallucinations, and seizures.
On physical examination the patient was disoriented and unable to form cohesive sentences. He had bilateral tenderness, erythema, and edema of the auricles, which notably spared the lobules (Figure 1). The conjunctivae were injected bilaterally, and joint involvement included bilateral knee tenderness and swelling. Neurologic examination revealed questionable meningeal signs but no motor or sensory deficits. An extensive laboratory workup for the etiology of his altered mental status was unremarkable, except for a mildly elevated white blood cell count in the cerebrospinal fluid with predominantly lymphocytes. No infectious etiologies were identified on laboratory testing, and rheumatologic markers were negative including antinuclear antibody, rheumatoid factor, and anti–Sjögren syndrome antigen A/Sjögren syndrome antigen B. Magnetic resonance imaging revealed nonspecific findings of bilateral T2 hyperdensities in the subcortical white matter; however, cerebral angiography revealed no evidence of vasculitis. A biopsy of the right antihelix revealed prominent perichondritis and a neutrophilic inflammatory infiltrate with several lymphocytes and histiocytes (Figure 2). There was degeneration of the cartilaginous tissue with evidence of pyknotic nuclei, eosinophilia, and vacuolization of the chondrocytes. He was diagnosed with RP on the basis of clinical and histologic inflammation of the auricular cartilage, polyarthritis, and ocular inflammation.
The patient was treated with high-dose immunosuppression with methylprednisolone (1000 mg intravenous once daily for 5 days) and cyclophosphamide (one dose at 500 mg/m2), which resulted in remarkable improvement in his mental status, auricular inflammation, and knee pain. After 31 days of hospitalization the patient was discharged with a course of oral prednisone (starting at 60 mg/d, then tapered over the following 2 months) and monthly cyclophosphamide infusions (5 months total; starting at 500 mg/m2, then uptitrated to goal of 1000 mg/m2). Maintenance suppression was achieved with azathioprine (starting at 50 mg daily, then uptitrated to 100 mg daily), which was continued without any evidence of relapsed disease through his last outpatient visit 1 year after the diagnosis.
Comment
Auricular inflammation is a hallmark of RP and is present in 83% to 95% of patients.1,3 The affected ears can appear erythematous to violaceous with tender edema of the auricle that spares the lobules where no cartilage is present. The inflammation can extend into the ear canal and cause hearing loss, tinnitus, and vertigo. Histologically, RP can present with a nonspecific leukocytoclastic vasculitis and inflammatory destruction of the cartilage. Therefore, diagnosis of RP is reliant mainly on clinical characteristics rather than pathologic findings. In 1976, McAdam et al5 established diagnostic criteria for RP based on the presence of common clinical manifestations (eg, auricular chondritis, seronegative inflammatory polyarthritis, nasal chondritis, ocular inflammation). Michet et al6 later proposed major and minor criteria to classify and diagnose RP based on clinical manifestations. Diagnosis of our patient was confirmed by the presence of auricular chondritis, polyarthritis, and ocular inflammation. Diagnosing RP can be difficult because it has many systemic manifestations that can evoke a broad differential diagnosis. The time to diagnosis in our patient was 3 months, but the mean delay in diagnosis for patients with RP and ME is 2.9 years.4
The etiology of RP remains unclear, but current evidence supports an immune-mediated process directed toward proteins found in cartilage. Animal studies have suggested that RP may be driven by antibodies to matrillin 1 and type II collagen. There also may be a familial association with HLA-DR4 and genetic predisposition to autoimmune diseases in individuals affected by RP.1,3 The pathogenesis of CNS involvement in RP is thought to be due to a localized small vessel vasculitis.7,8 In our patient, however, cerebral angiography was negative for vasculitis, and thus our case may represent another mechanism for CNS involvement. There have been cases of encephalitis in RP caused by pathways other than CNS vasculitis. Kashihara et al9 reported a case of RP with encephalitis associated with antiglutamate receptor antibodies found in the cerebrospinal fluid and blood.
Treatment of RP has been based on pathophysiological considerations rather than empiric data due to its rarity. Relapsing polychondritis has been responsive to steroid treatment in reported cases as well as in our patient; however, in cases in which RP did not respond to steroids, infliximab may be effective for RP with ME.10 Further research regarding the treatment outcomes of RP with ME may be warranted.
Although rare, additional cases of RP with ME have been reported (Table). Wang et al4 described a series of 28 patients with RP and ME from 1960 to 2010. A PubMed search of articles indexed for MEDLINE that were published in the English-language literature from 2010 to 2016 was performed using the search terms relapsing polychondritis and nervous system. Including our patient, RP with ME was reported in 17 additional cases since Wang et al4 published their findings. These cases involved adults ranging in age from 44 to 73 years who were mainly men (14/17 [82%]). All of the patients presented with bilateral auricular chondritis, except for a case of unilateral ear involvement reported by Storey et al.11 Common neurologic manifestations included fever, headache, and altered mental status. Motor symptoms ranged from dysarthria and agraphia12 to hemiparesis.13 The mechanism of CNS involvement in RP was not identified in most cases; however, Mattiassich et al14 documented cerebral vasculitis in their patient, and Niwa et al16 found diffuse cerebral vasculitis on autopsy. Eleven of 17 (65%) cases responded to steroid treatment. Of the 6 cases in which RP did not respond to steroids, 2 patients died despite high-dose steroid treatment,11,20 2 responded to infliximab,10,15 1 responded to tocilizumab,21 and 1 was lost to follow-up after initial treatment failure.20
Conclusion
Although rare, RP should not be overlooked in the inpatient setting due to its potential for life-threatening systemic effects. Early diagnosis of this condition may be of benefit to this select population of patients, and further research regarding the prognosis, mechanisms, and treatment of RP may be necessary in the future.
- Arnaud L, Mathian A, Haroche J, et al. Pathogenesis of relapsing polychondritis: a 2013 update. Autoimmun Rev. 2014;13:90-95.
- Ostrowski RA, Takagishi T, Robinson J. Rheumatoid arthritis, spondyloarthropathies, and relapsing polychondritis. Handb Clin Neurol. 2014;119:449-461.
- Lahmer T, Treiber M, von Werder A, et al. Relapsing polychondritis: an autoimmune disease with many faces. Autoimmun Rev. 2010;9:540-546.
- Wang ZJ, Pu CQ, Wang ZJ, et al. Meningoencephalitis or meningitis in relapsing polychondritis: four case reports and a literature review. J Clin Neurosci. 2011;18:1608-1615.
- McAdam LP, O’Hanlan MA, Bluestone R, et al. Relapsing polychondritis: prospective study of 23 patients and a review of the literature. Medicine (Baltimore). 1976;55:193-215.
- Michet C, McKenna C, Luthra H, et al. Relapsing polychondritis: survival and predictive role of early disease manifestations. Ann Intern Med. 1986;104:74-78.
- Sampaio L, Silva L, Mariz E, et al. CNS involvement in relapsing polychondritis. Joint Bone Spine. 2010;77:619-620.
- Prinz S, Dafotakis M, Schneider RK, et al. The red puffy ear sign—a clinical sign to diagnose a rare cause of meningoencephalitis. Fortschr Neurol Psychiatr. 2012;80:463-467.
- Kashihara K, Kawada S, Takahashi Y. Autoantibodies to glutamate receptor GluR2 in a patient with limic encephalitis associated with relapsing polychondritis. J Neurol Sci. 2009;287:275-277.
- Garcia-Egido A, Gutierrez C, de la Fuente C, et al. Relapsing polychondritis-associated meningitis and encephalitis: response to infliximab. Rheumatology (Oxford). 2011;50:1721-1723.
- Storey K, Matej R, Rusina R. Unusual association of seronegative, nonparaneoplastic limbic encephalitis and relapsing polychondritis in a patient with history of thymectomy for myasthemia: a case study. J Neurol. 2010;258:159-161.
- Choi HJ, Lee HJ. Relapsing polychondritis with encephalitis. J Clin Rheum. 2011;6:329-331.
- Fujiwara S, Zenke K, Iwata S, et al. Relapsing polychondritis presenting as encephalitis. No Shinkei Geka. 2012;40:247-253.
