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In Throwers With Posterior Instability, Rotator Cuff Tears Are Common but Do Not Affect Surgical Outcomes

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In Throwers With Posterior Instability, Rotator Cuff Tears Are Common but Do Not Affect Surgical Outcomes

ABSTRACT

In a previous study, compared with throwing athletes with superior labral anterior posterior (SLAP) tears, those with concomitant SLAP tears and rotator cuff tears (RCTs) had significantly poorer outcome scores and return to play. Posterior shoulder instability also occurs in throwing athletes, but no studies currently exist regarding outcomes of these patients with concomitant RCTs.

The authors hypothesized that throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent rotator cuff pathology would have poorer outcome scores and return to play.

Fifty-six consecutive throwing athletes with unidirectional posterior shoulder instability underwent arthroscopic capsulolabral repair. Preoperative and postoperative patient-centered outcomes of pain, stability, function, range of motion, strength, and American Shoulder and Elbow Surgeons Shoulder (ASES) scores, as well as return to play, were evaluated. Patients with and without rotator cuff pathology were compared.

Forty-three percent (24/56) of throwing athletes had rotator cuff pathology in addition to posterior capsulolabral pathology. All RCTs were débrided. At a mean of 3 years, there were no differences in preoperative and postoperative patient-centered outcomes between those with and without RCTs. Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport (P = .414) and 67% (16/24) returned to the same level (P = .430).

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike the previous study evaluating throwers outcomes after surgical treatment for concomitant SLAP tears and RCTs, the authors found no difference in patient-reported outcome measures or return to play for throwing athletes with concomitant posterior shoulder instability and RCTs. In throwing athletes with concomitant posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

Continue to: Posterior shoulder instability...

 

 

Posterior shoulder instability is an important and increasingly recognized pathology among throwers. Like the superior labrum, the posterior capsulolabral complex is also susceptible to injury during the throwing motion; the posterior labrum being most at risk during the late cocking and follow-through phases. Recent studies have found that arthroscopic capsulolabral reconstruction in posterior shoulder instability is successful in allowing athletes to return to their preinjury sports activities, with 2 studies detailing outcomes in throwing athletes.1-4 However, superior labral anterior posterior (SLAP) tears are common in throwing athletes and have been treated with varying and limited success. Further, in a study of outcomes of arthroscopic repair of SLAP lesions, Neri and colleagues5 found that, compared with throwing athletes with SLAP tears, throwing athletes with concomitant SLAP tears and partial-thickness rotator cuff tears (RCTs) had significantly poorer outcomes and return-to-play rates after surgical repair.

The purpose of this study was to determine outcome scores and return to play of throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent RCTs and to compare them with outcome scores as well as return to play of throwing athletes with isolated posterior shoulder instability. It was hypothesized that throwing athletes with a combination of posterior shoulder instability and RCT would have poorer outcomes and poorer return to play after surgery.5

METHODS

PATIENT SELECTION

After Institutional Review Board approval, informed consent was obtained, and consecutive throwing athletes who underwent arthroscopic posterior capsulolabral reconstruction for posterior shoulder instability were followed in the perioperative period. Inclusion criteria were throwing athletes participating in competitive sports at the high school, collegiate, or professional level, minimum 1-year follow-up, presence of unidirectional posterior instability, and absence of symptoms of instability in any direction other than posterior. Patients with inferior instability, SLAP pathology on examination and on magnetic resonance imaging, multidirectional instability, or habitual or psychogenic voluntary shoulder subluxations were excluded. Patients with diagnoses of both posterior shoulder instability and impingement treated with subacromial decompression and distal clavicle resection were also excluded.

After this cohort was identified, patient records were reviewed for pertinent operative data, such as procedure, complications, and evidence of RCT by operative report and arthroscopic photographs. A partial RCT was defined as a tear of 10% to 50%; those with rotator cuff fraying were determined not to be significant.

PATIENT EVALUATION

Surgeries were performed between January 1998 and December 2009 by the senior author (JPB). All patients were followed with clinical examinations, radiographs, and subjective grading scales. Recorded patient demographic data included age, sex, sport, position, competition level, and follow-up duration.

Continue to: All patients had...

 

 

All patients had symptomatic posterior shoulder instability, including posterior shoulder pain, clicking, a sensation of subluxation, or instability/apprehension with motion. Each athlete’s shoulder was palpated for tenderness and tested for impingement. Specific posterior glenohumeral instability tests, including the Kim test,6 the circumduction test, the jerk test,7 the posterior load-and-shift test,8 and the posterior stress test,9 were performed on all patients. Patients with multidirectional instability on the sulcus test, as well as provocative tests indicating SLAP pathology, such as the Crank test and the active compression test, were not included. Standard radiography and magnetic resonance arthrography (MRA) were performed to further narrow inclusion and exclusion criteria.

Both before surgery and at latest follow-up, patient outcomes were evaluated using the American Shoulder and Elbow Surgeons (ASES) score (range, 0-100) which combines a subjective functional scale measuring activities of daily living (0-3 for each of 10 tasks, with a total of 0-30) and a subjective pain scale (0-10, with 10 being worst pain). Values >80 were described as excellent, and failures were defined as scores <60 after surgery.10 A subjective stability scale (0-10, with 0 indicating completely stable and 10 completely unstable), strength scale (0-3, with 0 indicating none, 1 markedly decreased, 2 slightly decreased, and 3 normal), and ROM scale (0-3, with 0 indicating poor, 1 limited, 2 satisfactory, and 3 full) were evaluated both before surgery and at the latest follow-up. A stability score >5 after surgery was defined as a failure.1,2,11 Patients were also asked if, based on their current state, they would undergo surgery again. Intraoperative findings and specific surgical procedures performed were correlated with the aforementioned subjective and objective outcome scores.

OPERATIVE TREATMENT

Throwing athletes who met inclusion criteria and failed nonoperative management underwent surgery by the senior author (JPB). Each patient was examined under anesthesia and, with the patient in the lateral decubitus position, a diagnostic arthroscopy was performed to identify posterior capsulolabral complex pathology, including a patulous capsule, capsular tears, labral fraying, and labral tears. A careful examination for rotator cuff pathology was also performed. Based on preoperative clinical examination, MRA, examination under anesthesia, pathologic findings at diagnostic arthroscopic surgery, and surgeon experience, capsulolabral plication was performed with or without suture anchors.2,5 After capsulolabral repair, the capsule was evaluated for residual laxity, and additional plication sutures were placed, as indicated, with care to avoid overconstraint in these throwing athletes.1 Posterior glenohumeral stability restoration was judged by removing traction and performing posterior load-and-shift and posterior stress tests. Any RCT with <50% thickness was débrided. Postoperative care and rehabilitation were carried out as previously described and were not altered by the presence or absence of a RCT.3

STATISTICAL ANALYSIS

Preoperative and latest follow-up ASES scores, stability scores, functional scores, and pain-level findings were compared using paired-samples Comparisons between groups, including throwing athletes with and without rotator cuff pathology, were done using the Student t test. Outcome comparisons between multiple groups, which included intraoperative findings and surgical fixation methods, were analyzed with c2 modeling for nonparametric data. Statistical significance was set at P < .05. A power analysis found that this study was able to detect a meaningful difference of 10 ASES points.

RESULTS

PATIENT DEMOGRAPHIC CHARACTERISTICS

Of the 56 throwing athletes who met the inclusion criteria, 24 were found to have rotator cuff pathology in addition to posterior capsulolabral pathology, while 32 were found to have capsulolabral pathology alone. Demographic data are listed in Table 1. Mean age was 20.1 years for patients with rotator cuff pathology and 17.8 years for patients without RCTs. All 24 athletes with rotator cuff pathology were treated with arthroscopic débridement. Mean follow-up was 38.6 months (range, 16.5-63.6 months) for patients with RCTs and 39.1 months (range, 12-98.8 months) for patients without RCTs. No significant difference was found in age, sports level, or follow-up between groups.

Table 1. Demographic Data for Athletes With Posterior Instability With and Without Rotator Cuff Tears (N = 56 Shoulders)a

Characteristic

Rotator Cuff Tears

 

Yes

No

Total2432
Sex 
Male1627
Female85
Mean age, y20.117.8
Mean follow up, mo38.639.1
Participation level 
 Professional10
 College44
 High school1726
 Recreational22

aThe majority of athletes were males in high school and their mean follow-up was 3 years.

Continue to: Outcomes

 

 

OUTCOMES

Table 2 lists the preoperative and postoperative scores for shoulder performance in throwing athletes with posterior shoulder instability, with and without RCTs.

Table 2. Preoperative and Postoperative Scores for Shoulder Performance in Throwing Athletes With Posterior Shoulder Instability With and Without Rotator Cuff Tearsa
 With Rotator Cuff Tears (n=24 shoulders)Without Rotator Cuff Tears (n=32 shoulders)
 Preoperative Latest Follow-Up PreoperativeLatest Follow-Up 
Outcome MeasureMean ScoreRangeMean ScoreRangePMean ScoreRangeMean ScoreRangeP

ASES

0-100

0 = worst

41.820-7085.467-100<.0549.720-8583.125-100<.05

Stability

0-10

0 = most stable

6.72-102.40-6<.057.80-102.40-8<.05

Pain

0-10

10 = worst

7.65-101.90-5<.056.30-102.20-7<.05

Function

0-30

0 = worst

18.56-272716-30<.0519.08-2626.46-30<.05

aThere was no difference in ASES, stability, pain, or functional scores between athletes with posterior instability alone compared with patients with concomitant rotator cuff tears.

Abbreviation: ASES, American Shoulder and Elbow Surgeons.

ASES Scores. Mean preoperative ASES scores for patients with RCTs improved significantly (t = –13.8, P < .001), as did those for patients without rotator cuff pathology (t = –8.9, P < .001). No significant differences in ASES score were found between patients with and without rotator cuff pathology before or after surgery (t = 1.9, P = .07; t = .58, P = .06). In addition, 70.8% (17/24) of throwing athletes with rotator cuff pathology had an excellent postoperative outcome (ASES score >80), and 29.2% (7/24) had a satisfactory outcome (ASES score, 60-80). Thus, 100% of those with concomitant posterior shoulder instability and RCTs had a good or excellent outcome after surgical intervention. In those without rotator cuff pathology, 78.1% (25/32) had an excellent outcome, 12.5% (4/32) had a satisfactory outcome, and 9.4% (3/32) had a poor outcome. Thus, 91% of those without rotator cuff pathology had a good or excellent outcome after surgery.

Stability. Preoperative stability scores improved significantly after surgery in both groups (t = 7.2, P < .001; t = 10.5, P < .001). There were no statistical differences between preoperative or postoperative stability scores in those with or without rotator cuff pathology (t = 1.7, P = .095; t = .03, P = .975). Of throwing athletes with RCTs, 54.2% (13/24) had an excellent outcome, 33.3% (8/24) a good outcome, and 12.5% (3/24) a satisfactory outcome. Thus, 87.5% (21/24) of those with RCTs had a good or excellent outcome in terms of stability. In those without rotator cuff pathology, 46.9% (15/32) had excellent stability, 46.9% (15/32) had good stability, and 3.1% (1/32) had satisfactory stability after surgery. Thus, 93.8% (30/32) of throwing athletes without rotator cuff pathology had good or excellent stability after surgery.

Pain. Mean preoperative pain scores for those with and without rotator cuff pathology improved significantly (t = 13.4, P < .001; t = 7.1, P < .001). There was no statistical difference in preoperative or postoperative pain scores between those with and without rotator cuff pathology (t = 1.99, P = .051; t = .49, P = .627).

Function. Mean preoperative function scores for both groups improved significantly (t = 7.7, P < .001; t = 8.0, P < .001). There was no difference in improvement in functional scores between the two groups before or after surgery (t = .36, P = .721; t = .5, P = .622).

Continue to: ROM

 

 

ROM. Of those with rotator cuff pathology, 54% (13/24) had normal ROM, 42% (10/24) had satisfactory ROM, and 4% (1/24) had limited ROM. In throwing athletes without rotator cuff pathology, 34% (11/32) had normal ROM, 53.1% (17/32) had satisfactory ROM, and 9% (3/32) had limited ROM after surgery. There was no significant difference in ROM between the groups (c2 = 2.7, P = .260).

Strength. Of those with RCTs, 67% (16/24) reported normal strength, 29% (7/24) slightly decreased strength, and 4% (1/24) markedly decreased strength. Of those throwing athletes without rotator cuff pathology, 50% (16/32) had normal strength, 41% (13/32) had slightly decreased strength, and 9% (3/32) had markedly decreased strength. No statistical difference was noted between the two groups (c2 = 1.7, P = .429).

Return to Sport. Of those with RCTs, 92% (22/24) returned to sport while 84% (27/32) of throwing athletes without RCTs returned to sport. There was no difference between the two groups (c2 = .667, P = .414). Sixty-seven percent (16/24) of those with RCTs and 56% (18/32) of those without RCTs returned to the same level of sport. No statistical difference was found in return to play between throwing athletes with and without rotator cuff pathology (c2 = .624, P = .430).

Failures. According to ASES scores, no throwers with RCTs failed, while 9.4% (3/32) with posterior instability alone failed. Regarding stability, 8.3% (2/24) of athletes with RCTs failed, while 6.3% (2/32) with posterior instability alone failed. 

SURGICAL FINDINGS AND PROCEDURES

Of the 24 throwing athletes with rotator cuff pathology, 92% (22/24) had labral tears, while 78% (25/32) of those without RCTs had labral tears. The majority of RCTs were in the posterior supraspinatus and anterior infraspinatus regions. This was not significantly different between groups (c2 = 1.86, P = .172). All labral pathology was posterior-inferior, and all RCTs were <50% thickness, and therefore were débrided. Fifty-four percent (13/24) of those with RCTs had a patulous capsule and 63% (20/32) of throwing athletes without rotator cuff pathology had a patulous capsule. There was no significant difference between groups (c2 = .393, P = .530). Of those with RCTs, 92% (22/24) had surgical fixation with anchors, while 78% (25/32) of those without rotator cuff pathology underwent repair with anchor fixation. There was no statistically significant difference in anchor use between groups (c2 = 1.86, P = .172).

Continue to: Discussion

 

 

DISCUSSION

Throwing athletes with and without RCTs had similar rates of recovery and return to play after arthroscopic capsular labral repair, with rotator cuff débridement if a tear was present. The mean follow-up was 3.2 years. Further, there was no difference in return to play (92% vs 84%), ASES score, stability, pain, function, ROM, or strength between the 2 groups before or after surgery. In this cohort of 56 patients, 24 throwing athletes (43%) were found to have RCTs.

Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport, and 67% (16/24) returned to the same level. Eight percent of throwing athletes with RCTs were unable to return to sport after surgery. These return-to-play rates are an improvement over most previously reported rates in throwing athletes and in posterior shoulder instability in general.1-4,11 When these athletes are compared with their counterparts with combined SLAP tears and RCTs, return-to-play rates are notably higher. There may be discrepancies in interpreting return-to-play between the two studies, but in the current study, 67% of those with concomitant RCTs achieved return to preinjury level of play. This is 10% higher than the rate reported in athletes with SLAP tears alone (57%) and even higher than in those with concomitant SLAP and RCTs. It is also essential to note that a number of this cohort’s athletes who did not return to play did so for factors (eg, graduation) unrelated to the shoulder. However, the study by Neri and colleagues5 included professional athletes who likely all attempted to return to play and, if unable to perform at the same level, likely were unable to continue their professional career.5

All patients with RCTs had a good or excellent outcome (ASES score), and 70.8% had an excellent outcome. Similarly, 97% of those without rotator cuff pathology had a good or excellent outcome, and 81.3% had an excellent outcome. There was no significant difference between the two groups. These results parallel those of Neri and colleagues’5 study of SLAP tears with RCTs, where 96% (22/23) of throwing athletes had a good or excellent outcome. Despite these high outcome scores in patients with SLAP tears, only 57% were able to return to elite pitching.5 In the current study, pain was slightly higher for those with rotator cuff pathology before surgery—a finding consistent with pain frequently being found in patients with isolated partial-thickness RCTs. Their postoperative pain scores were actually lower on average than those of patients without RCTs, which suggests simple débridement of undersurface tears adequately addressed the pathology. The authors theorize that the main pain generator in this population may be posterior instability, and that the rotator cuff has less of an influence. In the SLAP population, the main pain generator likely is the RCT.

Failures by ASES score or strength were fairly rare in this cohort. Many patients opted to have revision surgery because of continued instability, pain, decreased function, or reinjury. One potential cause of failure in this cohort is inadequate capsular shift. However, capsular plication in throwing athletes is difficult to address, as overtensioning the repair can lead to the inability to adequately perform overhead activites.3,4 This cannot be overemphasized, particularly with pitchers.

Partial-thickness RCTs, particularly those on the articular side, are common in throwing athletes because of high tensile and compressive loads.12 Despite the known risk of RCTs with posterior shoulder instability in throwing athletes, the authors are unaware of reports of the incidence or treatment of this pathology. RCTs in this posterior instability group likely represent a pathology other than internal impingement. The high proportion of throwing athletes with RCTs in this study (43%) indicates a need for close evaluation of rotator cuff pathology in young throwing athletes. Ide et al found that 75% of patients with SLAP tears had partial articular-sided RCTs.13 In the current study, all RCTs were small partial tears, and arthroscopic débridement was performed. It is unknown whether repair of these RCTs would impact return to play. However, rotator cuff repair in this population has been shown to have poor outcomes. Tear thickness typically is used to determine treatment, with débridement performed if <50% tendon thickness is affected. More recently, many have advocated having greater tendon involvement in throwers before repair, because of poor outcomes. Although studies are limited, tear size does seem to correlate with outcomes.14

Continue to: Study Limitations

 

 

STUDY LIMITATIONS

Limitations of this study include its small number of professional throwing athletes, with the majority being high school athletes. Further, although ASES scores are consistently used in posterior shoulder instability studies, these scores are influenced highly by pain scores, and some argue that other scoring systems may provide more useful information. However, none of the more modern scoring systems have been studied extensively in posterior glenohumeral instability. Further, because the authors used the present scoring systems previously,1-4 they were continued to be used for comparison and consistency. Outcomes such as ROM and strength may carry more weight if measured and documented by clinical examination. Further testing, such as clinical evaluation of the jerk test or the posterior load-and-shift test, and their comparison before and after surgery may provide more objective data.

CONCLUSION

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike a previous study of throwing athletes’ outcomes after surgery for concomitant SLAP tears and RCTs,5 this study of throwing athletes with concomitant posterior shoulder instability and RCTs found no difference in patient-reported outcome measures or return to play. In throwing athletes with posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

References

1. Bradley JP, Baker CL 3rd, Kline AJ, Armfield DR, Chhabra A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071.

2. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014.

3. McClincy MP, Arner JW, Bradley JP. Posterior shoulder instability in throwing athletes: a case-matched comparison of throwers and non-throwers. Arthroscopy. 2015;31(6):1041-1051.

4. Radkowski CA, Chhabra A, Baker CL 3rd, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699.

5. Neri BR, ElAttrache NS, Owsley KC, Mohr K, Yocum LA. Outcome of type II superior labral anterior posterior repairs in elite overhead athletes: effect of concomitant partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(1):114-120.

6. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192.

7. Antoniou J, Duckworth DT, Harryman DT 2nd. Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am. 2000;82(9):1220-1230.

8. Altchek DW, Hobbs WR. Evaluation and management of shoulder instability in the elite overhead thrower. Orthop Clin North Am. 2001;32(3):423-430, viii.

9. Fuchs B, Jost B, Gerber C. Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am. 2000;82(1):16-25.

10. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

11. Arner JW, McClincy MP, Bradley JP. Arthroscopic stabilization of posterior shoulder instability is successful in American football players. Arthroscopy. 2015;31(8):1466-1471.

12. Mazoue CG, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34(2):182-189.

13. Ide J, Maeda S, Takagi K. Sports activity after arthroscopic superior labral repair using suture anchors in overhead-throwing athletes. Am J Sports Med. 2005;33(4):507-514.

14. Economopoulos KJ, Brockmeier SF. Rotator cuff tears in overhead athletes. Clin Sports Med. 2012;31(4):675-692.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

Dr. Arner is an Orthopaedic Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. McClincy is a Fellow, Sports Medicine Division, Harvard University, Boston Children’s Hospital, Boston, Massachusetts. Dr. Bradley is a Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

Justin W. Arner, MD Michael P. McClincy, MD James P. Bradley, MD . In Throwers With Posterior Instability, Rotator Cuff Tears Are Common but Do Not Affect Surgical Outcomes. Am J Orthop. January 30, 2018

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Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

Dr. Arner is an Orthopaedic Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. McClincy is a Fellow, Sports Medicine Division, Harvard University, Boston Children’s Hospital, Boston, Massachusetts. Dr. Bradley is a Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

Justin W. Arner, MD Michael P. McClincy, MD James P. Bradley, MD . In Throwers With Posterior Instability, Rotator Cuff Tears Are Common but Do Not Affect Surgical Outcomes. Am J Orthop. January 30, 2018

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

Dr. Arner is an Orthopaedic Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. McClincy is a Fellow, Sports Medicine Division, Harvard University, Boston Children’s Hospital, Boston, Massachusetts. Dr. Bradley is a Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

Justin W. Arner, MD Michael P. McClincy, MD James P. Bradley, MD . In Throwers With Posterior Instability, Rotator Cuff Tears Are Common but Do Not Affect Surgical Outcomes. Am J Orthop. January 30, 2018

ABSTRACT

In a previous study, compared with throwing athletes with superior labral anterior posterior (SLAP) tears, those with concomitant SLAP tears and rotator cuff tears (RCTs) had significantly poorer outcome scores and return to play. Posterior shoulder instability also occurs in throwing athletes, but no studies currently exist regarding outcomes of these patients with concomitant RCTs.

The authors hypothesized that throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent rotator cuff pathology would have poorer outcome scores and return to play.

Fifty-six consecutive throwing athletes with unidirectional posterior shoulder instability underwent arthroscopic capsulolabral repair. Preoperative and postoperative patient-centered outcomes of pain, stability, function, range of motion, strength, and American Shoulder and Elbow Surgeons Shoulder (ASES) scores, as well as return to play, were evaluated. Patients with and without rotator cuff pathology were compared.

Forty-three percent (24/56) of throwing athletes had rotator cuff pathology in addition to posterior capsulolabral pathology. All RCTs were débrided. At a mean of 3 years, there were no differences in preoperative and postoperative patient-centered outcomes between those with and without RCTs. Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport (P = .414) and 67% (16/24) returned to the same level (P = .430).

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike the previous study evaluating throwers outcomes after surgical treatment for concomitant SLAP tears and RCTs, the authors found no difference in patient-reported outcome measures or return to play for throwing athletes with concomitant posterior shoulder instability and RCTs. In throwing athletes with concomitant posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

Continue to: Posterior shoulder instability...

 

 

Posterior shoulder instability is an important and increasingly recognized pathology among throwers. Like the superior labrum, the posterior capsulolabral complex is also susceptible to injury during the throwing motion; the posterior labrum being most at risk during the late cocking and follow-through phases. Recent studies have found that arthroscopic capsulolabral reconstruction in posterior shoulder instability is successful in allowing athletes to return to their preinjury sports activities, with 2 studies detailing outcomes in throwing athletes.1-4 However, superior labral anterior posterior (SLAP) tears are common in throwing athletes and have been treated with varying and limited success. Further, in a study of outcomes of arthroscopic repair of SLAP lesions, Neri and colleagues5 found that, compared with throwing athletes with SLAP tears, throwing athletes with concomitant SLAP tears and partial-thickness rotator cuff tears (RCTs) had significantly poorer outcomes and return-to-play rates after surgical repair.

The purpose of this study was to determine outcome scores and return to play of throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent RCTs and to compare them with outcome scores as well as return to play of throwing athletes with isolated posterior shoulder instability. It was hypothesized that throwing athletes with a combination of posterior shoulder instability and RCT would have poorer outcomes and poorer return to play after surgery.5

METHODS

PATIENT SELECTION

After Institutional Review Board approval, informed consent was obtained, and consecutive throwing athletes who underwent arthroscopic posterior capsulolabral reconstruction for posterior shoulder instability were followed in the perioperative period. Inclusion criteria were throwing athletes participating in competitive sports at the high school, collegiate, or professional level, minimum 1-year follow-up, presence of unidirectional posterior instability, and absence of symptoms of instability in any direction other than posterior. Patients with inferior instability, SLAP pathology on examination and on magnetic resonance imaging, multidirectional instability, or habitual or psychogenic voluntary shoulder subluxations were excluded. Patients with diagnoses of both posterior shoulder instability and impingement treated with subacromial decompression and distal clavicle resection were also excluded.

After this cohort was identified, patient records were reviewed for pertinent operative data, such as procedure, complications, and evidence of RCT by operative report and arthroscopic photographs. A partial RCT was defined as a tear of 10% to 50%; those with rotator cuff fraying were determined not to be significant.

PATIENT EVALUATION

Surgeries were performed between January 1998 and December 2009 by the senior author (JPB). All patients were followed with clinical examinations, radiographs, and subjective grading scales. Recorded patient demographic data included age, sex, sport, position, competition level, and follow-up duration.

Continue to: All patients had...

 

 

All patients had symptomatic posterior shoulder instability, including posterior shoulder pain, clicking, a sensation of subluxation, or instability/apprehension with motion. Each athlete’s shoulder was palpated for tenderness and tested for impingement. Specific posterior glenohumeral instability tests, including the Kim test,6 the circumduction test, the jerk test,7 the posterior load-and-shift test,8 and the posterior stress test,9 were performed on all patients. Patients with multidirectional instability on the sulcus test, as well as provocative tests indicating SLAP pathology, such as the Crank test and the active compression test, were not included. Standard radiography and magnetic resonance arthrography (MRA) were performed to further narrow inclusion and exclusion criteria.

Both before surgery and at latest follow-up, patient outcomes were evaluated using the American Shoulder and Elbow Surgeons (ASES) score (range, 0-100) which combines a subjective functional scale measuring activities of daily living (0-3 for each of 10 tasks, with a total of 0-30) and a subjective pain scale (0-10, with 10 being worst pain). Values >80 were described as excellent, and failures were defined as scores <60 after surgery.10 A subjective stability scale (0-10, with 0 indicating completely stable and 10 completely unstable), strength scale (0-3, with 0 indicating none, 1 markedly decreased, 2 slightly decreased, and 3 normal), and ROM scale (0-3, with 0 indicating poor, 1 limited, 2 satisfactory, and 3 full) were evaluated both before surgery and at the latest follow-up. A stability score >5 after surgery was defined as a failure.1,2,11 Patients were also asked if, based on their current state, they would undergo surgery again. Intraoperative findings and specific surgical procedures performed were correlated with the aforementioned subjective and objective outcome scores.

OPERATIVE TREATMENT

Throwing athletes who met inclusion criteria and failed nonoperative management underwent surgery by the senior author (JPB). Each patient was examined under anesthesia and, with the patient in the lateral decubitus position, a diagnostic arthroscopy was performed to identify posterior capsulolabral complex pathology, including a patulous capsule, capsular tears, labral fraying, and labral tears. A careful examination for rotator cuff pathology was also performed. Based on preoperative clinical examination, MRA, examination under anesthesia, pathologic findings at diagnostic arthroscopic surgery, and surgeon experience, capsulolabral plication was performed with or without suture anchors.2,5 After capsulolabral repair, the capsule was evaluated for residual laxity, and additional plication sutures were placed, as indicated, with care to avoid overconstraint in these throwing athletes.1 Posterior glenohumeral stability restoration was judged by removing traction and performing posterior load-and-shift and posterior stress tests. Any RCT with <50% thickness was débrided. Postoperative care and rehabilitation were carried out as previously described and were not altered by the presence or absence of a RCT.3

STATISTICAL ANALYSIS

Preoperative and latest follow-up ASES scores, stability scores, functional scores, and pain-level findings were compared using paired-samples Comparisons between groups, including throwing athletes with and without rotator cuff pathology, were done using the Student t test. Outcome comparisons between multiple groups, which included intraoperative findings and surgical fixation methods, were analyzed with c2 modeling for nonparametric data. Statistical significance was set at P < .05. A power analysis found that this study was able to detect a meaningful difference of 10 ASES points.

RESULTS

PATIENT DEMOGRAPHIC CHARACTERISTICS

Of the 56 throwing athletes who met the inclusion criteria, 24 were found to have rotator cuff pathology in addition to posterior capsulolabral pathology, while 32 were found to have capsulolabral pathology alone. Demographic data are listed in Table 1. Mean age was 20.1 years for patients with rotator cuff pathology and 17.8 years for patients without RCTs. All 24 athletes with rotator cuff pathology were treated with arthroscopic débridement. Mean follow-up was 38.6 months (range, 16.5-63.6 months) for patients with RCTs and 39.1 months (range, 12-98.8 months) for patients without RCTs. No significant difference was found in age, sports level, or follow-up between groups.

Table 1. Demographic Data for Athletes With Posterior Instability With and Without Rotator Cuff Tears (N = 56 Shoulders)a

Characteristic

Rotator Cuff Tears

 

Yes

No

Total2432
Sex 
Male1627
Female85
Mean age, y20.117.8
Mean follow up, mo38.639.1
Participation level 
 Professional10
 College44
 High school1726
 Recreational22

aThe majority of athletes were males in high school and their mean follow-up was 3 years.

Continue to: Outcomes

 

 

OUTCOMES

Table 2 lists the preoperative and postoperative scores for shoulder performance in throwing athletes with posterior shoulder instability, with and without RCTs.

Table 2. Preoperative and Postoperative Scores for Shoulder Performance in Throwing Athletes With Posterior Shoulder Instability With and Without Rotator Cuff Tearsa
 With Rotator Cuff Tears (n=24 shoulders)Without Rotator Cuff Tears (n=32 shoulders)
 Preoperative Latest Follow-Up PreoperativeLatest Follow-Up 
Outcome MeasureMean ScoreRangeMean ScoreRangePMean ScoreRangeMean ScoreRangeP

ASES

0-100

0 = worst

41.820-7085.467-100<.0549.720-8583.125-100<.05

Stability

0-10

0 = most stable

6.72-102.40-6<.057.80-102.40-8<.05

Pain

0-10

10 = worst

7.65-101.90-5<.056.30-102.20-7<.05

Function

0-30

0 = worst

18.56-272716-30<.0519.08-2626.46-30<.05

aThere was no difference in ASES, stability, pain, or functional scores between athletes with posterior instability alone compared with patients with concomitant rotator cuff tears.

Abbreviation: ASES, American Shoulder and Elbow Surgeons.

ASES Scores. Mean preoperative ASES scores for patients with RCTs improved significantly (t = –13.8, P < .001), as did those for patients without rotator cuff pathology (t = –8.9, P < .001). No significant differences in ASES score were found between patients with and without rotator cuff pathology before or after surgery (t = 1.9, P = .07; t = .58, P = .06). In addition, 70.8% (17/24) of throwing athletes with rotator cuff pathology had an excellent postoperative outcome (ASES score >80), and 29.2% (7/24) had a satisfactory outcome (ASES score, 60-80). Thus, 100% of those with concomitant posterior shoulder instability and RCTs had a good or excellent outcome after surgical intervention. In those without rotator cuff pathology, 78.1% (25/32) had an excellent outcome, 12.5% (4/32) had a satisfactory outcome, and 9.4% (3/32) had a poor outcome. Thus, 91% of those without rotator cuff pathology had a good or excellent outcome after surgery.

Stability. Preoperative stability scores improved significantly after surgery in both groups (t = 7.2, P < .001; t = 10.5, P < .001). There were no statistical differences between preoperative or postoperative stability scores in those with or without rotator cuff pathology (t = 1.7, P = .095; t = .03, P = .975). Of throwing athletes with RCTs, 54.2% (13/24) had an excellent outcome, 33.3% (8/24) a good outcome, and 12.5% (3/24) a satisfactory outcome. Thus, 87.5% (21/24) of those with RCTs had a good or excellent outcome in terms of stability. In those without rotator cuff pathology, 46.9% (15/32) had excellent stability, 46.9% (15/32) had good stability, and 3.1% (1/32) had satisfactory stability after surgery. Thus, 93.8% (30/32) of throwing athletes without rotator cuff pathology had good or excellent stability after surgery.

Pain. Mean preoperative pain scores for those with and without rotator cuff pathology improved significantly (t = 13.4, P < .001; t = 7.1, P < .001). There was no statistical difference in preoperative or postoperative pain scores between those with and without rotator cuff pathology (t = 1.99, P = .051; t = .49, P = .627).

Function. Mean preoperative function scores for both groups improved significantly (t = 7.7, P < .001; t = 8.0, P < .001). There was no difference in improvement in functional scores between the two groups before or after surgery (t = .36, P = .721; t = .5, P = .622).

Continue to: ROM

 

 

ROM. Of those with rotator cuff pathology, 54% (13/24) had normal ROM, 42% (10/24) had satisfactory ROM, and 4% (1/24) had limited ROM. In throwing athletes without rotator cuff pathology, 34% (11/32) had normal ROM, 53.1% (17/32) had satisfactory ROM, and 9% (3/32) had limited ROM after surgery. There was no significant difference in ROM between the groups (c2 = 2.7, P = .260).

Strength. Of those with RCTs, 67% (16/24) reported normal strength, 29% (7/24) slightly decreased strength, and 4% (1/24) markedly decreased strength. Of those throwing athletes without rotator cuff pathology, 50% (16/32) had normal strength, 41% (13/32) had slightly decreased strength, and 9% (3/32) had markedly decreased strength. No statistical difference was noted between the two groups (c2 = 1.7, P = .429).

Return to Sport. Of those with RCTs, 92% (22/24) returned to sport while 84% (27/32) of throwing athletes without RCTs returned to sport. There was no difference between the two groups (c2 = .667, P = .414). Sixty-seven percent (16/24) of those with RCTs and 56% (18/32) of those without RCTs returned to the same level of sport. No statistical difference was found in return to play between throwing athletes with and without rotator cuff pathology (c2 = .624, P = .430).

Failures. According to ASES scores, no throwers with RCTs failed, while 9.4% (3/32) with posterior instability alone failed. Regarding stability, 8.3% (2/24) of athletes with RCTs failed, while 6.3% (2/32) with posterior instability alone failed. 

SURGICAL FINDINGS AND PROCEDURES

Of the 24 throwing athletes with rotator cuff pathology, 92% (22/24) had labral tears, while 78% (25/32) of those without RCTs had labral tears. The majority of RCTs were in the posterior supraspinatus and anterior infraspinatus regions. This was not significantly different between groups (c2 = 1.86, P = .172). All labral pathology was posterior-inferior, and all RCTs were <50% thickness, and therefore were débrided. Fifty-four percent (13/24) of those with RCTs had a patulous capsule and 63% (20/32) of throwing athletes without rotator cuff pathology had a patulous capsule. There was no significant difference between groups (c2 = .393, P = .530). Of those with RCTs, 92% (22/24) had surgical fixation with anchors, while 78% (25/32) of those without rotator cuff pathology underwent repair with anchor fixation. There was no statistically significant difference in anchor use between groups (c2 = 1.86, P = .172).

Continue to: Discussion

 

 

DISCUSSION

Throwing athletes with and without RCTs had similar rates of recovery and return to play after arthroscopic capsular labral repair, with rotator cuff débridement if a tear was present. The mean follow-up was 3.2 years. Further, there was no difference in return to play (92% vs 84%), ASES score, stability, pain, function, ROM, or strength between the 2 groups before or after surgery. In this cohort of 56 patients, 24 throwing athletes (43%) were found to have RCTs.

Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport, and 67% (16/24) returned to the same level. Eight percent of throwing athletes with RCTs were unable to return to sport after surgery. These return-to-play rates are an improvement over most previously reported rates in throwing athletes and in posterior shoulder instability in general.1-4,11 When these athletes are compared with their counterparts with combined SLAP tears and RCTs, return-to-play rates are notably higher. There may be discrepancies in interpreting return-to-play between the two studies, but in the current study, 67% of those with concomitant RCTs achieved return to preinjury level of play. This is 10% higher than the rate reported in athletes with SLAP tears alone (57%) and even higher than in those with concomitant SLAP and RCTs. It is also essential to note that a number of this cohort’s athletes who did not return to play did so for factors (eg, graduation) unrelated to the shoulder. However, the study by Neri and colleagues5 included professional athletes who likely all attempted to return to play and, if unable to perform at the same level, likely were unable to continue their professional career.5

All patients with RCTs had a good or excellent outcome (ASES score), and 70.8% had an excellent outcome. Similarly, 97% of those without rotator cuff pathology had a good or excellent outcome, and 81.3% had an excellent outcome. There was no significant difference between the two groups. These results parallel those of Neri and colleagues’5 study of SLAP tears with RCTs, where 96% (22/23) of throwing athletes had a good or excellent outcome. Despite these high outcome scores in patients with SLAP tears, only 57% were able to return to elite pitching.5 In the current study, pain was slightly higher for those with rotator cuff pathology before surgery—a finding consistent with pain frequently being found in patients with isolated partial-thickness RCTs. Their postoperative pain scores were actually lower on average than those of patients without RCTs, which suggests simple débridement of undersurface tears adequately addressed the pathology. The authors theorize that the main pain generator in this population may be posterior instability, and that the rotator cuff has less of an influence. In the SLAP population, the main pain generator likely is the RCT.

Failures by ASES score or strength were fairly rare in this cohort. Many patients opted to have revision surgery because of continued instability, pain, decreased function, or reinjury. One potential cause of failure in this cohort is inadequate capsular shift. However, capsular plication in throwing athletes is difficult to address, as overtensioning the repair can lead to the inability to adequately perform overhead activites.3,4 This cannot be overemphasized, particularly with pitchers.