- Mattiassich G, Egger M, Semlitsch G, et al. Occurrence of relapsing polychondritis with a rising cANCA titre in a cANCA-positive systemic and cerebral vasculitis patient [published online February 5, 2013]. BMJ Case Rep. doi:10.1136/bcr-2013-008717.
- Kondo T, Fukuta M, Takemoto A, et al. Limbic encephalitis associated with relapsing polychondritis responded to infliximab and maintained its condition without recurrence after discontinuation: a case report and review of the literature. Nagoya J Med Sci. 2014;76:361-368.
- Niwa A, Okamoto Y, Kondo T, et al. Perivasculitic pancencephalitis with relapsing polychondritis: an autopsy case report and review of previous cases. Intern Med. 2014;53:1191-1195.
- Coban EK, Xanmemmedoy E, Colak M, et al. A rare complication of a rare disease; stroke due to relapsing polychondritis. Ideggyogy Sz. 2015;68:429-432.
- Ducci R, Germiniani F, Czecko L, et al. Relapsing polychondritis and lymphocytic meningitis with varied neurological symptoms [published online February 5, 2016]. Rev Bras Reumatol. doi:10.1016/j.rbr.2015.09.005.
- Baba T, Kanno S, Shijo T, et al. Callosal disconnection syndrome associated with relapsing polychondritis. Intern Med. 2016;55:1191-1193.
- Jeon C. Relapsing polychondritis with central nervous system involvement: experience of three different cases in a single center. J Korean Med. 2016;31:1846-1850.
- Liu L, Liu S, Guan W, et al. Efficacy of tocilizumab for psychiatric symptoms associated with relapsing polychondritis: the first case report and review of the literature. Rheumatol Int. 2016;36:1185-1189.
Relapsing polychondritis (RP) is an autoimmune disease affecting cartilaginous structures such as the ears, respiratory passages, joints, and cardiovascular system.1,2 In rare cases, the systemic effects of this autoimmune process can cause central nervous system (CNS) involvement such as meningoencephalitis (ME).3 In 2011, Wang et al4 described 4 cases of RP with ME and reviewed 24 cases from the literature. We present a case of a man with RP-associated ME that was responsive to steroid treatment. We also provide an updated review of the literature.
Case Report
A 44-year-old man developed gradually worsening bilateral ear pain, headaches, and seizures. He was briefly hospitalized and discharged with levetiracetam and quetiapine. However, his mental status continued to deteriorate and he was subsequently hospitalized 3 months later with confusion, hallucinations, and seizures.
On physical examination the patient was disoriented and unable to form cohesive sentences. He had bilateral tenderness, erythema, and edema of the auricles, which notably spared the lobules (Figure 1). The conjunctivae were injected bilaterally, and joint involvement included bilateral knee tenderness and swelling. Neurologic examination revealed questionable meningeal signs but no motor or sensory deficits. An extensive laboratory workup for the etiology of his altered mental status was unremarkable, except for a mildly elevated white blood cell count in the cerebrospinal fluid with predominantly lymphocytes. No infectious etiologies were identified on laboratory testing, and rheumatologic markers were negative including antinuclear antibody, rheumatoid factor, and anti–Sjögren syndrome antigen A/Sjögren syndrome antigen B. Magnetic resonance imaging revealed nonspecific findings of bilateral T2 hyperdensities in the subcortical white matter; however, cerebral angiography revealed no evidence of vasculitis. A biopsy of the right antihelix revealed prominent perichondritis and a neutrophilic inflammatory infiltrate with several lymphocytes and histiocytes (Figure 2). There was degeneration of the cartilaginous tissue with evidence of pyknotic nuclei, eosinophilia, and vacuolization of the chondrocytes. He was diagnosed with RP on the basis of clinical and histologic inflammation of the auricular cartilage, polyarthritis, and ocular inflammation.
The patient was treated with high-dose immunosuppression with methylprednisolone (1000 mg intravenous once daily for 5 days) and cyclophosphamide (one dose at 500 mg/m2), which resulted in remarkable improvement in his mental status, auricular inflammation, and knee pain. After 31 days of hospitalization the patient was discharged with a course of oral prednisone (starting at 60 mg/d, then tapered over the following 2 months) and monthly cyclophosphamide infusions (5 months total; starting at 500 mg/m2, then uptitrated to goal of 1000 mg/m2). Maintenance suppression was achieved with azathioprine (starting at 50 mg daily, then uptitrated to 100 mg daily), which was continued without any evidence of relapsed disease through his last outpatient visit 1 year after the diagnosis.
Comment
Auricular inflammation is a hallmark of RP and is present in 83% to 95% of patients.1,3 The affected ears can appear erythematous to violaceous with tender edema of the auricle that spares the lobules where no cartilage is present. The inflammation can extend into the ear canal and cause hearing loss, tinnitus, and vertigo. Histologically, RP can present with a nonspecific leukocytoclastic vasculitis and inflammatory destruction of the cartilage. Therefore, diagnosis of RP is reliant mainly on clinical characteristics rather than pathologic findings. In 1976, McAdam et al5 established diagnostic criteria for RP based on the presence of common clinical manifestations (eg, auricular chondritis, seronegative inflammatory polyarthritis, nasal chondritis, ocular inflammation). Michet et al6 later proposed major and minor criteria to classify and diagnose RP based on clinical manifestations. Diagnosis of our patient was confirmed by the presence of auricular chondritis, polyarthritis, and ocular inflammation. Diagnosing RP can be difficult because it has many systemic manifestations that can evoke a broad differential diagnosis. The time to diagnosis in our patient was 3 months, but the mean delay in diagnosis for patients with RP and ME is 2.9 years.4
The etiology of RP remains unclear, but current evidence supports an immune-mediated process directed toward proteins found in cartilage. Animal studies have suggested that RP may be driven by antibodies to matrillin 1 and type II collagen. There also may be a familial association with HLA-DR4 and genetic predisposition to autoimmune diseases in individuals affected by RP.1,3 The pathogenesis of CNS involvement in RP is thought to be due to a localized small vessel vasculitis.7,8 In our patient, however, cerebral angiography was negative for vasculitis, and thus our case may represent another mechanism for CNS involvement. There have been cases of encephalitis in RP caused by pathways other than CNS vasculitis. Kashihara et al9 reported a case of RP with encephalitis associated with antiglutamate receptor antibodies found in the cerebrospinal fluid and blood.
Treatment of RP has been based on pathophysiological considerations rather than empiric data due to its rarity. Relapsing polychondritis has been responsive to steroid treatment in reported cases as well as in our patient; however, in cases in which RP did not respond to steroids, infliximab may be effective for RP with ME.10 Further research regarding the treatment outcomes of RP with ME may be warranted.
Although rare, additional cases of RP with ME have been reported (Table). Wang et al4 described a series of 28 patients with RP and ME from 1960 to 2010. A PubMed search of articles indexed for MEDLINE that were published in the English-language literature from 2010 to 2016 was performed using the search terms relapsing polychondritis and nervous system. Including our patient, RP with ME was reported in 17 additional cases since Wang et al4 published their findings. These cases involved adults ranging in age from 44 to 73 years who were mainly men (14/17 [82%]). All of the patients presented with bilateral auricular chondritis, except for a case of unilateral ear involvement reported by Storey et al.11 Common neurologic manifestations included fever, headache, and altered mental status. Motor symptoms ranged from dysarthria and agraphia12 to hemiparesis.13 The mechanism of CNS involvement in RP was not identified in most cases; however, Mattiassich et al14 documented cerebral vasculitis in their patient, and Niwa et al16 found diffuse cerebral vasculitis on autopsy. Eleven of 17 (65%) cases responded to steroid treatment. Of the 6 cases in which RP did not respond to steroids, 2 patients died despite high-dose steroid treatment,11,20 2 responded to infliximab,10,15 1 responded to tocilizumab,21 and 1 was lost to follow-up after initial treatment failure.20
Conclusion
Although rare, RP should not be overlooked in the inpatient setting due to its potential for life-threatening systemic effects. Early diagnosis of this condition may be of benefit to this select population of patients, and further research regarding the prognosis, mechanisms, and treatment of RP may be necessary in the future.