Partial-thickness RCTs, particularly those on the articular side, are common in throwing athletes because of high tensile and compressive loads.12 Despite the known risk of RCTs with posterior shoulder instability in throwing athletes, the authors are unaware of reports of the incidence or treatment of this pathology. RCTs in this posterior instability group likely represent a pathology other than internal impingement. The high proportion of throwing athletes with RCTs in this study (43%) indicates a need for close evaluation of rotator cuff pathology in young throwing athletes. Ide et al found that 75% of patients with SLAP tears had partial articular-sided RCTs.13 In the current study, all RCTs were small partial tears, and arthroscopic débridement was performed. It is unknown whether repair of these RCTs would impact return to play. However, rotator cuff repair in this population has been shown to have poor outcomes. Tear thickness typically is used to determine treatment, with débridement performed if <50% tendon thickness is affected. More recently, many have advocated having greater tendon involvement in throwers before repair, because of poor outcomes. Although studies are limited, tear size does seem to correlate with outcomes.14

Continue to: Study Limitations

 

 

STUDY LIMITATIONS

Limitations of this study include its small number of professional throwing athletes, with the majority being high school athletes. Further, although ASES scores are consistently used in posterior shoulder instability studies, these scores are influenced highly by pain scores, and some argue that other scoring systems may provide more useful information. However, none of the more modern scoring systems have been studied extensively in posterior glenohumeral instability. Further, because the authors used the present scoring systems previously,1-4 they were continued to be used for comparison and consistency. Outcomes such as ROM and strength may carry more weight if measured and documented by clinical examination. Further testing, such as clinical evaluation of the jerk test or the posterior load-and-shift test, and their comparison before and after surgery may provide more objective data.

CONCLUSION

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike a previous study of throwing athletes’ outcomes after surgery for concomitant SLAP tears and RCTs,5 this study of throwing athletes with concomitant posterior shoulder instability and RCTs found no difference in patient-reported outcome measures or return to play. In throwing athletes with posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

ABSTRACT

In a previous study, compared with throwing athletes with superior labral anterior posterior (SLAP) tears, those with concomitant SLAP tears and rotator cuff tears (RCTs) had significantly poorer outcome scores and return to play. Posterior shoulder instability also occurs in throwing athletes, but no studies currently exist regarding outcomes of these patients with concomitant RCTs.

The authors hypothesized that throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent rotator cuff pathology would have poorer outcome scores and return to play.

Fifty-six consecutive throwing athletes with unidirectional posterior shoulder instability underwent arthroscopic capsulolabral repair. Preoperative and postoperative patient-centered outcomes of pain, stability, function, range of motion, strength, and American Shoulder and Elbow Surgeons Shoulder (ASES) scores, as well as return to play, were evaluated. Patients with and without rotator cuff pathology were compared.

Forty-three percent (24/56) of throwing athletes had rotator cuff pathology in addition to posterior capsulolabral pathology. All RCTs were débrided. At a mean of 3 years, there were no differences in preoperative and postoperative patient-centered outcomes between those with and without RCTs. Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport (P = .414) and 67% (16/24) returned to the same level (P = .430).

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike the previous study evaluating throwers outcomes after surgical treatment for concomitant SLAP tears and RCTs, the authors found no difference in patient-reported outcome measures or return to play for throwing athletes with concomitant posterior shoulder instability and RCTs. In throwing athletes with concomitant posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

Continue to: Posterior shoulder instability...

 

 

Posterior shoulder instability is an important and increasingly recognized pathology among throwers. Like the superior labrum, the posterior capsulolabral complex is also susceptible to injury during the throwing motion; the posterior labrum being most at risk during the late cocking and follow-through phases. Recent studies have found that arthroscopic capsulolabral reconstruction in posterior shoulder instability is successful in allowing athletes to return to their preinjury sports activities, with 2 studies detailing outcomes in throwing athletes.1-4 However, superior labral anterior posterior (SLAP) tears are common in throwing athletes and have been treated with varying and limited success. Further, in a study of outcomes of arthroscopic repair of SLAP lesions, Neri and colleagues5 found that, compared with throwing athletes with SLAP tears, throwing athletes with concomitant SLAP tears and partial-thickness rotator cuff tears (RCTs) had significantly poorer outcomes and return-to-play rates after surgical repair.

The purpose of this study was to determine outcome scores and return to play of throwing athletes treated with arthroscopic capsulolabral repair for posterior shoulder instability with coexistent RCTs and to compare them with outcome scores as well as return to play of throwing athletes with isolated posterior shoulder instability. It was hypothesized that throwing athletes with a combination of posterior shoulder instability and RCT would have poorer outcomes and poorer return to play after surgery.5

METHODS

PATIENT SELECTION

After Institutional Review Board approval, informed consent was obtained, and consecutive throwing athletes who underwent arthroscopic posterior capsulolabral reconstruction for posterior shoulder instability were followed in the perioperative period. Inclusion criteria were throwing athletes participating in competitive sports at the high school, collegiate, or professional level, minimum 1-year follow-up, presence of unidirectional posterior instability, and absence of symptoms of instability in any direction other than posterior. Patients with inferior instability, SLAP pathology on examination and on magnetic resonance imaging, multidirectional instability, or habitual or psychogenic voluntary shoulder subluxations were excluded. Patients with diagnoses of both posterior shoulder instability and impingement treated with subacromial decompression and distal clavicle resection were also excluded.

After this cohort was identified, patient records were reviewed for pertinent operative data, such as procedure, complications, and evidence of RCT by operative report and arthroscopic photographs. A partial RCT was defined as a tear of 10% to 50%; those with rotator cuff fraying were determined not to be significant.

PATIENT EVALUATION

Surgeries were performed between January 1998 and December 2009 by the senior author (JPB). All patients were followed with clinical examinations, radiographs, and subjective grading scales. Recorded patient demographic data included age, sex, sport, position, competition level, and follow-up duration.

Continue to: All patients had...

 

 

All patients had symptomatic posterior shoulder instability, including posterior shoulder pain, clicking, a sensation of subluxation, or instability/apprehension with motion. Each athlete’s shoulder was palpated for tenderness and tested for impingement. Specific posterior glenohumeral instability tests, including the Kim test,6 the circumduction test, the jerk test,7 the posterior load-and-shift test,8 and the posterior stress test,9 were performed on all patients. Patients with multidirectional instability on the sulcus test, as well as provocative tests indicating SLAP pathology, such as the Crank test and the active compression test, were not included. Standard radiography and magnetic resonance arthrography (MRA) were performed to further narrow inclusion and exclusion criteria.

Both before surgery and at latest follow-up, patient outcomes were evaluated using the American Shoulder and Elbow Surgeons (ASES) score (range, 0-100) which combines a subjective functional scale measuring activities of daily living (0-3 for each of 10 tasks, with a total of 0-30) and a subjective pain scale (0-10, with 10 being worst pain). Values >80 were described as excellent, and failures were defined as scores <60 after surgery.10 A subjective stability scale (0-10, with 0 indicating completely stable and 10 completely unstable), strength scale (0-3, with 0 indicating none, 1 markedly decreased, 2 slightly decreased, and 3 normal), and ROM scale (0-3, with 0 indicating poor, 1 limited, 2 satisfactory, and 3 full) were evaluated both before surgery and at the latest follow-up. A stability score >5 after surgery was defined as a failure.1,2,11 Patients were also asked if, based on their current state, they would undergo surgery again. Intraoperative findings and specific surgical procedures performed were correlated with the aforementioned subjective and objective outcome scores.

OPERATIVE TREATMENT

Throwing athletes who met inclusion criteria and failed nonoperative management underwent surgery by the senior author (JPB). Each patient was examined under anesthesia and, with the patient in the lateral decubitus position, a diagnostic arthroscopy was performed to identify posterior capsulolabral complex pathology, including a patulous capsule, capsular tears, labral fraying, and labral tears. A careful examination for rotator cuff pathology was also performed. Based on preoperative clinical examination, MRA, examination under anesthesia, pathologic findings at diagnostic arthroscopic surgery, and surgeon experience, capsulolabral plication was performed with or without suture anchors.2,5 After capsulolabral repair, the capsule was evaluated for residual laxity, and additional plication sutures were placed, as indicated, with care to avoid overconstraint in these throwing athletes.1 Posterior glenohumeral stability restoration was judged by removing traction and performing posterior load-and-shift and posterior stress tests. Any RCT with <50% thickness was débrided. Postoperative care and rehabilitation were carried out as previously described and were not altered by the presence or absence of a RCT.3

STATISTICAL ANALYSIS

Preoperative and latest follow-up ASES scores, stability scores, functional scores, and pain-level findings were compared using paired-samples Comparisons between groups, including throwing athletes with and without rotator cuff pathology, were done using the Student t test. Outcome comparisons between multiple groups, which included intraoperative findings and surgical fixation methods, were analyzed with c2 modeling for nonparametric data. Statistical significance was set at P < .05. A power analysis found that this study was able to detect a meaningful difference of 10 ASES points.

RESULTS

PATIENT DEMOGRAPHIC CHARACTERISTICS

Of the 56 throwing athletes who met the inclusion criteria, 24 were found to have rotator cuff pathology in addition to posterior capsulolabral pathology, while 32 were found to have capsulolabral pathology alone. Demographic data are listed in Table 1. Mean age was 20.1 years for patients with rotator cuff pathology and 17.8 years for patients without RCTs. All 24 athletes with rotator cuff pathology were treated with arthroscopic débridement. Mean follow-up was 38.6 months (range, 16.5-63.6 months) for patients with RCTs and 39.1 months (range, 12-98.8 months) for patients without RCTs. No significant difference was found in age, sports level, or follow-up between groups.

Table 1. Demographic Data for Athletes With Posterior Instability With and Without Rotator Cuff Tears (N = 56 Shoulders)a

Characteristic

Rotator Cuff Tears

 

Yes

No

Total2432
Sex 
Male1627
Female85
Mean age, y20.117.8
Mean follow up, mo38.639.1
Participation level 
 Professional10
 College44
 High school1726
 Recreational22

aThe majority of athletes were males in high school and their mean follow-up was 3 years.

Continue to: Outcomes

 

 

OUTCOMES

Table 2 lists the preoperative and postoperative scores for shoulder performance in throwing athletes with posterior shoulder instability, with and without RCTs.

Table 2. Preoperative and Postoperative Scores for Shoulder Performance in Throwing Athletes With Posterior Shoulder Instability With and Without Rotator Cuff Tearsa
 With Rotator Cuff Tears (n=24 shoulders)Without Rotator Cuff Tears (n=32 shoulders)
 Preoperative Latest Follow-Up PreoperativeLatest Follow-Up 
Outcome MeasureMean ScoreRangeMean ScoreRangePMean ScoreRangeMean ScoreRangeP

ASES

0-100

0 = worst

41.820-7085.467-100<.0549.720-8583.125-100<.05

Stability

0-10

0 = most stable

6.72-102.40-6<.057.80-102.40-8<.05

Pain

0-10

10 = worst

7.65-101.90-5<.056.30-102.20-7<.05

Function

0-30

0 = worst

18.56-272716-30<.0519.08-2626.46-30<.05

aThere was no difference in ASES, stability, pain, or functional scores between athletes with posterior instability alone compared with patients with concomitant rotator cuff tears.

Abbreviation: ASES, American Shoulder and Elbow Surgeons.

ASES Scores. Mean preoperative ASES scores for patients with RCTs improved significantly (t = –13.8, P < .001), as did those for patients without rotator cuff pathology (t = –8.9, P < .001). No significant differences in ASES score were found between patients with and without rotator cuff pathology before or after surgery (t = 1.9, P = .07; t = .58, P = .06). In addition, 70.8% (17/24) of throwing athletes with rotator cuff pathology had an excellent postoperative outcome (ASES score >80), and 29.2% (7/24) had a satisfactory outcome (ASES score, 60-80). Thus, 100% of those with concomitant posterior shoulder instability and RCTs had a good or excellent outcome after surgical intervention. In those without rotator cuff pathology, 78.1% (25/32) had an excellent outcome, 12.5% (4/32) had a satisfactory outcome, and 9.4% (3/32) had a poor outcome. Thus, 91% of those without rotator cuff pathology had a good or excellent outcome after surgery.

Stability. Preoperative stability scores improved significantly after surgery in both groups (t = 7.2, P < .001; t = 10.5, P < .001). There were no statistical differences between preoperative or postoperative stability scores in those with or without rotator cuff pathology (t = 1.7, P = .095; t = .03, P = .975). Of throwing athletes with RCTs, 54.2% (13/24) had an excellent outcome, 33.3% (8/24) a good outcome, and 12.5% (3/24) a satisfactory outcome. Thus, 87.5% (21/24) of those with RCTs had a good or excellent outcome in terms of stability. In those without rotator cuff pathology, 46.9% (15/32) had excellent stability, 46.9% (15/32) had good stability, and 3.1% (1/32) had satisfactory stability after surgery. Thus, 93.8% (30/32) of throwing athletes without rotator cuff pathology had good or excellent stability after surgery.

Pain. Mean preoperative pain scores for those with and without rotator cuff pathology improved significantly (t = 13.4, P < .001; t = 7.1, P < .001). There was no statistical difference in preoperative or postoperative pain scores between those with and without rotator cuff pathology (t = 1.99, P = .051; t = .49, P = .627).

Function. Mean preoperative function scores for both groups improved significantly (t = 7.7, P < .001; t = 8.0, P < .001). There was no difference in improvement in functional scores between the two groups before or after surgery (t = .36, P = .721; t = .5, P = .622).

Continue to: ROM

 

 

ROM. Of those with rotator cuff pathology, 54% (13/24) had normal ROM, 42% (10/24) had satisfactory ROM, and 4% (1/24) had limited ROM. In throwing athletes without rotator cuff pathology, 34% (11/32) had normal ROM, 53.1% (17/32) had satisfactory ROM, and 9% (3/32) had limited ROM after surgery. There was no significant difference in ROM between the groups (c2 = 2.7, P = .260).

Strength. Of those with RCTs, 67% (16/24) reported normal strength, 29% (7/24) slightly decreased strength, and 4% (1/24) markedly decreased strength. Of those throwing athletes without rotator cuff pathology, 50% (16/32) had normal strength, 41% (13/32) had slightly decreased strength, and 9% (3/32) had markedly decreased strength. No statistical difference was noted between the two groups (c2 = 1.7, P = .429).

Return to Sport. Of those with RCTs, 92% (22/24) returned to sport while 84% (27/32) of throwing athletes without RCTs returned to sport. There was no difference between the two groups (c2 = .667, P = .414). Sixty-seven percent (16/24) of those with RCTs and 56% (18/32) of those without RCTs returned to the same level of sport. No statistical difference was found in return to play between throwing athletes with and without rotator cuff pathology (c2 = .624, P = .430).

Failures. According to ASES scores, no throwers with RCTs failed, while 9.4% (3/32) with posterior instability alone failed. Regarding stability, 8.3% (2/24) of athletes with RCTs failed, while 6.3% (2/32) with posterior instability alone failed. 

SURGICAL FINDINGS AND PROCEDURES

Of the 24 throwing athletes with rotator cuff pathology, 92% (22/24) had labral tears, while 78% (25/32) of those without RCTs had labral tears. The majority of RCTs were in the posterior supraspinatus and anterior infraspinatus regions. This was not significantly different between groups (c2 = 1.86, P = .172). All labral pathology was posterior-inferior, and all RCTs were <50% thickness, and therefore were débrided. Fifty-four percent (13/24) of those with RCTs had a patulous capsule and 63% (20/32) of throwing athletes without rotator cuff pathology had a patulous capsule. There was no significant difference between groups (c2 = .393, P = .530). Of those with RCTs, 92% (22/24) had surgical fixation with anchors, while 78% (25/32) of those without rotator cuff pathology underwent repair with anchor fixation. There was no statistically significant difference in anchor use between groups (c2 = 1.86, P = .172).

Continue to: Discussion

 

 

DISCUSSION

Throwing athletes with and without RCTs had similar rates of recovery and return to play after arthroscopic capsular labral repair, with rotator cuff débridement if a tear was present. The mean follow-up was 3.2 years. Further, there was no difference in return to play (92% vs 84%), ASES score, stability, pain, function, ROM, or strength between the 2 groups before or after surgery. In this cohort of 56 patients, 24 throwing athletes (43%) were found to have RCTs.

Return-to-play rates showed no between-group differences; 92% (22/24) of athletes with concomitant RCTs returned to sport, and 67% (16/24) returned to the same level. Eight percent of throwing athletes with RCTs were unable to return to sport after surgery. These return-to-play rates are an improvement over most previously reported rates in throwing athletes and in posterior shoulder instability in general.1-4,11 When these athletes are compared with their counterparts with combined SLAP tears and RCTs, return-to-play rates are notably higher. There may be discrepancies in interpreting return-to-play between the two studies, but in the current study, 67% of those with concomitant RCTs achieved return to preinjury level of play. This is 10% higher than the rate reported in athletes with SLAP tears alone (57%) and even higher than in those with concomitant SLAP and RCTs. It is also essential to note that a number of this cohort’s athletes who did not return to play did so for factors (eg, graduation) unrelated to the shoulder. However, the study by Neri and colleagues5 included professional athletes who likely all attempted to return to play and, if unable to perform at the same level, likely were unable to continue their professional career.5

All patients with RCTs had a good or excellent outcome (ASES score), and 70.8% had an excellent outcome. Similarly, 97% of those without rotator cuff pathology had a good or excellent outcome, and 81.3% had an excellent outcome. There was no significant difference between the two groups. These results parallel those of Neri and colleagues’5 study of SLAP tears with RCTs, where 96% (22/23) of throwing athletes had a good or excellent outcome. Despite these high outcome scores in patients with SLAP tears, only 57% were able to return to elite pitching.5 In the current study, pain was slightly higher for those with rotator cuff pathology before surgery—a finding consistent with pain frequently being found in patients with isolated partial-thickness RCTs. Their postoperative pain scores were actually lower on average than those of patients without RCTs, which suggests simple débridement of undersurface tears adequately addressed the pathology. The authors theorize that the main pain generator in this population may be posterior instability, and that the rotator cuff has less of an influence. In the SLAP population, the main pain generator likely is the RCT.

Failures by ASES score or strength were fairly rare in this cohort. Many patients opted to have revision surgery because of continued instability, pain, decreased function, or reinjury. One potential cause of failure in this cohort is inadequate capsular shift. However, capsular plication in throwing athletes is difficult to address, as overtensioning the repair can lead to the inability to adequately perform overhead activites.3,4 This cannot be overemphasized, particularly with pitchers.

Partial-thickness RCTs, particularly those on the articular side, are common in throwing athletes because of high tensile and compressive loads.12 Despite the known risk of RCTs with posterior shoulder instability in throwing athletes, the authors are unaware of reports of the incidence or treatment of this pathology. RCTs in this posterior instability group likely represent a pathology other than internal impingement. The high proportion of throwing athletes with RCTs in this study (43%) indicates a need for close evaluation of rotator cuff pathology in young throwing athletes. Ide et al found that 75% of patients with SLAP tears had partial articular-sided RCTs.13 In the current study, all RCTs were small partial tears, and arthroscopic débridement was performed. It is unknown whether repair of these RCTs would impact return to play. However, rotator cuff repair in this population has been shown to have poor outcomes. Tear thickness typically is used to determine treatment, with débridement performed if <50% tendon thickness is affected. More recently, many have advocated having greater tendon involvement in throwers before repair, because of poor outcomes. Although studies are limited, tear size does seem to correlate with outcomes.14

Continue to: Study Limitations

 

 

STUDY LIMITATIONS

Limitations of this study include its small number of professional throwing athletes, with the majority being high school athletes. Further, although ASES scores are consistently used in posterior shoulder instability studies, these scores are influenced highly by pain scores, and some argue that other scoring systems may provide more useful information. However, none of the more modern scoring systems have been studied extensively in posterior glenohumeral instability. Further, because the authors used the present scoring systems previously,1-4 they were continued to be used for comparison and consistency. Outcomes such as ROM and strength may carry more weight if measured and documented by clinical examination. Further testing, such as clinical evaluation of the jerk test or the posterior load-and-shift test, and their comparison before and after surgery may provide more objective data.

CONCLUSION

Arthroscopic capsulolabral reconstruction is successful in throwing athletes with RCTs treated with arthroscopic débridement. Unlike a previous study of throwing athletes’ outcomes after surgery for concomitant SLAP tears and RCTs,5 this study of throwing athletes with concomitant posterior shoulder instability and RCTs found no difference in patient-reported outcome measures or return to play. In throwing athletes with posterior instability and RCTs, arthroscopic posterior capsulolabral repair with rotator cuff débridement is successful.

References

1. Bradley JP, Baker CL 3rd, Kline AJ, Armfield DR, Chhabra A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071.

2. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014.

3. McClincy MP, Arner JW, Bradley JP. Posterior shoulder instability in throwing athletes: a case-matched comparison of throwers and non-throwers. Arthroscopy. 2015;31(6):1041-1051.

4. Radkowski CA, Chhabra A, Baker CL 3rd, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699.

5. Neri BR, ElAttrache NS, Owsley KC, Mohr K, Yocum LA. Outcome of type II superior labral anterior posterior repairs in elite overhead athletes: effect of concomitant partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(1):114-120.

6. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192.

7. Antoniou J, Duckworth DT, Harryman DT 2nd. Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am. 2000;82(9):1220-1230.

8. Altchek DW, Hobbs WR. Evaluation and management of shoulder instability in the elite overhead thrower. Orthop Clin North Am. 2001;32(3):423-430, viii.

9. Fuchs B, Jost B, Gerber C. Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am. 2000;82(1):16-25.

10. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

11. Arner JW, McClincy MP, Bradley JP. Arthroscopic stabilization of posterior shoulder instability is successful in American football players. Arthroscopy. 2015;31(8):1466-1471.

12. Mazoue CG, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34(2):182-189.

13. Ide J, Maeda S, Takagi K. Sports activity after arthroscopic superior labral repair using suture anchors in overhead-throwing athletes. Am J Sports Med. 2005;33(4):507-514.

14. Economopoulos KJ, Brockmeier SF. Rotator cuff tears in overhead athletes. Clin Sports Med. 2012;31(4):675-692.

References

1. Bradley JP, Baker CL 3rd, Kline AJ, Armfield DR, Chhabra A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071.

2. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014.

3. McClincy MP, Arner JW, Bradley JP. Posterior shoulder instability in throwing athletes: a case-matched comparison of throwers and non-throwers. Arthroscopy. 2015;31(6):1041-1051.

4. Radkowski CA, Chhabra A, Baker CL 3rd, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699.

5. Neri BR, ElAttrache NS, Owsley KC, Mohr K, Yocum LA. Outcome of type II superior labral anterior posterior repairs in elite overhead athletes: effect of concomitant partial-thickness rotator cuff tears. Am J Sports Med. 2011;39(1):114-120.

6. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192.

7. Antoniou J, Duckworth DT, Harryman DT 2nd. Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am. 2000;82(9):1220-1230.

8. Altchek DW, Hobbs WR. Evaluation and management of shoulder instability in the elite overhead thrower. Orthop Clin North Am. 2001;32(3):423-430, viii.

9. Fuchs B, Jost B, Gerber C. Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am. 2000;82(1):16-25.

10. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3(6):347-352.

11. Arner JW, McClincy MP, Bradley JP. Arthroscopic stabilization of posterior shoulder instability is successful in American football players. Arthroscopy. 2015;31(8):1466-1471.

12. Mazoue CG, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34(2):182-189.

13. Ide J, Maeda S, Takagi K. Sports activity after arthroscopic superior labral repair using suture anchors in overhead-throwing athletes. Am J Sports Med. 2005;33(4):507-514.

14. Economopoulos KJ, Brockmeier SF. Rotator cuff tears in overhead athletes. Clin Sports Med. 2012;31(4):675-692.

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TAKE-HOME POINTS

  • Arthroscopic capsulolabral reconstruction is successful in throwing athletes with concomitant RCTs treated with arthroscopic débridement.
  • A previous study of throwing athletes found poor outcomes after surgery for concomitant SLAP tears and RCTs.
  • Throwing athletes with concomitant posterior shoulder instability and RCTs were no different in patient-reported outcomes or return to play.
  • The high proportion of throwing athletes with partial thickness RCTs in this study (43%) indicates a need for close evaluation of rotator cuff pathology in young throwing athletes.
  • The authors theorize the main pain generator in this population may be posterior instability and that the rotator cuff has less of an influence.
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Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview

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Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview

Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.

Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.

The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.

HUMERAL BONE LOSS

Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.

In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.

Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.

For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.

Continue to: GLENOID BONE LOSS

 

 

GLENOID BONE LOSS

Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.

We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.

Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4

Modified Walch classification of glenoid deformity in primary glenohumeral osteoarthritis with the B3 glenoid defined as a monoconcave ad posteriorly worn glenoid

In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.

In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.

Continue to: All these classification systems...

 

 

All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.

Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.

Frankle classification of glenoid morphology in reverse shoulder arthroplasty using 3-dimensional imaging

With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11

Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.

This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.

4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.

5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.

6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.

7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.

8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.

10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.

11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc. 

Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.

Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, dinesd@hss.edu).

David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018

David M. Dines, MD

Joshua S. Dines, MD

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Author and Disclosure Information

Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc. 

Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.

Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, dinesd@hss.edu).

David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018

David M. Dines, MD

Joshua S. Dines, MD

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. David M. Dines reports that he has a financial relationship involving royalties with Zimmer Biomet and Thieme Inc. Dr. Joshua S. Dines reports that he has a financial relationship with Arthrex, and receives royalties from Thieme Inc. 

Dr. D.M. Dines is Co-Director, Shoulder Fellowship, and an Attending, Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Professor of Orthopedic Surgery, Weill Cornell Medical College, New York, New York. Dr. J.S. Dines is an Attending Orthopedic Surgeon, Shoulder Fellowship and Sports and Shoulder Fellowship, Hospital for Special Surgery, New York, New York, and Assistant Professor, Weill Cornell Medical College, New York, New York.

Address correspondence to: David M. Dines, MD, Hospital for Special Surgery, 535 E 70th Street, New York, NY 10021 (tel, 516-482-1037; email, dinesd@hss.edu).

David M. Dines, MD Joshua S. Dines, MD . Shoulder Arthroplasty in Cases of Significant Bone Loss: An Overview. Am J Orthop. January 29, 2018

David M. Dines, MD

Joshua S. Dines, MD

Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.

Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.

The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.

HUMERAL BONE LOSS

Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.

In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.

Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.

For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.

Continue to: GLENOID BONE LOSS

 

 

GLENOID BONE LOSS

Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.

We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.

Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4

Modified Walch classification of glenoid deformity in primary glenohumeral osteoarthritis with the B3 glenoid defined as a monoconcave ad posteriorly worn glenoid

In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.

In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.

Continue to: All these classification systems...

 

 

All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.

Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.

Frankle classification of glenoid morphology in reverse shoulder arthroplasty using 3-dimensional imaging

With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11

Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.

This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.

Over the past few decades, there has been a dramatic increase in the number of shoulder arthroplasties performed around the world. This increase is the result of an aging and increasingly more active population, better implant technology, and the advent of reverse shoulder arthroplasty (RSA) for rotator cuff arthropathy. Additionally, as the indications for RSA have expanded to include pathologies such as rotator cuff insufficiency, chronic instabilities, trauma, and tumors, the number of arthroplasties will continue to increase. Although the results of most arthroplasties are good and predictable, any glenoid and/or humeral bone deficiencies can have detrimental effects on the clinical outcomes of these procedures. Bone loss becomes more of a problem in revision cases, and, as the number of primary arthroplasties increases, it follows that the number of revision procedures will also increase.

Many of the disease- or procedure-specific processes indicated for shoulder arthroplasty have predictable patterns of bone loss, especially on the glenoid side. Walch and colleagues1 and Bercik and colleagues2 made us aware that many patients with primary osteoarthritis have significant glenoid bone deformity. Similarly, there have been a number of first- and second-generation classification systems for delineating glenoid deformity in rotator cuff tear arthropathy and in revision settings. In revision settings, both glenoid and humeral bone deficiencies can occur as a result of implant removal, iatrogenic fracture, and even infection. Each of these bone loss patterns must be recognized and treated appropriately for the best surgical outcome.

The articles in this month of The American Journal of Orthopedics address the most up-to-date concepts and solutions regarding both humeral and glenoid bone loss in shoulder arthroplasty of all types.

HUMERAL BONE LOSS

Humeral bone loss is typically encountered in proximal humerus fractures, in revision surgery necessitating humeral component removal, and, less commonly, in tumors and infection.

In many displaced proximal humeral fractures indicated for shoulder arthroplasty, the bone is comminuted with displacement of the lesser and greater tuberosities. In these situations, failure of tuberosity healing may result in loss of rotator cuff function with loss of elevation, rotation, and even instability. Humeral shortening can also occur as a result of bone loss and can compromise deltoid function by loss of proper muscle tension, leading to instability, dysfunction, or both. In addition to possible instability, humeral shortening with metaphyseal bone loss can adversely affect long-term fixation of the humeral component, leading to stem loosening or failure. Cuff and colleagues3 showed significantly more rotational micromotion in cases lacking metaphyseal support, leading to aseptic loosening of the humeral stem.

Humeral bone loss can also result from humeral stem component removal in revision shoulder arthroplasty for infection, component failure or loosening, and even periprosthetic fracture resulting from surgery or trauma.

For the surgeon, humeral bone loss can create a complex set of circumstances related to rotator cuff attachment failure, soft-tissue balancing effects, and component fixation issues. Any such issue must be recognized and addressed for best outcomes. Best results can be obtained with preoperative imaging, planning, use of bone graft techniques, proximal humeral allografts, and, more recently, modular and patient-specific implants. All of these issues are discussed comprehensively in the articles this month.

Continue to: GLENOID BONE LOSS

 

 

GLENOID BONE LOSS

Proper glenoid component placement with durable fixation is crucial for success in anatomical total shoulder arthroplasty and RSA. Glenoid bone deformity and loss can result from intrinsic deformity characteristics seen in primary osteoarthritis, cuff tear arthropathy, or glenoid component removal in revision situations and infection. These bone deformity complications can be extremely difficult to treat and in some cases lead to catastrophic failure of the index arthroplasty.

We are now aware that one key to success in the face of moderate to severe deformity is proper recognition. Newer imaging techniques, including 2-dimensional (2-D) computed tomography (CT) and 3-dimensional (3-D) modeling and surgical planning software tools, which are outlined in an upcoming article, have given surgeons important new instruments that can help in treating these difficult cases.

Glenoid bone deformity in primary osteoarthritis was well delineated in the 1999 seminal study of CT changes by Walch and colleagues.1 The Walch classification system, which characterized glenoid morphology based on 2-D CT findings, was recently upgraded, based on 3-D imaging technology, to include Walch B3 and D patterns (Figure 1).2 Recognition of certain primary deformities in osteoarthritis has led to increased use of RSA in some cases of Walch B2, B3, and C deformities with substantial glenoid retroversion and/or humeral head subluxation.4

Modified Walch classification of glenoid deformity in primary glenohumeral osteoarthritis with the B3 glenoid defined as a monoconcave ad posteriorly worn glenoid

In cases of rotator cuff tear arthropathy, glenoid bone deformities are well described with several classification systems based on degree and dimension of bone insufficiency. The Hamada classification system defines the degree of medial glenoid erosion and superior bone loss, as well as acetabularization of the acromion in 5 grades; 5 Rispoli and colleagues6 defined and graded the degree of medicalization of the glenohumeral joint based on degree of subchondral plate erosion; and Visotsky and colleagues7 based their classification system on wear patterns of bone loss, alignment, and concomitant soft-tissue insufficiencies leading to instability and rotation loss.

In severe glenoid bone deficiency after glenoid component removal, Antuna and colleagues8 described the classic findings related to medial bone loss, anterior and posterior wall failure, and combinations thereof.

Continue to: All these classification systems...

 

 

All these classification systems are based on the 2-D appearance of the glenoid and should be considered cautiously. The glenoid is a complex 3-D structure that can be affected by any number of disease processes, trauma, and surgical intervention. Using more modern CT techniques and 3-D imaging, we now know that many deformities previously classified as unidirectional are, instead, complex and multidirectional.

Frankle and colleagues9 developed a classification based more 3-D CT models which has further classified severe glenoid vault deformities in relation to direction and degree of bone loss (Figures 2A-2E). Using this system, they were better able to determine degree and direction of deformity than in previous 2-D evaluations, and they were able to determine the amount of glenoid vault bone available for baseplate fixation. Scalise and colleagues10 further defined the influence of such 3-D planning in total shoulder arthroplasty.

Frankle classification of glenoid morphology in reverse shoulder arthroplasty using 3-dimensional imaging

With knowledge of these classification systems and use of contemporary imaging systems, shoulder arthroplasty in cases of severe glenoid deficiency can be more successful. Potentially, we can improve outcomes even more in the more severe cases of bone loss with use of patient-specific planning tools, including the guides and patient-specific implants that are now readily available with many implant systems.11

Preoperative planning tools, bone-grafting techniques, augmented and specialized glenoid and humeral implants, and patient-specific implants are discussed this month to give our readers a comprehensive review of the latest concepts in shoulder arthroplasty in cases of significant bone loss or deformity.

This month of The American Journal of Orthopedics presents the most current and cutting-edge solutions for humeral and glenoid bone deformities and deficiencies in contemporary shoulder arthroplasties.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.

4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.

5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.

6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.

7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.

8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.

10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.

11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

3. Cuff D, Levy JC, Gutiérrez S, Frankle M. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651.

4. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598.

5. Hamada K, Fukuda H, Mikasa M, Kobayashi Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;(254):92-96.

6. Rispoli D, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Humeral head replacement for the treatment of osteoarthritis. J Bone Joint Surg Am. 2006;88(12):2637-2644.

7. Visotsky JL, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am. 2004;86(suppl 2):35-40.

8. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

9. Frankle MA, Teramoto A, Luo ZP, Levy JC, Pupello D. Glenoid morphology in reverse shoulder arthroplasty: classification and surgical implications. J Shoulder Elbow Surg. 2009;18(6):874-885.

10. Scalise JJ, Codsi MJ, Bryan J, Brems JJ, Iannotti JP. The influence of three-dimensional computed tomography images of the shoulder in preoperative planning for total shoulder arthroplasty. J Bone Joint Surg Am. 2008;90(11):2438-2445.

11. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.

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Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages

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Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages

ABSTRACT

We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.

We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.

Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.

Continue to: Bone morphogenetic proteins...

 

 

Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30

Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.

METHODS

After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.

Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.

To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).

Continue to: RESULTS

 

 

RESULTS

All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:

Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications

PtSympton Onset, moSurgery Level(s)Side(s)Complication(s)
13L3-L5 (2)BothRadiculopathy, pseudo-pedicle, urine
23L4-L5 (2)RRadiculopathy, pseudo-pedicle
34L5-S1 (1)RRadiculopathy, pseudo-pedicle
45L5-S1 (1)LRadiculopathy, pseudo-pedicle
54L4-S1 (2)LRadiculopathy, pseudo-pedicle, subsidence
65L5-S1 (1)LRadiculopathy, pseudo-pedicle
74L5-S1 (1)LRadiculopathy, pseudo-pedicle
84L5-S1 (1)LRadiculopathy, pseudo-pedicle
93L5-S1 (1)LRadiculopathy, pseudo-pedicle
102L5-S1 (1)LRadiculopathy, pseudo-pedicle
112L5-S1 (1)LRadiculopathy, pseudo-pedicle, subsidence, neurologic
126L5-S1 (1)LRadiculopathy, pseudo-pedicle
133L5-S1 (1)LRadiculopathy, pseudo-pedicle, neurologic
142L2-L3 (1)RRadiculopathy, pseudo-pedicle
154L5-S1 (1)LRadiculopathy, pseudo-pedicle
163L4-L5 (1)LRadiculopathy, pseudo-pedicle
173L2-L3, L4-L5 (2)LRadiculopathy, pseudo-pedicle
183L4-L5, L2-L3 (1)LRadiculopathy, pseudo-pedicle, nonunion
194L4-L5 (1)RRadiculopathy, pseudo-pedicle
205L4-L5 (1)LRadiculopathy, pseudo-pedicle
215L5-S1 (1)RRadiculopathy, pseudo-pedicle
223L3-L4, L5-S1 (2)BothRadiculopathy, pseudo-pedicle
234L4-L5 (1)LRadiculopathy, pseudo-pedicle
246L5-S1 (1)LRadiculopathy, pseudo-pedicle
254L5-S1 (1)LRadiculopathy, pseudo-pedicle
263L5-S1 (1)LRadiculopathy, pseudo-pedicle, urine, bowel
274L5-S1 (1)LRadiculopathy, pseudo-pedicle
284L4-L5 (1)LRadiculopathy, pseudo-pedicle
296L5-S1 (1)LRadiculopathy, pseudo-pedicle
303L5-S1 (1)LRadiculopathy, pseudo-pedicle
313L5-S1 (1)LRadiculopathy, pseudo-pedicle
324L5-S1 (1)LRadiculopathy, pseudo-pedicle
333L5-S1 (1)LRadiculopathy, pseudo-pedicle
344L5-S1 (1)LRadiculopathy, pseudo-pedicle
354L5-S1 (1)LRadiculopathy, pseudo-pedicle
363L5-S1 (1)LRadiculopathy, pseudo-pedicle
374L4-L5 (1)LRadiculopathy, pseudo-pedicle
384L4-L5 (1)LRadiculopathy, pseudo-pedicle

1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.

Magnetic resonance imaging shows that recombinant human bone morphogenetic protein 2 used in the disk space during transforaminal lumbar interbody fusion can leak out of the space and cause heterotopic bone formation around nerve roots and the thecal sac

2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.

As heterotopic ossification is often interpreted as postoperative fibrous or granulation tissue on magnetic resonance imaging, computed tomography is needed to fully appreciate heterotopic bone.

3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.

Computed tomography shows pseudo-pedicle-like heterotopic ossification of varying extent. Bone arising from the annulotomy site for transforaminal lumbar interbody fusion was universally present in all pateints.

4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.

Continue to: Bone formation with rhBMP-2...

 

 

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

DISCUSSION

We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.

In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.

Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.

This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

References

1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.

2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.

3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.

4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.

5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.

6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.

7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.

8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.

9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.

10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.

11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.

12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.

13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.

14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.

15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.

16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.

17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.

18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.

19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.

20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.

21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.

22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.

23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.

24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.

25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.

26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.

27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.

28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.

29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.

30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.

31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.

32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.

33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. 

Dr. Rosen and Dr. Kiester are Clinical Professors, Department of Orthopaedic Surgery, University of California Irvine School of Medicine, Orange, California. Dr. Lee is Senior Research Career Scientist, Veterans Affairs Rehabilitation Research and Development, Professor and Vice Chairman for Research and Academic Affairs, Department of Orthopaedic Surgery, and Professor, Department of Biomedical Engineering, Henry Samueli School of Engineering, University of California Irvine, Orange, California.

Address correspondence to: Charles D. Rosen, MD, Department of Orthopaedic Surgery, University of California Irvine (UCI) Medical Center, 101 City Drive S, Pavilion III, Orange, CA 92868 (tel, 714-456-1699; email, crosen@uci.edu).

Charles D. Rosen, MD P. Douglas Kiester, MD Thay Q. Lee, PhD . Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages. Am J Orthop. January 29, 2018

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Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. 

Dr. Rosen and Dr. Kiester are Clinical Professors, Department of Orthopaedic Surgery, University of California Irvine School of Medicine, Orange, California. Dr. Lee is Senior Research Career Scientist, Veterans Affairs Rehabilitation Research and Development, Professor and Vice Chairman for Research and Academic Affairs, Department of Orthopaedic Surgery, and Professor, Department of Biomedical Engineering, Henry Samueli School of Engineering, University of California Irvine, Orange, California.

Address correspondence to: Charles D. Rosen, MD, Department of Orthopaedic Surgery, University of California Irvine (UCI) Medical Center, 101 City Drive S, Pavilion III, Orange, CA 92868 (tel, 714-456-1699; email, crosen@uci.edu).

Charles D. Rosen, MD P. Douglas Kiester, MD Thay Q. Lee, PhD . Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages. Am J Orthop. January 29, 2018

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. 

Dr. Rosen and Dr. Kiester are Clinical Professors, Department of Orthopaedic Surgery, University of California Irvine School of Medicine, Orange, California. Dr. Lee is Senior Research Career Scientist, Veterans Affairs Rehabilitation Research and Development, Professor and Vice Chairman for Research and Academic Affairs, Department of Orthopaedic Surgery, and Professor, Department of Biomedical Engineering, Henry Samueli School of Engineering, University of California Irvine, Orange, California.

Address correspondence to: Charles D. Rosen, MD, Department of Orthopaedic Surgery, University of California Irvine (UCI) Medical Center, 101 City Drive S, Pavilion III, Orange, CA 92868 (tel, 714-456-1699; email, crosen@uci.edu).

Charles D. Rosen, MD P. Douglas Kiester, MD Thay Q. Lee, PhD . Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages. Am J Orthop. January 29, 2018

ABSTRACT

We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.

We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.

Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.

Continue to: Bone morphogenetic proteins...

 

 

Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30

Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.

METHODS

After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.

Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.

To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).

Continue to: RESULTS

 

 

RESULTS

All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:

Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications

PtSympton Onset, moSurgery Level(s)Side(s)Complication(s)
13L3-L5 (2)BothRadiculopathy, pseudo-pedicle, urine
23L4-L5 (2)RRadiculopathy, pseudo-pedicle
34L5-S1 (1)RRadiculopathy, pseudo-pedicle
45L5-S1 (1)LRadiculopathy, pseudo-pedicle
54L4-S1 (2)LRadiculopathy, pseudo-pedicle, subsidence
65L5-S1 (1)LRadiculopathy, pseudo-pedicle
74L5-S1 (1)LRadiculopathy, pseudo-pedicle
84L5-S1 (1)LRadiculopathy, pseudo-pedicle
93L5-S1 (1)LRadiculopathy, pseudo-pedicle
102L5-S1 (1)LRadiculopathy, pseudo-pedicle
112L5-S1 (1)LRadiculopathy, pseudo-pedicle, subsidence, neurologic
126L5-S1 (1)LRadiculopathy, pseudo-pedicle
133L5-S1 (1)LRadiculopathy, pseudo-pedicle, neurologic
142L2-L3 (1)RRadiculopathy, pseudo-pedicle
154L5-S1 (1)LRadiculopathy, pseudo-pedicle
163L4-L5 (1)LRadiculopathy, pseudo-pedicle
173L2-L3, L4-L5 (2)LRadiculopathy, pseudo-pedicle
183L4-L5, L2-L3 (1)LRadiculopathy, pseudo-pedicle, nonunion
194L4-L5 (1)RRadiculopathy, pseudo-pedicle
205L4-L5 (1)LRadiculopathy, pseudo-pedicle
215L5-S1 (1)RRadiculopathy, pseudo-pedicle
223L3-L4, L5-S1 (2)BothRadiculopathy, pseudo-pedicle
234L4-L5 (1)LRadiculopathy, pseudo-pedicle
246L5-S1 (1)LRadiculopathy, pseudo-pedicle
254L5-S1 (1)LRadiculopathy, pseudo-pedicle
263L5-S1 (1)LRadiculopathy, pseudo-pedicle, urine, bowel
274L5-S1 (1)LRadiculopathy, pseudo-pedicle
284L4-L5 (1)LRadiculopathy, pseudo-pedicle
296L5-S1 (1)LRadiculopathy, pseudo-pedicle
303L5-S1 (1)LRadiculopathy, pseudo-pedicle
313L5-S1 (1)LRadiculopathy, pseudo-pedicle
324L5-S1 (1)LRadiculopathy, pseudo-pedicle
333L5-S1 (1)LRadiculopathy, pseudo-pedicle
344L5-S1 (1)LRadiculopathy, pseudo-pedicle
354L5-S1 (1)LRadiculopathy, pseudo-pedicle
363L5-S1 (1)LRadiculopathy, pseudo-pedicle
374L4-L5 (1)LRadiculopathy, pseudo-pedicle
384L4-L5 (1)LRadiculopathy, pseudo-pedicle

1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.

Magnetic resonance imaging shows that recombinant human bone morphogenetic protein 2 used in the disk space during transforaminal lumbar interbody fusion can leak out of the space and cause heterotopic bone formation around nerve roots and the thecal sac

2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.

As heterotopic ossification is often interpreted as postoperative fibrous or granulation tissue on magnetic resonance imaging, computed tomography is needed to fully appreciate heterotopic bone.

3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.

Computed tomography shows pseudo-pedicle-like heterotopic ossification of varying extent. Bone arising from the annulotomy site for transforaminal lumbar interbody fusion was universally present in all pateints.

4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.

Continue to: Bone formation with rhBMP-2...

 

 

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

DISCUSSION

We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.

In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.

Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.

This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

ABSTRACT

We conducted a study to determine the common characteristics of patients who developed radiculopathy symptoms and corresponding heterotopic ossification (HO) from transforaminal lumbar interbody fusions (TLIF) using recombinant human bone morphogenetic protein 2 (rhBMP-2). HO can arise from a disk space with rhBMP-2 use in TLIF. Formation of bone around nerve roots or the thecal sac can cause a radiculopathy with a consistent pattern of symptoms.

We identified 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years who developed radiculopathy symptoms and corresponding HO from TLIF with rhBMP-2 in the disk space between 2002 and 2015. To document this complication and improve its recognition, we recorded common patterns of symptom development and radiologic findings: specifically, time from implantation of rhBMP-2 to symptom development, consistency with side of TLIF placement, and radiologic findings.

Radicular pain generally developed a mean (SD) of 3.8 (1.0) months after TLIF with rhBMP-2. Development of radiculopathy symptoms corresponded to consistent “pseudo-pedicle”-like HO. In all 38 patients, HO arising from the annulotomy site showed a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. In addition, development of radiculopathy symptoms and corresponding HO appear to be independent of amount of rhBMP-2. HO resulting from TLIF with rhBMP-2 in the disk space is a pain generator and a recognizable complication that can be diagnosed by assessment of symptoms and computed tomography characteristics.

Continue to: Bone morphogenetic proteins...

 

 

Bone morphogenetic proteins (BMPs), first isolated by Urist in 19641, are a family of growth factors that stimulate the cascade of bone formation. Recombinant human BMP (rhBMP), specifically rhBMP-2 and rhBMP-7 (also known as osteogenic protein 1 [OP-1]), was developed in the 1990s after the advent of gene splicing. Then, in 2002, the US Food and Drug Administration (FDA) approved use of rhBMP to stimulate fusion in the human spine. Specifically, rhBMP-2 (Medtronic) was approved for use in combination with a specific brand of interbody cage in 1-level anterior lumbar interbody fusion.2 Over the past decade, off-label use of rhBMP-2 to achieve osseous union has increased dramatically, particularly in spinal surgery: transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion, and posterolateral lumbar fusion.3-9 However, this widespread off-label use for posterior spinal fusion began despite FDA data indicating that specific complications were underreported in the peer-reviewed literature.10,11 Although rhBMP-2 is very effective in increasing osteoblast formation and improving osteogenesis and subsequent bone healing in spinal surgery,12,13 its use in TLIF resulted in significant adverse side effects, including radiculopathy with and without neuroforaminal heterotopic ossification (HO); 14-24 complications in the FDA studies; 14,22,25-27 and osteolysis causing intervertebral cage subsidence, inflammatory radiculitis, genitourinary complications, infections, possible systemic effects, and significant HO complications.10,28-30 Of these, HO complications involved rhBMP leakage through the annulotomy to the disk space that led to HO. Specifically, rhBMP leaked directly out of the disk space and formed a pillar of bone that encased the nerve roots and dura, which led to occlusion of the foramen and symptoms of radiculopathy.10,28-30

Despite this frequent finding of HO in the intervertebral space outside the target fusion area, use of rhBMP-2 with intervertebral cages increased so rapidly that rhBMP-2 was used more often than autologous bone.5,11,17,31 In this study, we reviewed the common characteristics of patients who developed HO and subsequent radiculopathy from TLIF with rhBMP.

METHODS

After this study received Institutional Review Board approval, we retrospectively reviewed cases of radiculopathy symptoms that developed after TLIF with rhBMP between January 2002 and January 2015. During this period, 38 patients (26 males, 12 females) with a mean (SD) age of 50.8 (7.5) years and radiculopathy symptoms arising from TLIF with rhBMP-2 were identified to determine commonalities and defining characteristics that will help facilitate diagnosis.

Inclusion criteria were computed tomography (CT)–documented HO arising from the TLIF annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell with contouring around the thecal sac or nerve roots, as well as recurrence or initial occurrence of radiculopathy with signs and symptoms corresponding to the CT site of aberrant bone growth in terms of laterality and particular nerve root(s) involved. Exclusion criteria were malplacement of interbody cage or pedicle screws, disk herniation, systemic neuropathic disease, and new or unresolved radiculopathy immediately after index surgery.

To improve recognition of this complication, we also documented the amount of BMP used, common patterns of radiculopathy symptom development, and radiologic findings. Type and timing of radiculopathy symptom onset and consistency with side of TLIF placement were documented as well. Radiculopathy symptoms included shooting pain in the legs, incontinence, sexual dysfunction, and severe paralysis. Radiologic findings were specific to bone formation from the disk space (detected with CT).

Continue to: RESULTS

 

 

RESULTS

All 38 selected patients had radiculopathy symptoms from HO out of the intervertebral space. The Table lists the patients’ overall characteristics. The left side had the most radiculopathy symptoms (31/38 patients), followed by the right side (5/38) and both sides (2/38). Radiculopathy symptoms began a mean (SD) of 3.8 (1.0) months (range, 2-6 months) after index surgery. The 38 patients had 4 characteristics in common:

Table. Transforaminal Lumbar Interbody Fusion With Recombinant Human Bone Morphogenetic Protein 2: Onset Time for Radiculopathy Symptoms, Surgery Level, Side of Pseudo-Pedicle Bone Formation, and Subsequent Complications

PtSympton Onset, moSurgery Level(s)Side(s)Complication(s)
13L3-L5 (2)BothRadiculopathy, pseudo-pedicle, urine
23L4-L5 (2)RRadiculopathy, pseudo-pedicle
34L5-S1 (1)RRadiculopathy, pseudo-pedicle
45L5-S1 (1)LRadiculopathy, pseudo-pedicle
54L4-S1 (2)LRadiculopathy, pseudo-pedicle, subsidence
65L5-S1 (1)LRadiculopathy, pseudo-pedicle
74L5-S1 (1)LRadiculopathy, pseudo-pedicle
84L5-S1 (1)LRadiculopathy, pseudo-pedicle
93L5-S1 (1)LRadiculopathy, pseudo-pedicle
102L5-S1 (1)LRadiculopathy, pseudo-pedicle
112L5-S1 (1)LRadiculopathy, pseudo-pedicle, subsidence, neurologic
126L5-S1 (1)LRadiculopathy, pseudo-pedicle
133L5-S1 (1)LRadiculopathy, pseudo-pedicle, neurologic
142L2-L3 (1)RRadiculopathy, pseudo-pedicle
154L5-S1 (1)LRadiculopathy, pseudo-pedicle
163L4-L5 (1)LRadiculopathy, pseudo-pedicle
173L2-L3, L4-L5 (2)LRadiculopathy, pseudo-pedicle
183L4-L5, L2-L3 (1)LRadiculopathy, pseudo-pedicle, nonunion
194L4-L5 (1)RRadiculopathy, pseudo-pedicle
205L4-L5 (1)LRadiculopathy, pseudo-pedicle
215L5-S1 (1)RRadiculopathy, pseudo-pedicle
223L3-L4, L5-S1 (2)BothRadiculopathy, pseudo-pedicle
234L4-L5 (1)LRadiculopathy, pseudo-pedicle
246L5-S1 (1)LRadiculopathy, pseudo-pedicle
254L5-S1 (1)LRadiculopathy, pseudo-pedicle
263L5-S1 (1)LRadiculopathy, pseudo-pedicle, urine, bowel
274L5-S1 (1)LRadiculopathy, pseudo-pedicle
284L4-L5 (1)LRadiculopathy, pseudo-pedicle
296L5-S1 (1)LRadiculopathy, pseudo-pedicle
303L5-S1 (1)LRadiculopathy, pseudo-pedicle
313L5-S1 (1)LRadiculopathy, pseudo-pedicle
324L5-S1 (1)LRadiculopathy, pseudo-pedicle
333L5-S1 (1)LRadiculopathy, pseudo-pedicle
344L5-S1 (1)LRadiculopathy, pseudo-pedicle
354L5-S1 (1)LRadiculopathy, pseudo-pedicle
363L5-S1 (1)LRadiculopathy, pseudo-pedicle
374L4-L5 (1)LRadiculopathy, pseudo-pedicle
384L4-L5 (1)LRadiculopathy, pseudo-pedicle

1. Bone growing out of the annulotomy site for TLIF cage placement was present and in continuity with the disk space in 33 (87%) of the 38 cases. In the other 5 cases (13%), HO was present around the neural tissue, but not necessarily in continuity with the disk space. This bone appeared ectopic and not osteophytic and facet-related, as it formed a shell around either the nerve root or the thecal sac, contouring to the structure.

Magnetic resonance imaging shows that recombinant human bone morphogenetic protein 2 used in the disk space during transforaminal lumbar interbody fusion can leak out of the space and cause heterotopic bone formation around nerve roots and the thecal sac

2. The common, novel finding on CT was a “pseudo-pedicle” (Figures 1A, 1B), which appeared as ectopic growth from the disk space—a solid piece of bone in the same direction as the anatomical pedicle. Confusing similarity to the anatomical pedicle is present on axial cuts and during surgery. The pseudo-pedicle varied in thickness and extent out of the disk space, but was always presented as a bar of bone arising from the annulotomy site. After arising from the disk space, the HO could disperse in any direction, further calcifying neural structures or the facet joints above or below. There was no apparent distinguishable repeating pattern, given the variable nature of arthritic facet changes, scoliotic deformities, size of annulotomies, amount of rhBMP used, and placement in cage and disk space or only in cage.

As heterotopic ossification is often interpreted as postoperative fibrous or granulation tissue on magnetic resonance imaging, computed tomography is needed to fully appreciate heterotopic bone.

3. In 36 (95%) of the 38 cases, the initial interpretation of HO on magnetic resonance imaging (MRI) was of tissue other than bone, such as fibrous tissue, granulation tissue, recurrent disk herniation, or postoperative changes. However, this tissue was later determined to be bone from HO complications, which we confirmed with CT in all 38 cases. It is important to note that HO on MRI (Figures 2A, 2B) was initially interpreted by a radiologist as fibrous tissue, but same-level CT of the same case (Figures 3A, 3B) showed clear HO.

Computed tomography shows pseudo-pedicle-like heterotopic ossification of varying extent. Bone arising from the annulotomy site for transforaminal lumbar interbody fusion was universally present in all pateints.

4. The radiculopathy symptoms caused by HO were independent of the amount of rhBMP-2 used in TLIF. Of the 38 patients, 19 had 1 rhBMP-2 sponge placed in the cage, 12 had a small kit sponge (1.05 mg), 5 had 1 sponge placed in the cage and 1 sponge placed directly in the disk space before cage placement (no notation of precise size or amount of rhBMP-2), and 2 had 1 sponge placed in the cage (no notation of rhBMP-2 amount). The data showed that HO can occur with even a small amount of rhBMP-2.

Continue to: Bone formation with rhBMP-2...

 

 

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

DISCUSSION

We identified 38 patients with a recognizable and consistent pattern of complications of off-label use of rhBMP-2 in TLIF performed at our institution between 2002 and 2015. This pattern included consistent radiculopathy symptoms with corresponding HO at the annulotomy site in continuity with bone in the disk space or ectopic bone forming a distinctive shell around the thecal sac or nerve roots, as well as showing a distinct pseudo-pedicle pattern encompassing nerve roots and the thecal sac. Our finding differs from other findings of similar complication characteristics, but with much larger variations without consistency within the patient population.19,20,22,24 Specifically, previous studies found an association between off-label rhBMP-2 use in the posterior spine and radiculopathy with and without neuroforaminal HO. However, our study found consistent radiculopathy symptoms with pseudo-pedicle-like HO complications in all its 38 patients a mean (SD) of 3.8 (1.0) months after surgery.

In this study, consistent radiculopathy symptoms with pseudo-pedicle-like HO complications were independent of the amount of rhBMP-2 used, as some complications occurred with use of small pack rhBMP-2 with TLIF. It is well understood that high doses of rhBMP-2 may be required to improve fusion rates, but to our knowledge an optimal dosing strategy for TLIF has not been reported, particularly with respect to potential complications.8,20,31-33 For anterior lumbar interbody fusion surgery, the FDA-approved use of rhBMP-2 appears to have a significantly decreased risk of neuroforaminal HO complications. This may be attributable to the protective presence of the intact posterior annulus and longitudinal ligament for this procedure.20,33 For TLIF, it has been suggested that rhBMP-2 should be placed only along the anterior annulus with a posterior strut and morselized bone allograft barricade,33 and that fibrin glue should be used to limit BMP diffusion through the annulotomy site31 to prevent this complication.

Our study results suggest that radiculopathy symptoms with pseudo-pedicle-like HO complications appear to be caused by leakage of rhBMP-2 from the disk space through the annulotomy site. This was often initially interpreted incorrectly on MRI in the first year after surgery as being fibrous or granulation tissue, or even postoperative changes that the heterotopic tissue was bone was obvious only on CT. Even then the tissue may be incorrectly identified, as the encasing nerve roots in bone are similar to the scar tissue having no compressive effect. HO may compress, but it also has an inflammatory component that the scars lack. Additionally, the HO from the disk space, caused by leakage of the BMP placed in or around the fusion cage, can create a pseudo-pedicle of varying size and extent. This was present in all 38 of our cases.

This retrospective case series had its limitations. Its clinical and radiographic findings were not blinded. Confounding variables cannot be isolated for causal relationships, if any, to the complication in a case series such as this.

Bone formation with rhBMP-2 is robust and beneficial, but HO-related complications are significant, and identifiable on assessment of radiculopathy symptoms and CT characteristics.

References

1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.

2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.

3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.

4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.

5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.

6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.

7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.

8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.

9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.

10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.

11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.

12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.

13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.

14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.

15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.

16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.

17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.

18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.

19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.

20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.

21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.

22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.

23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.

24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.

25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.

26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.

27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.

28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.

29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.

30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.

31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.

32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.

33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.

References

1. Urist MR. Bone: formation by autoinduction. Science. 1965;150(3698):893-899.

2. Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA. Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and recombinant human bone morphogenetic protein-2. J Bone Joint Surg Am. 2009;91(5):1181-1189.

3. Boden SD, Kang J, Sandhu H, Heller JG. Use of recombinant human bone morphogenetic protein-2 to achieve posterolateral lumbar spine fusion in humans: a prospective, randomized clinical pilot trial: 2002 Volvo award in clinical studies. Spine. 2002;27(23):2662-2673.

4. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP-2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine. 2000;25(3):376-381.

5. Haid RW Jr, Branch CL Jr, Alexander JT, Burkus JK. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J. 2004;4(5):527-538.

6. Meisel HJ, Schnöring M, Hohaus C, et al. Posterior lumbar interbody fusion using rhBMP-2. Eur Spine J. 2008;17(12):1735-1744.

7. Mummaneni PV, Pan J, Haid RW, Rodts GE. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine. 2004;1(1):19-23.

8. Shimer AL, Oner FC, Vaccaro AR. Spinal reconstruction and bone morphogenetic proteins: open questions. Injury. 2009;40(suppl 3):S32-S38.

9. Slosar PJ, Josey R, Reynolds J. Accelerating lumbar fusions by combining rhBMP-2 with allograft bone: a prospective analysis of interbody fusion rates and clinical outcomes. Spine J. 2007;7(3):301-307.

10. Knox JB, Dai JM 3rd, Orchowski J. Osteolysis in transforaminal lumbar interbody fusion with bone morphogenetic protein-2. Spine. 2011;36(8):672-676.

11. Owens K, Glassman SD, Howard JM, Djurasovic M, Witten JL, Carreon LY. Perioperative complications with rhBMP-2 in transforaminal lumbar interbody fusion. Eur Spine J. 2011;20(4):612-617.

12. Mindea SA, Shih P, Song JK. Recombinant human bone morphogenetic protein-2-induced radiculitis in elective minimally invasive transforaminal lumbar interbody fusions: a series review. Spine. 2009;34(14):1480-1484.

13. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vitro and in vivo. Spine. 2004;29(23):2603-2611.

14. Cahill KS, Chi JH, Day A, Claus EB. Prevalence, complications, and hospital charges associated with use of bone-morphogenetic proteins in spinal fusion procedures. JAMA. 2009;302(1):58-66.

15. Carragee EJ, Hurwitz EL, Weiner BK. A critical review of recombinant human bone morphogenetic protein-2 trials in spinal surgery: emerging safety concerns and lessons learned. Spine J. 2011;11(6):471-491.

16. Chen NF, Smith ZA, Stiner E, Armin S, Sheikh H, Khoo LT. Symptomatic ectopic bone formation after off-label use of recombinant human bone morphogenetic protein-2 in transforaminal lumbar interbody fusion. J Neurosurg Spine. 2010;12(1):40-46.

17. Joseph V, Rampersaud YR. Heterotopic bone formation with the use of rhBMP2 in posterior minimal access interbody fusion: a CT analysis. Spine. 2007;32(25):2885-2890.

18. McClellan JW, Mulconrey DS, Forbes RJ, Fullmer N. Vertebral bone resorption after transforaminal lumbar interbody fusion with bone morphogenetic protein (rhBMP-2). J Spinal Disord Tech. 2006;19(7):483-486.

19. Mroz TE, Wang JC, Hashimoto R, Norvell DC. Complications related to osteobiologics use in spine surgery: a systematic review. Spine. 2010;35(9 suppl):S86-S104.

20. Muchow RD, Hsu WK, Anderson PA. Histopathologic inflammatory response induced by recombinant bone morphogenetic protein-2 causing radiculopathy after transforaminal lumbar interbody fusion. Spine J. 2010;10(9):e1-e6.

21. Ong KL, Villarraga ML, Lau E, Carreon LY, Kurtz SM, Glassman SD. Off-label use of bone morphogenetic proteins in the United States using administrative data. Spine. 2010;35(19):1794-1800.

22. Rihn JA, Patel R, Makda J, et al. Complications associated with single-level transforaminal lumbar interbody fusion. Spine J. 2009;9(8):623-629.

23. Vaidya R, Sethi A, Bartol S, Jacobson M, Coe C, Craig JG. Complications in the use of rhBMP-2 in PEEK cages for interbody spinal fusions. J Spinal Disord Tech. 2008;21(8):557-562.

24. Wong DA, Kumar A, Jatana S, Ghiselli G, Wong K. Neurologic impairment from ectopic bone in the lumbar canal: a potential complication of off-label PLIF/TLIF use of bone morphogenetic protein-2 (BMP-2). Spine J. 2008;8(6):1011-1018.

25. Delawi D, Dhert WJ, Rillardon L, et al. A prospective, randomized, controlled, multicenter study of osteogenic protein-1 in instrumented posterolateral fusions: report on safety and feasibility. Spine. 2010;35(12):1185-1191.

26. Vaccaro AR, Patel T, Fischgrund J, et al. A pilot study evaluating the safety and efficacy of OP-1 putty (rhBMP-7) as a replacement for iliac crest autograft in posterolateral lumbar arthrodesis for degenerative spondylolisthesis. Spine. 2004;29(17):1885-1892.

27. Vaidya R, Weir R, Sethi A, Meisterling S, Hakeos W, Wybo CD. Interbody fusion with allograft and rhBMP-2 leads to consistent fusion but early subsidence. J Bone Joint Surg Br. 2007;89(3):342-345.

28. Glassman SD, Howard J, Dimar J, Sweet A, Wilson G, Carreon L. Complications with recombinant human bone morphogenic protein-2 in posterolateral spine fusion: a consecutive series of 1037 cases. Spine. 2011;36(22):1849-1854.

29. Helgeson MD, Lehman RA Jr, Patzkowski JC, Dmitriev AE, Rosner MK, Mack AW. Adjacent vertebral body osteolysis with bone morphogenetic protein use in transforaminal lumbar interbody fusion. Spine J. 2011;11(6):507-510.

30. Hoffmann MF, Jones CB, Sietsema DL. Adjuncts in posterior lumbar spine fusion: comparison of complications and efficacy. Arch Orthop Trauma Surg. 2012;132(8):1105-1110.

31. Villavicencio AT, Burneikiene S, Nelson EL, Bulsara KR, Favors M, Thramann J. Safety of transforaminal lumbar interbody fusion and intervertebral recombinant human bone morphogenetic protein-2. J Neurosurg Spine. 2005;3(6):436-443.

32. Patel VV, Zhao L, Wong P, et al. Controlling bone morphogenetic protein diffusion and bone morphogenetic protein-stimulated bone growth using fibrin glue. Spine. 2006;31(11):1201-1206.

33. Zhang H, Sucato DJ, Welch RD. Recombinant human bone morphogenic protein-2-enhanced anterior spine fusion without bone encroachment into the spinal canal: a histomorphometric study in a thoracoscopically instrumented porcine model. Spine. 2005;30(5):512-518.

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Pseudo-Pedicle Heterotopic Ossification From Use of Recombinant Human Bone Morphogenetic Protein 2 (rhBMP-2) in Transforaminal Lumbar Interbody Fusion Cages
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TAKE-HOME POINTS

  • Use of rhBMP-2 in TLIF cages can result in HO out of the cage into the spinal canal.
  • HO from rhBMP-2 in TLIF cages can result in a radiculopathy from compression or inflammatory reaction.
  • HO out of the cage into the spinal canal resulting from use of rhBMP-2 in TLIF cages can be adequately diagnosed only with CT.
  • HO can appear as a pedicle or pseudo-pedicle.
  • Consider potential HO when using rhBMP-2 in TLIF cages.
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Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players

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Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players

    ABSTRACT

    Anterior ankle impingement is a frequent cause of pain and disability in athletes with impingement of soft-tissue or osseous structures along the anterior margin of the tibiotalar joint during dorsiflexion.

    In this study, we hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and range of motion (ROM), and would allow National Football League (NFL) players to return to their preoperative level of play.

    We reviewed 29 arthroscopic ankle débridements performed by a single surgeon. Each NFL player underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to return to play (RTP), events missed secondary to surgery, and complications were recorded.

    All athletes returned to the same level of NFL play at a mean (SD) of 8.4 (4.1) weeks after surgery and continued playing for a mean (SD) of 3.43 (2.57) years after surgery. Mean (SD) VAS pain scores decreased significantly (P < .001), to 0.38 (0.89) from 4.21 (1.52). Mean (SD) active ankle dorsiflexion increased significantly (P < .001), to 18.86° (2.62°) from 8.28° (4.14°). Mean (SD) AOFAS hindfoot scores increased significantly (P < .001), to 97.45 (4.72) from 70.62 (10.39). Degree of arthritis (r = 0.305) and age (r = 0.106) were poorly correlated to time to RTP.

    In all cases, arthroscopic débridement of anterior ankle impingement resulted in RTP at the same level at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM.

    Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

    Continue to: Anterior ankle impingement...

     

     

    Anterior ankle impingement is a frequent cause of disability in athletes.1 This condition results from repetitive trauma over time, which leads to osseous and soft-tissue impingement, pain, and decreased ankle range of motion (ROM).

    First termed footballer’s ankle, this condition is linked to repeated, forceful plantarflexion,2 though later studies attributed the phenomenon to repeated dorsiflexion resulting in periosteal hemorrhage.3 Both osseous and soft-tissue structures can cause impingement at the tibiotalar joint, often with osteophytes anteromedially at the tibial talar joint. Soft-tissue structures, including hypertrophic synovium, meniscoid lesions, and a thickened anterior talofibular ligament, more often cause anterolateral impingement.4-6 This process results in pain in extreme dorsiflexion, which comes into play in almost all football maneuvers, including sprinting, back-peddling, and offensive and defensive stances. Therefore, maintenance of pain-free dorsiflexion is required for high-level football. Decreased ROM can lead to decreased ability to perform these high-level athletic functions and can limit performance.

    Arthroscopic débridement improves functional outcomes and functional motion in both athletes and nonathletes.7,8 In addition, findings of a recent systematic review provide support for arthroscopic treatment of ankle impingement.9 Although arthroscopic treatment is effective in nonathletes and recreational athletes,10 there is a paucity of data on the efficacy of this procedure and on time to return to play (RTP) in professional football players.

    We conducted a study to evaluate the outcomes (pain, ROM, RTP) of arthroscopic débridement for anterior ankle impingement in National Football League (NFL) players. We hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and ROM, and would allow NFL players to return to their preoperative level of play.

    METHODS

    After this study was granted Institutional Review Board approval, we retrospectively reviewed a consecutive series of arthroscopically treated anterior ankle impingement athletes by a single surgeon (JPB). Indications for surgery were anterior ankle impingement resulting in ankle pain and decreased ROM that interfered with sport. Active NFL players who underwent ankle arthroscopy for symptomatic anterior ankle impingement were included. Excluded were players who underwent surgery after retirement or who retired before returning to play for reasons unrelated to the ankle. Medical records, operative reports, and rehabilitation reports were reviewed.

    Continue to: Preoperative and postoperative...

     

     

    Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to RTP, events missed secondary to surgery, and complications were recorded. These preoperative and postoperative variables were compared with paired Student 2-way t tests for continuous variables. Pearson correlation coefficients were calculated.

    PROCEDURE

    Ankle arthroscopy was performed with the patient supine after spinal or general anesthesia was induced. Prophylactic antibiotics were given in each case. Arthroscopy was performed with standard anterolateral and anteromedial portals. First, an incision was made through skin only, followed by blunt subcutaneous dissection down to the ankle capsule. A capsulotomy was then made bluntly. Care was taken to avoid all neurovascular structures. Posterior portals were not used. A 2.7-mm arthroscope was inserted and alternated between the anteromedial and anterolateral portals to maximally visualize the ankle joint. Diagnostic arthroscopy was performed to document synovitis, chondral injury, osseous, and soft-tissue impingement and any other noted pathology (Figures 1A-1C).

    Diagnostic ankle arthroscopic images

    A full radius resector was then used to perform a synovectomy and débridement of impinging soft tissue from the anterior talofibular ligament or anterior inferior talofibular ligament. All patients underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. A small burr was used to débride and remove the osteophytes on the talus and/or tibia. Soft-tissue and osseous structures were resected until the contours of the talus and tibia were normal. Any unstable articular defects were débrided and loose bodies were removed. Ankle ROM was checked to confirm complete resolution of impingement (Figures 2A-2D). Patients were not immobilized and were allowed progressive weight-bearing as tolerated. Crutches were used for assisted ambulation the first 3 to 5 postoperative days.

    Ankle arthroscopic images

    Physical therapy progressed through 3 phases: (1) inflammation control and ROM restoration, (2) initiation of ankle strengthening, including eversion and inversion, and (3) agility, proprioception, and functional rehabilitation.

    RESULTS

    Twenty-five NFL players (29 surgeries) were included in the study. Two players were excluded because they had retired at the end of the season before the surgery for reasons unrelated to the operative ankle. Mean (SD) age was 28.1 (2.9) years. Six included players had a history of ankle sprains, 1 had a history of ipsilateral ankle fracture, and 1 had a history of ipsilateral ankle dislocation. Table 1 lists the positions of players who underwent ankle arthroscopic decompression.

    Table 1. Positions of National Football League Players Who Underwent Ankle Arthroscopic Decompression for Anterior Ankle Impingement

    Position

    Surgeries, n

    Offensive line8
    Defensive line8
    Wide receiver4
    Running back4
    Linebacker3
    Quarterback1
    Defensive back1

    Continue to: During diagnostic arthroscopy...

     

     

    During diagnostic arthroscopy, changes to the articular cartilage were noted: grade 0 in 38% of patients, grade 1 in 17%, grade 2 in 21%, grade 3 in 21%, and grade 4 in 3%. Four patients had an osteochondral lesion (<1 cm in each case), which was treated with chondroplasty without microfracture.

    Each included patient returned to NFL play. Mean (SD) time to RTP without restrictions was 8.4 (4.1) weeks after surgery (range, 2-20 weeks). There was a poor correlation between degree of chondrosis and time to RTP (r = 0.305). In addition, there was a poor correlation between age and time to RTP (r = 0.106).

    Dorsiflexion improved significantly (P < .001), patients had significantly less pain after surgery (P < .001), and AOFAS hindfoot scores improved significantly (P < .001) (Table 2).

    Table 2. Preoperative and Postoperative Dorsiflexion, Pain, and AOFAS Score Before and After Arthroscopic Débridement of Anterior Ankle Impingementa
     Mean (SD)
     PreoperativePostoperative
    Dorsiflexion8.28º (4.14º)18.86° (2.62°)
    VAS pain score4.21 (1.52)0.38 (0.89)
    AOFAS score70.62 (10.39)97.45 (4.72)

    aAll values were significantly improved after surgery (P < .001).

    Abbreviations: AOFAS, American Orthopaedic Foot and Ankle Society; VAS, visual analog scale.

    The athletes played in the NFL for a mean (SD) of 3.43 (2.57) years after surgery (range, 1-10 seasons). These players included 6 who were still active at time of publication. No patient required revision surgery or additional surgery on the ipsilateral ankle. The one patient who was treated for superficial thrombophlebitis after surgery reported symptoms before surgery as well.

    DISCUSSION

    Arthroscopic decompression of anterior ankle impingement is safe and significantly improves pain and ROM in professional American football players. The procedure results in reliable RTP at an elite level, with durable results over the time remaining in their NFL careers.

    Continue to: before the 1988 study by Hawkins...

     

     

    Before the 1988 study by Hawkins,11 ankle spurs were removed with open procedures. Hawkins11 used arthroscopy for better and safer visualization of the ankle joint and used a burr for less painful removal of spurs from the tibia and the talus. In 2002, a series of 105 patients (median age, 35 years) had reduced pain and improved function a minimum of 2 years after arthroscopic débridement.12 These patients had a mix of pathology, including soft-tissue impingement, bony impingement, chondral lesions, loose bodies, and osteoarthritis.

    For many elite athletes, anterior ankle impingement can cause significant limitation. Reduced ankle dorsiflexion can alter all limb mechanics and predispose athletes to injury.13 In addition, because NFL players’ ankle ROM often approaches or exceeds normal physiologic limits,14 an ankle ROM limitation will often hinder their performance.

    Miyamoto and colleagues15 studied a series of 9 professional athletes (6 soccer players, 1 baseball pitcher, 1 mixed martial artist, 1 golfer) who underwent decompression of both anterior and posterior impingement. With regard to anterior impingement, they found anterior osteophytes in all the ankles, as was seen in the present study. Furthermore, they noted that mean dorsiflexion improved from 10° before surgery to 15° after surgery and that their athletes returned to play 12 to 15 weeks after surgery. Their results are similar to ours, though we noted more improvement in dorsiflexion, from 8.28° before surgery to 18.86° after surgery.

    One of the most important metrics in evaluating treatment options for professional athletes is time from surgery to RTP without restrictions. Mean time to full RTP was shorter in our study (8.4 weeks) than in the study by Miyamoto and colleagues15 (up to 20 weeks). However, many of their procedures were performed during the off-season, when there was no need to expeditiously clear patients for full sports participation. In addition, the patients in their study had both anterior and posterior pathology.

    Faster return to high-level athletics was supported in a study of 11 elite ballet dancers,16 whose pain and dance performance improved after arthroscopic débridement. Of the 11 patients, 9 returned to dance at a mean of 7 weeks after surgery; the other 2 required reoperation. Although the pathology differed in their study of elite professional soccer players, Calder and colleagues17 found that mean time to RTP after ankle arthroscopy for posterior impingement was 5 weeks.

    Continue to: For the NFL players in our study...

     

     

    For the NFL players in our study, RTP at their elite level was 100% after arthroscopic débridement of anterior ankle impingement. In the literature, time to RTP varies. Table 3 lists RTP rates for recreational athletes in published studies.18-27 In their recent systematic literature review, Zwiers and colleagues10 noted that 24% to 96.4% of recreational athletes returned to play after arthroscopic treatment for anterior ankle impingement. The percentage was significantly higher for the professional athletes in our study. Historical comparison supports an evolution in the indications and techniques for this procedure, with more recent literature suggesting a RTP rate much higher than earlier rates. In addition, compared with recreational athletes, professional athletes have strong financial incentives to return to their sports. Furthermore, our professional cohort was significantly younger than the recreational cohorts in those studies.