Relapsing polychondritis (RP) is an autoimmune disease affecting cartilaginous structures such as the ears, respiratory passages, joints, and cardiovascular system.1,2 In rare cases, the systemic effects of this autoimmune process can cause central nervous system (CNS) involvement such as meningoencephalitis (ME).3 In 2011, Wang et al4 described 4 cases of RP with ME and reviewed 24 cases from the literature. We present a case of a man with RP-associated ME that was responsive to steroid treatment. We also provide an updated review of the literature.
Case Report
A 44-year-old man developed gradually worsening bilateral ear pain, headaches, and seizures. He was briefly hospitalized and discharged with levetiracetam and quetiapine. However, his mental status continued to deteriorate and he was subsequently hospitalized 3 months later with confusion, hallucinations, and seizures.
On physical examination the patient was disoriented and unable to form cohesive sentences. He had bilateral tenderness, erythema, and edema of the auricles, which notably spared the lobules (Figure 1). The conjunctivae were injected bilaterally, and joint involvement included bilateral knee tenderness and swelling. Neurologic examination revealed questionable meningeal signs but no motor or sensory deficits. An extensive laboratory workup for the etiology of his altered mental status was unremarkable, except for a mildly elevated white blood cell count in the cerebrospinal fluid with predominantly lymphocytes. No infectious etiologies were identified on laboratory testing, and rheumatologic markers were negative including antinuclear antibody, rheumatoid factor, and anti–Sjögren syndrome antigen A/Sjögren syndrome antigen B. Magnetic resonance imaging revealed nonspecific findings of bilateral T2 hyperdensities in the subcortical white matter; however, cerebral angiography revealed no evidence of vasculitis. A biopsy of the right antihelix revealed prominent perichondritis and a neutrophilic inflammatory infiltrate with several lymphocytes and histiocytes (Figure 2). There was degeneration of the cartilaginous tissue with evidence of pyknotic nuclei, eosinophilia, and vacuolization of the chondrocytes. He was diagnosed with RP on the basis of clinical and histologic inflammation of the auricular cartilage, polyarthritis, and ocular inflammation.
The patient was treated with high-dose immunosuppression with methylprednisolone (1000 mg intravenous once daily for 5 days) and cyclophosphamide (one dose at 500 mg/m2), which resulted in remarkable improvement in his mental status, auricular inflammation, and knee pain. After 31 days of hospitalization the patient was discharged with a course of oral prednisone (starting at 60 mg/d, then tapered over the following 2 months) and monthly cyclophosphamide infusions (5 months total; starting at 500 mg/m2, then uptitrated to goal of 1000 mg/m2). Maintenance suppression was achieved with azathioprine (starting at 50 mg daily, then uptitrated to 100 mg daily), which was continued without any evidence of relapsed disease through his last outpatient visit 1 year after the diagnosis.
Comment
Auricular inflammation is a hallmark of RP and is present in 83% to 95% of patients.1,3 The affected ears can appear erythematous to violaceous with tender edema of the auricle that spares the lobules where no cartilage is present. The inflammation can extend into the ear canal and cause hearing loss, tinnitus, and vertigo. Histologically, RP can present with a nonspecific leukocytoclastic vasculitis and inflammatory destruction of the cartilage. Therefore, diagnosis of RP is reliant mainly on clinical characteristics rather than pathologic findings. In 1976, McAdam et al5 established diagnostic criteria for RP based on the presence of common clinical manifestations (eg, auricular chondritis, seronegative inflammatory polyarthritis, nasal chondritis, ocular inflammation). Michet et al6 later proposed major and minor criteria to classify and diagnose RP based on clinical manifestations. Diagnosis of our patient was confirmed by the presence of auricular chondritis, polyarthritis, and ocular inflammation. Diagnosing RP can be difficult because it has many systemic manifestations that can evoke a broad differential diagnosis. The time to diagnosis in our patient was 3 months, but the mean delay in diagnosis for patients with RP and ME is 2.9 years.4
The etiology of RP remains unclear, but current evidence supports an immune-mediated process directed toward proteins found in cartilage. Animal studies have suggested that RP may be driven by antibodies to matrillin 1 and type II collagen. There also may be a familial association with HLA-DR4 and genetic predisposition to autoimmune diseases in individuals affected by RP.1,3 The pathogenesis of CNS involvement in RP is thought to be due to a localized small vessel vasculitis.7,8 In our patient, however, cerebral angiography was negative for vasculitis, and thus our case may represent another mechanism for CNS involvement. There have been cases of encephalitis in RP caused by pathways other than CNS vasculitis. Kashihara et al9 reported a case of RP with encephalitis associated with antiglutamate receptor antibodies found in the cerebrospinal fluid and blood.
Treatment of RP has been based on pathophysiological considerations rather than empiric data due to its rarity. Relapsing polychondritis has been responsive to steroid treatment in reported cases as well as in our patient; however, in cases in which RP did not respond to steroids, infliximab may be effective for RP with ME.10 Further research regarding the treatment outcomes of RP with ME may be warranted.
Although rare, additional cases of RP with ME have been reported (Table). Wang et al4 described a series of 28 patients with RP and ME from 1960 to 2010. A PubMed search of articles indexed for MEDLINE that were published in the English-language literature from 2010 to 2016 was performed using the search terms relapsing polychondritis and nervous system. Including our patient, RP with ME was reported in 17 additional cases since Wang et al4 published their findings. These cases involved adults ranging in age from 44 to 73 years who were mainly men (14/17 [82%]). All of the patients presented with bilateral auricular chondritis, except for a case of unilateral ear involvement reported by Storey et al.11 Common neurologic manifestations included fever, headache, and altered mental status. Motor symptoms ranged from dysarthria and agraphia12 to hemiparesis.13 The mechanism of CNS involvement in RP was not identified in most cases; however, Mattiassich et al14 documented cerebral vasculitis in their patient, and Niwa et al16 found diffuse cerebral vasculitis on autopsy. Eleven of 17 (65%) cases responded to steroid treatment. Of the 6 cases in which RP did not respond to steroids, 2 patients died despite high-dose steroid treatment,11,20 2 responded to infliximab,10,15 1 responded to tocilizumab,21 and 1 was lost to follow-up after initial treatment failure.20
Conclusion
Although rare, RP should not be overlooked in the inpatient setting due to its potential for life-threatening systemic effects. Early diagnosis of this condition may be of benefit to this select population of patients, and further research regarding the prognosis, mechanisms, and treatment of RP may be necessary in the future.
- Arnaud L, Mathian A, Haroche J, et al. Pathogenesis of relapsing polychondritis: a 2013 update. Autoimmun Rev. 2014;13:90-95.
- Ostrowski RA, Takagishi T, Robinson J. Rheumatoid arthritis, spondyloarthropathies, and relapsing polychondritis. Handb Clin Neurol. 2014;119:449-461.
- Lahmer T, Treiber M, von Werder A, et al. Relapsing polychondritis: an autoimmune disease with many faces. Autoimmun Rev. 2010;9:540-546.
- Wang ZJ, Pu CQ, Wang ZJ, et al. Meningoencephalitis or meningitis in relapsing polychondritis: four case reports and a literature review. J Clin Neurosci. 2011;18:1608-1615.
- McAdam LP, O’Hanlan MA, Bluestone R, et al. Relapsing polychondritis: prospective study of 23 patients and a review of the literature. Medicine (Baltimore). 1976;55:193-215.
- Michet C, McKenna C, Luthra H, et al. Relapsing polychondritis: survival and predictive role of early disease manifestations. Ann Intern Med. 1986;104:74-78.
- Sampaio L, Silva L, Mariz E, et al. CNS involvement in relapsing polychondritis. Joint Bone Spine. 2010;77:619-620.
- Prinz S, Dafotakis M, Schneider RK, et al. The red puffy ear sign—a clinical sign to diagnose a rare cause of meningoencephalitis. Fortschr Neurol Psychiatr. 2012;80:463-467.
- Kashihara K, Kawada S, Takahashi Y. Autoantibodies to glutamate receptor GluR2 in a patient with limic encephalitis associated with relapsing polychondritis. J Neurol Sci. 2009;287:275-277.
- Garcia-Egido A, Gutierrez C, de la Fuente C, et al. Relapsing polychondritis-associated meningitis and encephalitis: response to infliximab. Rheumatology (Oxford). 2011;50:1721-1723.