    Table 3. Frequency of Recreational Athletes’ Return to Play After Arthroscopic Débridement of Anterior Ankle Impingement, as Reported in the Literature
    StudyYearJournalReturn to Play
       n/N%
    Akseki et al181999Acta Orthop Scand10/1191
    Baums et al192006Knee Surg Sports Traumatol Arthrosc25/2696
    Branca et al201997Foot Ankle Int13/2748
    Di Palma et al21   1999J Sports Traumatol Relat Res21/3266
    Ferkel et al221991Am J Sports Med27/3187.1
    Hassan232007Knee Surg Sports Traumatol Arthrosc9/1182
    Jerosch et al24     1994Knee Surg Sports Traumatol Arthrosc9/3824
    Murawski & Kennedy252010Am J Sports Med 27/2896.4
    Ogilvie-Harris et al261993J Bone Joint Surg Br21/2875
    Rouvillain et al272014Eur J Orthop Surg Traumatol10/1190

     

    Total

      172/24370

    Current recommendations for recreational athletes include initial conservative treatment with rest, ankle bracing, and avoidance of jumping and other repetitive dorsiflexing activities. Physical therapy should include joint mobilization and work along the entire kinetic chain. Night splints or a removable walking boot can be used temporarily, as can a single intra-articular corticosteroid injection to reduce inflammation and evaluate improvement in more refractory cases.28 Commonly, conservative treatments fail if patients remain active, and soft tissue and/or osteophytes can be resected, though resection typically is reserved for recreational athletes for whom nonoperative treatments have been exhausted.29,30

    This study had several limitations, including its retrospective nature and lack of control group. In addition, follow-up was relatively short, and we did not use more recently described outcome measures, such as the Sports subscale of the Foot and Ankle Ability Measure, which may be more sensitive in describing function in elite athletes. However, many of the cases in our study predated these measures, but the rate of RTP at the NFL level requires a very high degree of postoperative ankle function, making this outcome the most meaningful. In the context of professional athletes, specifically the length of their careers, our study results provide valuable information regarding expectations about RTP and the durability of arthroscopic débridement of anterior ankle impingement in a high-demand setting.

    CONCLUSION

    For all the NFL players in this study, arthroscopic débridement of anterior ankle impingement resulted in return to preoperative level of play at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM. Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

    References

    1. Lubowitz JH. Editorial commentary: ankle anterior impingement is common in athletes and could be under-recognized. Arthroscopy. 2015;31(8):1597.

    2. Mcdougall A. Footballer’s ankle. Lancet. 1955;269(6902):1219-1220.

    3. Kleiger B. Anterior tibiotalar impingement syndromes in dancers. Foot Ankle. 1982;3(2):69-73.

    4. Bassett FH 3rd, Gates HS 3rd, Billys JB, Morris HB, Nikolaou PK. Talar impingement by the anteroinferior tibiofibular ligament. A cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am. 1990;72(1):55-59.

    5. Liu SH, Raskin A, Osti L, et al. Arthroscopic treatment of anterolateral ankle impingement. Arthroscopy. 1994;10(2):215-218.

    6. Thein R, Eichenblat M. Arthroscopic treatment of sports-related synovitis of the ankle. Am J Sports Med. 1992;20(5):496-498.

    7. Arnold H. Posttraumatic impingement syndrome of the ankle—indication and results of arthroscopic therapy. Foot Ankle Surg. 2011;17(2):85-88.

    8. Walsh SJ, Twaddle BC, Rosenfeldt MP, Boyle MJ. Arthroscopic treatment of anterior ankle impingement: a prospective study of 46 patients with 5-year follow-up. Am J Sports Med. 2014;42(11):2722-2726.

    9. Glazebrook MA, Ganapathy V, Bridge MA, Stone JW, Allard JP. Evidence-based indications for ankle arthroscopy. Arthroscopy. 2009;25(12):1478-1490.

    10. Zwiers R, Wiegerinck JI, Murawski CD, Fraser EJ, Kennedy JG, van Dijk CN. Arthroscopic treatment for anterior ankle impingement: a systematic review of the current literature. Arthroscopy. 2015;31(8):1585-1596.

    11. Hawkins RB. Arthroscopic treatment of sports-related anterior osteophytes in the ankle. Foot Ankle. 1988;9(2):87-90.

    12. Rasmussen S, Hjorth Jensen C. Arthroscopic treatment of impingement of the ankle reduces pain and enhances function. Scand J Med Sci Sports. 2002;12(2):69-72.

    13. Mason-Mackay AR, Whatman C, Reid D. The effect of reduced ankle dorsiflexion on lower extremity mechanics during landing: a systematic review. J Sci Med Sport. 2017;20(5):451-458.

    14. Riley PO, Kent RW, Dierks TA, Lievers WB, Frimenko RE, Crandall JR. Foot kinematics and loading of professional athletes in American football-specific tasks. Gait Posture. 2013;38(4):563-569.

    15. Miyamoto W, Takao M, Matsui K, Matsushita T. Simultaneous ankle arthroscopy and hindfoot endoscopy for combined anterior and posterior ankle impingement syndrome in professional athletes. J Orthop Sci. 2015;20(4):642-648.

    16. Nihal A, Rose DJ, Trepman E. Arthroscopic treatment of anterior ankle impingement syndrome in dancers. Foot Ankle Int. 2005;26(11):908-912.

    17. Calder JD, Sexton SA, Pearce CJ. Return to training and playing after posterior ankle arthroscopy for posterior impingement in elite professional soccer. Am J Sports Med. 2010;38(1):120-124.

    18. Akseki D, Pinar H, Bozkurt M, Yaldiz K, Arag S. The distal fascicle of the anterior inferior tibiofibular ligament as a cause of anterolateral ankle impingement: results of arthroscopic resection. Acta Orthop Scand. 1999;70(5):478-482.

    19. Baums MH, Kahl E, Schultz W, Klinger HM. Clinical outcome of the arthroscopic management of sports-related “anterior ankle pain”: a prospective study. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):482-486.

    20. Branca A, Di Palma L, Bucca C, Visconti CS, Di Mille M. Arthroscopic treatment of anterior ankle impingement. Foot Ankle Int. 1997;18(7):418-423.

    21. Di Palma L, Bucca C, Di Mille M, Branca A. Diagnosis and arthroscopic treatment of fibrous impingement of the ankle. J Sports Traumatol Relat Res. 1999;21:170-177.

    22. Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP. Arthroscopic treatment of anterolateral impingement of the ankle. Am J Sports Med. 1991;19(5):440-446.

    23. Hassan AH. Treatment of anterolateral impingements of the ankle joint by arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1150-1154.

    24. Jerosch J, Steinbeck J, Schröder M, Halm H. Arthroscopic treatment of anterior synovitis of the ankle in athletes. Knee Surg Sports Traumatol Arthrosc. 1994;2(3):176-181.

    25. Murawski CD, Kennedy JG. Anteromedial impingement in the ankle joint: outcomes following arthroscopy. Am J Sports Med. 2010;38(10):2017-2024.

    26. Ogilvie-Harris DJ, Mahomed N, Demazière A. Anterior impingement of the ankle treated by arthroscopic removal of bony spurs. J Bone Joint Surg Br. 1993;75(3):437-440.

    27. Rouvillain JL, Daoud W, Donica A, Garron E, Uzel AP. Distraction-free ankle arthroscopy for anterolateral impingement. Eur J Orthop Surg Traumatol. 2014;24(6):1019-1023.

    28. O’Kane JW, Kadel N. Anterior impingement syndrome in dancers. Curr Rev Musculoskelet Med. 2008;1(1):12-16.

    29. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. J Orthop Surg Res. 2016;11(1):97.

    30. Talusan PG, Toy J, Perez JL, Milewski MD, Reach JS. Anterior ankle impingement: diagnosis and treatment. J Am Acad Orthop Surg. 2014;22(5):333-339.

    Author and Disclosure Information

    Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

    Dr. McCrum is an Orthopaedic Surgery Sports Fellow, Dr. Arner is an Orthopaedic Surgery Resident, and Dr. Lesniak is Associate Professor, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. Bradley is Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

    Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

    Christopher L. McCrum, MD Justin W. Arner, MD Bryson Lesniak, MD James P. Bradley, MD . Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players. Am J Orthop. January 26, 2018

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    Author and Disclosure Information

    Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

    Dr. McCrum is an Orthopaedic Surgery Sports Fellow, Dr. Arner is an Orthopaedic Surgery Resident, and Dr. Lesniak is Associate Professor, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. Bradley is Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

    Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

    Christopher L. McCrum, MD Justin W. Arner, MD Bryson Lesniak, MD James P. Bradley, MD . Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players. Am J Orthop. January 26, 2018

    Author and Disclosure Information

    Authors’ Disclosure Statement: Dr. Bradley reports that he receives royalties from Arthrex. The other authors report no actual or potential conflict of interest in relation to this article.  

    Dr. McCrum is an Orthopaedic Surgery Sports Fellow, Dr. Arner is an Orthopaedic Surgery Resident, and Dr. Lesniak is Associate Professor, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Dr. Bradley is Clinical Professor, University of Pittsburgh Medical Center and Burke and Bradley Orthopedics, Pittsburgh, Pennsylvania.

    Address correspondence to: James P. Bradley, MD, Burke and Bradley Orthopedics, 200 Medical Arts Building, Suite 4010, 200 Delafield Rd, Pittsburgh, PA 15215 (tel, 412-784-5770; fax, 412-784-5776; email, bradleyjp@upmc.edu).

    Christopher L. McCrum, MD Justin W. Arner, MD Bryson Lesniak, MD James P. Bradley, MD . Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players. Am J Orthop. January 26, 2018

      ABSTRACT

      Anterior ankle impingement is a frequent cause of pain and disability in athletes with impingement of soft-tissue or osseous structures along the anterior margin of the tibiotalar joint during dorsiflexion.

      In this study, we hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and range of motion (ROM), and would allow National Football League (NFL) players to return to their preoperative level of play.

      We reviewed 29 arthroscopic ankle débridements performed by a single surgeon. Each NFL player underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to return to play (RTP), events missed secondary to surgery, and complications were recorded.

      All athletes returned to the same level of NFL play at a mean (SD) of 8.4 (4.1) weeks after surgery and continued playing for a mean (SD) of 3.43 (2.57) years after surgery. Mean (SD) VAS pain scores decreased significantly (P < .001), to 0.38 (0.89) from 4.21 (1.52). Mean (SD) active ankle dorsiflexion increased significantly (P < .001), to 18.86° (2.62°) from 8.28° (4.14°). Mean (SD) AOFAS hindfoot scores increased significantly (P < .001), to 97.45 (4.72) from 70.62 (10.39). Degree of arthritis (r = 0.305) and age (r = 0.106) were poorly correlated to time to RTP.

      In all cases, arthroscopic débridement of anterior ankle impingement resulted in RTP at the same level at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM.

      Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

      Continue to: Anterior ankle impingement...

       

       

      Anterior ankle impingement is a frequent cause of disability in athletes.1 This condition results from repetitive trauma over time, which leads to osseous and soft-tissue impingement, pain, and decreased ankle range of motion (ROM).

      First termed footballer’s ankle, this condition is linked to repeated, forceful plantarflexion,2 though later studies attributed the phenomenon to repeated dorsiflexion resulting in periosteal hemorrhage.3 Both osseous and soft-tissue structures can cause impingement at the tibiotalar joint, often with osteophytes anteromedially at the tibial talar joint. Soft-tissue structures, including hypertrophic synovium, meniscoid lesions, and a thickened anterior talofibular ligament, more often cause anterolateral impingement.4-6 This process results in pain in extreme dorsiflexion, which comes into play in almost all football maneuvers, including sprinting, back-peddling, and offensive and defensive stances. Therefore, maintenance of pain-free dorsiflexion is required for high-level football. Decreased ROM can lead to decreased ability to perform these high-level athletic functions and can limit performance.

      Arthroscopic débridement improves functional outcomes and functional motion in both athletes and nonathletes.7,8 In addition, findings of a recent systematic review provide support for arthroscopic treatment of ankle impingement.9 Although arthroscopic treatment is effective in nonathletes and recreational athletes,10 there is a paucity of data on the efficacy of this procedure and on time to return to play (RTP) in professional football players.

      We conducted a study to evaluate the outcomes (pain, ROM, RTP) of arthroscopic débridement for anterior ankle impingement in National Football League (NFL) players. We hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and ROM, and would allow NFL players to return to their preoperative level of play.

      METHODS

      After this study was granted Institutional Review Board approval, we retrospectively reviewed a consecutive series of arthroscopically treated anterior ankle impingement athletes by a single surgeon (JPB). Indications for surgery were anterior ankle impingement resulting in ankle pain and decreased ROM that interfered with sport. Active NFL players who underwent ankle arthroscopy for symptomatic anterior ankle impingement were included. Excluded were players who underwent surgery after retirement or who retired before returning to play for reasons unrelated to the ankle. Medical records, operative reports, and rehabilitation reports were reviewed.

      Continue to: Preoperative and postoperative...

       

       

      Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to RTP, events missed secondary to surgery, and complications were recorded. These preoperative and postoperative variables were compared with paired Student 2-way t tests for continuous variables. Pearson correlation coefficients were calculated.

      PROCEDURE

      Ankle arthroscopy was performed with the patient supine after spinal or general anesthesia was induced. Prophylactic antibiotics were given in each case. Arthroscopy was performed with standard anterolateral and anteromedial portals. First, an incision was made through skin only, followed by blunt subcutaneous dissection down to the ankle capsule. A capsulotomy was then made bluntly. Care was taken to avoid all neurovascular structures. Posterior portals were not used. A 2.7-mm arthroscope was inserted and alternated between the anteromedial and anterolateral portals to maximally visualize the ankle joint. Diagnostic arthroscopy was performed to document synovitis, chondral injury, osseous, and soft-tissue impingement and any other noted pathology (Figures 1A-1C).

      Diagnostic ankle arthroscopic images

      A full radius resector was then used to perform a synovectomy and débridement of impinging soft tissue from the anterior talofibular ligament or anterior inferior talofibular ligament. All patients underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. A small burr was used to débride and remove the osteophytes on the talus and/or tibia. Soft-tissue and osseous structures were resected until the contours of the talus and tibia were normal. Any unstable articular defects were débrided and loose bodies were removed. Ankle ROM was checked to confirm complete resolution of impingement (Figures 2A-2D). Patients were not immobilized and were allowed progressive weight-bearing as tolerated. Crutches were used for assisted ambulation the first 3 to 5 postoperative days.

      Ankle arthroscopic images

      Physical therapy progressed through 3 phases: (1) inflammation control and ROM restoration, (2) initiation of ankle strengthening, including eversion and inversion, and (3) agility, proprioception, and functional rehabilitation.

      RESULTS

      Twenty-five NFL players (29 surgeries) were included in the study. Two players were excluded because they had retired at the end of the season before the surgery for reasons unrelated to the operative ankle. Mean (SD) age was 28.1 (2.9) years. Six included players had a history of ankle sprains, 1 had a history of ipsilateral ankle fracture, and 1 had a history of ipsilateral ankle dislocation. Table 1 lists the positions of players who underwent ankle arthroscopic decompression.

      Table 1. Positions of National Football League Players Who Underwent Ankle Arthroscopic Decompression for Anterior Ankle Impingement

      Position

      Surgeries, n

      Offensive line8
      Defensive line8
      Wide receiver4
      Running back4
      Linebacker3
      Quarterback1
      Defensive back1

      Continue to: During diagnostic arthroscopy...

       

       

      During diagnostic arthroscopy, changes to the articular cartilage were noted: grade 0 in 38% of patients, grade 1 in 17%, grade 2 in 21%, grade 3 in 21%, and grade 4 in 3%. Four patients had an osteochondral lesion (<1 cm in each case), which was treated with chondroplasty without microfracture.

      Each included patient returned to NFL play. Mean (SD) time to RTP without restrictions was 8.4 (4.1) weeks after surgery (range, 2-20 weeks). There was a poor correlation between degree of chondrosis and time to RTP (r = 0.305). In addition, there was a poor correlation between age and time to RTP (r = 0.106).

      Dorsiflexion improved significantly (P < .001), patients had significantly less pain after surgery (P < .001), and AOFAS hindfoot scores improved significantly (P < .001) (Table 2).

      Table 2. Preoperative and Postoperative Dorsiflexion, Pain, and AOFAS Score Before and After Arthroscopic Débridement of Anterior Ankle Impingementa
       Mean (SD)
       PreoperativePostoperative
      Dorsiflexion8.28º (4.14º)18.86° (2.62°)
      VAS pain score4.21 (1.52)0.38 (0.89)
      AOFAS score70.62 (10.39)97.45 (4.72)

      aAll values were significantly improved after surgery (P < .001).

      Abbreviations: AOFAS, American Orthopaedic Foot and Ankle Society; VAS, visual analog scale.

      The athletes played in the NFL for a mean (SD) of 3.43 (2.57) years after surgery (range, 1-10 seasons). These players included 6 who were still active at time of publication. No patient required revision surgery or additional surgery on the ipsilateral ankle. The one patient who was treated for superficial thrombophlebitis after surgery reported symptoms before surgery as well.

      DISCUSSION

      Arthroscopic decompression of anterior ankle impingement is safe and significantly improves pain and ROM in professional American football players. The procedure results in reliable RTP at an elite level, with durable results over the time remaining in their NFL careers.

      Continue to: before the 1988 study by Hawkins...

       

       

      Before the 1988 study by Hawkins,11 ankle spurs were removed with open procedures. Hawkins11 used arthroscopy for better and safer visualization of the ankle joint and used a burr for less painful removal of spurs from the tibia and the talus. In 2002, a series of 105 patients (median age, 35 years) had reduced pain and improved function a minimum of 2 years after arthroscopic débridement.12 These patients had a mix of pathology, including soft-tissue impingement, bony impingement, chondral lesions, loose bodies, and osteoarthritis.

      For many elite athletes, anterior ankle impingement can cause significant limitation. Reduced ankle dorsiflexion can alter all limb mechanics and predispose athletes to injury.13 In addition, because NFL players’ ankle ROM often approaches or exceeds normal physiologic limits,14 an ankle ROM limitation will often hinder their performance.

      Miyamoto and colleagues15 studied a series of 9 professional athletes (6 soccer players, 1 baseball pitcher, 1 mixed martial artist, 1 golfer) who underwent decompression of both anterior and posterior impingement. With regard to anterior impingement, they found anterior osteophytes in all the ankles, as was seen in the present study. Furthermore, they noted that mean dorsiflexion improved from 10° before surgery to 15° after surgery and that their athletes returned to play 12 to 15 weeks after surgery. Their results are similar to ours, though we noted more improvement in dorsiflexion, from 8.28° before surgery to 18.86° after surgery.

      One of the most important metrics in evaluating treatment options for professional athletes is time from surgery to RTP without restrictions. Mean time to full RTP was shorter in our study (8.4 weeks) than in the study by Miyamoto and colleagues15 (up to 20 weeks). However, many of their procedures were performed during the off-season, when there was no need to expeditiously clear patients for full sports participation. In addition, the patients in their study had both anterior and posterior pathology.

      Faster return to high-level athletics was supported in a study of 11 elite ballet dancers,16 whose pain and dance performance improved after arthroscopic débridement. Of the 11 patients, 9 returned to dance at a mean of 7 weeks after surgery; the other 2 required reoperation. Although the pathology differed in their study of elite professional soccer players, Calder and colleagues17 found that mean time to RTP after ankle arthroscopy for posterior impingement was 5 weeks.

      Continue to: For the NFL players in our study...

       

       

      For the NFL players in our study, RTP at their elite level was 100% after arthroscopic débridement of anterior ankle impingement. In the literature, time to RTP varies. Table 3 lists RTP rates for recreational athletes in published studies.18-27 In their recent systematic literature review, Zwiers and colleagues10 noted that 24% to 96.4% of recreational athletes returned to play after arthroscopic treatment for anterior ankle impingement. The percentage was significantly higher for the professional athletes in our study. Historical comparison supports an evolution in the indications and techniques for this procedure, with more recent literature suggesting a RTP rate much higher than earlier rates. In addition, compared with recreational athletes, professional athletes have strong financial incentives to return to their sports. Furthermore, our professional cohort was significantly younger than the recreational cohorts in those studies.

      Table 3. Frequency of Recreational Athletes’ Return to Play After Arthroscopic Débridement of Anterior Ankle Impingement, as Reported in the Literature
      StudyYearJournalReturn to Play
         n/N%
      Akseki et al181999Acta Orthop Scand10/1191
      Baums et al192006Knee Surg Sports Traumatol Arthrosc25/2696
      Branca et al201997Foot Ankle Int13/2748
      Di Palma et al21   1999J Sports Traumatol Relat Res21/3266
      Ferkel et al221991Am J Sports Med27/3187.1
      Hassan232007Knee Surg Sports Traumatol Arthrosc9/1182
      Jerosch et al24     1994Knee Surg Sports Traumatol Arthrosc9/3824
      Murawski & Kennedy252010Am J Sports Med 27/2896.4
      Ogilvie-Harris et al261993J Bone Joint Surg Br21/2875
      Rouvillain et al272014Eur J Orthop Surg Traumatol10/1190

       

      Total

        172/24370

      Current recommendations for recreational athletes include initial conservative treatment with rest, ankle bracing, and avoidance of jumping and other repetitive dorsiflexing activities. Physical therapy should include joint mobilization and work along the entire kinetic chain. Night splints or a removable walking boot can be used temporarily, as can a single intra-articular corticosteroid injection to reduce inflammation and evaluate improvement in more refractory cases.28 Commonly, conservative treatments fail if patients remain active, and soft tissue and/or osteophytes can be resected, though resection typically is reserved for recreational athletes for whom nonoperative treatments have been exhausted.29,30

      This study had several limitations, including its retrospective nature and lack of control group. In addition, follow-up was relatively short, and we did not use more recently described outcome measures, such as the Sports subscale of the Foot and Ankle Ability Measure, which may be more sensitive in describing function in elite athletes. However, many of the cases in our study predated these measures, but the rate of RTP at the NFL level requires a very high degree of postoperative ankle function, making this outcome the most meaningful. In the context of professional athletes, specifically the length of their careers, our study results provide valuable information regarding expectations about RTP and the durability of arthroscopic débridement of anterior ankle impingement in a high-demand setting.

      CONCLUSION

      For all the NFL players in this study, arthroscopic débridement of anterior ankle impingement resulted in return to preoperative level of play at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM. Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

        ABSTRACT

        Anterior ankle impingement is a frequent cause of pain and disability in athletes with impingement of soft-tissue or osseous structures along the anterior margin of the tibiotalar joint during dorsiflexion.

        In this study, we hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and range of motion (ROM), and would allow National Football League (NFL) players to return to their preoperative level of play.

        We reviewed 29 arthroscopic ankle débridements performed by a single surgeon. Each NFL player underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to return to play (RTP), events missed secondary to surgery, and complications were recorded.

        All athletes returned to the same level of NFL play at a mean (SD) of 8.4 (4.1) weeks after surgery and continued playing for a mean (SD) of 3.43 (2.57) years after surgery. Mean (SD) VAS pain scores decreased significantly (P < .001), to 0.38 (0.89) from 4.21 (1.52). Mean (SD) active ankle dorsiflexion increased significantly (P < .001), to 18.86° (2.62°) from 8.28° (4.14°). Mean (SD) AOFAS hindfoot scores increased significantly (P < .001), to 97.45 (4.72) from 70.62 (10.39). Degree of arthritis (r = 0.305) and age (r = 0.106) were poorly correlated to time to RTP.

        In all cases, arthroscopic débridement of anterior ankle impingement resulted in RTP at the same level at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM.

        Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

        Continue to: Anterior ankle impingement...

         

         

        Anterior ankle impingement is a frequent cause of disability in athletes.1 This condition results from repetitive trauma over time, which leads to osseous and soft-tissue impingement, pain, and decreased ankle range of motion (ROM).

        First termed footballer’s ankle, this condition is linked to repeated, forceful plantarflexion,2 though later studies attributed the phenomenon to repeated dorsiflexion resulting in periosteal hemorrhage.3 Both osseous and soft-tissue structures can cause impingement at the tibiotalar joint, often with osteophytes anteromedially at the tibial talar joint. Soft-tissue structures, including hypertrophic synovium, meniscoid lesions, and a thickened anterior talofibular ligament, more often cause anterolateral impingement.4-6 This process results in pain in extreme dorsiflexion, which comes into play in almost all football maneuvers, including sprinting, back-peddling, and offensive and defensive stances. Therefore, maintenance of pain-free dorsiflexion is required for high-level football. Decreased ROM can lead to decreased ability to perform these high-level athletic functions and can limit performance.

        Arthroscopic débridement improves functional outcomes and functional motion in both athletes and nonathletes.7,8 In addition, findings of a recent systematic review provide support for arthroscopic treatment of ankle impingement.9 Although arthroscopic treatment is effective in nonathletes and recreational athletes,10 there is a paucity of data on the efficacy of this procedure and on time to return to play (RTP) in professional football players.

        We conducted a study to evaluate the outcomes (pain, ROM, RTP) of arthroscopic débridement for anterior ankle impingement in National Football League (NFL) players. We hypothesized that arthroscopic decompression of anterior ankle impingement would result in significant, reliable, and durable improvement in pain and ROM, and would allow NFL players to return to their preoperative level of play.

        METHODS

        After this study was granted Institutional Review Board approval, we retrospectively reviewed a consecutive series of arthroscopically treated anterior ankle impingement athletes by a single surgeon (JPB). Indications for surgery were anterior ankle impingement resulting in ankle pain and decreased ROM that interfered with sport. Active NFL players who underwent ankle arthroscopy for symptomatic anterior ankle impingement were included. Excluded were players who underwent surgery after retirement or who retired before returning to play for reasons unrelated to the ankle. Medical records, operative reports, and rehabilitation reports were reviewed.

        Continue to: Preoperative and postoperative...

         

         

        Preoperative and postoperative visual analog scale (VAS) pain scores, American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot scores, and ankle ROM were compared; time to RTP, events missed secondary to surgery, and complications were recorded. These preoperative and postoperative variables were compared with paired Student 2-way t tests for continuous variables. Pearson correlation coefficients were calculated.

        PROCEDURE

        Ankle arthroscopy was performed with the patient supine after spinal or general anesthesia was induced. Prophylactic antibiotics were given in each case. Arthroscopy was performed with standard anterolateral and anteromedial portals. First, an incision was made through skin only, followed by blunt subcutaneous dissection down to the ankle capsule. A capsulotomy was then made bluntly. Care was taken to avoid all neurovascular structures. Posterior portals were not used. A 2.7-mm arthroscope was inserted and alternated between the anteromedial and anterolateral portals to maximally visualize the ankle joint. Diagnostic arthroscopy was performed to document synovitis, chondral injury, osseous, and soft-tissue impingement and any other noted pathology (Figures 1A-1C).

        Diagnostic ankle arthroscopic images

        A full radius resector was then used to perform a synovectomy and débridement of impinging soft tissue from the anterior talofibular ligament or anterior inferior talofibular ligament. All patients underwent arthroscopic débridement of pathologic soft tissue and of tibial and talar osteophytes in the anterior ankle. A small burr was used to débride and remove the osteophytes on the talus and/or tibia. Soft-tissue and osseous structures were resected until the contours of the talus and tibia were normal. Any unstable articular defects were débrided and loose bodies were removed. Ankle ROM was checked to confirm complete resolution of impingement (Figures 2A-2D). Patients were not immobilized and were allowed progressive weight-bearing as tolerated. Crutches were used for assisted ambulation the first 3 to 5 postoperative days.

        Ankle arthroscopic images

        Physical therapy progressed through 3 phases: (1) inflammation control and ROM restoration, (2) initiation of ankle strengthening, including eversion and inversion, and (3) agility, proprioception, and functional rehabilitation.

        RESULTS

        Twenty-five NFL players (29 surgeries) were included in the study. Two players were excluded because they had retired at the end of the season before the surgery for reasons unrelated to the operative ankle. Mean (SD) age was 28.1 (2.9) years. Six included players had a history of ankle sprains, 1 had a history of ipsilateral ankle fracture, and 1 had a history of ipsilateral ankle dislocation. Table 1 lists the positions of players who underwent ankle arthroscopic decompression.

        Table 1. Positions of National Football League Players Who Underwent Ankle Arthroscopic Decompression for Anterior Ankle Impingement

        Position

        Surgeries, n

        Offensive line8
        Defensive line8
        Wide receiver4
        Running back4
        Linebacker3
        Quarterback1
        Defensive back1

        Continue to: During diagnostic arthroscopy...

         

         

        During diagnostic arthroscopy, changes to the articular cartilage were noted: grade 0 in 38% of patients, grade 1 in 17%, grade 2 in 21%, grade 3 in 21%, and grade 4 in 3%. Four patients had an osteochondral lesion (<1 cm in each case), which was treated with chondroplasty without microfracture.

        Each included patient returned to NFL play. Mean (SD) time to RTP without restrictions was 8.4 (4.1) weeks after surgery (range, 2-20 weeks). There was a poor correlation between degree of chondrosis and time to RTP (r = 0.305). In addition, there was a poor correlation between age and time to RTP (r = 0.106).

        Dorsiflexion improved significantly (P < .001), patients had significantly less pain after surgery (P < .001), and AOFAS hindfoot scores improved significantly (P < .001) (Table 2).

        Table 2. Preoperative and Postoperative Dorsiflexion, Pain, and AOFAS Score Before and After Arthroscopic Débridement of Anterior Ankle Impingementa
         Mean (SD)
         PreoperativePostoperative
        Dorsiflexion8.28º (4.14º)18.86° (2.62°)
        VAS pain score4.21 (1.52)0.38 (0.89)
        AOFAS score70.62 (10.39)97.45 (4.72)

        aAll values were significantly improved after surgery (P < .001).

        Abbreviations: AOFAS, American Orthopaedic Foot and Ankle Society; VAS, visual analog scale.

        The athletes played in the NFL for a mean (SD) of 3.43 (2.57) years after surgery (range, 1-10 seasons). These players included 6 who were still active at time of publication. No patient required revision surgery or additional surgery on the ipsilateral ankle. The one patient who was treated for superficial thrombophlebitis after surgery reported symptoms before surgery as well.

        DISCUSSION

        Arthroscopic decompression of anterior ankle impingement is safe and significantly improves pain and ROM in professional American football players. The procedure results in reliable RTP at an elite level, with durable results over the time remaining in their NFL careers.

        Continue to: before the 1988 study by Hawkins...

         

         

        Before the 1988 study by Hawkins,11 ankle spurs were removed with open procedures. Hawkins11 used arthroscopy for better and safer visualization of the ankle joint and used a burr for less painful removal of spurs from the tibia and the talus. In 2002, a series of 105 patients (median age, 35 years) had reduced pain and improved function a minimum of 2 years after arthroscopic débridement.12 These patients had a mix of pathology, including soft-tissue impingement, bony impingement, chondral lesions, loose bodies, and osteoarthritis.

        For many elite athletes, anterior ankle impingement can cause significant limitation. Reduced ankle dorsiflexion can alter all limb mechanics and predispose athletes to injury.13 In addition, because NFL players’ ankle ROM often approaches or exceeds normal physiologic limits,14 an ankle ROM limitation will often hinder their performance.

        Miyamoto and colleagues15 studied a series of 9 professional athletes (6 soccer players, 1 baseball pitcher, 1 mixed martial artist, 1 golfer) who underwent decompression of both anterior and posterior impingement. With regard to anterior impingement, they found anterior osteophytes in all the ankles, as was seen in the present study. Furthermore, they noted that mean dorsiflexion improved from 10° before surgery to 15° after surgery and that their athletes returned to play 12 to 15 weeks after surgery. Their results are similar to ours, though we noted more improvement in dorsiflexion, from 8.28° before surgery to 18.86° after surgery.

        One of the most important metrics in evaluating treatment options for professional athletes is time from surgery to RTP without restrictions. Mean time to full RTP was shorter in our study (8.4 weeks) than in the study by Miyamoto and colleagues15 (up to 20 weeks). However, many of their procedures were performed during the off-season, when there was no need to expeditiously clear patients for full sports participation. In addition, the patients in their study had both anterior and posterior pathology.

        Faster return to high-level athletics was supported in a study of 11 elite ballet dancers,16 whose pain and dance performance improved after arthroscopic débridement. Of the 11 patients, 9 returned to dance at a mean of 7 weeks after surgery; the other 2 required reoperation. Although the pathology differed in their study of elite professional soccer players, Calder and colleagues17 found that mean time to RTP after ankle arthroscopy for posterior impingement was 5 weeks.

        Continue to: For the NFL players in our study...

         

         

        For the NFL players in our study, RTP at their elite level was 100% after arthroscopic débridement of anterior ankle impingement. In the literature, time to RTP varies. Table 3 lists RTP rates for recreational athletes in published studies.18-27 In their recent systematic literature review, Zwiers and colleagues10 noted that 24% to 96.4% of recreational athletes returned to play after arthroscopic treatment for anterior ankle impingement. The percentage was significantly higher for the professional athletes in our study. Historical comparison supports an evolution in the indications and techniques for this procedure, with more recent literature suggesting a RTP rate much higher than earlier rates. In addition, compared with recreational athletes, professional athletes have strong financial incentives to return to their sports. Furthermore, our professional cohort was significantly younger than the recreational cohorts in those studies.

        Table 3. Frequency of Recreational Athletes’ Return to Play After Arthroscopic Débridement of Anterior Ankle Impingement, as Reported in the Literature
        StudyYearJournalReturn to Play
           n/N%
        Akseki et al181999Acta Orthop Scand10/1191
        Baums et al192006Knee Surg Sports Traumatol Arthrosc25/2696
        Branca et al201997Foot Ankle Int13/2748
        Di Palma et al21   1999J Sports Traumatol Relat Res21/3266
        Ferkel et al221991Am J Sports Med27/3187.1
        Hassan232007Knee Surg Sports Traumatol Arthrosc9/1182
        Jerosch et al24     1994Knee Surg Sports Traumatol Arthrosc9/3824
        Murawski & Kennedy252010Am J Sports Med 27/2896.4
        Ogilvie-Harris et al261993J Bone Joint Surg Br21/2875
        Rouvillain et al272014Eur J Orthop Surg Traumatol10/1190

         

        Total

          172/24370

        Current recommendations for recreational athletes include initial conservative treatment with rest, ankle bracing, and avoidance of jumping and other repetitive dorsiflexing activities. Physical therapy should include joint mobilization and work along the entire kinetic chain. Night splints or a removable walking boot can be used temporarily, as can a single intra-articular corticosteroid injection to reduce inflammation and evaluate improvement in more refractory cases.28 Commonly, conservative treatments fail if patients remain active, and soft tissue and/or osteophytes can be resected, though resection typically is reserved for recreational athletes for whom nonoperative treatments have been exhausted.29,30

        This study had several limitations, including its retrospective nature and lack of control group. In addition, follow-up was relatively short, and we did not use more recently described outcome measures, such as the Sports subscale of the Foot and Ankle Ability Measure, which may be more sensitive in describing function in elite athletes. However, many of the cases in our study predated these measures, but the rate of RTP at the NFL level requires a very high degree of postoperative ankle function, making this outcome the most meaningful. In the context of professional athletes, specifically the length of their careers, our study results provide valuable information regarding expectations about RTP and the durability of arthroscopic débridement of anterior ankle impingement in a high-demand setting.

        CONCLUSION

        For all the NFL players in this study, arthroscopic débridement of anterior ankle impingement resulted in return to preoperative level of play at a mean of 2 months after surgery. There were significant improvements in VAS pain scores, AOFAS hindfoot scores, and ROM. Arthroscopic débridement of anterior ankle impingement relieves pain, restores ROM and function, and results in reliable RTP in professional football players.

        References

        1. Lubowitz JH. Editorial commentary: ankle anterior impingement is common in athletes and could be under-recognized. Arthroscopy. 2015;31(8):1597.

        2. Mcdougall A. Footballer’s ankle. Lancet. 1955;269(6902):1219-1220.

        3. Kleiger B. Anterior tibiotalar impingement syndromes in dancers. Foot Ankle. 1982;3(2):69-73.

        4. Bassett FH 3rd, Gates HS 3rd, Billys JB, Morris HB, Nikolaou PK. Talar impingement by the anteroinferior tibiofibular ligament. A cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am. 1990;72(1):55-59.

        5. Liu SH, Raskin A, Osti L, et al. Arthroscopic treatment of anterolateral ankle impingement. Arthroscopy. 1994;10(2):215-218.

        6. Thein R, Eichenblat M. Arthroscopic treatment of sports-related synovitis of the ankle. Am J Sports Med. 1992;20(5):496-498.

        7. Arnold H. Posttraumatic impingement syndrome of the ankle—indication and results of arthroscopic therapy. Foot Ankle Surg. 2011;17(2):85-88.

        8. Walsh SJ, Twaddle BC, Rosenfeldt MP, Boyle MJ. Arthroscopic treatment of anterior ankle impingement: a prospective study of 46 patients with 5-year follow-up. Am J Sports Med. 2014;42(11):2722-2726.

        9. Glazebrook MA, Ganapathy V, Bridge MA, Stone JW, Allard JP. Evidence-based indications for ankle arthroscopy. Arthroscopy. 2009;25(12):1478-1490.

        10. Zwiers R, Wiegerinck JI, Murawski CD, Fraser EJ, Kennedy JG, van Dijk CN. Arthroscopic treatment for anterior ankle impingement: a systematic review of the current literature. Arthroscopy. 2015;31(8):1585-1596.

        11. Hawkins RB. Arthroscopic treatment of sports-related anterior osteophytes in the ankle. Foot Ankle. 1988;9(2):87-90.

        12. Rasmussen S, Hjorth Jensen C. Arthroscopic treatment of impingement of the ankle reduces pain and enhances function. Scand J Med Sci Sports. 2002;12(2):69-72.

        13. Mason-Mackay AR, Whatman C, Reid D. The effect of reduced ankle dorsiflexion on lower extremity mechanics during landing: a systematic review. J Sci Med Sport. 2017;20(5):451-458.

        14. Riley PO, Kent RW, Dierks TA, Lievers WB, Frimenko RE, Crandall JR. Foot kinematics and loading of professional athletes in American football-specific tasks. Gait Posture. 2013;38(4):563-569.

        15. Miyamoto W, Takao M, Matsui K, Matsushita T. Simultaneous ankle arthroscopy and hindfoot endoscopy for combined anterior and posterior ankle impingement syndrome in professional athletes. J Orthop Sci. 2015;20(4):642-648.

        16. Nihal A, Rose DJ, Trepman E. Arthroscopic treatment of anterior ankle impingement syndrome in dancers. Foot Ankle Int. 2005;26(11):908-912.

        17. Calder JD, Sexton SA, Pearce CJ. Return to training and playing after posterior ankle arthroscopy for posterior impingement in elite professional soccer. Am J Sports Med. 2010;38(1):120-124.

        18. Akseki D, Pinar H, Bozkurt M, Yaldiz K, Arag S. The distal fascicle of the anterior inferior tibiofibular ligament as a cause of anterolateral ankle impingement: results of arthroscopic resection. Acta Orthop Scand. 1999;70(5):478-482.

        19. Baums MH, Kahl E, Schultz W, Klinger HM. Clinical outcome of the arthroscopic management of sports-related “anterior ankle pain”: a prospective study. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):482-486.

        20. Branca A, Di Palma L, Bucca C, Visconti CS, Di Mille M. Arthroscopic treatment of anterior ankle impingement. Foot Ankle Int. 1997;18(7):418-423.

        21. Di Palma L, Bucca C, Di Mille M, Branca A. Diagnosis and arthroscopic treatment of fibrous impingement of the ankle. J Sports Traumatol Relat Res. 1999;21:170-177.

        22. Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP. Arthroscopic treatment of anterolateral impingement of the ankle. Am J Sports Med. 1991;19(5):440-446.

        23. Hassan AH. Treatment of anterolateral impingements of the ankle joint by arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1150-1154.

        24. Jerosch J, Steinbeck J, Schröder M, Halm H. Arthroscopic treatment of anterior synovitis of the ankle in athletes. Knee Surg Sports Traumatol Arthrosc. 1994;2(3):176-181.

        25. Murawski CD, Kennedy JG. Anteromedial impingement in the ankle joint: outcomes following arthroscopy. Am J Sports Med. 2010;38(10):2017-2024.

        26. Ogilvie-Harris DJ, Mahomed N, Demazière A. Anterior impingement of the ankle treated by arthroscopic removal of bony spurs. J Bone Joint Surg Br. 1993;75(3):437-440.

        27. Rouvillain JL, Daoud W, Donica A, Garron E, Uzel AP. Distraction-free ankle arthroscopy for anterolateral impingement. Eur J Orthop Surg Traumatol. 2014;24(6):1019-1023.

        28. O’Kane JW, Kadel N. Anterior impingement syndrome in dancers. Curr Rev Musculoskelet Med. 2008;1(1):12-16.

        29. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. J Orthop Surg Res. 2016;11(1):97.

        30. Talusan PG, Toy J, Perez JL, Milewski MD, Reach JS. Anterior ankle impingement: diagnosis and treatment. J Am Acad Orthop Surg. 2014;22(5):333-339.

        References

        1. Lubowitz JH. Editorial commentary: ankle anterior impingement is common in athletes and could be under-recognized. Arthroscopy. 2015;31(8):1597.

        2. Mcdougall A. Footballer’s ankle. Lancet. 1955;269(6902):1219-1220.

        3. Kleiger B. Anterior tibiotalar impingement syndromes in dancers. Foot Ankle. 1982;3(2):69-73.

        4. Bassett FH 3rd, Gates HS 3rd, Billys JB, Morris HB, Nikolaou PK. Talar impingement by the anteroinferior tibiofibular ligament. A cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am. 1990;72(1):55-59.

        5. Liu SH, Raskin A, Osti L, et al. Arthroscopic treatment of anterolateral ankle impingement. Arthroscopy. 1994;10(2):215-218.

        6. Thein R, Eichenblat M. Arthroscopic treatment of sports-related synovitis of the ankle. Am J Sports Med. 1992;20(5):496-498.

        7. Arnold H. Posttraumatic impingement syndrome of the ankle—indication and results of arthroscopic therapy. Foot Ankle Surg. 2011;17(2):85-88.

        8. Walsh SJ, Twaddle BC, Rosenfeldt MP, Boyle MJ. Arthroscopic treatment of anterior ankle impingement: a prospective study of 46 patients with 5-year follow-up. Am J Sports Med. 2014;42(11):2722-2726.

        9. Glazebrook MA, Ganapathy V, Bridge MA, Stone JW, Allard JP. Evidence-based indications for ankle arthroscopy. Arthroscopy. 2009;25(12):1478-1490.

        10. Zwiers R, Wiegerinck JI, Murawski CD, Fraser EJ, Kennedy JG, van Dijk CN. Arthroscopic treatment for anterior ankle impingement: a systematic review of the current literature. Arthroscopy. 2015;31(8):1585-1596.

        11. Hawkins RB. Arthroscopic treatment of sports-related anterior osteophytes in the ankle. Foot Ankle. 1988;9(2):87-90.

        12. Rasmussen S, Hjorth Jensen C. Arthroscopic treatment of impingement of the ankle reduces pain and enhances function. Scand J Med Sci Sports. 2002;12(2):69-72.

        13. Mason-Mackay AR, Whatman C, Reid D. The effect of reduced ankle dorsiflexion on lower extremity mechanics during landing: a systematic review. J Sci Med Sport. 2017;20(5):451-458.

        14. Riley PO, Kent RW, Dierks TA, Lievers WB, Frimenko RE, Crandall JR. Foot kinematics and loading of professional athletes in American football-specific tasks. Gait Posture. 2013;38(4):563-569.

        15. Miyamoto W, Takao M, Matsui K, Matsushita T. Simultaneous ankle arthroscopy and hindfoot endoscopy for combined anterior and posterior ankle impingement syndrome in professional athletes. J Orthop Sci. 2015;20(4):642-648.

        16. Nihal A, Rose DJ, Trepman E. Arthroscopic treatment of anterior ankle impingement syndrome in dancers. Foot Ankle Int. 2005;26(11):908-912.

        17. Calder JD, Sexton SA, Pearce CJ. Return to training and playing after posterior ankle arthroscopy for posterior impingement in elite professional soccer. Am J Sports Med. 2010;38(1):120-124.

        18. Akseki D, Pinar H, Bozkurt M, Yaldiz K, Arag S. The distal fascicle of the anterior inferior tibiofibular ligament as a cause of anterolateral ankle impingement: results of arthroscopic resection. Acta Orthop Scand. 1999;70(5):478-482.

        19. Baums MH, Kahl E, Schultz W, Klinger HM. Clinical outcome of the arthroscopic management of sports-related “anterior ankle pain”: a prospective study. Knee Surg Sports Traumatol Arthrosc. 2006;14(5):482-486.

        20. Branca A, Di Palma L, Bucca C, Visconti CS, Di Mille M. Arthroscopic treatment of anterior ankle impingement. Foot Ankle Int. 1997;18(7):418-423.

        21. Di Palma L, Bucca C, Di Mille M, Branca A. Diagnosis and arthroscopic treatment of fibrous impingement of the ankle. J Sports Traumatol Relat Res. 1999;21:170-177.

        22. Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP. Arthroscopic treatment of anterolateral impingement of the ankle. Am J Sports Med. 1991;19(5):440-446.

        23. Hassan AH. Treatment of anterolateral impingements of the ankle joint by arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1150-1154.

        24. Jerosch J, Steinbeck J, Schröder M, Halm H. Arthroscopic treatment of anterior synovitis of the ankle in athletes. Knee Surg Sports Traumatol Arthrosc. 1994;2(3):176-181.

        25. Murawski CD, Kennedy JG. Anteromedial impingement in the ankle joint: outcomes following arthroscopy. Am J Sports Med. 2010;38(10):2017-2024.

        26. Ogilvie-Harris DJ, Mahomed N, Demazière A. Anterior impingement of the ankle treated by arthroscopic removal of bony spurs. J Bone Joint Surg Br. 1993;75(3):437-440.

        27. Rouvillain JL, Daoud W, Donica A, Garron E, Uzel AP. Distraction-free ankle arthroscopy for anterolateral impingement. Eur J Orthop Surg Traumatol. 2014;24(6):1019-1023.

        28. O’Kane JW, Kadel N. Anterior impingement syndrome in dancers. Curr Rev Musculoskelet Med. 2008;1(1):12-16.

        29. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. J Orthop Surg Res. 2016;11(1):97.

        30. Talusan PG, Toy J, Perez JL, Milewski MD, Reach JS. Anterior ankle impingement: diagnosis and treatment. J Am Acad Orthop Surg. 2014;22(5):333-339.

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        TAKE-HOME POINTS

        • Anterior ankle impingement can be very debilitating in elite athletes and may lead to significantly decreased performance.
        • First line treatment for anterior ankle impingement is conservative which includes rest, ankle bracing, and avoidance of repetitive dorsiflexing activities such as jumping.
        • Arthroscopic débridement of anterior ankle impingement reliably relieves pain, and restores ROM and function.
        • Arthroscopic débridement of anterior ankle impingement results in reliable RTP in professional football players.
        • RTP after arthroscopic anterior ankle débridement for impingement averaged 2 months in professional football players.
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        Knotless Tape Suture Fixation of Quadriceps Tendon Rupture: A Novel Technique

        Article Type
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        Display Headline
        Knotless Tape Suture Fixation of Quadriceps Tendon Rupture: A Novel Technique

        ABSTRACT

        Quadriceps tendon ruptures disrupt the extensor mechanism of the knee and require urgent surgical management. Traditional repair techniques have had mixed biomechanical and clinical results risking weakness and extensor lag. We describe a novel technique using tape suture and knotless anchors, which has performed superiorly during biomechanical testing and yielded terrific early clinical results. 

        Continue to: Quadriceps tendon rupture...

         

         

        Quadriceps tendon rupture is an uncommon yet potentially devastating knee injury with an estimated incidence of 1.37 in 100,000.1 It most often occurs in male, middle-aged or older patients with degenerative tendon changes and serious systemic diseases, such as chronic renal failure, diabetes mellitus, rheumatoid arthritis, and disorders requiring long-term steroid use (tissue quality is often compromised by patient age and comorbidities).2-10 Whereas partial tears with an intact extensor mechanism may be managed nonoperatively, prompt operative intervention is indicated in cases of complete tear or an incompetent extensor mechanism to facilitate early range of motion (ROM) and return of knee function.2-4,8,9

        The standard of care is repair with a nonabsorbable suture passed through transosseous patellar tunnels, often with several weeks of postoperative immobilization to protect the repair.3,4,7,10-12 Reported complications of this method include significant extension lag, decreased strength, and ROM compared with the contralateral knee, chronic pain, and iatrogenic patellar fracture.8,13-18 Repair techniques using suture anchors have been proposed as viable alternatives, but biomechanical studies comparing them with standard transosseous repair have reported mixed results.7,10-12,18-20 Two studies found improved biomechanical characteristics with suture anchors,10,21 but 2 others found the characteristics of suture anchor fixation equal to11 or worse than12 those of transosseous fixation. In light of the controversy regarding strength and clinical outcomes of suture anchor repair compared with transosseous repair, new and potentially superior surgical interventions should be considered.

        We recently completed a cadaveric study comparing the biomechanical properties of a novel quadriceps tendon repair technique using 4.75-mm biocomposite knotless suture anchors with suture tape and the properties of conventional techniques using either transosseous or suture anchor repair alone.22 In the cadaveric model, compared with transosseous and fully threaded suture anchor techniques, repair of quadriceps tendon ruptures with this knotless suture anchor with suture tape technique was biomechanically superior in cyclic displacement, construct stiffness, and ultimate load to failure.22 Additionally, this method allows for less extensive dissection, shorter operative times, and the potential for earlier and more aggressive rehabilitation protocols.22 We propose this technique, presented in this article, as a superior alternative to traditional quadriceps tendon repair techniques.

        TECHNIQUE

        The patient is placed in supine position with a tourniquet placed on the proximal thigh. A midline incision is made from the proximal pole of the patella, proximally by 5 cm. A combination of sharp and blunt dissection is performed through skin and subcutaneous tissues down to the extensor mechanism, exposing the proximal pole of the patella and the torn quadriceps tendon.

        The distal aspect of the quadriceps tendon is then débrided of any devitalized tissue and secured with an Allis clamp. A long tape suture (FiberTape; Arthrex) is then used to place a locking Krackow stitch in a distal-to-proximal and then proximal-to-distal direction for 5 throws in each direction within the quadriceps tendon, with the tails exiting distally at the tear site. Care is taken with each pass to ensure that there is no slack within the system.

        Continue to: The proximal pole of the patella...

         

         

        The proximal pole of the patella is then prepared by débriding any remaining soft tissue back to an area of exposed subcortical bone, which is débrided to a bleeding bony bed. Holes are drilled in the medial and lateral thirds of the patella at the proximal pole using the drill for 4.75-mm biocomposite knotless suture anchors (SwiveLock; Arthrex). The tap for the 4.75-mm anchors is then passed at each guide hole. In hard bone, double-tapping is recommended.

        Next, the medial strand of tape suture is loaded within a 4.75-mm biocomposite knotless suture anchor eyelet and reduced to the patella. The medial anchor is malleted and screwed into place, while tension is kept on the lateral strand with the knee in full extension. The lateral strand is then placed into its 4.75-mm biocomposite knotless suture anchor, reduced to the patella, and then malleted and screwed into place in the lateral hole, thereby completing the core portion of the repair (Figures A-D). The core strands from the 4.75-mm biocomposite knotless suture anchors are then back-passed in mattress fashion and tied, and medial and lateral retinacular repairs are then performed using supersuture tape (SutureTape or FiberWire; Arthrex).

        Suture tape repair, anterior view.

        After surgery, the patient is placed in a knee brace locked in full extension and allowed to weight-bear as tolerated using crutches. During the first week, knee ROM is allowed up to 30°. During weeks 2 to 6 passive ROM is gradually increased to 90°, and use of crutches is tapered. At week 6 the brace is unlocked for ambulation; it may be discontinued after 7 to 8 weeks or when determined safe. Light activity is permitted from month 4 to month 6. A patient who achieves satisfactory strength, is clinically examined, and progresses through rehabilitation is allowed to return to fully unrestricted sport.

        DISCUSSION

        Quadriceps tendon rupture is an uncommon clinical entity that requires early surgical management.1-5,12,17,19 The standard of care is passage of nonabsorbable sutures through transosseous patellar bone tunnels, but repair with suture anchors has been studied as an alternative that allows for less tissue trauma, decreased operative time, safe early initiation of rehabilitation protocols, and reduced risk of patella fracture or damage.3,7,10-12,18-20,21,23 Despite these potential advantages, biomechanical studies have yielded inconsistent results regarding the superiority of suture anchor repair over repair with transosseous tunnels.7,10-12,18-20 We propose quadriceps tendon repair using the 4.75-mm biocomposite knotless suture anchor with tape suture technique as a biomechanically superior alternative to either transosseous tunnels or suture anchor repair alone, with significant advantages both in and out of the operating room.

        Results of biomechanical studies comparing transosseous tunnel repair and standard suture anchor repair have been mixed, though the heterogeneity of their study methods and endpoints makes direct comparisons difficult.7,10-12,18-20 Petri and colleagues10 and Sherman and colleagues21 reported statistically significant higher load to failure10 and reduced gapping during cyclic loading10,21 with suture anchor repair relative to transosseous repair. However, Hart and colleagues12 found that repair with suture anchors had lower ultimate tensile load, and they concluded that transosseous repair is superior. Lighthart and colleagues11 found no significant difference in displacement between the 2 repairs.

        Continue to: In our cadaveric biomechanical study...

         

         

        In our cadaveric biomechanical study, a novel 4.75-mm biocomposite knotless suture anchor with suture tape repair was compared with traditional 3-tunnel transosseous repair and with standard 2-anchor suture anchor repair.22 Statistically significant superiority was found across multiple parameters, including initial tendon displacement, stiffness, and ultimate load to failure (vs 5.5-mm biocomposite fully threaded suture anchor repair), as well as initial and late tendon displacement, stiffness, and ultimate load to failure (vs transosseous repair).22 Although definitive conclusions are difficult to draw on the basis of prior cadaveric studies comparing standard suture anchor repair and transosseous repair, our results decidedly favor the biomechanical characteristics of this 4.75-mm biocomposite knotless suture anchor with suture tape repair and make it a potentially superior repair technique based on biomechanics alone.22

        Similarly to standard repair with suture anchors, repair using a 4.75-mm biocomposite knotless suture anchor with tape suture eliminates the need to expose the distal pole of the patella.7,10-12,21 This allows for a smaller surgical incision, less extensive dissection, and prevents possible interference with the patellar tendon.7,10-12,21 Additionally, it eliminates the risk of iatrogenic patellar fracture and damage to the articular surface from drilling the transpatellar tunnels.17,18 Both our own review of cases repaired with our 4.75-mm biocomposite knotless suture anchor with suture tape technique as well as studies of suture anchor repair have consistently found operative times of <1 hour.21 Shorter operative times and smaller surgical wounds are advantageous given that many of these patients have medical comorbidities that predispose them to intraoperative and wound-healing complications.12,19-22

        Optimal rehabilitation protocols for quadriceps tendon repair are a matter of controversy. Multiple studies of repair with transosseous patellar tunnels describe immobilization for 6 weeks after surgery, but there has been a recent push toward early motion.7,13,23,24 Reported complications of extended immobilization include limited flexion, pain, weakness, decreased patellar mobility, and patella baja.14 Studies have suggested that, while excessive loading can cause gap formation and weaken the repair, some controlled motion is necessary to heal the tendon23,25 and reduce the risks of stiffness and atrophy.14 The improved biomechanical characteristics of the 4.75-mm biocomposite knotless suture anchor with tape suture technique allow for safe early initiation of ROM exercises and accelerated rehabilitation protocols.

        In our early experience with this technique, functional outcomes have been excellent. A formal 2-year outcome study of patients who have undergone quadriceps tendon repair with this 4.75-mm biocomposite knotless suture anchor with tape suture technique is under way.

        References

        1. Clayton RA, Court-Brown CM. The epidemiology of musculoskeletal tendinous and ligamentous injuries. Injury. 2008;39(12):1338-1344.

        2. Rasul AT Jr, Fischer DA. Primary repair of quadriceps tendon ruptures. Clin Orthop Relat Res. 1993;(289):205-207.

        3. Ilan DI, Tejwani N, Keschner M, Leibman M. Quadriceps tendon rupture. J Am Acad Orthop Surg. 2003;11(3):192-200.

        4. Ramseier LE, Werner CM, Heinzelmann M. Quadriceps and patellar tendon rupture. Injury. 2006;37(6):516-519.

        5. Ciriello V, Gudipati S, Tosounidis T, Soucacos PN, Giannoudis PV. Clinical outcomes after repair of quadriceps tendon rupture: a systematic review. Injury. 2012;43(11):1931-1938.

        6. O’Shea K, Kenny P, Donovan J, Condon F, McElwain JP. Outcomes following quadriceps tendon ruptures. Injury. 2002;33(3):257-260.

        7. Richards DP, Barber FA. Repair of quadriceps tendon ruptures using suture anchors. Arthroscopy. 2002;18(5):556-559.

        8. Wenzl ME, Kirchner R, Seide K, Strametz S, Jürgens C. Quadriceps tendon ruptures—is there a complete functional restitution? Injury. 2004;35(9):922-926.

        9. Boudissa M, Roudet A, Rubens-Duval B, Chaussard C, Saragaglia D. Acute quadriceps tendon ruptures: a series of 50 knees with an average follow-up of more than 6 years. Orthop Traumatol Surg Res. 2014;100(2):213-216.

        10. Petri M, Dratzidis A, Brand S, et al. Suture anchor repair yields better biomechanical properties than transosseous sutures in ruptured quadriceps tendons. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1039-1045.

        11. Lighthart WC, Cohen DA, Levine RG, Parks BG, Boucher HR. Suture anchor versus suture through tunnel fixation for quadriceps tendon rupture: a biomechanical study. Orthopedics. 2008;31(5):441.

        12. Hart ND, Wallace MK, Scovell JF, Krupp RJ, Cook C, Wyland DJ. Quadriceps tendon rupture: a biomechanical comparison of transosseous equivalent double-row suture anchor versus transosseous tunnel repair. J Knee Surg. 2012;25(4):335-339.

        13. Rougraff BT, Reeck CC, Essenmacher J. Complete quadriceps tendon ruptures. Orthopedics. 1996;19(6):509-514.

        14. West JL, Keene JS, Kaplan LD. Early motion after quadriceps and patellar tendon repairs: outcomes with single-suture augmentation. Am J Sports Med. 2008;36(2):316-323.

        15. De Baere T, Geulette B, Manche E, Barras L. Functional results after surgical repair of quadriceps tendon rupture. Acta Orthop Belg. 2002;68(2):146-149.

        16. Konrath GA, Chen D, Lock T, et al. Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma. 1998;12(4):273-279.

        17. Gregory JM, Sherman SL, Mather R, Bach BR Jr. Patellar stress fracture after transosseous extensor mechanism repair: report of 3 cases. Am J Sports Med. 2012;40(7):1668-1672.

        18. Bushnell BD, Whitener GB, Rubright JH, Creighton RA, Logel KJ, Wood ML. The use of suture anchors to repair the ruptured quadriceps tendon. J Orthop Trauma. 2007;21(6):407-413.

        19. Harris JD, Abrams GD, Yanke AB, Hellman MD, Erickson BJ, Bach BR Jr. Suture anchor repair of quadriceps tendon rupture. Orthopedics. 2014;37(3):183-186.

        20. Maniscalco P, Bertone C, Rivera F, Bocchi L. A new method of repair for quadriceps tendon ruptures. A case report. Panminerva Med. 2000;42(3):223-225.

        21. Sherman SL, Copeland ME, Milles JL, Flood DA, Pfeiffer FM. Biomechanical evaluation of suture anchor versus transosseous tunnel quadriceps tendon repair techniques. Arthroscopy. 2016;32(6):1117-1124.

        22. Kindya MC, Konicek J, Rizzi A, Komatsu DE, Paci JM. Knotless suture anchor with suture tape quadriceps tendon repair is biomechanically superior to transosseous and traditional suture anchor-based repairs in a cadaveric model. Arthroscopy. 2017;33(1):190-198.

        23. Brossard P, Le Roux G, Vasse B; Orthopedics, Traumatology Society of Western France (SOO). Acute quadriceps tendon rupture repaired by suture anchors: outcomes at 7 years’ follow-up in 25 cases. Orthop Traumatol Surg Res. 2017;103(4):597-601.

        24. Langenhan R, Baumann M, Ricart P, et al. Postoperative functional rehabilitation after repair of quadriceps tendon ruptures: a comparison of two different protocols. Knee Surg Sports Traumatol Arthrosc. 2012;20(11):2275-2278.

        25. Killian ML, Cavinatto L, Galatz LM, Thomopoulos S. The role of mechanobiology in tendon healing. J Shoulder Elbow Surg. 2012;21(2):228-237.

        Author and Disclosure Information

        Authors’ Disclosure Statement: Dr. Paci reports that he receives research support and is an educational consultant for Arthrex, Rotation Medical, and Zimmer Biomet. Dr. Pawlak reports no actual or potential conflict of interest in relation to this article. 

        Dr. Paci is a Team Physician for Stony Brook University and an Associate Professor, and Dr. Pawlak is a Resident, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, Stony Brook, New York.

        Address correspondence to: James M. Paci, MD, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, 101 Nicolls Road, Stony Brook, NY 11794 (tel, 631-444-1496; email, james_paci@yahoo.com).

        James M. Paci, MD Amanda Pawlak, MD . Knotless Tape Suture Fixation of Quadriceps Tendon Rupture: A Novel Technique. Am J Orthop. January 26, 2018

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        Author and Disclosure Information

        Authors’ Disclosure Statement: Dr. Paci reports that he receives research support and is an educational consultant for Arthrex, Rotation Medical, and Zimmer Biomet. Dr. Pawlak reports no actual or potential conflict of interest in relation to this article. 

        Dr. Paci is a Team Physician for Stony Brook University and an Associate Professor, and Dr. Pawlak is a Resident, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, Stony Brook, New York.

        Address correspondence to: James M. Paci, MD, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, 101 Nicolls Road, Stony Brook, NY 11794 (tel, 631-444-1496; email, james_paci@yahoo.com).

        James M. Paci, MD Amanda Pawlak, MD . Knotless Tape Suture Fixation of Quadriceps Tendon Rupture: A Novel Technique. Am J Orthop. January 26, 2018

        Author and Disclosure Information

        Authors’ Disclosure Statement: Dr. Paci reports that he receives research support and is an educational consultant for Arthrex, Rotation Medical, and Zimmer Biomet. Dr. Pawlak reports no actual or potential conflict of interest in relation to this article. 

        Dr. Paci is a Team Physician for Stony Brook University and an Associate Professor, and Dr. Pawlak is a Resident, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, Stony Brook, New York.

        Address correspondence to: James M. Paci, MD, Department of Orthopaedic Surgery, Stony Brook University School of Medicine, 101 Nicolls Road, Stony Brook, NY 11794 (tel, 631-444-1496; email, james_paci@yahoo.com).

        James M. Paci, MD Amanda Pawlak, MD . Knotless Tape Suture Fixation of Quadriceps Tendon Rupture: A Novel Technique. Am J Orthop. January 26, 2018

        ABSTRACT

        Quadriceps tendon ruptures disrupt the extensor mechanism of the knee and require urgent surgical management. Traditional repair techniques have had mixed biomechanical and clinical results risking weakness and extensor lag. We describe a novel technique using tape suture and knotless anchors, which has performed superiorly during biomechanical testing and yielded terrific early clinical results. 

        Continue to: Quadriceps tendon rupture...

         

         

        Quadriceps tendon rupture is an uncommon yet potentially devastating knee injury with an estimated incidence of 1.37 in 100,000.1 It most often occurs in male, middle-aged or older patients with degenerative tendon changes and serious systemic diseases, such as chronic renal failure, diabetes mellitus, rheumatoid arthritis, and disorders requiring long-term steroid use (tissue quality is often compromised by patient age and comorbidities).2-10 Whereas partial tears with an intact extensor mechanism may be managed nonoperatively, prompt operative intervention is indicated in cases of complete tear or an incompetent extensor mechanism to facilitate early range of motion (ROM) and return of knee function.2-4,8,9

        The standard of care is repair with a nonabsorbable suture passed through transosseous patellar tunnels, often with several weeks of postoperative immobilization to protect the repair.3,4,7,10-12 Reported complications of this method include significant extension lag, decreased strength, and ROM compared with the contralateral knee, chronic pain, and iatrogenic patellar fracture.8,13-18 Repair techniques using suture anchors have been proposed as viable alternatives, but biomechanical studies comparing them with standard transosseous repair have reported mixed results.7,10-12,18-20 Two studies found improved biomechanical characteristics with suture anchors,10,21 but 2 others found the characteristics of suture anchor fixation equal to11 or worse than12 those of transosseous fixation. In light of the controversy regarding strength and clinical outcomes of suture anchor repair compared with transosseous repair, new and potentially superior surgical interventions should be considered.

        We recently completed a cadaveric study comparing the biomechanical properties of a novel quadriceps tendon repair technique using 4.75-mm biocomposite knotless suture anchors with suture tape and the properties of conventional techniques using either transosseous or suture anchor repair alone.22 In the cadaveric model, compared with transosseous and fully threaded suture anchor techniques, repair of quadriceps tendon ruptures with this knotless suture anchor with suture tape technique was biomechanically superior in cyclic displacement, construct stiffness, and ultimate load to failure.22 Additionally, this method allows for less extensive dissection, shorter operative times, and the potential for earlier and more aggressive rehabilitation protocols.22 We propose this technique, presented in this article, as a superior alternative to traditional quadriceps tendon repair techniques.

        TECHNIQUE

        The patient is placed in supine position with a tourniquet placed on the proximal thigh. A midline incision is made from the proximal pole of the patella, proximally by 5 cm. A combination of sharp and blunt dissection is performed through skin and subcutaneous tissues down to the extensor mechanism, exposing the proximal pole of the patella and the torn quadriceps tendon.

        The distal aspect of the quadriceps tendon is then débrided of any devitalized tissue and secured with an Allis clamp. A long tape suture (FiberTape; Arthrex) is then used to place a locking Krackow stitch in a distal-to-proximal and then proximal-to-distal direction for 5 throws in each direction within the quadriceps tendon, with the tails exiting distally at the tear site. Care is taken with each pass to ensure that there is no slack within the system.

        Continue to: The proximal pole of the patella...

         

         

        The proximal pole of the patella is then prepared by débriding any remaining soft tissue back to an area of exposed subcortical bone, which is débrided to a bleeding bony bed. Holes are drilled in the medial and lateral thirds of the patella at the proximal pole using the drill for 4.75-mm biocomposite knotless suture anchors (SwiveLock; Arthrex). The tap for the 4.75-mm anchors is then passed at each guide hole. In hard bone, double-tapping is recommended.

        Next, the medial strand of tape suture is loaded within a 4.75-mm biocomposite knotless suture anchor eyelet and reduced to the patella. The medial anchor is malleted and screwed into place, while tension is kept on the lateral strand with the knee in full extension. The lateral strand is then placed into its 4.75-mm biocomposite knotless suture anchor, reduced to the patella, and then malleted and screwed into place in the lateral hole, thereby completing the core portion of the repair (Figures A-D). The core strands from the 4.75-mm biocomposite knotless suture anchors are then back-passed in mattress fashion and tied, and medial and lateral retinacular repairs are then performed using supersuture tape (SutureTape or FiberWire; Arthrex).

        Suture tape repair, anterior view.

        After surgery, the patient is placed in a knee brace locked in full extension and allowed to weight-bear as tolerated using crutches. During the first week, knee ROM is allowed up to 30°. During weeks 2 to 6 passive ROM is gradually increased to 90°, and use of crutches is tapered. At week 6 the brace is unlocked for ambulation; it may be discontinued after 7 to 8 weeks or when determined safe. Light activity is permitted from month 4 to month 6. A patient who achieves satisfactory strength, is clinically examined, and progresses through rehabilitation is allowed to return to fully unrestricted sport.

        DISCUSSION

        Quadriceps tendon rupture is an uncommon clinical entity that requires early surgical management.1-5,12,17,19 The standard of care is passage of nonabsorbable sutures through transosseous patellar bone tunnels, but repair with suture anchors has been studied as an alternative that allows for less tissue trauma, decreased operative time, safe early initiation of rehabilitation protocols, and reduced risk of patella fracture or damage.3,7,10-12,18-20,21,23 Despite these potential advantages, biomechanical studies have yielded inconsistent results regarding the superiority of suture anchor repair over repair with transosseous tunnels.7,10-12,18-20 We propose quadriceps tendon repair using the 4.75-mm biocomposite knotless suture anchor with tape suture technique as a biomechanically superior alternative to either transosseous tunnels or suture anchor repair alone, with significant advantages both in and out of the operating room.

        Results of biomechanical studies comparing transosseous tunnel repair and standard suture anchor repair have been mixed, though the heterogeneity of their study methods and endpoints makes direct comparisons difficult.7,10-12,18-20 Petri and colleagues10 and Sherman and colleagues21 reported statistically significant higher load to failure10 and reduced gapping during cyclic loading10,21 with suture anchor repair relative to transosseous repair. However, Hart and colleagues12 found that repair with suture anchors had lower ultimate tensile load, and they concluded that transosseous repair is superior. Lighthart and colleagues11 found no significant difference in displacement between the 2 repairs.

        Continue to: In our cadaveric biomechanical study...

         

         

        In our cadaveric biomechanical study, a novel 4.75-mm biocomposite knotless suture anchor with suture tape repair was compared with traditional 3-tunnel transosseous repair and with standard 2-anchor suture anchor repair.22 Statistically significant superiority was found across multiple parameters, including initial tendon displacement, stiffness, and ultimate load to failure (vs 5.5-mm biocomposite fully threaded suture anchor repair), as well as initial and late tendon displacement, stiffness, and ultimate load to failure (vs transosseous repair).22 Although definitive conclusions are difficult to draw on the basis of prior cadaveric studies comparing standard suture anchor repair and transosseous repair, our results decidedly favor the biomechanical characteristics of this 4.75-mm biocomposite knotless suture anchor with suture tape repair and make it a potentially superior repair technique based on biomechanics alone.22

        Similarly to standard repair with suture anchors, repair using a 4.75-mm biocomposite knotless suture anchor with tape suture eliminates the need to expose the distal pole of the patella.7,10-12,21 This allows for a smaller surgical incision, less extensive dissection, and prevents possible interference with the patellar tendon.7,10-12,21 Additionally, it eliminates the risk of iatrogenic patellar fracture and damage to the articular surface from drilling the transpatellar tunnels.17,18 Both our own review of cases repaired with our 4.75-mm biocomposite knotless suture anchor with suture tape technique as well as studies of suture anchor repair have consistently found operative times of <1 hour.21 Shorter operative times and smaller surgical wounds are advantageous given that many of these patients have medical comorbidities that predispose them to intraoperative and wound-healing complications.12,19-22

        Optimal rehabilitation protocols for quadriceps tendon repair are a matter of controversy. Multiple studies of repair with transosseous patellar tunnels describe immobilization for 6 weeks after surgery, but there has been a recent push toward early motion.7,13,23,24 Reported complications of extended immobilization include limited flexion, pain, weakness, decreased patellar mobility, and patella baja.14 Studies have suggested that, while excessive loading can cause gap formation and weaken the repair, some controlled motion is necessary to heal the tendon23,25 and reduce the risks of stiffness and atrophy.14 The improved biomechanical characteristics of the 4.75-mm biocomposite knotless suture anchor with tape suture technique allow for safe early initiation of ROM exercises and accelerated rehabilitation protocols.

        In our early experience with this technique, functional outcomes have been excellent. A formal 2-year outcome study of patients who have undergone quadriceps tendon repair with this 4.75-mm biocomposite knotless suture anchor with tape suture technique is under way.

        ABSTRACT

        Quadriceps tendon ruptures disrupt the extensor mechanism of the knee and require urgent surgical management. Traditional repair techniques have had mixed biomechanical and clinical results risking weakness and extensor lag. We describe a novel technique using tape suture and knotless anchors, which has performed superiorly during biomechanical testing and yielded terrific early clinical results. 

        Continue to: Quadriceps tendon rupture...

         

         

        Quadriceps tendon rupture is an uncommon yet potentially devastating knee injury with an estimated incidence of 1.37 in 100,000.1 It most often occurs in male, middle-aged or older patients with degenerative tendon changes and serious systemic diseases, such as chronic renal failure, diabetes mellitus, rheumatoid arthritis, and disorders requiring long-term steroid use (tissue quality is often compromised by patient age and comorbidities).2-10 Whereas partial tears with an intact extensor mechanism may be managed nonoperatively, prompt operative intervention is indicated in cases of complete tear or an incompetent extensor mechanism to facilitate early range of motion (ROM) and return of knee function.2-4,8,9

        The standard of care is repair with a nonabsorbable suture passed through transosseous patellar tunnels, often with several weeks of postoperative immobilization to protect the repair.3,4,7,10-12 Reported complications of this method include significant extension lag, decreased strength, and ROM compared with the contralateral knee, chronic pain, and iatrogenic patellar fracture.8,13-18 Repair techniques using suture anchors have been proposed as viable alternatives, but biomechanical studies comparing them with standard transosseous repair have reported mixed results.7,10-12,18-20 Two studies found improved biomechanical characteristics with suture anchors,10,21 but 2 others found the characteristics of suture anchor fixation equal to11 or worse than12 those of transosseous fixation. In light of the controversy regarding strength and clinical outcomes of suture anchor repair compared with transosseous repair, new and potentially superior surgical interventions should be considered.

        We recently completed a cadaveric study comparing the biomechanical properties of a novel quadriceps tendon repair technique using 4.75-mm biocomposite knotless suture anchors with suture tape and the properties of conventional techniques using either transosseous or suture anchor repair alone.22 In the cadaveric model, compared with transosseous and fully threaded suture anchor techniques, repair of quadriceps tendon ruptures with this knotless suture anchor with suture tape technique was biomechanically superior in cyclic displacement, construct stiffness, and ultimate load to failure.22 Additionally, this method allows for less extensive dissection, shorter operative times, and the potential for earlier and more aggressive rehabilitation protocols.22 We propose this technique, presented in this article, as a superior alternative to traditional quadriceps tendon repair techniques.

        TECHNIQUE

        The patient is placed in supine position with a tourniquet placed on the proximal thigh. A midline incision is made from the proximal pole of the patella, proximally by 5 cm. A combination of sharp and blunt dissection is performed through skin and subcutaneous tissues down to the extensor mechanism, exposing the proximal pole of the patella and the torn quadriceps tendon.

        The distal aspect of the quadriceps tendon is then débrided of any devitalized tissue and secured with an Allis clamp. A long tape suture (FiberTape; Arthrex) is then used to place a locking Krackow stitch in a distal-to-proximal and then proximal-to-distal direction for 5 throws in each direction within the quadriceps tendon, with the tails exiting distally at the tear site. Care is taken with each pass to ensure that there is no slack within the system.

        Continue to: The proximal pole of the patella...

         

         

        The proximal pole of the patella is then prepared by débriding any remaining soft tissue back to an area of exposed subcortical bone, which is débrided to a bleeding bony bed. Holes are drilled in the medial and lateral thirds of the patella at the proximal pole using the drill for 4.75-mm biocomposite knotless suture anchors (SwiveLock; Arthrex). The tap for the 4.75-mm anchors is then passed at each guide hole. In hard bone, double-tapping is recommended.

        Next, the medial strand of tape suture is loaded within a 4.75-mm biocomposite knotless suture anchor eyelet and reduced to the patella. The medial anchor is malleted and screwed into place, while tension is kept on the lateral strand with the knee in full extension. The lateral strand is then placed into its 4.75-mm biocomposite knotless suture anchor, reduced to the patella, and then malleted and screwed into place in the lateral hole, thereby completing the core portion of the repair (Figures A-D). The core strands from the 4.75-mm biocomposite knotless suture anchors are then back-passed in mattress fashion and tied, and medial and lateral retinacular repairs are then performed using supersuture tape (SutureTape or FiberWire; Arthrex).

        Suture tape repair, anterior view.

        After surgery, the patient is placed in a knee brace locked in full extension and allowed to weight-bear as tolerated using crutches. During the first week, knee ROM is allowed up to 30°. During weeks 2 to 6 passive ROM is gradually increased to 90°, and use of crutches is tapered. At week 6 the brace is unlocked for ambulation; it may be discontinued after 7 to 8 weeks or when determined safe. Light activity is permitted from month 4 to month 6. A patient who achieves satisfactory strength, is clinically examined, and progresses through rehabilitation is allowed to return to fully unrestricted sport.

        DISCUSSION

        Quadriceps tendon rupture is an uncommon clinical entity that requires early surgical management.1-5,12,17,19 The standard of care is passage of nonabsorbable sutures through transosseous patellar bone tunnels, but repair with suture anchors has been studied as an alternative that allows for less tissue trauma, decreased operative time, safe early initiation of rehabilitation protocols, and reduced risk of patella fracture or damage.3,7,10-12,18-20,21,23 Despite these potential advantages, biomechanical studies have yielded inconsistent results regarding the superiority of suture anchor repair over repair with transosseous tunnels.7,10-12,18-20 We propose quadriceps tendon repair using the 4.75-mm biocomposite knotless suture anchor with tape suture technique as a biomechanically superior alternative to either transosseous tunnels or suture anchor repair alone, with significant advantages both in and out of the operating room.