- Storey K, Matej R, Rusina R. Unusual association of seronegative, nonparaneoplastic limbic encephalitis and relapsing polychondritis in a patient with history of thymectomy for myasthemia: a case study. J Neurol. 2010;258:159-161.
- Choi HJ, Lee HJ. Relapsing polychondritis with encephalitis. J Clin Rheum. 2011;6:329-331.
- Fujiwara S, Zenke K, Iwata S, et al. Relapsing polychondritis presenting as encephalitis. No Shinkei Geka. 2012;40:247-253.
- Mattiassich G, Egger M, Semlitsch G, et al. Occurrence of relapsing polychondritis with a rising cANCA titre in a cANCA-positive systemic and cerebral vasculitis patient [published online February 5, 2013]. BMJ Case Rep. doi:10.1136/bcr-2013-008717.
- Kondo T, Fukuta M, Takemoto A, et al. Limbic encephalitis associated with relapsing polychondritis responded to infliximab and maintained its condition without recurrence after discontinuation: a case report and review of the literature. Nagoya J Med Sci. 2014;76:361-368.
- Niwa A, Okamoto Y, Kondo T, et al. Perivasculitic pancencephalitis with relapsing polychondritis: an autopsy case report and review of previous cases. Intern Med. 2014;53:1191-1195.
- Coban EK, Xanmemmedoy E, Colak M, et al. A rare complication of a rare disease; stroke due to relapsing polychondritis. Ideggyogy Sz. 2015;68:429-432.
- Ducci R, Germiniani F, Czecko L, et al. Relapsing polychondritis and lymphocytic meningitis with varied neurological symptoms [published online February 5, 2016]. Rev Bras Reumatol. doi:10.1016/j.rbr.2015.09.005.
- Baba T, Kanno S, Shijo T, et al. Callosal disconnection syndrome associated with relapsing polychondritis. Intern Med. 2016;55:1191-1193.
- Jeon C. Relapsing polychondritis with central nervous system involvement: experience of three different cases in a single center. J Korean Med. 2016;31:1846-1850.
- Liu L, Liu S, Guan W, et al. Efficacy of tocilizumab for psychiatric symptoms associated with relapsing polychondritis: the first case report and review of the literature. Rheumatol Int. 2016;36:1185-1189.
- Arnaud L, Mathian A, Haroche J, et al. Pathogenesis of relapsing polychondritis: a 2013 update. Autoimmun Rev. 2014;13:90-95.
- Ostrowski RA, Takagishi T, Robinson J. Rheumatoid arthritis, spondyloarthropathies, and relapsing polychondritis. Handb Clin Neurol. 2014;119:449-461.
- Lahmer T, Treiber M, von Werder A, et al. Relapsing polychondritis: an autoimmune disease with many faces. Autoimmun Rev. 2010;9:540-546.
- Wang ZJ, Pu CQ, Wang ZJ, et al. Meningoencephalitis or meningitis in relapsing polychondritis: four case reports and a literature review. J Clin Neurosci. 2011;18:1608-1615.
- McAdam LP, O’Hanlan MA, Bluestone R, et al. Relapsing polychondritis: prospective study of 23 patients and a review of the literature. Medicine (Baltimore). 1976;55:193-215.
- Michet C, McKenna C, Luthra H, et al. Relapsing polychondritis: survival and predictive role of early disease manifestations. Ann Intern Med. 1986;104:74-78.
- Sampaio L, Silva L, Mariz E, et al. CNS involvement in relapsing polychondritis. Joint Bone Spine. 2010;77:619-620.
- Prinz S, Dafotakis M, Schneider RK, et al. The red puffy ear sign—a clinical sign to diagnose a rare cause of meningoencephalitis. Fortschr Neurol Psychiatr. 2012;80:463-467.
- Kashihara K, Kawada S, Takahashi Y. Autoantibodies to glutamate receptor GluR2 in a patient with limic encephalitis associated with relapsing polychondritis. J Neurol Sci. 2009;287:275-277.
- Garcia-Egido A, Gutierrez C, de la Fuente C, et al. Relapsing polychondritis-associated meningitis and encephalitis: response to infliximab. Rheumatology (Oxford). 2011;50:1721-1723.
- Storey K, Matej R, Rusina R. Unusual association of seronegative, nonparaneoplastic limbic encephalitis and relapsing polychondritis in a patient with history of thymectomy for myasthemia: a case study. J Neurol. 2010;258:159-161.
- Choi HJ, Lee HJ. Relapsing polychondritis with encephalitis. J Clin Rheum. 2011;6:329-331.
- Fujiwara S, Zenke K, Iwata S, et al. Relapsing polychondritis presenting as encephalitis. No Shinkei Geka. 2012;40:247-253.
- Mattiassich G, Egger M, Semlitsch G, et al. Occurrence of relapsing polychondritis with a rising cANCA titre in a cANCA-positive systemic and cerebral vasculitis patient [published online February 5, 2013]. BMJ Case Rep. doi:10.1136/bcr-2013-008717.
- Kondo T, Fukuta M, Takemoto A, et al. Limbic encephalitis associated with relapsing polychondritis responded to infliximab and maintained its condition without recurrence after discontinuation: a case report and review of the literature. Nagoya J Med Sci. 2014;76:361-368.
- Niwa A, Okamoto Y, Kondo T, et al. Perivasculitic pancencephalitis with relapsing polychondritis: an autopsy case report and review of previous cases. Intern Med. 2014;53:1191-1195.
- Coban EK, Xanmemmedoy E, Colak M, et al. A rare complication of a rare disease; stroke due to relapsing polychondritis. Ideggyogy Sz. 2015;68:429-432.
- Ducci R, Germiniani F, Czecko L, et al. Relapsing polychondritis and lymphocytic meningitis with varied neurological symptoms [published online February 5, 2016]. Rev Bras Reumatol. doi:10.1016/j.rbr.2015.09.005.
- Baba T, Kanno S, Shijo T, et al. Callosal disconnection syndrome associated with relapsing polychondritis. Intern Med. 2016;55:1191-1193.
- Jeon C. Relapsing polychondritis with central nervous system involvement: experience of three different cases in a single center. J Korean Med. 2016;31:1846-1850.
- Liu L, Liu S, Guan W, et al. Efficacy of tocilizumab for psychiatric symptoms associated with relapsing polychondritis: the first case report and review of the literature. Rheumatol Int. 2016;36:1185-1189.
Practice Points
- Meningoencephalitis (ME) is a potentially rare complication of relapsing polychondritis (RP).
- Treatment of ME due to RP can include high-dose steroids and biologics.
Clinicians Should Retain the Ability to Choose a Pathologist
As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?
Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.
The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.1 A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.2 The degree of discordance would be expected to vary based on the range of diagnoses included in each study.
Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).3 The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.4 Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.
As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).5 These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.6 These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.
Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,7 which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.
All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.
- Trotter MJ, Bruecks AK. Interpretation of skin biopsies by general pathologists: diagnostic discrepancy rate measured by blinded review. Arch Pathol Lab Med. 2003;127:1489-1492.
- Shoo BA, Sagebiel RW, Kashani-Sabet M. Discordance in the histopathologic diagnosis of melanoma at a melanoma referral center [published online March 19, 2010]. J Am Acad Dermatol. 2010;62:751-756.
- Gerami P, Busam K, Cochran A, et al. Histomorphologic assessment and interobserver diagnostic reproducibility of atypical spitzoid melanocytic neoplasms with long-term follow-up. Am J Surg Pathol. 2014;38:934-940.
- Puri PK, Ferringer TC, Tyler WB, et al. Statistical analysis of the concordance of immunohistochemical stains with the final diagnosis in spitzoid neoplasms. Am J Dermatopathol. 2011;33:72-77.
- Braun RP, Gutkowicz-Krusin D, Rabinovitz H, et al. Agreement of dermatopathologists in the evaluation of clinically difficult melanocytic lesions: how golden is the ‘gold standard’? Dermatology. 2012;224:51-58.
- Urso C, Rongioletti F, Innocenzi D, et al. Interobserver reproducibility of histological features in cutaneous malignant melanoma. J Clin Pathol. 2005;58:1194-1198.
- Harvey NT, Budgeon CA, Leecy T, et al. Interobserver variability in the diagnosis of circumscribed sebaceous neoplasms of the skin. Pathology. 2013;45:581-586.
As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?
Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.
The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.1 A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.2 The degree of discordance would be expected to vary based on the range of diagnoses included in each study.
Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).3 The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.4 Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.
As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).5 These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.6 These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.
Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,7 which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.
All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.
As employers search for ways to reduce the cost of providing health care to their employees, there is a growing trend toward narrowed provider networks and exclusive laboratory contracts. In the case of clinical pathology, some of these choices make sense from the employer’s perspective. A complete blood cell count or comprehensive metabolic panel is done on a machine and the result is much the same regardless of the laboratory. So why not have all laboratory tests performed by the lowest bidder?
Laboratories vary in quality and anatomic pathology services are different from blood tests. Each slide must be interpreted by a physician and skill in the interpretation of skin specimens varies widely. Dermatopathology was one of the first subspecialties to be recognized within pathology, as it requires a high level of expertise. Clinicopathological correlation often is key to the accurate interpretation of a specimen. The stakes are high, and a delay in diagnosis of melanoma remains one of the most serious errors in medicine and one of the most common causes for litigation in dermatology.
The accurate interpretation of skin biopsy specimens becomes especially difficult when inadequate or misleading clinical information accompanies the specimen. A study of 589 biopsies submitted by primary care physicians and reported by general pathologists demonstrated a 6.5% error rate. False-negative errors were the most common, but false-positives also were observed.1 A study of pigmented lesions referred to the University of California, San Francisco, demonstrated a discordance rate of 14.3%.2 The degree of discordance would be expected to vary based on the range of diagnoses included in each study.
Board-certified dermatopathologists have varying areas of expertise and there is notable subjectivity in the interpretation of biopsy specimens. In the case of problematic pigmented lesions such as atypical Spitz nevi, there can be low interobserver agreement even among the experts in categorizing lesions as malignant versus nonmalignant (κ=0.30).3 The low concordance among expert dermatopathologists demonstrates that light microscopic features alone often are inadequate for diagnosis. Advanced studies, including immunohistochemical stains, can help to clarify the diagnosis. In the case of atypical Spitz tumors, the contribution of special stains to the final diagnosis is statistically similar to that of hematoxylin and eosin sections and age, suggesting that nothing alone is sufficiently reliable to establish a definitive diagnosis in every case.4 Although helpful, these studies are costly, and savings obtained by sending cases to the lowest bidder can evaporate quickly. Costs are higher when factoring in molecular studies, which can run upwards of $3000 per slide; the cost of litigation related to incorrect diagnoses; or the human costs of an incorrect diagnosis.
As a group, dermatopathologists are highly skilled in the interpretation of skin specimens, but challenging lesions are common in the routine practice of dermatopathology. A study of 1249 pigmented melanocytic lesions demonstrated substantial agreement among expert dermatopathologists for less problematic lesions, though agreement was greater for patients 40 years and older (κ=0.67) than for younger patients (κ=0.49). Agreement was lower for patients with atypical mole syndrome (κ=0.31).5 These discrepancies occur despite the fact that there is good interobserver reproducibility for grading of individual histological features such as asymmetry, circumscription, irregular confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, symmetrical melanin, deep melanin, cytological atypia, mitoses, dermal lymphocytic infiltrate, and necrosis.6 These results indicate that accurate diagnoses cannot be reliably established simply by grading a list of histological features. Accurate diagnosis requires complex pattern recognition and integration of findings. Conflicting criteria often are present and an accurate interpretation requires considerable judgment as to which features are significant and which are not.
Separation of sebaceous adenoma, sebaceoma, and well-differentiated sebaceous carcinoma is another challenging area, and interobserver consensus can be as low as 11%,7 which suggests notable subjectivity in the criteria for diagnosis of nonmelanocytic tumors and emphasizes the importance of communication between the dermatopathologist and clinician when determining how to manage an ambiguous lesion. The interpretation of inflammatory skin diseases, alopecia, and lymphoid proliferations also can be problematic, and expert consultation often is required.
All dermatologists receive substantial training in dermatopathology, which puts them in an excellent position to interpret ambiguous findings in the context of the clinical presentation. Sometimes the dermatologist who has seen the clinical presentation can be in the best position to make the diagnosis. All clinicians must be wary of bias and an objective set of eyes often can be helpful. Communication is crucial to ensure appropriate care for each patient, and policies that restrict the choice of pathologist can be damaging.
- Trotter MJ, Bruecks AK. Interpretation of skin biopsies by general pathologists: diagnostic discrepancy rate measured by blinded review. Arch Pathol Lab Med. 2003;127:1489-1492.
- Shoo BA, Sagebiel RW, Kashani-Sabet M. Discordance in the histopathologic diagnosis of melanoma at a melanoma referral center [published online March 19, 2010]. J Am Acad Dermatol. 2010;62:751-756.
- Gerami P, Busam K, Cochran A, et al. Histomorphologic assessment and interobserver diagnostic reproducibility of atypical spitzoid melanocytic neoplasms with long-term follow-up. Am J Surg Pathol. 2014;38:934-940.
- Puri PK, Ferringer TC, Tyler WB, et al. Statistical analysis of the concordance of immunohistochemical stains with the final diagnosis in spitzoid neoplasms. Am J Dermatopathol. 2011;33:72-77.
- Braun RP, Gutkowicz-Krusin D, Rabinovitz H, et al. Agreement of dermatopathologists in the evaluation of clinically difficult melanocytic lesions: how golden is the ‘gold standard’? Dermatology. 2012;224:51-58.
- Urso C, Rongioletti F, Innocenzi D, et al. Interobserver reproducibility of histological features in cutaneous malignant melanoma. J Clin Pathol. 2005;58:1194-1198.
- Harvey NT, Budgeon CA, Leecy T, et al. Interobserver variability in the diagnosis of circumscribed sebaceous neoplasms of the skin. Pathology. 2013;45:581-586.
- Trotter MJ, Bruecks AK. Interpretation of skin biopsies by general pathologists: diagnostic discrepancy rate measured by blinded review. Arch Pathol Lab Med. 2003;127:1489-1492.
- Shoo BA, Sagebiel RW, Kashani-Sabet M. Discordance in the histopathologic diagnosis of melanoma at a melanoma referral center [published online March 19, 2010]. J Am Acad Dermatol. 2010;62:751-756.
- Gerami P, Busam K, Cochran A, et al. Histomorphologic assessment and interobserver diagnostic reproducibility of atypical spitzoid melanocytic neoplasms with long-term follow-up. Am J Surg Pathol. 2014;38:934-940.
- Puri PK, Ferringer TC, Tyler WB, et al. Statistical analysis of the concordance of immunohistochemical stains with the final diagnosis in spitzoid neoplasms. Am J Dermatopathol. 2011;33:72-77.
- Braun RP, Gutkowicz-Krusin D, Rabinovitz H, et al. Agreement of dermatopathologists in the evaluation of clinically difficult melanocytic lesions: how golden is the ‘gold standard’? Dermatology. 2012;224:51-58.
- Urso C, Rongioletti F, Innocenzi D, et al. Interobserver reproducibility of histological features in cutaneous malignant melanoma. J Clin Pathol. 2005;58:1194-1198.
- Harvey NT, Budgeon CA, Leecy T, et al. Interobserver variability in the diagnosis of circumscribed sebaceous neoplasms of the skin. Pathology. 2013;45:581-586.
French psychiatrist condemned for society’s deficiency
On Dec. 14, 2016, a French psychiatrist was sentenced to an 18-month suspended prison sentence. Lekhraj Gujadhur, MD, was the supervisor of unit 101 at the Psychiatric Hospital Center of Saint-Egrève in France. In November 2008, he had approved the nonsupervised release of a schizophrenia patient, Jean-Pierre Guillaud, to outside of his unit but within the hospital facility. Mr. Guillaud, while outside supervision, escaped. He subsequently purchased a large knife and murdered a 26-year-old student, Luc Meunier, Le Monde reported.1
This is reminiscent of a similar case in 2012 in Marseille, where a psychiatrist received a suspended prison sentence after his patient committed murder. That prior case was later dismissed in appellate court. In my opinion, both trials point to a failure in psychiatry’s responsibility to educate the public in our limitations and roles. They also highlight the necessary discourse that society should have on the role of mental illness when it comes to crime.