        Results of biomechanical studies comparing transosseous tunnel repair and standard suture anchor repair have been mixed, though the heterogeneity of their study methods and endpoints makes direct comparisons difficult.7,10-12,18-20 Petri and colleagues10 and Sherman and colleagues21 reported statistically significant higher load to failure10 and reduced gapping during cyclic loading10,21 with suture anchor repair relative to transosseous repair. However, Hart and colleagues12 found that repair with suture anchors had lower ultimate tensile load, and they concluded that transosseous repair is superior. Lighthart and colleagues11 found no significant difference in displacement between the 2 repairs.

        Continue to: In our cadaveric biomechanical study...

         

         

        In our cadaveric biomechanical study, a novel 4.75-mm biocomposite knotless suture anchor with suture tape repair was compared with traditional 3-tunnel transosseous repair and with standard 2-anchor suture anchor repair.22 Statistically significant superiority was found across multiple parameters, including initial tendon displacement, stiffness, and ultimate load to failure (vs 5.5-mm biocomposite fully threaded suture anchor repair), as well as initial and late tendon displacement, stiffness, and ultimate load to failure (vs transosseous repair).22 Although definitive conclusions are difficult to draw on the basis of prior cadaveric studies comparing standard suture anchor repair and transosseous repair, our results decidedly favor the biomechanical characteristics of this 4.75-mm biocomposite knotless suture anchor with suture tape repair and make it a potentially superior repair technique based on biomechanics alone.22

        Similarly to standard repair with suture anchors, repair using a 4.75-mm biocomposite knotless suture anchor with tape suture eliminates the need to expose the distal pole of the patella.7,10-12,21 This allows for a smaller surgical incision, less extensive dissection, and prevents possible interference with the patellar tendon.7,10-12,21 Additionally, it eliminates the risk of iatrogenic patellar fracture and damage to the articular surface from drilling the transpatellar tunnels.17,18 Both our own review of cases repaired with our 4.75-mm biocomposite knotless suture anchor with suture tape technique as well as studies of suture anchor repair have consistently found operative times of <1 hour.21 Shorter operative times and smaller surgical wounds are advantageous given that many of these patients have medical comorbidities that predispose them to intraoperative and wound-healing complications.12,19-22

        Optimal rehabilitation protocols for quadriceps tendon repair are a matter of controversy. Multiple studies of repair with transosseous patellar tunnels describe immobilization for 6 weeks after surgery, but there has been a recent push toward early motion.7,13,23,24 Reported complications of extended immobilization include limited flexion, pain, weakness, decreased patellar mobility, and patella baja.14 Studies have suggested that, while excessive loading can cause gap formation and weaken the repair, some controlled motion is necessary to heal the tendon23,25 and reduce the risks of stiffness and atrophy.14 The improved biomechanical characteristics of the 4.75-mm biocomposite knotless suture anchor with tape suture technique allow for safe early initiation of ROM exercises and accelerated rehabilitation protocols.

        In our early experience with this technique, functional outcomes have been excellent. A formal 2-year outcome study of patients who have undergone quadriceps tendon repair with this 4.75-mm biocomposite knotless suture anchor with tape suture technique is under way.

        References

        1. Clayton RA, Court-Brown CM. The epidemiology of musculoskeletal tendinous and ligamentous injuries. Injury. 2008;39(12):1338-1344.

        2. Rasul AT Jr, Fischer DA. Primary repair of quadriceps tendon ruptures. Clin Orthop Relat Res. 1993;(289):205-207.

        3. Ilan DI, Tejwani N, Keschner M, Leibman M. Quadriceps tendon rupture. J Am Acad Orthop Surg. 2003;11(3):192-200.

        4. Ramseier LE, Werner CM, Heinzelmann M. Quadriceps and patellar tendon rupture. Injury. 2006;37(6):516-519.

        5. Ciriello V, Gudipati S, Tosounidis T, Soucacos PN, Giannoudis PV. Clinical outcomes after repair of quadriceps tendon rupture: a systematic review. Injury. 2012;43(11):1931-1938.

        6. O’Shea K, Kenny P, Donovan J, Condon F, McElwain JP. Outcomes following quadriceps tendon ruptures. Injury. 2002;33(3):257-260.

        7. Richards DP, Barber FA. Repair of quadriceps tendon ruptures using suture anchors. Arthroscopy. 2002;18(5):556-559.

        8. Wenzl ME, Kirchner R, Seide K, Strametz S, Jürgens C. Quadriceps tendon ruptures—is there a complete functional restitution? Injury. 2004;35(9):922-926.

        9. Boudissa M, Roudet A, Rubens-Duval B, Chaussard C, Saragaglia D. Acute quadriceps tendon ruptures: a series of 50 knees with an average follow-up of more than 6 years. Orthop Traumatol Surg Res. 2014;100(2):213-216.

        10. Petri M, Dratzidis A, Brand S, et al. Suture anchor repair yields better biomechanical properties than transosseous sutures in ruptured quadriceps tendons. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1039-1045.

        11. Lighthart WC, Cohen DA, Levine RG, Parks BG, Boucher HR. Suture anchor versus suture through tunnel fixation for quadriceps tendon rupture: a biomechanical study. Orthopedics. 2008;31(5):441.

        12. Hart ND, Wallace MK, Scovell JF, Krupp RJ, Cook C, Wyland DJ. Quadriceps tendon rupture: a biomechanical comparison of transosseous equivalent double-row suture anchor versus transosseous tunnel repair. J Knee Surg. 2012;25(4):335-339.

        13. Rougraff BT, Reeck CC, Essenmacher J. Complete quadriceps tendon ruptures. Orthopedics. 1996;19(6):509-514.

        14. West JL, Keene JS, Kaplan LD. Early motion after quadriceps and patellar tendon repairs: outcomes with single-suture augmentation. Am J Sports Med. 2008;36(2):316-323.

        15. De Baere T, Geulette B, Manche E, Barras L. Functional results after surgical repair of quadriceps tendon rupture. Acta Orthop Belg. 2002;68(2):146-149.

        16. Konrath GA, Chen D, Lock T, et al. Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma. 1998;12(4):273-279.

        17. Gregory JM, Sherman SL, Mather R, Bach BR Jr. Patellar stress fracture after transosseous extensor mechanism repair: report of 3 cases. Am J Sports Med. 2012;40(7):1668-1672.

        18. Bushnell BD, Whitener GB, Rubright JH, Creighton RA, Logel KJ, Wood ML. The use of suture anchors to repair the ruptured quadriceps tendon. J Orthop Trauma. 2007;21(6):407-413.

        19. Harris JD, Abrams GD, Yanke AB, Hellman MD, Erickson BJ, Bach BR Jr. Suture anchor repair of quadriceps tendon rupture. Orthopedics. 2014;37(3):183-186.

        20. Maniscalco P, Bertone C, Rivera F, Bocchi L. A new method of repair for quadriceps tendon ruptures. A case report. Panminerva Med. 2000;42(3):223-225.

        21. Sherman SL, Copeland ME, Milles JL, Flood DA, Pfeiffer FM. Biomechanical evaluation of suture anchor versus transosseous tunnel quadriceps tendon repair techniques. Arthroscopy. 2016;32(6):1117-1124.

        22. Kindya MC, Konicek J, Rizzi A, Komatsu DE, Paci JM. Knotless suture anchor with suture tape quadriceps tendon repair is biomechanically superior to transosseous and traditional suture anchor-based repairs in a cadaveric model. Arthroscopy. 2017;33(1):190-198.

        23. Brossard P, Le Roux G, Vasse B; Orthopedics, Traumatology Society of Western France (SOO). Acute quadriceps tendon rupture repaired by suture anchors: outcomes at 7 years’ follow-up in 25 cases. Orthop Traumatol Surg Res. 2017;103(4):597-601.

        24. Langenhan R, Baumann M, Ricart P, et al. Postoperative functional rehabilitation after repair of quadriceps tendon ruptures: a comparison of two different protocols. Knee Surg Sports Traumatol Arthrosc. 2012;20(11):2275-2278.

        25. Killian ML, Cavinatto L, Galatz LM, Thomopoulos S. The role of mechanobiology in tendon healing. J Shoulder Elbow Surg. 2012;21(2):228-237.

        References

        1. Clayton RA, Court-Brown CM. The epidemiology of musculoskeletal tendinous and ligamentous injuries. Injury. 2008;39(12):1338-1344.

        2. Rasul AT Jr, Fischer DA. Primary repair of quadriceps tendon ruptures. Clin Orthop Relat Res. 1993;(289):205-207.

        3. Ilan DI, Tejwani N, Keschner M, Leibman M. Quadriceps tendon rupture. J Am Acad Orthop Surg. 2003;11(3):192-200.

        4. Ramseier LE, Werner CM, Heinzelmann M. Quadriceps and patellar tendon rupture. Injury. 2006;37(6):516-519.

        5. Ciriello V, Gudipati S, Tosounidis T, Soucacos PN, Giannoudis PV. Clinical outcomes after repair of quadriceps tendon rupture: a systematic review. Injury. 2012;43(11):1931-1938.

        6. O’Shea K, Kenny P, Donovan J, Condon F, McElwain JP. Outcomes following quadriceps tendon ruptures. Injury. 2002;33(3):257-260.

        7. Richards DP, Barber FA. Repair of quadriceps tendon ruptures using suture anchors. Arthroscopy. 2002;18(5):556-559.

        8. Wenzl ME, Kirchner R, Seide K, Strametz S, Jürgens C. Quadriceps tendon ruptures—is there a complete functional restitution? Injury. 2004;35(9):922-926.

        9. Boudissa M, Roudet A, Rubens-Duval B, Chaussard C, Saragaglia D. Acute quadriceps tendon ruptures: a series of 50 knees with an average follow-up of more than 6 years. Orthop Traumatol Surg Res. 2014;100(2):213-216.

        10. Petri M, Dratzidis A, Brand S, et al. Suture anchor repair yields better biomechanical properties than transosseous sutures in ruptured quadriceps tendons. Knee Surg Sports Traumatol Arthrosc. 2015;23(4):1039-1045.

        11. Lighthart WC, Cohen DA, Levine RG, Parks BG, Boucher HR. Suture anchor versus suture through tunnel fixation for quadriceps tendon rupture: a biomechanical study. Orthopedics. 2008;31(5):441.

        12. Hart ND, Wallace MK, Scovell JF, Krupp RJ, Cook C, Wyland DJ. Quadriceps tendon rupture: a biomechanical comparison of transosseous equivalent double-row suture anchor versus transosseous tunnel repair. J Knee Surg. 2012;25(4):335-339.

        13. Rougraff BT, Reeck CC, Essenmacher J. Complete quadriceps tendon ruptures. Orthopedics. 1996;19(6):509-514.

        14. West JL, Keene JS, Kaplan LD. Early motion after quadriceps and patellar tendon repairs: outcomes with single-suture augmentation. Am J Sports Med. 2008;36(2):316-323.

        15. De Baere T, Geulette B, Manche E, Barras L. Functional results after surgical repair of quadriceps tendon rupture. Acta Orthop Belg. 2002;68(2):146-149.

        16. Konrath GA, Chen D, Lock T, et al. Outcomes following repair of quadriceps tendon ruptures. J Orthop Trauma. 1998;12(4):273-279.

        17. Gregory JM, Sherman SL, Mather R, Bach BR Jr. Patellar stress fracture after transosseous extensor mechanism repair: report of 3 cases. Am J Sports Med. 2012;40(7):1668-1672.

        18. Bushnell BD, Whitener GB, Rubright JH, Creighton RA, Logel KJ, Wood ML. The use of suture anchors to repair the ruptured quadriceps tendon. J Orthop Trauma. 2007;21(6):407-413.

        19. Harris JD, Abrams GD, Yanke AB, Hellman MD, Erickson BJ, Bach BR Jr. Suture anchor repair of quadriceps tendon rupture. Orthopedics. 2014;37(3):183-186.

        20. Maniscalco P, Bertone C, Rivera F, Bocchi L. A new method of repair for quadriceps tendon ruptures. A case report. Panminerva Med. 2000;42(3):223-225.

        21. Sherman SL, Copeland ME, Milles JL, Flood DA, Pfeiffer FM. Biomechanical evaluation of suture anchor versus transosseous tunnel quadriceps tendon repair techniques. Arthroscopy. 2016;32(6):1117-1124.

        22. Kindya MC, Konicek J, Rizzi A, Komatsu DE, Paci JM. Knotless suture anchor with suture tape quadriceps tendon repair is biomechanically superior to transosseous and traditional suture anchor-based repairs in a cadaveric model. Arthroscopy. 2017;33(1):190-198.

        23. Brossard P, Le Roux G, Vasse B; Orthopedics, Traumatology Society of Western France (SOO). Acute quadriceps tendon rupture repaired by suture anchors: outcomes at 7 years’ follow-up in 25 cases. Orthop Traumatol Surg Res. 2017;103(4):597-601.

        24. Langenhan R, Baumann M, Ricart P, et al. Postoperative functional rehabilitation after repair of quadriceps tendon ruptures: a comparison of two different protocols. Knee Surg Sports Traumatol Arthrosc. 2012;20(11):2275-2278.

        25. Killian ML, Cavinatto L, Galatz LM, Thomopoulos S. The role of mechanobiology in tendon healing. J Shoulder Elbow Surg. 2012;21(2):228-237.

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        TAKE-HOME POINTS

        • Knotless tape suture fixation of the quadriceps tendon is biomechanically superior to traditional fixation techniques.
        • When passing locking Krackow stitches, be sure to take all slack out with each pass.
        • Consider double tapping the patella pilot holes prior to placing anchors, as the bone is very hard.
        • Palpate the articular surface of the patella when drilling pilot holes for safe placement.
        • Perform an adequate retinacular repair to complete the repair.
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        Diagnosing Multiple Myeloma in Primary Care

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        Diagnosing Multiple Myeloma in Primary Care

        IN THIS ARTICLE

        • Presenting symptoms
        • Diagnostic tests
        • Differential diagnostic criteria

        Multiple myeloma (MM) is a fatal, malignant neoplasm that originates in the plasma cells of bone marrow. A genetic mutation in the plasma cells creates myeloma cells, which replicate and produce monoclonal protein (M-protein). This accumulation of cells and abnormal protein can result in destruction and eventual marrow failure.1,2

        MM’s insidious nature means it often goes undetected or misdiagnosed in its early stages; this delayed diagnosis can cause sequelae that limit quality of life. Furthermore, the five-year survival rate for myeloma varies by stage at which the disease is diagnosed: from 48% for distant (metastasized) myeloma to 71% for localized disease.3 It has also been noted that, in the past two decades, improvements in available treatment options and supportive care have contributed to a doubling of median survival time (from three years to six years).4 It is therefore paramount that providers be aware of MM and its signs to facilitate early diagnosis and treatment.

        INCIDENCE AND EPIDEMIOLOGY

        MM accounts for 1% of all cancers and about 10% of all hematologic malignancies.5 In 2017, the American Cancer Society estimated that more than 30,000 new cases of MM would be diagnosed in the United States.6 Additionally, MM was expected to cause more than 12,000 deaths last year.6

        Median age at diagnosis is 69.3 In fact, 75% of men are older than 75 and 79% of women are older than 70 at diagnosis.1

        Apart from age, other risk factors for MM have been identified but not fully explicated. For example, the disease is more common in men than in women (with men comprising two-thirds of new cases per year).3 MM is also two to three times more common in black than in white persons, making it the most common hematologic malignancy in this demographic group.3,7

        The possibility of a genetic predisposition has also been studied. Several analyses have indicated an increased risk for MM in patients with a family history of the disease—as much as four times higher in those with an affected first-degree relative. This risk was further elevated in black compared with white patients (odds ratios, 17.4 and 1.5, respectively).7 However, many patients with MM have no relatives with this disorder.6,8

        DISEASE PROGRESSION

        Almost all patients who develop MM also experience an asymptomatic premalignant stage called monoclonal gammopathy of undetermined significance (MGUS). MGUS is present in 3% to 4% of the general population older than 50 and is often an incidental finding. This stage almost always precedes MM—but because it is asymptomatic, only 10% of individuals diagnosed with MM have a known history of MGUS.8

        In some patients, an asymptomatic intermediate stage called smoldering multiple myeloma (SMM) can be identified. SMM progresses to MM at a rate of 10% per year for the first five years; the rate decreases to 3% per year over the following five years, and 1% per year after that.8

        MM is not curable, but as noted, the survival rate is steadily increasing due to rapidly evolving treatment regimens. Discussion of treatment is outside the scope of this article, but early diagnosis can improve quality of life and clinical outcomes and prolong life expectancy.

        SYMPTOMS

        The initial symptoms of MM can be nonspecific and may lead the provider to suspect a host of other conditions.2,6 (Those for advanced disease are also vague but tend to be more pronounced.) These may include fatigue, weakness, easy bruising or bleeding, and bone pain. Other common clinical manifestations of MM are anemia, chronic infection, bone disease, and/or renal failure.1,4 Patients may also experience loss of appetite, nausea, vomiting, increased thirst, and increased urination.9

        Recent studies have shown that patients with SMM and/or MGUS also exhibit early signs of bone disease and increased risk for fracture.10 Eighty percent of patients who progress to MM have evidence of pathologic bone fractures.10 It is also possible for bones in the spine to weaken and collapse, pressing on the spinal nerves. This is known as spinal cord compression, which can manifest with sudden, severe back pain or numbness and/or muscle weakness (most often in the legs).6

        MM must be included in the differential diagnosis, particularly when symptoms do not point to one specific disease process. Without early diagnosis, disease progression can result in complications such as bone fracture and osteoporosis, reduced kidney function, peripheral neuropathy, chronic anemia, and ultimately, death.2,6 The presence of bone fractures increases mortality risk by 20%.10

         

         

        DIAGNOSTIC WORKUP

        Evidence of MM may be discovered during routine bloodwork and screening tests, while presenting symptoms or subtle changes in lab results can raise suspicion for the disease. Initial bloodwork abnormalities include anemia, elevated calcium levels, renal insufficiency, and/or elevated protein levels.8

        A combination of abnormalities in the complete blood count (CBC) and complete metabolic panel (CMP), along with symptoms, should alert the provider to the possibility of MM, prompting additional workup. Table 1 outlines suggested diagnostic tests; the possible findings are discussed below.

        CBC. The CBC may reveal abnormalities including anemia (which occurs in 75% of patients with MM), thrombocytopenia, and leukopenia.1,8 These findings can contribute to fatigue, increased incidence of infection, and abnormal bruising of the skin.2,8

        CMP. A CMP may show increases in ­serum calcium or protein. Hypercalcemia occurs in 15% of patients with MM, leading to symptoms such as loss of appetite, nausea, vomiting, increased urination, weakness, and confusion.8 An increase in protein may alter the albumin/globulin ratio, which should raise suspicion for MM. A decrease in albumin can signify disease severity. Also, the CMP may show worsening renal function and elevated serum creatinine, which occurs in 20% of patients with MM.8

        Serum protein electrophoresis (SPEP). Suspicion of MM should prompt the clinician to evaluate proteins via SPEP. This test may be indicated for patients with anemia, hypercalcemia, bone pain, and unexplained neuropathy.9 The electrophoresis separates proteins based on their physical properties. This identifies the presence and amount of M-protein, which can determine the extent of the disease.1 M-protein is identified in approximately 82% of patients with MM using this test.8

        Serum free light chain (FLC) assay. This diagnostic test can identify MM in individuals with high clinical suspicion for the disease but no discernible M-protein on SPEP; it increases sensitivity to 97%.8 The serum FLC assay evaluates for presence and ratio of free light chains—proteins produced by plasma cells. This test is also useful for monitoring treatment response and disease progression.1

        Urine protein electrophoresis (UPEP). The UPEP separates proteins according to charge, which is helpful for classifying renal injury. Protein patterns are interpreted and may be reported as glomerular, tubular, or mixed. UPEP also tests for M-protein in the urine.1,11

        24-hour urine. The 24-h urine test quantifies the amount and type of protein excreted in the urine and helps determine the extent of kidney disease.1

        Skeletal survey. MM causes significant bone changes that can be identified with radiographic studies. The most common locations for fractures are the vertebral, pelvic, and clavicular areas.10 Currently, the skeletal survey is the gold standard for detecting fractures and osteolytic lesions associated with MM.10 Radiographic films ordered for other purposes may uncover abnormalities in bones.

        Bone mineral density (BMD) test. Most often, BMD testing is used to evaluate treatment and progression of bone involvement. Because it can uncover osteopenia or osteoporosis, however, it can also be used to corroborate the diagnosis of MM.10

        Once the presence of M-protein is identified, patients are referred for specialty care. At that time, further workup will include a bone marrow biopsy and imaging studies, such as additional radiographic films, CT scans (without contrast, as contrast dye can damage frail kidneys), and MRI.1,8 These diagnostic tests provide useful information for the classification of the disease and guide initiation of treatment.

        CLASSIFICATION OF DISEASE

        MM can be classified into three stages—MGUS, SMM, and MM—based on recommendations from the International Myeloma Working Group.12 Table 2 outlines the diagnostic criteria for each stage.

        Individuals with MGUS and SMM are considered asymptomatic; guidelines do not recommend treatment for these patients. Those who are diagnosed with MM are referred to oncologists and treated based on current clinical practice guidelines.1

        CONCLUSION

        Multiple myeloma is a malignant neoplasm without a cure. Presenting symptoms may include anemia, bone pain, elevated creatinine or serum protein, fatigue, and hypercalcemia. Early diagnosis is key to early intervention and treatment, which can improve quality of life and clinical outcomes for those affected. Primary care providers play a major role in recognizing the subtle symptoms and ordering the appropriate diagnostic tests.

        References

        1. National Comprehensive Cancer Network. Multiple myeloma. NCCN clinical practice guidelines in oncology version 2.2015.
        2. Rajkumar VS. Multiple myeloma symptoms, diagnosis, and staging. www.uptodate.com/contents/clinical-features-laboratory-manifestations-and-diagnosis-of-multiple-myeloma?source=machineLearning&search=multiple+myeloma&selectedTitle=1%7E150&sectionRank=1&anchor=H25#H26. Accessed October 16, 2017.
        3. National Cancer Institute Surveillance, Epidemiology, and End Results Program. Cancer stat facts: myeloma. https://seer.cancer.gov/statfacts/html/mulmy.html. Accessed October 26, 2017.
        4. Röllig C, Knop S, Bornhäuser M. Multiple myeloma. Lancet. 2015;385(9983):2197-2208.
        5. Moreau P, San Miguel J, Sonneveld M, et al. Multiple myeloma: ESMO clinical practice guidelines. Ann Oncol. 2017;28(4):iv52-iv61.
        6. American Cancer Society. Multiple myeloma. www.cancer.org/cancer/multiplemyeloma/detailedguide. Accessed October 16, 2017.
        7. Koura DT, Langston AA. Inherited predisposition to multiple myeloma. Ther Adv Hematol. 2013;4(4):291-297.
        8. Rajkumar SV, Kumar S. Multiple myeloma: diagnosis and treatment. Mayo Clin Proc. 2016;91:101-119.
        9. O’Connell T, Horita TJ, Kasravi B. Understanding and interpreting serum electrophoresis. Am Fam Physician. 2005; 71(1):105-112.
        10. Kristinsson SY, Minter AR, Korde N, et al. Bone disease in multiple myeloma and precursor disease; novel diagnostic approaches and implications on clinical management. Expert Rev Mol Diagn. 2011;11(6):593-603.
        11. Jacobs D, DeMott W, Oxley D. Laboratory Test Handbook: Concise With Disease Index. Hudson, OH: Lexi-Comp; 2004.
        12. Kyle RA, Rajkumar SV. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma. Leukemia. 2009;23(1):3-9.

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        Denise Schentrup is Clinical Associate Professor and Associate Dean for Clinical Affairs at the University of Florida College of Nursing in Gainesville, and Clinic Director at Archer Family Health Care.

        The author has no financial relationships to disclose.

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        The author has no financial relationships to disclose.

        Article PDF
        Article PDF

        IN THIS ARTICLE

        • Presenting symptoms
        • Diagnostic tests
        • Differential diagnostic criteria

        Multiple myeloma (MM) is a fatal, malignant neoplasm that originates in the plasma cells of bone marrow. A genetic mutation in the plasma cells creates myeloma cells, which replicate and produce monoclonal protein (M-protein). This accumulation of cells and abnormal protein can result in destruction and eventual marrow failure.1,2

        MM’s insidious nature means it often goes undetected or misdiagnosed in its early stages; this delayed diagnosis can cause sequelae that limit quality of life. Furthermore, the five-year survival rate for myeloma varies by stage at which the disease is diagnosed: from 48% for distant (metastasized) myeloma to 71% for localized disease.3 It has also been noted that, in the past two decades, improvements in available treatment options and supportive care have contributed to a doubling of median survival time (from three years to six years).4 It is therefore paramount that providers be aware of MM and its signs to facilitate early diagnosis and treatment.

        INCIDENCE AND EPIDEMIOLOGY

        MM accounts for 1% of all cancers and about 10% of all hematologic malignancies.5 In 2017, the American Cancer Society estimated that more than 30,000 new cases of MM would be diagnosed in the United States.6 Additionally, MM was expected to cause more than 12,000 deaths last year.6

        Median age at diagnosis is 69.3 In fact, 75% of men are older than 75 and 79% of women are older than 70 at diagnosis.1

        Apart from age, other risk factors for MM have been identified but not fully explicated. For example, the disease is more common in men than in women (with men comprising two-thirds of new cases per year).3 MM is also two to three times more common in black than in white persons, making it the most common hematologic malignancy in this demographic group.3,7

        The possibility of a genetic predisposition has also been studied. Several analyses have indicated an increased risk for MM in patients with a family history of the disease—as much as four times higher in those with an affected first-degree relative. This risk was further elevated in black compared with white patients (odds ratios, 17.4 and 1.5, respectively).7 However, many patients with MM have no relatives with this disorder.6,8

        DISEASE PROGRESSION

        Almost all patients who develop MM also experience an asymptomatic premalignant stage called monoclonal gammopathy of undetermined significance (MGUS). MGUS is present in 3% to 4% of the general population older than 50 and is often an incidental finding. This stage almost always precedes MM—but because it is asymptomatic, only 10% of individuals diagnosed with MM have a known history of MGUS.8

        In some patients, an asymptomatic intermediate stage called smoldering multiple myeloma (SMM) can be identified. SMM progresses to MM at a rate of 10% per year for the first five years; the rate decreases to 3% per year over the following five years, and 1% per year after that.8

        MM is not curable, but as noted, the survival rate is steadily increasing due to rapidly evolving treatment regimens. Discussion of treatment is outside the scope of this article, but early diagnosis can improve quality of life and clinical outcomes and prolong life expectancy.

        SYMPTOMS

        The initial symptoms of MM can be nonspecific and may lead the provider to suspect a host of other conditions.2,6 (Those for advanced disease are also vague but tend to be more pronounced.) These may include fatigue, weakness, easy bruising or bleeding, and bone pain. Other common clinical manifestations of MM are anemia, chronic infection, bone disease, and/or renal failure.1,4 Patients may also experience loss of appetite, nausea, vomiting, increased thirst, and increased urination.9

        Recent studies have shown that patients with SMM and/or MGUS also exhibit early signs of bone disease and increased risk for fracture.10 Eighty percent of patients who progress to MM have evidence of pathologic bone fractures.10 It is also possible for bones in the spine to weaken and collapse, pressing on the spinal nerves. This is known as spinal cord compression, which can manifest with sudden, severe back pain or numbness and/or muscle weakness (most often in the legs).6

        MM must be included in the differential diagnosis, particularly when symptoms do not point to one specific disease process. Without early diagnosis, disease progression can result in complications such as bone fracture and osteoporosis, reduced kidney function, peripheral neuropathy, chronic anemia, and ultimately, death.2,6 The presence of bone fractures increases mortality risk by 20%.10

         

         

        DIAGNOSTIC WORKUP

        Evidence of MM may be discovered during routine bloodwork and screening tests, while presenting symptoms or subtle changes in lab results can raise suspicion for the disease. Initial bloodwork abnormalities include anemia, elevated calcium levels, renal insufficiency, and/or elevated protein levels.8

        A combination of abnormalities in the complete blood count (CBC) and complete metabolic panel (CMP), along with symptoms, should alert the provider to the possibility of MM, prompting additional workup. Table 1 outlines suggested diagnostic tests; the possible findings are discussed below.

        CBC. The CBC may reveal abnormalities including anemia (which occurs in 75% of patients with MM), thrombocytopenia, and leukopenia.1,8 These findings can contribute to fatigue, increased incidence of infection, and abnormal bruising of the skin.2,8

        CMP. A CMP may show increases in ­serum calcium or protein. Hypercalcemia occurs in 15% of patients with MM, leading to symptoms such as loss of appetite, nausea, vomiting, increased urination, weakness, and confusion.8 An increase in protein may alter the albumin/globulin ratio, which should raise suspicion for MM. A decrease in albumin can signify disease severity. Also, the CMP may show worsening renal function and elevated serum creatinine, which occurs in 20% of patients with MM.8

        Serum protein electrophoresis (SPEP). Suspicion of MM should prompt the clinician to evaluate proteins via SPEP. This test may be indicated for patients with anemia, hypercalcemia, bone pain, and unexplained neuropathy.9 The electrophoresis separates proteins based on their physical properties. This identifies the presence and amount of M-protein, which can determine the extent of the disease.1 M-protein is identified in approximately 82% of patients with MM using this test.8

        Serum free light chain (FLC) assay. This diagnostic test can identify MM in individuals with high clinical suspicion for the disease but no discernible M-protein on SPEP; it increases sensitivity to 97%.8 The serum FLC assay evaluates for presence and ratio of free light chains—proteins produced by plasma cells. This test is also useful for monitoring treatment response and disease progression.1

        Urine protein electrophoresis (UPEP). The UPEP separates proteins according to charge, which is helpful for classifying renal injury. Protein patterns are interpreted and may be reported as glomerular, tubular, or mixed. UPEP also tests for M-protein in the urine.1,11

        24-hour urine. The 24-h urine test quantifies the amount and type of protein excreted in the urine and helps determine the extent of kidney disease.1

        Skeletal survey. MM causes significant bone changes that can be identified with radiographic studies. The most common locations for fractures are the vertebral, pelvic, and clavicular areas.10 Currently, the skeletal survey is the gold standard for detecting fractures and osteolytic lesions associated with MM.10 Radiographic films ordered for other purposes may uncover abnormalities in bones.

        Bone mineral density (BMD) test. Most often, BMD testing is used to evaluate treatment and progression of bone involvement. Because it can uncover osteopenia or osteoporosis, however, it can also be used to corroborate the diagnosis of MM.10

        Once the presence of M-protein is identified, patients are referred for specialty care. At that time, further workup will include a bone marrow biopsy and imaging studies, such as additional radiographic films, CT scans (without contrast, as contrast dye can damage frail kidneys), and MRI.1,8 These diagnostic tests provide useful information for the classification of the disease and guide initiation of treatment.

        CLASSIFICATION OF DISEASE

        MM can be classified into three stages—MGUS, SMM, and MM—based on recommendations from the International Myeloma Working Group.12 Table 2 outlines the diagnostic criteria for each stage.

        Individuals with MGUS and SMM are considered asymptomatic; guidelines do not recommend treatment for these patients. Those who are diagnosed with MM are referred to oncologists and treated based on current clinical practice guidelines.1

        CONCLUSION

        Multiple myeloma is a malignant neoplasm without a cure. Presenting symptoms may include anemia, bone pain, elevated creatinine or serum protein, fatigue, and hypercalcemia. Early diagnosis is key to early intervention and treatment, which can improve quality of life and clinical outcomes for those affected. Primary care providers play a major role in recognizing the subtle symptoms and ordering the appropriate diagnostic tests.

        IN THIS ARTICLE

        • Presenting symptoms
        • Diagnostic tests
        • Differential diagnostic criteria

        Multiple myeloma (MM) is a fatal, malignant neoplasm that originates in the plasma cells of bone marrow. A genetic mutation in the plasma cells creates myeloma cells, which replicate and produce monoclonal protein (M-protein). This accumulation of cells and abnormal protein can result in destruction and eventual marrow failure.1,2

        MM’s insidious nature means it often goes undetected or misdiagnosed in its early stages; this delayed diagnosis can cause sequelae that limit quality of life. Furthermore, the five-year survival rate for myeloma varies by stage at which the disease is diagnosed: from 48% for distant (metastasized) myeloma to 71% for localized disease.3 It has also been noted that, in the past two decades, improvements in available treatment options and supportive care have contributed to a doubling of median survival time (from three years to six years).4 It is therefore paramount that providers be aware of MM and its signs to facilitate early diagnosis and treatment.

        INCIDENCE AND EPIDEMIOLOGY

        MM accounts for 1% of all cancers and about 10% of all hematologic malignancies.5 In 2017, the American Cancer Society estimated that more than 30,000 new cases of MM would be diagnosed in the United States.6 Additionally, MM was expected to cause more than 12,000 deaths last year.6

        Median age at diagnosis is 69.3 In fact, 75% of men are older than 75 and 79% of women are older than 70 at diagnosis.1

        Apart from age, other risk factors for MM have been identified but not fully explicated. For example, the disease is more common in men than in women (with men comprising two-thirds of new cases per year).3 MM is also two to three times more common in black than in white persons, making it the most common hematologic malignancy in this demographic group.3,7

        The possibility of a genetic predisposition has also been studied. Several analyses have indicated an increased risk for MM in patients with a family history of the disease—as much as four times higher in those with an affected first-degree relative. This risk was further elevated in black compared with white patients (odds ratios, 17.4 and 1.5, respectively).7 However, many patients with MM have no relatives with this disorder.6,8

        DISEASE PROGRESSION

        Almost all patients who develop MM also experience an asymptomatic premalignant stage called monoclonal gammopathy of undetermined significance (MGUS). MGUS is present in 3% to 4% of the general population older than 50 and is often an incidental finding. This stage almost always precedes MM—but because it is asymptomatic, only 10% of individuals diagnosed with MM have a known history of MGUS.8

        In some patients, an asymptomatic intermediate stage called smoldering multiple myeloma (SMM) can be identified. SMM progresses to MM at a rate of 10% per year for the first five years; the rate decreases to 3% per year over the following five years, and 1% per year after that.8

        MM is not curable, but as noted, the survival rate is steadily increasing due to rapidly evolving treatment regimens. Discussion of treatment is outside the scope of this article, but early diagnosis can improve quality of life and clinical outcomes and prolong life expectancy.

        SYMPTOMS

        The initial symptoms of MM can be nonspecific and may lead the provider to suspect a host of other conditions.2,6 (Those for advanced disease are also vague but tend to be more pronounced.) These may include fatigue, weakness, easy bruising or bleeding, and bone pain. Other common clinical manifestations of MM are anemia, chronic infection, bone disease, and/or renal failure.1,4 Patients may also experience loss of appetite, nausea, vomiting, increased thirst, and increased urination.9

        Recent studies have shown that patients with SMM and/or MGUS also exhibit early signs of bone disease and increased risk for fracture.10 Eighty percent of patients who progress to MM have evidence of pathologic bone fractures.10 It is also possible for bones in the spine to weaken and collapse, pressing on the spinal nerves. This is known as spinal cord compression, which can manifest with sudden, severe back pain or numbness and/or muscle weakness (most often in the legs).6

        MM must be included in the differential diagnosis, particularly when symptoms do not point to one specific disease process. Without early diagnosis, disease progression can result in complications such as bone fracture and osteoporosis, reduced kidney function, peripheral neuropathy, chronic anemia, and ultimately, death.2,6 The presence of bone fractures increases mortality risk by 20%.10

         

         

        DIAGNOSTIC WORKUP

        Evidence of MM may be discovered during routine bloodwork and screening tests, while presenting symptoms or subtle changes in lab results can raise suspicion for the disease. Initial bloodwork abnormalities include anemia, elevated calcium levels, renal insufficiency, and/or elevated protein levels.8

        A combination of abnormalities in the complete blood count (CBC) and complete metabolic panel (CMP), along with symptoms, should alert the provider to the possibility of MM, prompting additional workup. Table 1 outlines suggested diagnostic tests; the possible findings are discussed below.

        CBC. The CBC may reveal abnormalities including anemia (which occurs in 75% of patients with MM), thrombocytopenia, and leukopenia.1,8 These findings can contribute to fatigue, increased incidence of infection, and abnormal bruising of the skin.2,8

        CMP. A CMP may show increases in ­serum calcium or protein. Hypercalcemia occurs in 15% of patients with MM, leading to symptoms such as loss of appetite, nausea, vomiting, increased urination, weakness, and confusion.8 An increase in protein may alter the albumin/globulin ratio, which should raise suspicion for MM. A decrease in albumin can signify disease severity. Also, the CMP may show worsening renal function and elevated serum creatinine, which occurs in 20% of patients with MM.8

        Serum protein electrophoresis (SPEP). Suspicion of MM should prompt the clinician to evaluate proteins via SPEP. This test may be indicated for patients with anemia, hypercalcemia, bone pain, and unexplained neuropathy.9 The electrophoresis separates proteins based on their physical properties. This identifies the presence and amount of M-protein, which can determine the extent of the disease.1 M-protein is identified in approximately 82% of patients with MM using this test.8

        Serum free light chain (FLC) assay. This diagnostic test can identify MM in individuals with high clinical suspicion for the disease but no discernible M-protein on SPEP; it increases sensitivity to 97%.8 The serum FLC assay evaluates for presence and ratio of free light chains—proteins produced by plasma cells. This test is also useful for monitoring treatment response and disease progression.1

        Urine protein electrophoresis (UPEP). The UPEP separates proteins according to charge, which is helpful for classifying renal injury. Protein patterns are interpreted and may be reported as glomerular, tubular, or mixed. UPEP also tests for M-protein in the urine.1,11

        24-hour urine. The 24-h urine test quantifies the amount and type of protein excreted in the urine and helps determine the extent of kidney disease.1

        Skeletal survey. MM causes significant bone changes that can be identified with radiographic studies. The most common locations for fractures are the vertebral, pelvic, and clavicular areas.10 Currently, the skeletal survey is the gold standard for detecting fractures and osteolytic lesions associated with MM.10 Radiographic films ordered for other purposes may uncover abnormalities in bones.

        Bone mineral density (BMD) test. Most often, BMD testing is used to evaluate treatment and progression of bone involvement. Because it can uncover osteopenia or osteoporosis, however, it can also be used to corroborate the diagnosis of MM.10

        Once the presence of M-protein is identified, patients are referred for specialty care. At that time, further workup will include a bone marrow biopsy and imaging studies, such as additional radiographic films, CT scans (without contrast, as contrast dye can damage frail kidneys), and MRI.1,8 These diagnostic tests provide useful information for the classification of the disease and guide initiation of treatment.