Although I appreciate society’s concern about such crimes, I think that displacement of our anger onto Dr. Gujadhur is misguided, and instead, allows us to forget to look at our own poor judgment. Dr. Gujadhur, other psychiatrists, and mental hospitals do not have the responsibility to enact sentences for crimes; the legal system does. Law enforcement and prosecutors had numerous opportunities to charge and commit Mr. Guillaud over the years but chose not to do so, instead permitting him to stay within society under the care of the mental health system.
Asking Dr. Gujadhur to primarily focus on becoming an agent of the law, instead of treating his patient, is unfair. Schizophrenia, and in particular paranoia, are greatly worsened by social isolation. Confining Mr. Guillaud would be countertherapeutic and possibly lead to his suicide. Would Dr. Gujadhur have been responsible for the suicide? Mental health providers have to understand and support the psychological functioning of their patients. Creating a dual agency blurs and effaces the doctor-patient relationship, already so fragile in the treatment of paranoid patients.
The publicity of such cases, and of Mr. Guillaud’s mental illness, seems to go against current mental health research. Recent work has suggested that mental illness is not a significant risk factor for violence but rather a risk factor for being the victim of violence. Certainly, some patients with mental illness commit acts of violence, but studies suggest that this is mostly independent of their mental illness (Law Hum Behav. 2014 Oct;38[5];439-49).2 Our overemphasis on the mental status of criminals belittles their crimes and suggests that psychiatrists are responsible for the failings of our legal system.
As a supervising psychiatrist at one of the largest jail systems in America, I am familiar with the challenges in such cases. All of my patients are facing legal charges, and many suffer from severe mental illness like schizophrenia. As their treating psychiatrist, I am not asked to also sentence them for the charges they are facing. Simply working for the sheriff makes my ability to gain the trust of my patients much more difficult. Conspiring with the city or district attorney in an attempt to protect society would obliterate any chance at rapport building.
Working in corrections, I am deeply familiar with the current debate on the solitary confinement of our mentally ill offenders. Ironically, in that context, society has blamed the legal system for socially isolating our mentally ill offenders, especially ones with severe mental illness.3 In our jail, we meet regularly and discuss in an interdisciplinary fashion the role and consequences of social isolation. During our weekly sessions, a case involving stabbing someone 2 years prior would not have justified the punishment of social isolation and constant monitoring.
As a field, psychiatry must educate society on its ability to create a therapeutic environment and its ability to provide risk assessment of violence. We must also remind others of the impossibility of doing both simultaneously. Decisions on removing patients’ right to freedom can be informed by the mental health perspective but should be left to the courts. Society’s need to find a target after such tragedies is understandable, but blaming the treating psychiatrists will not help past or future victims.
References
1. Le psychiatre d’un schizophrène meurtrier condamné pour homicide involontaire, Le Monde, Dec. 14, 2016.
2. How often and how consistently do symptoms directly precede criminal behavior among offenders with mental illness? (Law Hum Behav. 2014 Oct;38[5]:439-49).
3. How to fix solitary confinement in American prisons, Los Angeles Times, Oct. 17, 2016.
Dr. Badre is a supervising psychiatric contractor at the San Diego Central Jail. He also holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches on medical education, psychopharmacology, ethics in psychiatry, and correctional care. He mentors several residents on projects, including reduction in the use of solitary confinement of patients with mental illness, reduction in the use of involuntary treatment of the mentally ill, and examination of the mentally ill offender.
On Dec. 14, 2016, a French psychiatrist was sentenced to an 18-month suspended prison sentence. Lekhraj Gujadhur, MD, was the supervisor of unit 101 at the Psychiatric Hospital Center of Saint-Egrève in France. In November 2008, he had approved the nonsupervised release of a schizophrenia patient, Jean-Pierre Guillaud, to outside of his unit but within the hospital facility. Mr. Guillaud, while outside supervision, escaped. He subsequently purchased a large knife and murdered a 26-year-old student, Luc Meunier, Le Monde reported.1
This is reminiscent of a similar case in 2012 in Marseille, where a psychiatrist received a suspended prison sentence after his patient committed murder. That prior case was later dismissed in appellate court. In my opinion, both trials point to a failure in psychiatry’s responsibility to educate the public in our limitations and roles. They also highlight the necessary discourse that society should have on the role of mental illness when it comes to crime.
Although I appreciate society’s concern about such crimes, I think that displacement of our anger onto Dr. Gujadhur is misguided, and instead, allows us to forget to look at our own poor judgment. Dr. Gujadhur, other psychiatrists, and mental hospitals do not have the responsibility to enact sentences for crimes; the legal system does. Law enforcement and prosecutors had numerous opportunities to charge and commit Mr. Guillaud over the years but chose not to do so, instead permitting him to stay within society under the care of the mental health system.
Asking Dr. Gujadhur to primarily focus on becoming an agent of the law, instead of treating his patient, is unfair. Schizophrenia, and in particular paranoia, are greatly worsened by social isolation. Confining Mr. Guillaud would be countertherapeutic and possibly lead to his suicide. Would Dr. Gujadhur have been responsible for the suicide? Mental health providers have to understand and support the psychological functioning of their patients. Creating a dual agency blurs and effaces the doctor-patient relationship, already so fragile in the treatment of paranoid patients.
The publicity of such cases, and of Mr. Guillaud’s mental illness, seems to go against current mental health research. Recent work has suggested that mental illness is not a significant risk factor for violence but rather a risk factor for being the victim of violence. Certainly, some patients with mental illness commit acts of violence, but studies suggest that this is mostly independent of their mental illness (Law Hum Behav. 2014 Oct;38[5];439-49).2 Our overemphasis on the mental status of criminals belittles their crimes and suggests that psychiatrists are responsible for the failings of our legal system.
As a supervising psychiatrist at one of the largest jail systems in America, I am familiar with the challenges in such cases. All of my patients are facing legal charges, and many suffer from severe mental illness like schizophrenia. As their treating psychiatrist, I am not asked to also sentence them for the charges they are facing. Simply working for the sheriff makes my ability to gain the trust of my patients much more difficult. Conspiring with the city or district attorney in an attempt to protect society would obliterate any chance at rapport building.
Working in corrections, I am deeply familiar with the current debate on the solitary confinement of our mentally ill offenders. Ironically, in that context, society has blamed the legal system for socially isolating our mentally ill offenders, especially ones with severe mental illness.3 In our jail, we meet regularly and discuss in an interdisciplinary fashion the role and consequences of social isolation. During our weekly sessions, a case involving stabbing someone 2 years prior would not have justified the punishment of social isolation and constant monitoring.
As a field, psychiatry must educate society on its ability to create a therapeutic environment and its ability to provide risk assessment of violence. We must also remind others of the impossibility of doing both simultaneously. Decisions on removing patients’ right to freedom can be informed by the mental health perspective but should be left to the courts. Society’s need to find a target after such tragedies is understandable, but blaming the treating psychiatrists will not help past or future victims.
References
1. Le psychiatre d’un schizophrène meurtrier condamné pour homicide involontaire, Le Monde, Dec. 14, 2016.
2. How often and how consistently do symptoms directly precede criminal behavior among offenders with mental illness? (Law Hum Behav. 2014 Oct;38[5]:439-49).
3. How to fix solitary confinement in American prisons, Los Angeles Times, Oct. 17, 2016.
Dr. Badre is a supervising psychiatric contractor at the San Diego Central Jail. He also holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches on medical education, psychopharmacology, ethics in psychiatry, and correctional care. He mentors several residents on projects, including reduction in the use of solitary confinement of patients with mental illness, reduction in the use of involuntary treatment of the mentally ill, and examination of the mentally ill offender.