        CLASSIFICATION OF DISEASE

        MM can be classified into three stages—MGUS, SMM, and MM—based on recommendations from the International Myeloma Working Group.12 Table 2 outlines the diagnostic criteria for each stage.

        Individuals with MGUS and SMM are considered asymptomatic; guidelines do not recommend treatment for these patients. Those who are diagnosed with MM are referred to oncologists and treated based on current clinical practice guidelines.1

        CONCLUSION

        Multiple myeloma is a malignant neoplasm without a cure. Presenting symptoms may include anemia, bone pain, elevated creatinine or serum protein, fatigue, and hypercalcemia. Early diagnosis is key to early intervention and treatment, which can improve quality of life and clinical outcomes for those affected. Primary care providers play a major role in recognizing the subtle symptoms and ordering the appropriate diagnostic tests.

        References

        1. National Comprehensive Cancer Network. Multiple myeloma. NCCN clinical practice guidelines in oncology version 2.2015.
        2. Rajkumar VS. Multiple myeloma symptoms, diagnosis, and staging. www.uptodate.com/contents/clinical-features-laboratory-manifestations-and-diagnosis-of-multiple-myeloma?source=machineLearning&search=multiple+myeloma&selectedTitle=1%7E150&sectionRank=1&anchor=H25#H26. Accessed October 16, 2017.
        3. National Cancer Institute Surveillance, Epidemiology, and End Results Program. Cancer stat facts: myeloma. https://seer.cancer.gov/statfacts/html/mulmy.html. Accessed October 26, 2017.
        4. Röllig C, Knop S, Bornhäuser M. Multiple myeloma. Lancet. 2015;385(9983):2197-2208.
        5. Moreau P, San Miguel J, Sonneveld M, et al. Multiple myeloma: ESMO clinical practice guidelines. Ann Oncol. 2017;28(4):iv52-iv61.
        6. American Cancer Society. Multiple myeloma. www.cancer.org/cancer/multiplemyeloma/detailedguide. Accessed October 16, 2017.
        7. Koura DT, Langston AA. Inherited predisposition to multiple myeloma. Ther Adv Hematol. 2013;4(4):291-297.
        8. Rajkumar SV, Kumar S. Multiple myeloma: diagnosis and treatment. Mayo Clin Proc. 2016;91:101-119.
        9. O’Connell T, Horita TJ, Kasravi B. Understanding and interpreting serum electrophoresis. Am Fam Physician. 2005; 71(1):105-112.
        10. Kristinsson SY, Minter AR, Korde N, et al. Bone disease in multiple myeloma and precursor disease; novel diagnostic approaches and implications on clinical management. Expert Rev Mol Diagn. 2011;11(6):593-603.
        11. Jacobs D, DeMott W, Oxley D. Laboratory Test Handbook: Concise With Disease Index. Hudson, OH: Lexi-Comp; 2004.
        12. Kyle RA, Rajkumar SV. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma. Leukemia. 2009;23(1):3-9.

        References

        1. National Comprehensive Cancer Network. Multiple myeloma. NCCN clinical practice guidelines in oncology version 2.2015.
        2. Rajkumar VS. Multiple myeloma symptoms, diagnosis, and staging. www.uptodate.com/contents/clinical-features-laboratory-manifestations-and-diagnosis-of-multiple-myeloma?source=machineLearning&search=multiple+myeloma&selectedTitle=1%7E150&sectionRank=1&anchor=H25#H26. Accessed October 16, 2017.
        3. National Cancer Institute Surveillance, Epidemiology, and End Results Program. Cancer stat facts: myeloma. https://seer.cancer.gov/statfacts/html/mulmy.html. Accessed October 26, 2017.
        4. Röllig C, Knop S, Bornhäuser M. Multiple myeloma. Lancet. 2015;385(9983):2197-2208.
        5. Moreau P, San Miguel J, Sonneveld M, et al. Multiple myeloma: ESMO clinical practice guidelines. Ann Oncol. 2017;28(4):iv52-iv61.
        6. American Cancer Society. Multiple myeloma. www.cancer.org/cancer/multiplemyeloma/detailedguide. Accessed October 16, 2017.
        7. Koura DT, Langston AA. Inherited predisposition to multiple myeloma. Ther Adv Hematol. 2013;4(4):291-297.
        8. Rajkumar SV, Kumar S. Multiple myeloma: diagnosis and treatment. Mayo Clin Proc. 2016;91:101-119.
        9. O’Connell T, Horita TJ, Kasravi B. Understanding and interpreting serum electrophoresis. Am Fam Physician. 2005; 71(1):105-112.
        10. Kristinsson SY, Minter AR, Korde N, et al. Bone disease in multiple myeloma and precursor disease; novel diagnostic approaches and implications on clinical management. Expert Rev Mol Diagn. 2011;11(6):593-603.
        11. Jacobs D, DeMott W, Oxley D. Laboratory Test Handbook: Concise With Disease Index. Hudson, OH: Lexi-Comp; 2004.
        12. Kyle RA, Rajkumar SV. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma. Leukemia. 2009;23(1):3-9.

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        Biomechanical Evaluation of a Novel Suture Augment in Patella Fixation

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        Take-Home Points

        • Suture augmentation improves construct strength for patella fixation.
        • Krackow sutures may be placed in the quadriceps and patella tendons, then secured over the anterior patella (much like an anterior tension band).
        • The Krackow technique described was superior to the suture cerclage technique based on mean load values, but did not reach statistical significance.
        • The Krackow suture technique is a viable and easily applied technique for suture augmentation of patella fixation constructs.

        Patella fractures are relatively uncommon, accounting for only 1% of skeletal injuries.1 Restoration of the function of the patella and the extensor mechanism is vital for knee extension and gait. However, patella fractures have an inherently high rate of complications, making these injuries challenging to treat.2-4 In patients with intact extensor function, displacement of <4 mm, and articular step-off of <3 mm, nonoperative management is extremely effective, with 99% of patients reporting favorable results.5 However, for fractures in which the extensor mechanism is disrupted, surgical intervention typically is indicated.6

        Authors have reported various surgical interventions, one of the most commonly used being the anterior tension band (ATB) technique, first described by the AO (Arbeitsgemeinschaft für Osteosynthesefragen) group in the 1950s.7 By converting distractive anterior force during knee flexion to compressive force at the fracture site, the ATB technique provides a repair stronger than the previously used cerclage repair.8 Although initially considered standard of care, the ATB technique was soon found to be associated with implant failure and subcutaneous irritation prompting implant removal.9

        To address these issues, Berg10 and Carpenter and colleagues11 evaluated an ATB technique that used cannulated screws instead of Kirschner wires (K-wires). This variation on the ATB technique reduced the implant-related issues while maintaining the mechanical advantage of the tension band. The more rigid design also permitted earlier postoperative rehabilitation, which significantly reduced development of arthrofibrosis.6,7,10 This modified ATB (MATB) technique has since been investigated for additional augments, mainly focusing on use of different tension band materials, including polyester suture and braided composite suture.12-14

        However, there is little research on augments that incorporate the surrounding soft tissue, specifically the quadriceps and patellar tendons. In a recent retrospective clinical study, Oh and colleagues15 found positive clinical results with use of Krackow sutures, though 2 or 3 vertically oriented stainless steel wires were used instead of cannulated screws.

        We conducted a study to determine the biomechanical efficacy of using a cerclage suture augment and a Krackow suture augment coupled with and compared with conventional MATB repair. If effective, this technique may represent another strategy for increasing repair strength and thereby improve postoperative outcomes.

         

         

        Materials and Methods

        Specimen Preparation

        Fresh-frozen cadaver extensor mechanisms (quadriceps tendon, patella, surrounding retinaculum, patellar tendon) were kept frozen at –4°C until preparation. Fifteen specimens were selected. Mean (SD) age at death was 68 (10) years (range, 51-85 years). One specimen was excluded for a short patella tendon, which precluded adequate attachment for testing. All specimens were free of overt osseous pathology.

        After specimens were thawed overnight, the patellae were transversely osteotomized with an osteotome at the junction of the middle and distal thirds of the patella. Sharp dissection was performed to carry the division through the medial and lateral retinaculum at the same level. All 14 specimens were then repaired using the MATB technique. First, the transverse fracture was reduced with a reduction clamp. Then, two 4-mm cannulated screws (DePuy Synthes) were inserted parallel to each other and perpendicular to the fracture. An 18-gauge stainless steel wire was then passed through each screw, crossed anteriorly, and tightened to create a figure-of-8 ATB. The specimens were then randomly divided into 3 groups—MATB; MATB with cerclage suture augment; MATB with Krackow suture augment—while ensuring specimens from a single cadaver were placed in different groups to avoid confounding based on bone density differences.

        Figure 1.
        Figure 2.
        A braided composite suture (No. 5 FiberWire; Arthrex) was used for the cerclage augment on 4 specimens, and a Krackow augment was used for 5 specimens (Figures 1A-1C). The cerclage augment was placed by circumferentially passing the suture at 8 points in the surrounding retinaculum. For the Krackow augment, 4 locking passes were made on both the medial and the lateral sides of the quadriceps and patella tendon, yielding a total of 4 free suture ends (Figure 2). Free ends were then crossed anteriorly in a fashion similar to that used for the 18-gauge wires and tied. Last, overlying subcutaneous tissue and paratenon were stripped from the quadriceps and patellar tendons to maximize friction during clamping for testing. After completion of all repairs, specimens were biomechanically tested.

        Experimental Setup

        Repaired specimens were secured with tissue clamps at the quadriceps and patellar tendons on an MTS Bionix 858 (MTS Systems) hydraulic arm.

        Figure 3.
        Anatomical conditions were simulated by using a bracket to connect a distal femur sawbone model to the MTS machine and orienting the model on the posterior surface of the patella to produce a flexion angle of 45° (Figure 3), which maximizes tensile forces.16

        Each patella was secured for cyclic testing. Initially it was placed under 10 N of tension. Then it underwent tensile loading from 10 N to 300 N at 50 N/s for 10 cycles. These parameters were based on previous biomechanical patella studies.10,11 Load was measured with the MTS load cell and displacement with the displacement transducer. Fracture displacement associated with 300-N cyclic tension was recorded. Displacement was calculated as the difference between 10th cycle and 2nd cycle values, which accounted for any degree of initial tissue slippage. After cyclic testing, the patella was placed back in 10 N of tensile loading and subjected to maximum force loading to determine ultimate repair strength. For maximum loading, the patella was stretched progressively at 50 N/s until failure. Again, load and displacement were measured with MTS.

        Statistical Analysis

        After testing, fracture displacement and maximum load force data were compiled for analysis. One-way analysis of variance with Bonferroni correction was used to determine if there were significant differences between groups. Significance level was set at P < .05.

         

         

        Results

        For cyclic testing, mean total displacement was measured over 10 cycles for each group. Again, displacement was determined by taking the difference between 10th cycle and 2nd cycle values, allowing for system stabilization.

        Figure 4.
        Figure 5.
        Mean (SD) displacement was 3.57 (1.63) mm with MATB repair, 2.50 (0.80) mm with cerclage augment repair, and 2.17 (0.77) mm with Krackow augment repair (Figure 4). Among all specimens, displacement followed a hyperbolic arrangement, with the majority of total displacement occurring during initial cycles and tapering off during later cycles (Figure 5). Mean displacement was 30% lower with cerclage repair (vs MATB repair) and 40% lower with Krackow repair (vs MATB repair). However, this trend was not statistically significant (P > .05), owing to sample size and presence of an outlier in all 3 groups.

        Figure 6.
        After cyclic loading, load-to-failure testing was performed by applying increasing tension until repair failure. None of our 14 specimens showed significant failure after cyclic testing, so all were subjected to load-to-failure testing. Mean (SD) maximum tension force was found to be 753 (16) N for MATB, 793 (177) N for cerclage, and 863 (104) N for Krackow (Figure 6). Similar to the cyclic testing findings, maximum load strength was 5% higher with cerclage repair (vs MATB repair) and 14% higher with Krackow repair (vs MATB repair). Again, with the small sample size and the presence of outliers (and other variation among data), the trend was not statistically significant (P > .05). In addition, pairwise comparisons of the 3 groups revealed no statistically significant differences.

        Discussion

        Our main objective was to compare the efficacy of a novel suture augment technique with that of other patella fracture repair techniques. Our hypothesis—that adding a Krackow suture augment would increase strength in both cyclic and maximum loading—was supported. Although testing results were not statistically significant because of the small sample size, we think this novel technique has clinically relevant descriptive significance and warrants further investigation.

        Proper anatomical reduction and postoperative stabilization are of utmost importance in clinical approaches to patella fractures. In addition, regardless of which technical procedure is used, open reduction should also allow for early range of motion to prevent joint arthrofibrosis. Ever since the ATB technique was first described by the AO group, postoperative outcomes have improved significantly. In a retrospective study by Levack and colleagues,17 30 of 64 patients with patella fractures underwent internal fixation. Mean follow-up was 6.2 years. By both objective and subjective measures, the best functional outcomes were associated with internal tension band fixation (vs cerclage repair). Lotke and Ecker18 also documented the efficacy of the tension band technique. Sixteen patients with patella fractures underwent anterior tension banding; those with a comminuted fracture also underwent cerclage repair for patella stabilization during tension banding. At 6-week follow-up, all patients had good range of motion (≥90° flexion), relatively few symptoms, and no implant failures. Results were similar to those of Levack and colleagues.17

        Although it improves stability and functional outcomes over conventional patellectomy and cerclage wiring, the ATB technique has been associated with subcutaneous irritation caused by the K-wires used to secure the band. Hung and colleagues9 followed up 68 patients with patellar fractures. Five of these patients underwent tension banding. Although there was a high level of adequate functional outcomes, implant irritation was found to be “quite frequent.”

        To address this issue, Carpenter and colleagues11 evaluated an ATB technique that uses K-wires instead of cannulated screws. Biomechanical testing in a cadaver model revealed less fracture displacement and overall more repair strength through cyclic and maximum load testing. Clinically, these results were supported by Berg,10 who followed up 10 patients with transverse patella fractures repaired with the MATB technique. At a mean follow-up of 24 months, 7 of the 10 patients had good to excellent outcomes, and there were no implant failures.

         

         

        Further investigation into patella repairs has mainly focused on improving the MATB technique and experimenting with different tension band materials. Rabalais and colleagues13 biomechanically tested high-strength polyethylene suture as a replacement for standard 18-gauge wire, and Bryant and colleagues14 tested a braided composite suture (FiberWire; Arthrex) as a replacement for standard 18-gauge stainless steel wire. Both found no significant difference with use of augmented tension band material, but Rabalais and colleagues13 did find more advantages with a parallel tension band construct than with a standard figure-of-8 arrangement.

        In developing our novel technique, we considered that Krackow sutures are routinely used in both quadriceps tendon repair and patellar tendon repair, including partial patellectomy for distal patella fracture. With a suture placed in both tendons, the augment could be expected to resist longitudinal gapping and augment the tension band across the anterior patella. First described by Krackow and colleagues,19 the Krackow suture is widely used for tendon reconstruction. In an interlocking system of sutures, the Krackow suture provides a repair that is more stable than repair with conventional suture techniques, specifically in the context of tendon repair.20 Given the sesamoidal nature of the patella, its repair shares the goal of gap prevention with other tendon repairs. In theory, anchoring the supporting structures that are above and below the patella provides support for the intervening patella and ultimately improves fracture fixation strength.

        Oh and colleagues15 reported on the clinical efficacy of a Krackow augment in distal pole patella repairs. Similarly, we found a Krackow augment to be efficacious, supporting its potential in clinical approaches to patella repairs. Our results indicate this augment can be a useful clinical adjunct in biomechanical evaluation. 

        Limitations of this study include its use of dissected extensor mechanisms, which may have less biofidelity than whole-knee specimens. In our model, specimens were secured at the patellar tendon and the quadriceps tendons, as opposed to the quadriceps tendon and the tibia distally. Use of this model could have led to an increase in early displacement during cyclic testing as a result of tissue slippage. Furthermore, our small sample size could have affected our ability to demonstrate a difference between these techniques.

        Given its increased strength as demonstrated by mean displacement during cyclic loading and mean load to failure, as well as the early clinical data recently published, the Krackow suture augment represents a feasible technique for patella fixation. It likely will be most useful in cases in which conventional techniques are prone to failure or cannot be applied, such as severe distal comminution or poor bone density. Further biomechanical testing with a larger number of specimens may be required for statistical significance.

        Conclusion

        In patella fracture repair strategies, the Krackow suture augment increased strength when used with a MATB technique. Failure to reach statistical significance likely resulted from our small sample size. Further biomechanical testing and clinical studies are needed for more complete evaluation of this technique. We think it will be most useful in the setting of poor bone quality or severe comminution, which can limit fixation options. As increased repair strength allows earlier postoperative rehabilitation and maintains fracture reduction, patient outcomes should improve. This novel technique represents another strategy for managing challenging patella fractures.

        References

        1. Boström Å. Fracture of the patella. A study of 422 patellar fractures. Acta Orthop Scand Suppl. 1972;143:1-80. 

        2. Hungerford DS, Barry M. Biomechanics of the patellofemoral joint. Clin Orthop Relat Res. 1979;(144):9-15.

        3. LeBrun CT, Langford JR, Sagi HC. Functional outcomes after operatively treated patella fractures. J Orthop Trauma. 2012;26(7):422-426. 

        4. Kaufer H. Mechanical function of the patella. J Bone Joint Surg Am. 1971;53(8):1551-1560. 

        5. Braun W, Wiedemann M, Rüter A, Kundel K, Kolbinger S. Indications and results of nonoperative treatment of patellar fractures. Clin Orthop Relat Res. 1993;(289):197-201.

        6. Melvin JS, Mehta S. Patellar fractures in adults. J Am Acad Orthop Surg. 2011;19(4):198-207. 

        7. Müller M, Allgöwer M, Schneider R, Willeneger H. Manual of Internal Fixation: Techniques Recommended by the AO Group. Berlin, Germany: Springer; 1979.

        8. Weber MJ, Janecki CJ, McLeod P, Nelson CL, Thompson JA. Efficacy of various forms of fixation of transverse fractures of the patella. J Bone Joint Surg Am. 1980;62(2):215-220.

        9. Hung LK, Chan KM, Chow YN, Leung PC. Fractured patella: operative treatment using the tension band principle. Injury. 1985;16(5):343-347. 

        10. Berg EE. Open reduction internal fixation of displaced transverse patella fractures with figure-eight wiring through parallel cannulated compression screws. J Orthop Trauma. 1997;11(8):573-576.

        11. Carpenter JE, Kasman RA, Patel N, Lee ML, Goldstein SA. Biomechanical evaluation of current patella fracture fixation techniques. J Orthop Trauma. 1997;11(5):351-356.

        12. Hughes SC, Stott PM, Hearnden AJ, Ripley LG. A new and effective tension-band braided polyester suture technique for transverse patellar fracture fixation. Injury. 2007;38(2):212-222. 

        13. Rabalais RD, Burger E, Lu Y, Mansour A, Baratta RV. Comparison of two tension-band fixation materials and techniques in transverse patella fractures: a biomechanical study. Orthopedics. 2008;31(2):128.

        14. Bryant TL, Anderson CL, Stevens CG, Conrad BP, Vincent HK, Sadasivan KK. Comparison of cannulated screws with FiberWire or stainless steel wire for patella fracture fixation: a pilot study. J Orthop. 2014;12(2):92-96.

        15. Oh HK, Choo SK, Kim JW, Lee M. Internal fixation of displaced inferior pole of the patella fractures using vertical wiring augmented with Krachow suturing. Injury. 2015;46(12):2512-2515.

        16. Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional anatomy of the patello-femoral joint. J Bone Joint Surg Br. 1976;58(3):287-290. 

        17. Levack B, Flannagan JP, Hobbs S. Results of surgical treatment of patellar fractures. J Bone Joint Surg Br. 1985;67(3):416-419. 

        18. Lotke PA, Ecker ML. Transverse fractures of the patella. Clin Orthop Relat Res. 1981;(158):180-184.

        19. Krackow KA, Thomas SC, Jones LC. Ligament-tendon fixation: analysis of a new stitch and comparison with standard techniques. Orthopedics. 1988;11(6):909-917.

        20. Hahn JM, Inceoğlu S, Wongworawat MD. Biomechanical comparison of Krackow locking stitch versus nonlocking loop stitch with varying number of throws. Am J Sports Med. 2014;42(12):3003-3008.

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        Authors’ Disclosure Statement: DePuy Synthes provided the cannulated screws used in the study reported here. The authors report no actual or potential conflict of interest in relation to this article. 

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        Take-Home Points

        • Suture augmentation improves construct strength for patella fixation.
        • Krackow sutures may be placed in the quadriceps and patella tendons, then secured over the anterior patella (much like an anterior tension band).
        • The Krackow technique described was superior to the suture cerclage technique based on mean load values, but did not reach statistical significance.
        • The Krackow suture technique is a viable and easily applied technique for suture augmentation of patella fixation constructs.

        Patella fractures are relatively uncommon, accounting for only 1% of skeletal injuries.1 Restoration of the function of the patella and the extensor mechanism is vital for knee extension and gait. However, patella fractures have an inherently high rate of complications, making these injuries challenging to treat.2-4 In patients with intact extensor function, displacement of <4 mm, and articular step-off of <3 mm, nonoperative management is extremely effective, with 99% of patients reporting favorable results.5 However, for fractures in which the extensor mechanism is disrupted, surgical intervention typically is indicated.6

        Authors have reported various surgical interventions, one of the most commonly used being the anterior tension band (ATB) technique, first described by the AO (Arbeitsgemeinschaft für Osteosynthesefragen) group in the 1950s.7 By converting distractive anterior force during knee flexion to compressive force at the fracture site, the ATB technique provides a repair stronger than the previously used cerclage repair.8 Although initially considered standard of care, the ATB technique was soon found to be associated with implant failure and subcutaneous irritation prompting implant removal.9

        To address these issues, Berg10 and Carpenter and colleagues11 evaluated an ATB technique that used cannulated screws instead of Kirschner wires (K-wires). This variation on the ATB technique reduced the implant-related issues while maintaining the mechanical advantage of the tension band. The more rigid design also permitted earlier postoperative rehabilitation, which significantly reduced development of arthrofibrosis.6,7,10 This modified ATB (MATB) technique has since been investigated for additional augments, mainly focusing on use of different tension band materials, including polyester suture and braided composite suture.12-14

        However, there is little research on augments that incorporate the surrounding soft tissue, specifically the quadriceps and patellar tendons. In a recent retrospective clinical study, Oh and colleagues15 found positive clinical results with use of Krackow sutures, though 2 or 3 vertically oriented stainless steel wires were used instead of cannulated screws.

        We conducted a study to determine the biomechanical efficacy of using a cerclage suture augment and a Krackow suture augment coupled with and compared with conventional MATB repair. If effective, this technique may represent another strategy for increasing repair strength and thereby improve postoperative outcomes.

         

         

        Materials and Methods

        Specimen Preparation

        Fresh-frozen cadaver extensor mechanisms (quadriceps tendon, patella, surrounding retinaculum, patellar tendon) were kept frozen at –4°C until preparation. Fifteen specimens were selected. Mean (SD) age at death was 68 (10) years (range, 51-85 years). One specimen was excluded for a short patella tendon, which precluded adequate attachment for testing. All specimens were free of overt osseous pathology.

        After specimens were thawed overnight, the patellae were transversely osteotomized with an osteotome at the junction of the middle and distal thirds of the patella. Sharp dissection was performed to carry the division through the medial and lateral retinaculum at the same level. All 14 specimens were then repaired using the MATB technique. First, the transverse fracture was reduced with a reduction clamp. Then, two 4-mm cannulated screws (DePuy Synthes) were inserted parallel to each other and perpendicular to the fracture. An 18-gauge stainless steel wire was then passed through each screw, crossed anteriorly, and tightened to create a figure-of-8 ATB. The specimens were then randomly divided into 3 groups—MATB; MATB with cerclage suture augment; MATB with Krackow suture augment—while ensuring specimens from a single cadaver were placed in different groups to avoid confounding based on bone density differences.

        Figure 1.
        Figure 2.
        A braided composite suture (No. 5 FiberWire; Arthrex) was used for the cerclage augment on 4 specimens, and a Krackow augment was used for 5 specimens (Figures 1A-1C). The cerclage augment was placed by circumferentially passing the suture at 8 points in the surrounding retinaculum. For the Krackow augment, 4 locking passes were made on both the medial and the lateral sides of the quadriceps and patella tendon, yielding a total of 4 free suture ends (Figure 2). Free ends were then crossed anteriorly in a fashion similar to that used for the 18-gauge wires and tied. Last, overlying subcutaneous tissue and paratenon were stripped from the quadriceps and patellar tendons to maximize friction during clamping for testing. After completion of all repairs, specimens were biomechanically tested.

        Experimental Setup

        Repaired specimens were secured with tissue clamps at the quadriceps and patellar tendons on an MTS Bionix 858 (MTS Systems) hydraulic arm.

        Figure 3.
        Anatomical conditions were simulated by using a bracket to connect a distal femur sawbone model to the MTS machine and orienting the model on the posterior surface of the patella to produce a flexion angle of 45° (Figure 3), which maximizes tensile forces.16

        Each patella was secured for cyclic testing. Initially it was placed under 10 N of tension. Then it underwent tensile loading from 10 N to 300 N at 50 N/s for 10 cycles. These parameters were based on previous biomechanical patella studies.10,11 Load was measured with the MTS load cell and displacement with the displacement transducer. Fracture displacement associated with 300-N cyclic tension was recorded. Displacement was calculated as the difference between 10th cycle and 2nd cycle values, which accounted for any degree of initial tissue slippage. After cyclic testing, the patella was placed back in 10 N of tensile loading and subjected to maximum force loading to determine ultimate repair strength. For maximum loading, the patella was stretched progressively at 50 N/s until failure. Again, load and displacement were measured with MTS.

        Statistical Analysis

        After testing, fracture displacement and maximum load force data were compiled for analysis. One-way analysis of variance with Bonferroni correction was used to determine if there were significant differences between groups. Significance level was set at P < .05.

         

         

        Results

        For cyclic testing, mean total displacement was measured over 10 cycles for each group. Again, displacement was determined by taking the difference between 10th cycle and 2nd cycle values, allowing for system stabilization.

        Figure 4.
        Figure 5.
        Mean (SD) displacement was 3.57 (1.63) mm with MATB repair, 2.50 (0.80) mm with cerclage augment repair, and 2.17 (0.77) mm with Krackow augment repair (Figure 4). Among all specimens, displacement followed a hyperbolic arrangement, with the majority of total displacement occurring during initial cycles and tapering off during later cycles (Figure 5). Mean displacement was 30% lower with cerclage repair (vs MATB repair) and 40% lower with Krackow repair (vs MATB repair). However, this trend was not statistically significant (P > .05), owing to sample size and presence of an outlier in all 3 groups.

        Figure 6.
        After cyclic loading, load-to-failure testing was performed by applying increasing tension until repair failure. None of our 14 specimens showed significant failure after cyclic testing, so all were subjected to load-to-failure testing. Mean (SD) maximum tension force was found to be 753 (16) N for MATB, 793 (177) N for cerclage, and 863 (104) N for Krackow (Figure 6). Similar to the cyclic testing findings, maximum load strength was 5% higher with cerclage repair (vs MATB repair) and 14% higher with Krackow repair (vs MATB repair). Again, with the small sample size and the presence of outliers (and other variation among data), the trend was not statistically significant (P > .05). In addition, pairwise comparisons of the 3 groups revealed no statistically significant differences.

        Discussion

        Our main objective was to compare the efficacy of a novel suture augment technique with that of other patella fracture repair techniques. Our hypothesis—that adding a Krackow suture augment would increase strength in both cyclic and maximum loading—was supported. Although testing results were not statistically significant because of the small sample size, we think this novel technique has clinically relevant descriptive significance and warrants further investigation.

        Proper anatomical reduction and postoperative stabilization are of utmost importance in clinical approaches to patella fractures. In addition, regardless of which technical procedure is used, open reduction should also allow for early range of motion to prevent joint arthrofibrosis. Ever since the ATB technique was first described by the AO group, postoperative outcomes have improved significantly. In a retrospective study by Levack and colleagues,17 30 of 64 patients with patella fractures underwent internal fixation. Mean follow-up was 6.2 years. By both objective and subjective measures, the best functional outcomes were associated with internal tension band fixation (vs cerclage repair). Lotke and Ecker18 also documented the efficacy of the tension band technique. Sixteen patients with patella fractures underwent anterior tension banding; those with a comminuted fracture also underwent cerclage repair for patella stabilization during tension banding. At 6-week follow-up, all patients had good range of motion (≥90° flexion), relatively few symptoms, and no implant failures. Results were similar to those of Levack and colleagues.17

        Although it improves stability and functional outcomes over conventional patellectomy and cerclage wiring, the ATB technique has been associated with subcutaneous irritation caused by the K-wires used to secure the band. Hung and colleagues9 followed up 68 patients with patellar fractures. Five of these patients underwent tension banding. Although there was a high level of adequate functional outcomes, implant irritation was found to be “quite frequent.”

        To address this issue, Carpenter and colleagues11 evaluated an ATB technique that uses K-wires instead of cannulated screws. Biomechanical testing in a cadaver model revealed less fracture displacement and overall more repair strength through cyclic and maximum load testing. Clinically, these results were supported by Berg,10 who followed up 10 patients with transverse patella fractures repaired with the MATB technique. At a mean follow-up of 24 months, 7 of the 10 patients had good to excellent outcomes, and there were no implant failures.

         

         

        Further investigation into patella repairs has mainly focused on improving the MATB technique and experimenting with different tension band materials. Rabalais and colleagues13 biomechanically tested high-strength polyethylene suture as a replacement for standard 18-gauge wire, and Bryant and colleagues14 tested a braided composite suture (FiberWire; Arthrex) as a replacement for standard 18-gauge stainless steel wire. Both found no significant difference with use of augmented tension band material, but Rabalais and colleagues13 did find more advantages with a parallel tension band construct than with a standard figure-of-8 arrangement.

        In developing our novel technique, we considered that Krackow sutures are routinely used in both quadriceps tendon repair and patellar tendon repair, including partial patellectomy for distal patella fracture. With a suture placed in both tendons, the augment could be expected to resist longitudinal gapping and augment the tension band across the anterior patella. First described by Krackow and colleagues,19 the Krackow suture is widely used for tendon reconstruction. In an interlocking system of sutures, the Krackow suture provides a repair that is more stable than repair with conventional suture techniques, specifically in the context of tendon repair.20 Given the sesamoidal nature of the patella, its repair shares the goal of gap prevention with other tendon repairs. In theory, anchoring the supporting structures that are above and below the patella provides support for the intervening patella and ultimately improves fracture fixation strength.

        Oh and colleagues15 reported on the clinical efficacy of a Krackow augment in distal pole patella repairs. Similarly, we found a Krackow augment to be efficacious, supporting its potential in clinical approaches to patella repairs. Our results indicate this augment can be a useful clinical adjunct in biomechanical evaluation. 

        Limitations of this study include its use of dissected extensor mechanisms, which may have less biofidelity than whole-knee specimens. In our model, specimens were secured at the patellar tendon and the quadriceps tendons, as opposed to the quadriceps tendon and the tibia distally. Use of this model could have led to an increase in early displacement during cyclic testing as a result of tissue slippage. Furthermore, our small sample size could have affected our ability to demonstrate a difference between these techniques.

        Given its increased strength as demonstrated by mean displacement during cyclic loading and mean load to failure, as well as the early clinical data recently published, the Krackow suture augment represents a feasible technique for patella fixation. It likely will be most useful in cases in which conventional techniques are prone to failure or cannot be applied, such as severe distal comminution or poor bone density. Further biomechanical testing with a larger number of specimens may be required for statistical significance.

        Conclusion

        In patella fracture repair strategies, the Krackow suture augment increased strength when used with a MATB technique. Failure to reach statistical significance likely resulted from our small sample size. Further biomechanical testing and clinical studies are needed for more complete evaluation of this technique. We think it will be most useful in the setting of poor bone quality or severe comminution, which can limit fixation options. As increased repair strength allows earlier postoperative rehabilitation and maintains fracture reduction, patient outcomes should improve. This novel technique represents another strategy for managing challenging patella fractures.

        Take-Home Points

        • Suture augmentation improves construct strength for patella fixation.
        • Krackow sutures may be placed in the quadriceps and patella tendons, then secured over the anterior patella (much like an anterior tension band).
        • The Krackow technique described was superior to the suture cerclage technique based on mean load values, but did not reach statistical significance.
        • The Krackow suture technique is a viable and easily applied technique for suture augmentation of patella fixation constructs.

        Patella fractures are relatively uncommon, accounting for only 1% of skeletal injuries.1 Restoration of the function of the patella and the extensor mechanism is vital for knee extension and gait. However, patella fractures have an inherently high rate of complications, making these injuries challenging to treat.2-4 In patients with intact extensor function, displacement of <4 mm, and articular step-off of <3 mm, nonoperative management is extremely effective, with 99% of patients reporting favorable results.5 However, for fractures in which the extensor mechanism is disrupted, surgical intervention typically is indicated.6

        Authors have reported various surgical interventions, one of the most commonly used being the anterior tension band (ATB) technique, first described by the AO (Arbeitsgemeinschaft für Osteosynthesefragen) group in the 1950s.7 By converting distractive anterior force during knee flexion to compressive force at the fracture site, the ATB technique provides a repair stronger than the previously used cerclage repair.8 Although initially considered standard of care, the ATB technique was soon found to be associated with implant failure and subcutaneous irritation prompting implant removal.9

        To address these issues, Berg10 and Carpenter and colleagues11 evaluated an ATB technique that used cannulated screws instead of Kirschner wires (K-wires). This variation on the ATB technique reduced the implant-related issues while maintaining the mechanical advantage of the tension band. The more rigid design also permitted earlier postoperative rehabilitation, which significantly reduced development of arthrofibrosis.6,7,10 This modified ATB (MATB) technique has since been investigated for additional augments, mainly focusing on use of different tension band materials, including polyester suture and braided composite suture.12-14

        However, there is little research on augments that incorporate the surrounding soft tissue, specifically the quadriceps and patellar tendons. In a recent retrospective clinical study, Oh and colleagues15 found positive clinical results with use of Krackow sutures, though 2 or 3 vertically oriented stainless steel wires were used instead of cannulated screws.

        We conducted a study to determine the biomechanical efficacy of using a cerclage suture augment and a Krackow suture augment coupled with and compared with conventional MATB repair. If effective, this technique may represent another strategy for increasing repair strength and thereby improve postoperative outcomes.

         

         

        Materials and Methods

        Specimen Preparation

        Fresh-frozen cadaver extensor mechanisms (quadriceps tendon, patella, surrounding retinaculum, patellar tendon) were kept frozen at –4°C until preparation. Fifteen specimens were selected. Mean (SD) age at death was 68 (10) years (range, 51-85 years). One specimen was excluded for a short patella tendon, which precluded adequate attachment for testing. All specimens were free of overt osseous pathology.

        After specimens were thawed overnight, the patellae were transversely osteotomized with an osteotome at the junction of the middle and distal thirds of the patella. Sharp dissection was performed to carry the division through the medial and lateral retinaculum at the same level. All 14 specimens were then repaired using the MATB technique. First, the transverse fracture was reduced with a reduction clamp. Then, two 4-mm cannulated screws (DePuy Synthes) were inserted parallel to each other and perpendicular to the fracture. An 18-gauge stainless steel wire was then passed through each screw, crossed anteriorly, and tightened to create a figure-of-8 ATB. The specimens were then randomly divided into 3 groups—MATB; MATB with cerclage suture augment; MATB with Krackow suture augment—while ensuring specimens from a single cadaver were placed in different groups to avoid confounding based on bone density differences.

        Figure 1.
        Figure 2.
        A braided composite suture (No. 5 FiberWire; Arthrex) was used for the cerclage augment on 4 specimens, and a Krackow augment was used for 5 specimens (Figures 1A-1C). The cerclage augment was placed by circumferentially passing the suture at 8 points in the surrounding retinaculum. For the Krackow augment, 4 locking passes were made on both the medial and the lateral sides of the quadriceps and patella tendon, yielding a total of 4 free suture ends (Figure 2). Free ends were then crossed anteriorly in a fashion similar to that used for the 18-gauge wires and tied. Last, overlying subcutaneous tissue and paratenon were stripped from the quadriceps and patellar tendons to maximize friction during clamping for testing. After completion of all repairs, specimens were biomechanically tested.

        Experimental Setup

        Repaired specimens were secured with tissue clamps at the quadriceps and patellar tendons on an MTS Bionix 858 (MTS Systems) hydraulic arm.

        Figure 3.
        Anatomical conditions were simulated by using a bracket to connect a distal femur sawbone model to the MTS machine and orienting the model on the posterior surface of the patella to produce a flexion angle of 45° (Figure 3), which maximizes tensile forces.16

        Each patella was secured for cyclic testing. Initially it was placed under 10 N of tension. Then it underwent tensile loading from 10 N to 300 N at 50 N/s for 10 cycles. These parameters were based on previous biomechanical patella studies.10,11 Load was measured with the MTS load cell and displacement with the displacement transducer. Fracture displacement associated with 300-N cyclic tension was recorded. Displacement was calculated as the difference between 10th cycle and 2nd cycle values, which accounted for any degree of initial tissue slippage. After cyclic testing, the patella was placed back in 10 N of tensile loading and subjected to maximum force loading to determine ultimate repair strength. For maximum loading, the patella was stretched progressively at 50 N/s until failure. Again, load and displacement were measured with MTS.

        Statistical Analysis

        After testing, fracture displacement and maximum load force data were compiled for analysis. One-way analysis of variance with Bonferroni correction was used to determine if there were significant differences between groups. Significance level was set at P < .05.

         

         

        Results

        For cyclic testing, mean total displacement was measured over 10 cycles for each group. Again, displacement was determined by taking the difference between 10th cycle and 2nd cycle values, allowing for system stabilization.

        Figure 4.
        Figure 5.
        Mean (SD) displacement was 3.57 (1.63) mm with MATB repair, 2.50 (0.80) mm with cerclage augment repair, and 2.17 (0.77) mm with Krackow augment repair (Figure 4). Among all specimens, displacement followed a hyperbolic arrangement, with the majority of total displacement occurring during initial cycles and tapering off during later cycles (Figure 5). Mean displacement was 30% lower with cerclage repair (vs MATB repair) and 40% lower with Krackow repair (vs MATB repair). However, this trend was not statistically significant (P > .05), owing to sample size and presence of an outlier in all 3 groups.