On Dec. 14, 2016, a French psychiatrist was sentenced to an 18-month suspended prison sentence. Lekhraj Gujadhur, MD, was the supervisor of unit 101 at the Psychiatric Hospital Center of Saint-Egrève in France. In November 2008, he had approved the nonsupervised release of a schizophrenia patient, Jean-Pierre Guillaud, to outside of his unit but within the hospital facility. Mr. Guillaud, while outside supervision, escaped. He subsequently purchased a large knife and murdered a 26-year-old student, Luc Meunier, Le Monde reported.1
This is reminiscent of a similar case in 2012 in Marseille, where a psychiatrist received a suspended prison sentence after his patient committed murder. That prior case was later dismissed in appellate court. In my opinion, both trials point to a failure in psychiatry’s responsibility to educate the public in our limitations and roles. They also highlight the necessary discourse that society should have on the role of mental illness when it comes to crime.
Although I appreciate society’s concern about such crimes, I think that displacement of our anger onto Dr. Gujadhur is misguided, and instead, allows us to forget to look at our own poor judgment. Dr. Gujadhur, other psychiatrists, and mental hospitals do not have the responsibility to enact sentences for crimes; the legal system does. Law enforcement and prosecutors had numerous opportunities to charge and commit Mr. Guillaud over the years but chose not to do so, instead permitting him to stay within society under the care of the mental health system.
Asking Dr. Gujadhur to primarily focus on becoming an agent of the law, instead of treating his patient, is unfair. Schizophrenia, and in particular paranoia, are greatly worsened by social isolation. Confining Mr. Guillaud would be countertherapeutic and possibly lead to his suicide. Would Dr. Gujadhur have been responsible for the suicide? Mental health providers have to understand and support the psychological functioning of their patients. Creating a dual agency blurs and effaces the doctor-patient relationship, already so fragile in the treatment of paranoid patients.
The publicity of such cases, and of Mr. Guillaud’s mental illness, seems to go against current mental health research. Recent work has suggested that mental illness is not a significant risk factor for violence but rather a risk factor for being the victim of violence. Certainly, some patients with mental illness commit acts of violence, but studies suggest that this is mostly independent of their mental illness (Law Hum Behav. 2014 Oct;38[5];439-49).2 Our overemphasis on the mental status of criminals belittles their crimes and suggests that psychiatrists are responsible for the failings of our legal system.
As a supervising psychiatrist at one of the largest jail systems in America, I am familiar with the challenges in such cases. All of my patients are facing legal charges, and many suffer from severe mental illness like schizophrenia. As their treating psychiatrist, I am not asked to also sentence them for the charges they are facing. Simply working for the sheriff makes my ability to gain the trust of my patients much more difficult. Conspiring with the city or district attorney in an attempt to protect society would obliterate any chance at rapport building.
Working in corrections, I am deeply familiar with the current debate on the solitary confinement of our mentally ill offenders. Ironically, in that context, society has blamed the legal system for socially isolating our mentally ill offenders, especially ones with severe mental illness.3 In our jail, we meet regularly and discuss in an interdisciplinary fashion the role and consequences of social isolation. During our weekly sessions, a case involving stabbing someone 2 years prior would not have justified the punishment of social isolation and constant monitoring.
As a field, psychiatry must educate society on its ability to create a therapeutic environment and its ability to provide risk assessment of violence. We must also remind others of the impossibility of doing both simultaneously. Decisions on removing patients’ right to freedom can be informed by the mental health perspective but should be left to the courts. Society’s need to find a target after such tragedies is understandable, but blaming the treating psychiatrists will not help past or future victims.
References
1. Le psychiatre d’un schizophrène meurtrier condamné pour homicide involontaire, Le Monde, Dec. 14, 2016.
2. How often and how consistently do symptoms directly precede criminal behavior among offenders with mental illness? (Law Hum Behav. 2014 Oct;38[5]:439-49).
3. How to fix solitary confinement in American prisons, Los Angeles Times, Oct. 17, 2016.
Dr. Badre is a supervising psychiatric contractor at the San Diego Central Jail. He also holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches on medical education, psychopharmacology, ethics in psychiatry, and correctional care. He mentors several residents on projects, including reduction in the use of solitary confinement of patients with mental illness, reduction in the use of involuntary treatment of the mentally ill, and examination of the mentally ill offender.
Endoscopy during pregnancy increases risk of preterm, SGA birth
Women who undergo an endoscopy during pregnancy are increasing the chances that their baby will be born preterm, or be small for gestational age (SGA), according to research published in the February issue of Gastroenterology (doi: 10.1053/j.gastro.2016.10.016).
“Research in pregnancy outcome in women undergoing endoscopy during pregnancy is scarce,” wrote the authors, led by Jonas F. Ludvigsson, MD, of the Karolinska Institutet in Stockholm, adding that there are nine studies with original data on a total of 379 pregnant women undergoing endoscopy; two of these studies examined pregnancy outcome in upper endoscopy (n = 143), two examined pregnancy outcome in sigmoidoscopy or colonoscopy (n = 116), and four examined pregnancy outcome in endoscopic retrograde cholangiopancreatography (n = 120).
Additionally, the authors noted that, to their knowledge, there are no studies that offer data on the relative risk of endoscopy during pregnancy, and none that followed up subjects after birth. Of the few studies that do exist, a handful conclude that endoscopy during pregnancy is actually safe, but do not include data on stillbirths and neonatal deaths that did not occur immediately after patients underwent endoscopy, which could compromise that data.
To address the lack of reliable research on the effect of endoscopy on pregnancy, Dr. Ludvigsson and his coinvestigators launched a nationwide study of pregnancies in Sweden that occurred between 1992 and 2011, all of which were registered in the Swedish Medical Birth Registry and the Swedish Patient Registry. The databases revealed 2,025 upper endoscopies, 1,109 lower endoscopies, and 58 endoscopic retrograde cholangiopancreatographies, for a total of 3,052 pregnancies exposed to endoscopy over that time period.
The primary endpoint of the study was the frequency of preterm birth and stillbirth in this population. To measure this, the investigators used adjusted relative risk (ARR), calculated via Poisson regression by using data on 1,589,173 pregnancies that were not exposed to endoscopy as reference.
“Stillbirth is recorded from 22 completed gestational weeks since mid-2008, and before that from gestational week 28. Gestational age was determined using ultrasound, and when ultrasound data were missing, we used the first day of the last menstrual period for pregnancy start,” the authors wrote.
The results showed that mothers who had any kind of endoscopy during pregnancy were more likely to experience a preterm birth or give birth to a baby who was SGA, with the ARR being 1.54 (95% confidence interval, 1.36-1.75) and 1.30 (95% CI, 1.07-1.57), respectively. However, the risk of other adverse effects, such as stillbirth or congenital malformation, was not significant: Stillbirth ARR was 1.45 (95% CI, 0.87-2.40) and congenital malformation ARR was 1.00 (95% CI, 0.83-1.20).
Women who were exposed to endoscopy during pregnancy were more likely to have a preterm birth, compared with women who had endoscopy 1 year before or after pregnancy, but were not more highly predisposed to SGA, stillbirth, or congenital malformations. Additionally, when data on multiple pregnancies carried by the same mother were compared, no correlation was found between endoscopy and gestational age or birth weight, if the mother was exposed to endoscopy during only one of the pregnancies.
“Earlier recommendations suggest that endoscopy should only be performed during pregnancy if there are strong indications, and if so, not during the second trimester, [but] our study shows that endoscopy is unlikely to have a more than marginal influence on pregnancy outcome independently of trimester,” the authors concluded. “Neither does it seem that sigmoidoscopy is preferable to a full colonoscopy in the pregnant woman.”
Regarding the latter conclusion, the authors clarified that “it is possible that in women with particularly severe gastrointestinal disease where endoscopy is inevitable, the physician will prefer a sigmoidoscopy rather than a full colonoscopy, and under such circumstances the sigmoidoscopy will signal a more severe disease.”
The investigators also noted that their study had several limitations, including not knowing the length of time each endoscopy took, the sedatives and bowel preparations that were used, the patient’s position during the procedure, and the indication that prompted the endoscopy in the first place.
The study was funded by grants from the Swedish Society of Medicine and the Stockholm County Council, and the Swedish Research Council. Dr. Ludvigsson and his coauthors did not report any relevant financial disclosures.
Women who undergo an endoscopy during pregnancy are increasing the chances that their baby will be born preterm, or be small for gestational age (SGA), according to research published in the February issue of Gastroenterology (doi: 10.1053/j.gastro.2016.10.016).
“Research in pregnancy outcome in women undergoing endoscopy during pregnancy is scarce,” wrote the authors, led by Jonas F. Ludvigsson, MD, of the Karolinska Institutet in Stockholm, adding that there are nine studies with original data on a total of 379 pregnant women undergoing endoscopy; two of these studies examined pregnancy outcome in upper endoscopy (n = 143), two examined pregnancy outcome in sigmoidoscopy or colonoscopy (n = 116), and four examined pregnancy outcome in endoscopic retrograde cholangiopancreatography (n = 120).
Additionally, the authors noted that, to their knowledge, there are no studies that offer data on the relative risk of endoscopy during pregnancy, and none that followed up subjects after birth. Of the few studies that do exist, a handful conclude that endoscopy during pregnancy is actually safe, but do not include data on stillbirths and neonatal deaths that did not occur immediately after patients underwent endoscopy, which could compromise that data.
To address the lack of reliable research on the effect of endoscopy on pregnancy, Dr. Ludvigsson and his coinvestigators launched a nationwide study of pregnancies in Sweden that occurred between 1992 and 2011, all of which were registered in the Swedish Medical Birth Registry and the Swedish Patient Registry. The databases revealed 2,025 upper endoscopies, 1,109 lower endoscopies, and 58 endoscopic retrograde cholangiopancreatographies, for a total of 3,052 pregnancies exposed to endoscopy over that time period.
The primary endpoint of the study was the frequency of preterm birth and stillbirth in this population. To measure this, the investigators used adjusted relative risk (ARR), calculated via Poisson regression by using data on 1,589,173 pregnancies that were not exposed to endoscopy as reference.
“Stillbirth is recorded from 22 completed gestational weeks since mid-2008, and before that from gestational week 28. Gestational age was determined using ultrasound, and when ultrasound data were missing, we used the first day of the last menstrual period for pregnancy start,” the authors wrote.
The results showed that mothers who had any kind of endoscopy during pregnancy were more likely to experience a preterm birth or give birth to a baby who was SGA, with the ARR being 1.54 (95% confidence interval, 1.36-1.75) and 1.30 (95% CI, 1.07-1.57), respectively. However, the risk of other adverse effects, such as stillbirth or congenital malformation, was not significant: Stillbirth ARR was 1.45 (95% CI, 0.87-2.40) and congenital malformation ARR was 1.00 (95% CI, 0.83-1.20).
Women who were exposed to endoscopy during pregnancy were more likely to have a preterm birth, compared with women who had endoscopy 1 year before or after pregnancy, but were not more highly predisposed to SGA, stillbirth, or congenital malformations. Additionally, when data on multiple pregnancies carried by the same mother were compared, no correlation was found between endoscopy and gestational age or birth weight, if the mother was exposed to endoscopy during only one of the pregnancies.
“Earlier recommendations suggest that endoscopy should only be performed during pregnancy if there are strong indications, and if so, not during the second trimester, [but] our study shows that endoscopy is unlikely to have a more than marginal influence on pregnancy outcome independently of trimester,” the authors concluded. “Neither does it seem that sigmoidoscopy is preferable to a full colonoscopy in the pregnant woman.”
Regarding the latter conclusion, the authors clarified that “it is possible that in women with particularly severe gastrointestinal disease where endoscopy is inevitable, the physician will prefer a sigmoidoscopy rather than a full colonoscopy, and under such circumstances the sigmoidoscopy will signal a more severe disease.”
The investigators also noted that their study had several limitations, including not knowing the length of time each endoscopy took, the sedatives and bowel preparations that were used, the patient’s position during the procedure, and the indication that prompted the endoscopy in the first place.
The study was funded by grants from the Swedish Society of Medicine and the Stockholm County Council, and the Swedish Research Council. Dr. Ludvigsson and his coauthors did not report any relevant financial disclosures.
Women who undergo an endoscopy during pregnancy are increasing the chances that their baby will be born preterm, or be small for gestational age (SGA), according to research published in the February issue of Gastroenterology (doi: 10.1053/j.gastro.2016.10.016).
“Research in pregnancy outcome in women undergoing endoscopy during pregnancy is scarce,” wrote the authors, led by Jonas F. Ludvigsson, MD, of the Karolinska Institutet in Stockholm, adding that there are nine studies with original data on a total of 379 pregnant women undergoing endoscopy; two of these studies examined pregnancy outcome in upper endoscopy (n = 143), two examined pregnancy outcome in sigmoidoscopy or colonoscopy (n = 116), and four examined pregnancy outcome in endoscopic retrograde cholangiopancreatography (n = 120).
Additionally, the authors noted that, to their knowledge, there are no studies that offer data on the relative risk of endoscopy during pregnancy, and none that followed up subjects after birth. Of the few studies that do exist, a handful conclude that endoscopy during pregnancy is actually safe, but do not include data on stillbirths and neonatal deaths that did not occur immediately after patients underwent endoscopy, which could compromise that data.
To address the lack of reliable research on the effect of endoscopy on pregnancy, Dr. Ludvigsson and his coinvestigators launched a nationwide study of pregnancies in Sweden that occurred between 1992 and 2011, all of which were registered in the Swedish Medical Birth Registry and the Swedish Patient Registry. The databases revealed 2,025 upper endoscopies, 1,109 lower endoscopies, and 58 endoscopic retrograde cholangiopancreatographies, for a total of 3,052 pregnancies exposed to endoscopy over that time period.
The primary endpoint of the study was the frequency of preterm birth and stillbirth in this population. To measure this, the investigators used adjusted relative risk (ARR), calculated via Poisson regression by using data on 1,589,173 pregnancies that were not exposed to endoscopy as reference.
“Stillbirth is recorded from 22 completed gestational weeks since mid-2008, and before that from gestational week 28. Gestational age was determined using ultrasound, and when ultrasound data were missing, we used the first day of the last menstrual period for pregnancy start,” the authors wrote.
The results showed that mothers who had any kind of endoscopy during pregnancy were more likely to experience a preterm birth or give birth to a baby who was SGA, with the ARR being 1.54 (95% confidence interval, 1.36-1.75) and 1.30 (95% CI, 1.07-1.57), respectively. However, the risk of other adverse effects, such as stillbirth or congenital malformation, was not significant: Stillbirth ARR was 1.45 (95% CI, 0.87-2.40) and congenital malformation ARR was 1.00 (95% CI, 0.83-1.20).
Women who were exposed to endoscopy during pregnancy were more likely to have a preterm birth, compared with women who had endoscopy 1 year before or after pregnancy, but were not more highly predisposed to SGA, stillbirth, or congenital malformations. Additionally, when data on multiple pregnancies carried by the same mother were compared, no correlation was found between endoscopy and gestational age or birth weight, if the mother was exposed to endoscopy during only one of the pregnancies.
“Earlier recommendations suggest that endoscopy should only be performed during pregnancy if there are strong indications, and if so, not during the second trimester, [but] our study shows that endoscopy is unlikely to have a more than marginal influence on pregnancy outcome independently of trimester,” the authors concluded. “Neither does it seem that sigmoidoscopy is preferable to a full colonoscopy in the pregnant woman.”
Regarding the latter conclusion, the authors clarified that “it is possible that in women with particularly severe gastrointestinal disease where endoscopy is inevitable, the physician will prefer a sigmoidoscopy rather than a full colonoscopy, and under such circumstances the sigmoidoscopy will signal a more severe disease.”
The investigators also noted that their study had several limitations, including not knowing the length of time each endoscopy took, the sedatives and bowel preparations that were used, the patient’s position during the procedure, and the indication that prompted the endoscopy in the first place.
The study was funded by grants from the Swedish Society of Medicine and the Stockholm County Council, and the Swedish Research Council. Dr. Ludvigsson and his coauthors did not report any relevant financial disclosures.
FROM GASTROENTEROLOGY
Key clinical point:
Major finding: The adjusted relative risk of preterm birth was 1.54 (95% CI, 1.36-1.75) and was 1.30 (95% CI, 1.07-1.57) for SGA.
Data source: A population-based cohort study of 3,052 pregnancies in Sweden exposed to endoscopy from 1992 through 2011.
Disclosures: The study was funded by the Swedish Society of Medicine and the Stockholm County Council, and the Swedish Research Council. The authors did not report any relevant financial disclosures.