        Figure 6.
        After cyclic loading, load-to-failure testing was performed by applying increasing tension until repair failure. None of our 14 specimens showed significant failure after cyclic testing, so all were subjected to load-to-failure testing. Mean (SD) maximum tension force was found to be 753 (16) N for MATB, 793 (177) N for cerclage, and 863 (104) N for Krackow (Figure 6). Similar to the cyclic testing findings, maximum load strength was 5% higher with cerclage repair (vs MATB repair) and 14% higher with Krackow repair (vs MATB repair). Again, with the small sample size and the presence of outliers (and other variation among data), the trend was not statistically significant (P > .05). In addition, pairwise comparisons of the 3 groups revealed no statistically significant differences.

        Discussion

        Our main objective was to compare the efficacy of a novel suture augment technique with that of other patella fracture repair techniques. Our hypothesis—that adding a Krackow suture augment would increase strength in both cyclic and maximum loading—was supported. Although testing results were not statistically significant because of the small sample size, we think this novel technique has clinically relevant descriptive significance and warrants further investigation.

        Proper anatomical reduction and postoperative stabilization are of utmost importance in clinical approaches to patella fractures. In addition, regardless of which technical procedure is used, open reduction should also allow for early range of motion to prevent joint arthrofibrosis. Ever since the ATB technique was first described by the AO group, postoperative outcomes have improved significantly. In a retrospective study by Levack and colleagues,17 30 of 64 patients with patella fractures underwent internal fixation. Mean follow-up was 6.2 years. By both objective and subjective measures, the best functional outcomes were associated with internal tension band fixation (vs cerclage repair). Lotke and Ecker18 also documented the efficacy of the tension band technique. Sixteen patients with patella fractures underwent anterior tension banding; those with a comminuted fracture also underwent cerclage repair for patella stabilization during tension banding. At 6-week follow-up, all patients had good range of motion (≥90° flexion), relatively few symptoms, and no implant failures. Results were similar to those of Levack and colleagues.17

        Although it improves stability and functional outcomes over conventional patellectomy and cerclage wiring, the ATB technique has been associated with subcutaneous irritation caused by the K-wires used to secure the band. Hung and colleagues9 followed up 68 patients with patellar fractures. Five of these patients underwent tension banding. Although there was a high level of adequate functional outcomes, implant irritation was found to be “quite frequent.”

        To address this issue, Carpenter and colleagues11 evaluated an ATB technique that uses K-wires instead of cannulated screws. Biomechanical testing in a cadaver model revealed less fracture displacement and overall more repair strength through cyclic and maximum load testing. Clinically, these results were supported by Berg,10 who followed up 10 patients with transverse patella fractures repaired with the MATB technique. At a mean follow-up of 24 months, 7 of the 10 patients had good to excellent outcomes, and there were no implant failures.

         

         

        Further investigation into patella repairs has mainly focused on improving the MATB technique and experimenting with different tension band materials. Rabalais and colleagues13 biomechanically tested high-strength polyethylene suture as a replacement for standard 18-gauge wire, and Bryant and colleagues14 tested a braided composite suture (FiberWire; Arthrex) as a replacement for standard 18-gauge stainless steel wire. Both found no significant difference with use of augmented tension band material, but Rabalais and colleagues13 did find more advantages with a parallel tension band construct than with a standard figure-of-8 arrangement.

        In developing our novel technique, we considered that Krackow sutures are routinely used in both quadriceps tendon repair and patellar tendon repair, including partial patellectomy for distal patella fracture. With a suture placed in both tendons, the augment could be expected to resist longitudinal gapping and augment the tension band across the anterior patella. First described by Krackow and colleagues,19 the Krackow suture is widely used for tendon reconstruction. In an interlocking system of sutures, the Krackow suture provides a repair that is more stable than repair with conventional suture techniques, specifically in the context of tendon repair.20 Given the sesamoidal nature of the patella, its repair shares the goal of gap prevention with other tendon repairs. In theory, anchoring the supporting structures that are above and below the patella provides support for the intervening patella and ultimately improves fracture fixation strength.

        Oh and colleagues15 reported on the clinical efficacy of a Krackow augment in distal pole patella repairs. Similarly, we found a Krackow augment to be efficacious, supporting its potential in clinical approaches to patella repairs. Our results indicate this augment can be a useful clinical adjunct in biomechanical evaluation. 

        Limitations of this study include its use of dissected extensor mechanisms, which may have less biofidelity than whole-knee specimens. In our model, specimens were secured at the patellar tendon and the quadriceps tendons, as opposed to the quadriceps tendon and the tibia distally. Use of this model could have led to an increase in early displacement during cyclic testing as a result of tissue slippage. Furthermore, our small sample size could have affected our ability to demonstrate a difference between these techniques.

        Given its increased strength as demonstrated by mean displacement during cyclic loading and mean load to failure, as well as the early clinical data recently published, the Krackow suture augment represents a feasible technique for patella fixation. It likely will be most useful in cases in which conventional techniques are prone to failure or cannot be applied, such as severe distal comminution or poor bone density. Further biomechanical testing with a larger number of specimens may be required for statistical significance.

        Conclusion

        In patella fracture repair strategies, the Krackow suture augment increased strength when used with a MATB technique. Failure to reach statistical significance likely resulted from our small sample size. Further biomechanical testing and clinical studies are needed for more complete evaluation of this technique. We think it will be most useful in the setting of poor bone quality or severe comminution, which can limit fixation options. As increased repair strength allows earlier postoperative rehabilitation and maintains fracture reduction, patient outcomes should improve. This novel technique represents another strategy for managing challenging patella fractures.

        References

        1. Boström Å. Fracture of the patella. A study of 422 patellar fractures. Acta Orthop Scand Suppl. 1972;143:1-80. 

        2. Hungerford DS, Barry M. Biomechanics of the patellofemoral joint. Clin Orthop Relat Res. 1979;(144):9-15.

        3. LeBrun CT, Langford JR, Sagi HC. Functional outcomes after operatively treated patella fractures. J Orthop Trauma. 2012;26(7):422-426. 

        4. Kaufer H. Mechanical function of the patella. J Bone Joint Surg Am. 1971;53(8):1551-1560. 

        5. Braun W, Wiedemann M, Rüter A, Kundel K, Kolbinger S. Indications and results of nonoperative treatment of patellar fractures. Clin Orthop Relat Res. 1993;(289):197-201.

        6. Melvin JS, Mehta S. Patellar fractures in adults. J Am Acad Orthop Surg. 2011;19(4):198-207. 

        7. Müller M, Allgöwer M, Schneider R, Willeneger H. Manual of Internal Fixation: Techniques Recommended by the AO Group. Berlin, Germany: Springer; 1979.

        8. Weber MJ, Janecki CJ, McLeod P, Nelson CL, Thompson JA. Efficacy of various forms of fixation of transverse fractures of the patella. J Bone Joint Surg Am. 1980;62(2):215-220.

        9. Hung LK, Chan KM, Chow YN, Leung PC. Fractured patella: operative treatment using the tension band principle. Injury. 1985;16(5):343-347. 

        10. Berg EE. Open reduction internal fixation of displaced transverse patella fractures with figure-eight wiring through parallel cannulated compression screws. J Orthop Trauma. 1997;11(8):573-576.

        11. Carpenter JE, Kasman RA, Patel N, Lee ML, Goldstein SA. Biomechanical evaluation of current patella fracture fixation techniques. J Orthop Trauma. 1997;11(5):351-356.

        12. Hughes SC, Stott PM, Hearnden AJ, Ripley LG. A new and effective tension-band braided polyester suture technique for transverse patellar fracture fixation. Injury. 2007;38(2):212-222. 

        13. Rabalais RD, Burger E, Lu Y, Mansour A, Baratta RV. Comparison of two tension-band fixation materials and techniques in transverse patella fractures: a biomechanical study. Orthopedics. 2008;31(2):128.

        14. Bryant TL, Anderson CL, Stevens CG, Conrad BP, Vincent HK, Sadasivan KK. Comparison of cannulated screws with FiberWire or stainless steel wire for patella fracture fixation: a pilot study. J Orthop. 2014;12(2):92-96.

        15. Oh HK, Choo SK, Kim JW, Lee M. Internal fixation of displaced inferior pole of the patella fractures using vertical wiring augmented with Krachow suturing. Injury. 2015;46(12):2512-2515.

        16. Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional anatomy of the patello-femoral joint. J Bone Joint Surg Br. 1976;58(3):287-290. 

        17. Levack B, Flannagan JP, Hobbs S. Results of surgical treatment of patellar fractures. J Bone Joint Surg Br. 1985;67(3):416-419. 

        18. Lotke PA, Ecker ML. Transverse fractures of the patella. Clin Orthop Relat Res. 1981;(158):180-184.

        19. Krackow KA, Thomas SC, Jones LC. Ligament-tendon fixation: analysis of a new stitch and comparison with standard techniques. Orthopedics. 1988;11(6):909-917.

        20. Hahn JM, Inceoğlu S, Wongworawat MD. Biomechanical comparison of Krackow locking stitch versus nonlocking loop stitch with varying number of throws. Am J Sports Med. 2014;42(12):3003-3008.

        References

        1. Boström Å. Fracture of the patella. A study of 422 patellar fractures. Acta Orthop Scand Suppl. 1972;143:1-80. 

        2. Hungerford DS, Barry M. Biomechanics of the patellofemoral joint. Clin Orthop Relat Res. 1979;(144):9-15.

        3. LeBrun CT, Langford JR, Sagi HC. Functional outcomes after operatively treated patella fractures. J Orthop Trauma. 2012;26(7):422-426. 

        4. Kaufer H. Mechanical function of the patella. J Bone Joint Surg Am. 1971;53(8):1551-1560. 

        5. Braun W, Wiedemann M, Rüter A, Kundel K, Kolbinger S. Indications and results of nonoperative treatment of patellar fractures. Clin Orthop Relat Res. 1993;(289):197-201.

        6. Melvin JS, Mehta S. Patellar fractures in adults. J Am Acad Orthop Surg. 2011;19(4):198-207. 

        7. Müller M, Allgöwer M, Schneider R, Willeneger H. Manual of Internal Fixation: Techniques Recommended by the AO Group. Berlin, Germany: Springer; 1979.

        8. Weber MJ, Janecki CJ, McLeod P, Nelson CL, Thompson JA. Efficacy of various forms of fixation of transverse fractures of the patella. J Bone Joint Surg Am. 1980;62(2):215-220.

        9. Hung LK, Chan KM, Chow YN, Leung PC. Fractured patella: operative treatment using the tension band principle. Injury. 1985;16(5):343-347. 

        10. Berg EE. Open reduction internal fixation of displaced transverse patella fractures with figure-eight wiring through parallel cannulated compression screws. J Orthop Trauma. 1997;11(8):573-576.

        11. Carpenter JE, Kasman RA, Patel N, Lee ML, Goldstein SA. Biomechanical evaluation of current patella fracture fixation techniques. J Orthop Trauma. 1997;11(5):351-356.

        12. Hughes SC, Stott PM, Hearnden AJ, Ripley LG. A new and effective tension-band braided polyester suture technique for transverse patellar fracture fixation. Injury. 2007;38(2):212-222. 

        13. Rabalais RD, Burger E, Lu Y, Mansour A, Baratta RV. Comparison of two tension-band fixation materials and techniques in transverse patella fractures: a biomechanical study. Orthopedics. 2008;31(2):128.

        14. Bryant TL, Anderson CL, Stevens CG, Conrad BP, Vincent HK, Sadasivan KK. Comparison of cannulated screws with FiberWire or stainless steel wire for patella fracture fixation: a pilot study. J Orthop. 2014;12(2):92-96.

        15. Oh HK, Choo SK, Kim JW, Lee M. Internal fixation of displaced inferior pole of the patella fractures using vertical wiring augmented with Krachow suturing. Injury. 2015;46(12):2512-2515.

        16. Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional anatomy of the patello-femoral joint. J Bone Joint Surg Br. 1976;58(3):287-290. 

        17. Levack B, Flannagan JP, Hobbs S. Results of surgical treatment of patellar fractures. J Bone Joint Surg Br. 1985;67(3):416-419. 

        18. Lotke PA, Ecker ML. Transverse fractures of the patella. Clin Orthop Relat Res. 1981;(158):180-184.

        19. Krackow KA, Thomas SC, Jones LC. Ligament-tendon fixation: analysis of a new stitch and comparison with standard techniques. Orthopedics. 1988;11(6):909-917.

        20. Hahn JM, Inceoğlu S, Wongworawat MD. Biomechanical comparison of Krackow locking stitch versus nonlocking loop stitch with varying number of throws. Am J Sports Med. 2014;42(12):3003-3008.

        Issue
        The American Journal of Orthopedics - 46(6)
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        ANSWER

        The radiograph shows an oblique fracture through the radial styloid process. The patient was placed in a splint and referred to outpatient orthopedics for follow-up.

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        ANSWER

        The radiograph shows an oblique fracture through the radial styloid process. The patient was placed in a splint and referred to outpatient orthopedics for follow-up.

        ANSWER

        The radiograph shows an oblique fracture through the radial styloid process. The patient was placed in a splint and referred to outpatient orthopedics for follow-up.

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        Questionnaire Body

        A 35-year-old woman arrives at the emergency department following a motor vehicle accident. She was a restrained driver who was crossing an intersection when another vehicle pulled out in front of her. She recalls gripping the steering wheel in anticipation of impact. No air bags deployed. She complains of wrist pain, but denies any other ailment.

        Medical history is unremarkable. Vital signs are normal. Physical examination of the patient’s left wrist shows no obvious deformity. There is mild soft-tissue swelling, decreased range of motion, and moderate point tenderness along the radial aspect of the wrist. The nailbeds have good capillary refill. Strong pulses are present, as well.

        Triage has already obtained a radiograph of the left wrist (shown). What is your impression?

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        Total Hip Arthroplasty and Hemiarthroplasty: US National Trends in the Treatment of Femoral Neck Fractures

        Article Type
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        Take-Home Points

        • An increasing number of THAs and HAs were performed over time for FNF.
        • HA patients tended to be older.
        • Hospitalization and blood transfusion rates were higher for THA.
        • Hospital size affected the rate of HAs, while hospital location affected the rate of THAs.
        • A larger proportion of THA patients had private insurance.

        Femoral neck fractures (FNFs) are a common source of morbidity and mortality worldwide. The increasing number of FNFs in the United States is attributed to increases in number of US residents >65 years old, the average life span, and the incidence of osteoporosis.1 Three hundred forty thousand hip fractures occurred in the United States in 1996, and the number is expected to double by 2050.2 By that year, an estimated 6.3 million hip fractures will occur worldwide.3 Given the 1-year mortality rate of 14% to 36%, optimizing the management of these fractures is an important public health issue that must be addressed.4

        Treatment is based on preoperative ambulatory status, cognitive function, comorbidities, fracture type and displacement, and other factors. In physiologically elderly patients with displaced fractures, surgical treatment usually involves either hemiarthroplasty (HA) or total hip arthroplasty (THA). There is controversy regarding which modality is the preferred treatment.

        Proponents of HA point to a higher rate of dislocation for FNFs treated with THAs,5,6 attributed to increased range of motion.7 Proponents of THA point to superior short-term clinical results and fewer complications, especially in mobile, independent patients.8

        We conducted a study to assess recent US national trends in performing THA and HA for FNFs and to evaluate perioperative outcomes for each treatment group. 

        Materials and Methods

        Data for this study were obtained from the National Center for Health Statistics (NCHS) National Hospital Discharge Survey (NHDS) and were imported into Microsoft Office Excel 2010.9 The NHDS examines patient discharges from various hospitals across the US, including federal, military, and Veterans Administration hospitals.9 Only short-stay hospitals (mean stay, <30 days) and hospitals with a general specialty are included in the survey. Each year, about 1% of all hospital admissions from across the US are abstracted and weighted to provide nationwide estimates. The information collected from each hospital record includes age, sex, race, marital status, discharge month, discharge status, days of care, hospital location, hospital size (number of beds), hospital type (proprietary or for-profit, government, nonprofit/church), and up to 15 discharge diagnoses and 8 procedures performed during admission.9

        International Classification of Diseases, Ninth Revision (ICD-9) procedure codes were used to search the NHDS for patients admitted after FNF for each year from 2001 through 2010. These codes were then used to identify patients within this group who underwent THA or HA. We also collected data on patient demographics, hospitalization duration, discharge disposition, in-hospital adverse events (deep vein thrombosis [DVT], pulmonary embolism [PE], blood transfusion, mortality), form of primary medical insurance, number of hospital beds (0-99, 100-199, 200-299, 300-499, ≥500), hospital type (proprietary, government, nonprofit/church), and hospital region (Northeast, Midwest, South, West). 

         

         

        Trends were evaluated by linear regression with the Pearson correlation coefficient (r). Statistical comparisons were made using the Student t test for continuous data, and both the Fisher exact test and the χ2 test for categorical variables. Significance level was set at P < .05. All analyses were performed with IBM SPSS Statistics 22. 

        Results

        Figure 1.
        Of the 12,757 patients identified as having FNFs (Figure 1), 582 (4.6%) underwent THA, 6697 (52.5%) underwent HA, 3453 (27.1%) received internal fixation, and 1809 (14.2%) did not have their surgery documented. There were 164 men (28.2%) in the THA group and 1744 (26.0%) in the HA group (P = .27). Mean age was significantly (P < .01) higher for HA patients (81.1 years; range, 18-99 years) than for THA patients (76.9 years; range, 19-99 years), and there were significantly (P < .01) more medical comorbidities for HA patients (6.4 diagnoses; range, 1-7+ diagnoses) than for THA patients (6.1 diagnoses; range, 1-7 diagnoses).

        Figure 2.
        There was no clear trend in prevalence of FNFs between 2001 and 2010 (r = 0.25; Figure 2). During this period, fracture prevalence ranged from 406 to 477 per 100,000 admissions. However, there was increased frequency in use of both surgical techniques for FNFs over time: THA (r = 0.82; Figure 3) and HA (r = 0.80; Figure 4).
        Figure 3.
        Figure 4.
        The rate of THAs for FNFs increased from 4.2% for 2001 to 2005 to 5.0% for 2006 to 2010 (P = .04); similarly, the rate of HAs for FNFs increased from 51.0% for 2001 to 2005 to 54.7% for 2006 to 2010 (P < .01).

        Hospital stay was longer (P < .01) for THA patients (7.7 days; range, 1-312 days) than for HA patients (6.7 days; range, 1-118 days), and blood transfusion rate was higher (P = .02) for THA patients (30.4%) than for HA patients (25.7%), but the groups did not differ in their rates of DVT (THA, 1.2%; HA, 0.80%, P = .50), PE (THA, 0.52%; HA, 0.72%, P = .52), or mortality (THA, 1.8%; HA, 2.9%; P = .16). Discharge disposition varied with surgical status (P < .01): 23.2% of THA patients and 11.6% of HA patients were discharged directly home after their inpatient stay, and 76.8% of THA patients and 88.4% of HA patients were discharged or transferred to a short- or long-term care facility.

        Table.
        Figure 5.
        Hospital size (number of beds) affected the number of HAs performed (P < .01) but not the number of THAs performed (P = .10; Table). Hospital location (Northeast, Midwest, South, West) affected THA frequency (P = .01), but not HA frequency (P = .07; Figure 5). In contrast, hospital type (proprietary, government, nonprofit/church) affected the HA rate (P < .01) but not the THA rate (P = .12; Table). 

        Private medical insurance provided coverage for 14.3% of THAs and 9.1% of HAs, and Medicare provided coverage for 80.9% of THAs and 86.0% of HAs (P < .01).

         

         

        Discussion

        The NHDS data showed a preference for HA over THA in the treatment of FNFs and suggested THA was favored for younger, healthier patients while HA was reserved for older patients with more comorbidities. Despite being younger and healthier, the THA group had higher transfusion rates and longer hospitalizations, possibly because of the increased complexity of THA procedures, which generally involve more operative time and increased blood loss. The resultant higher transfusion rate for THAs likely contributed to longer hospitalizations for FNFs. However, the THA and HA groups did not differ in their rates of DVT, PE, or mortality.

        Multiple studies have noted no differences in mortality, infection, or general complications between THA and HA for FNF.8,10,11 THA patients have better functional outcomes, including Harris and Oxford hip scores and walking distance, but higher dislocation rates,8,10-12 and HA patients are at higher risk for reoperation because of progressive acetabular erosion.8,10,11

        We noted an increase in use of both THA and HA for FNF over the study period (2001-2010). In a review of operative treatment for FNF by surgeons applying for the American Board of Orthopaedic Surgery certification between 1999 and 2011, Miller and colleagues13 found a similar increase in the THA rate over time, but decreases in the HA and internal fixation rates, with candidates in the “adult reconstruction” subspecialty showing a particularly strong trend toward THA use.

        These findings reflect a general propensity toward femoral head replacement rather than preservation through open reduction and internal fixation (ORIF). Recent studies have found that ORIF carries a 39% to 43% rate of fixation failure and need for secondary revision, as well as risks of avascular necrosis, malunion, and nonunion.1,14-16 This need for secondary surgery makes ORIF ultimately less cost-effective than either THA or HA.16,17 Most authors would recommend arthroplasty for FNF in elderly patients with normal mental function1,16,18 and would reserve ORIF for young patients with good bone stock, joint space preservation, and reducible noncomminuted fractures.1,19

        Our study results suggest that smaller hospitals (<100 beds) tend to have lower rates of HA (P < .01, significant) and THA (P = .10, not significant; Table), possibly because FNF patients who present to these hospitals may be referred elsewhere because of regional differences in the availability of orthopedic traumatologists and arthroplasty subspecialists. Surgeon volume affects postoperative outcomes and may play a role in referral patterns.20 Ames and colleagues20 found that HA performed for FNF by surgeons with high-volume THA experience (vs non-hip-arthroplasty surgeons) had lower rates of dislocation, superficial infection, and mortality.

        Regional differences were significant for THA alone, with the highest THA rates in the South (5.2%) and the lowest in the West (3.3%; Figure 5). There were no clear regional trends for HA. Possible explanations include a propensity toward a more aggressive approach in these regions, increased regional prevalence of acetabular disease, regional surgeon preferences, and regional differences in patient characteristics (eg, increased prevalence of obesity in the South).21

         

         

        HA rates were highest for nonprofit/church hospitals and lowest for proprietary hospitals, whereas THA rates did not differ by hospital type. Possible explanations include an older, less mobile nonprofit/church patient cohort that is more amenable to HA, and surgeon preference. 

        THA patients were more likely to be covered by private medical insurance than by Medicare—a finding in agreement with Hochfelder and colleagues,22 who found that, compared with federal insurance and self-pay patients, private insurance patients were 41% more likely to undergo THA than HA or internal fixation for FNF. We think that the age difference between our THA and HA groups contributed to the insurance variability in our study.

        Our study had several limitations. It was conducted to examine the rates of THA and HA after FNF, not to survey treatment types, including ORIF and nonoperative management. The NHDS database does not provide information on HA implant type (unipolar, bipolar), use or nonuse of cement with HA, or surgical approach. Surgical approach could influence the rate of postoperative dislocation, an outcome measure that was not examined in this study. Last, the NHDS database tracks admissions and discharges, not patients. When a patient is discharged, collection of information on the patient’s postoperative course stops; a patient who returns even only 1 day later is recorded as a new or unique patient. Therefore, intermediate or long-term outcome information is unavailable, which likely led to an underrepresentation of DVT, PE, and mortality after these THA and HA procedures.

        There was a trend toward femoral head replacement rather than ORIF in the treatment of FNF. Cognitively functional and independent elderly patients, and patients with osteoarthritis or rheumatoid arthritis, may benefit from THA, whereas HA may be better suited to cognitively dysfunctional patients.23,24 The NHDS reflects an increasing trend toward arthroplasty over ORIF, but the exact treatment choice is affected by hospital type, size,  location and surgeon preference, training, and subspecialization.

        References

        1. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287-293.

        2. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596-607.

        3. Kannus P, Parkkari J, Sievänen H, Heinonen A, Vuori I, Järvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 suppl):57S-63S.

        4. Zuckerman JD. Hip fracture. N Engl J Med. 1996;334(23):1519-1525.

        5. Papandrea RF, Froimson MI. Total hip arthroplasty after acute displaced femoral neck fractures. Am J Orthop. 1996;25(2):85-88.

        6. Burgers PT, Van Geene AR, Van den Bekerom MP, et al. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures in the healthy elderly: a meta-analysis and systematic review of randomized trials. Int Orthop. 2012;36(8):1549-1560.

        7. Skinner P, Riley D, Ellery J, Beaumont A, Coumine R, Shafighian B. Displaced subcapital fractures of the femur: a prospective randomized comparison of internal fixation, hemiarthroplasty and total hip replacement. Injury. 1989;20(5):291-293.

        8. Baker RP, Squires B, Gargan MF, Bannister GC. Total hip arthroplasty and hemiarthroplasty in mobile, independent patients with a displaced intracapsular fracture of the femoral neck. A randomized, controlled trial. J Bone Joint Surg Am. 2006;88(12):2583-2589.

        9. Centers for Disease Control and Prevention, National Center for Health Statistics. National Hospital Discharge Survey. http://www.cdc.gov/nchs/nhds/about_nhds.htm. Last updated December 6, 2011. Accessed December 10, 2013.

        10. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplasty. 2012;27(4):583-590.

        11. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235-2243.

        12. Hopley C, Stengel D, Ekkernkamp A, Wich M. Primary total hip arthroplasty versus hemiarthroplasty for displaced intracapsular hip fractures in older patients: systematic review. BMJ. 2010;340:c2332.

        13. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg Am. 2014;96(17):e149.

        14. Rogmark C, Carlsson A, Johnell O, Sernbo I. A prospective randomised trial of internal fixation versus arthroplasty for displaced fractures of the neck of the femur. Functional outcome for 450 patients at two years. J Bone Joint Surg Br. 2002;84(2):183-188.

        15. Bhandari M, Devereaux PJ, Swiontkowski MF, et al. Internal fixation compared with arthroplasty for displaced fractures of the femoral neck. A meta-analysis. J Bone Joint Surg Am. 2003;85(9):1673-1681.

        16. Keating JF, Grant A, Masson M, Scott NW, Forbes JF. Randomized comparison of reduction and fixation, bipolar hemiarthroplasty, and total hip arthroplasty. Treatment of displaced intracapsular hip fractures in healthy older patients. J Bone Joint Surg Am. 2006;88(2):249-260.

        17. Iorio R, Healy WL, Lemos DW, Appleby D, Lucchesi CA, Saleh KJ. Displaced femoral neck fractures in the elderly: outcomes and cost effectiveness. Clin Orthop Relat Res. 2001;(383):229-242.

        18. Johansson T, Jacobsson SA, Ivarsson I, Knutsson A, Wahlström O. Internal fixation versus total hip arthroplasty in the treatment of displaced femoral neck fractures: a prospective randomized study of 100 hips. Acta Orthop Scand. 2000;71(6):597-602.

        19. Shah AK, Eissler J, Radomisli T. Algorithms for the treatment of femoral neck fractures. Clin Orthop Relat Res. 2002;(399):28-34.

        20. Ames JB, Lurie JD, Tomek IM, Zhou W, Koval KJ. Does surgeon volume for total hip arthroplasty affect outcomes after hemiarthroplasty for femoral neck fracture? Am J Orthop. 2010;39(8):E84-E89.

        21. Le A, Judd SE, Allison DB, et al. The geographic distribution of obesity in the US and the potential regional differences in misreporting of obesity. Obesity. 2014;22(1):300-306.

        22. Hochfelder JP, Khatib ON, Glait SA, Slover JD. Femoral neck fractures in New York state. Is the rate of THA increasing, and do race or payer influence decision making? J Orthop Trauma. 2014;28(7):422-426.

        23. Lowe JA, Crist BD, Bhandari M, Ferguson TA. Optimal treatment of femoral neck fractures according to patient’s physiologic age: an evidence-based review. Orthop Clin North Am. 2010;41(2):157-166.

        24. Callaghan JJ, Liu SS, Haidukewych GJ. Subcapital fractures: a changing paradigm. J Bone Joint Surg Br. 2012;94(11 suppl A):19-21.

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        Take-Home Points

        • An increasing number of THAs and HAs were performed over time for FNF.
        • HA patients tended to be older.
        • Hospitalization and blood transfusion rates were higher for THA.
        • Hospital size affected the rate of HAs, while hospital location affected the rate of THAs.
        • A larger proportion of THA patients had private insurance.

        Femoral neck fractures (FNFs) are a common source of morbidity and mortality worldwide. The increasing number of FNFs in the United States is attributed to increases in number of US residents >65 years old, the average life span, and the incidence of osteoporosis.1 Three hundred forty thousand hip fractures occurred in the United States in 1996, and the number is expected to double by 2050.2 By that year, an estimated 6.3 million hip fractures will occur worldwide.3 Given the 1-year mortality rate of 14% to 36%, optimizing the management of these fractures is an important public health issue that must be addressed.4

        Treatment is based on preoperative ambulatory status, cognitive function, comorbidities, fracture type and displacement, and other factors. In physiologically elderly patients with displaced fractures, surgical treatment usually involves either hemiarthroplasty (HA) or total hip arthroplasty (THA). There is controversy regarding which modality is the preferred treatment.

        Proponents of HA point to a higher rate of dislocation for FNFs treated with THAs,5,6 attributed to increased range of motion.7 Proponents of THA point to superior short-term clinical results and fewer complications, especially in mobile, independent patients.8

        We conducted a study to assess recent US national trends in performing THA and HA for FNFs and to evaluate perioperative outcomes for each treatment group. 

        Materials and Methods

        Data for this study were obtained from the National Center for Health Statistics (NCHS) National Hospital Discharge Survey (NHDS) and were imported into Microsoft Office Excel 2010.9 The NHDS examines patient discharges from various hospitals across the US, including federal, military, and Veterans Administration hospitals.9 Only short-stay hospitals (mean stay, <30 days) and hospitals with a general specialty are included in the survey. Each year, about 1% of all hospital admissions from across the US are abstracted and weighted to provide nationwide estimates. The information collected from each hospital record includes age, sex, race, marital status, discharge month, discharge status, days of care, hospital location, hospital size (number of beds), hospital type (proprietary or for-profit, government, nonprofit/church), and up to 15 discharge diagnoses and 8 procedures performed during admission.9

        International Classification of Diseases, Ninth Revision (ICD-9) procedure codes were used to search the NHDS for patients admitted after FNF for each year from 2001 through 2010. These codes were then used to identify patients within this group who underwent THA or HA. We also collected data on patient demographics, hospitalization duration, discharge disposition, in-hospital adverse events (deep vein thrombosis [DVT], pulmonary embolism [PE], blood transfusion, mortality), form of primary medical insurance, number of hospital beds (0-99, 100-199, 200-299, 300-499, ≥500), hospital type (proprietary, government, nonprofit/church), and hospital region (Northeast, Midwest, South, West). 

         

         

        Trends were evaluated by linear regression with the Pearson correlation coefficient (r). Statistical comparisons were made using the Student t test for continuous data, and both the Fisher exact test and the χ2 test for categorical variables. Significance level was set at P < .05. All analyses were performed with IBM SPSS Statistics 22. 

        Results

        Figure 1.
        Of the 12,757 patients identified as having FNFs (Figure 1), 582 (4.6%) underwent THA, 6697 (52.5%) underwent HA, 3453 (27.1%) received internal fixation, and 1809 (14.2%) did not have their surgery documented. There were 164 men (28.2%) in the THA group and 1744 (26.0%) in the HA group (P = .27). Mean age was significantly (P < .01) higher for HA patients (81.1 years; range, 18-99 years) than for THA patients (76.9 years; range, 19-99 years), and there were significantly (P < .01) more medical comorbidities for HA patients (6.4 diagnoses; range, 1-7+ diagnoses) than for THA patients (6.1 diagnoses; range, 1-7 diagnoses).

        Figure 2.
        There was no clear trend in prevalence of FNFs between 2001 and 2010 (r = 0.25; Figure 2). During this period, fracture prevalence ranged from 406 to 477 per 100,000 admissions. However, there was increased frequency in use of both surgical techniques for FNFs over time: THA (r = 0.82; Figure 3) and HA (r = 0.80; Figure 4).
        Figure 3.
        Figure 4.
        The rate of THAs for FNFs increased from 4.2% for 2001 to 2005 to 5.0% for 2006 to 2010 (P = .04); similarly, the rate of HAs for FNFs increased from 51.0% for 2001 to 2005 to 54.7% for 2006 to 2010 (P < .01).

        Hospital stay was longer (P < .01) for THA patients (7.7 days; range, 1-312 days) than for HA patients (6.7 days; range, 1-118 days), and blood transfusion rate was higher (P = .02) for THA patients (30.4%) than for HA patients (25.7%), but the groups did not differ in their rates of DVT (THA, 1.2%; HA, 0.80%, P = .50), PE (THA, 0.52%; HA, 0.72%, P = .52), or mortality (THA, 1.8%; HA, 2.9%; P = .16). Discharge disposition varied with surgical status (P < .01): 23.2% of THA patients and 11.6% of HA patients were discharged directly home after their inpatient stay, and 76.8% of THA patients and 88.4% of HA patients were discharged or transferred to a short- or long-term care facility.

        Table.
        Figure 5.
        Hospital size (number of beds) affected the number of HAs performed (P < .01) but not the number of THAs performed (P = .10; Table). Hospital location (Northeast, Midwest, South, West) affected THA frequency (P = .01), but not HA frequency (P = .07; Figure 5). In contrast, hospital type (proprietary, government, nonprofit/church) affected the HA rate (P < .01) but not the THA rate (P = .12; Table). 

        Private medical insurance provided coverage for 14.3% of THAs and 9.1% of HAs, and Medicare provided coverage for 80.9% of THAs and 86.0% of HAs (P < .01).

         

         

        Discussion

        The NHDS data showed a preference for HA over THA in the treatment of FNFs and suggested THA was favored for younger, healthier patients while HA was reserved for older patients with more comorbidities. Despite being younger and healthier, the THA group had higher transfusion rates and longer hospitalizations, possibly because of the increased complexity of THA procedures, which generally involve more operative time and increased blood loss. The resultant higher transfusion rate for THAs likely contributed to longer hospitalizations for FNFs. However, the THA and HA groups did not differ in their rates of DVT, PE, or mortality.

        Multiple studies have noted no differences in mortality, infection, or general complications between THA and HA for FNF.8,10,11 THA patients have better functional outcomes, including Harris and Oxford hip scores and walking distance, but higher dislocation rates,8,10-12 and HA patients are at higher risk for reoperation because of progressive acetabular erosion.8,10,11

        We noted an increase in use of both THA and HA for FNF over the study period (2001-2010). In a review of operative treatment for FNF by surgeons applying for the American Board of Orthopaedic Surgery certification between 1999 and 2011, Miller and colleagues13 found a similar increase in the THA rate over time, but decreases in the HA and internal fixation rates, with candidates in the “adult reconstruction” subspecialty showing a particularly strong trend toward THA use.

        These findings reflect a general propensity toward femoral head replacement rather than preservation through open reduction and internal fixation (ORIF). Recent studies have found that ORIF carries a 39% to 43% rate of fixation failure and need for secondary revision, as well as risks of avascular necrosis, malunion, and nonunion.1,14-16 This need for secondary surgery makes ORIF ultimately less cost-effective than either THA or HA.16,17 Most authors would recommend arthroplasty for FNF in elderly patients with normal mental function1,16,18 and would reserve ORIF for young patients with good bone stock, joint space preservation, and reducible noncomminuted fractures.1,19

        Our study results suggest that smaller hospitals (<100 beds) tend to have lower rates of HA (P < .01, significant) and THA (P = .10, not significant; Table), possibly because FNF patients who present to these hospitals may be referred elsewhere because of regional differences in the availability of orthopedic traumatologists and arthroplasty subspecialists. Surgeon volume affects postoperative outcomes and may play a role in referral patterns.20 Ames and colleagues20 found that HA performed for FNF by surgeons with high-volume THA experience (vs non-hip-arthroplasty surgeons) had lower rates of dislocation, superficial infection, and mortality.

        Regional differences were significant for THA alone, with the highest THA rates in the South (5.2%) and the lowest in the West (3.3%; Figure 5). There were no clear regional trends for HA. Possible explanations include a propensity toward a more aggressive approach in these regions, increased regional prevalence of acetabular disease, regional surgeon preferences, and regional differences in patient characteristics (eg, increased prevalence of obesity in the South).21

         

         

        HA rates were highest for nonprofit/church hospitals and lowest for proprietary hospitals, whereas THA rates did not differ by hospital type. Possible explanations include an older, less mobile nonprofit/church patient cohort that is more amenable to HA, and surgeon preference. 

        THA patients were more likely to be covered by private medical insurance than by Medicare—a finding in agreement with Hochfelder and colleagues,22 who found that, compared with federal insurance and self-pay patients, private insurance patients were 41% more likely to undergo THA than HA or internal fixation for FNF. We think that the age difference between our THA and HA groups contributed to the insurance variability in our study.

        Our study had several limitations. It was conducted to examine the rates of THA and HA after FNF, not to survey treatment types, including ORIF and nonoperative management. The NHDS database does not provide information on HA implant type (unipolar, bipolar), use or nonuse of cement with HA, or surgical approach. Surgical approach could influence the rate of postoperative dislocation, an outcome measure that was not examined in this study. Last, the NHDS database tracks admissions and discharges, not patients. When a patient is discharged, collection of information on the patient’s postoperative course stops; a patient who returns even only 1 day later is recorded as a new or unique patient. Therefore, intermediate or long-term outcome information is unavailable, which likely led to an underrepresentation of DVT, PE, and mortality after these THA and HA procedures.

        There was a trend toward femoral head replacement rather than ORIF in the treatment of FNF. Cognitively functional and independent elderly patients, and patients with osteoarthritis or rheumatoid arthritis, may benefit from THA, whereas HA may be better suited to cognitively dysfunctional patients.23,24 The NHDS reflects an increasing trend toward arthroplasty over ORIF, but the exact treatment choice is affected by hospital type, size,  location and surgeon preference, training, and subspecialization.

        Take-Home Points

        • An increasing number of THAs and HAs were performed over time for FNF.
        • HA patients tended to be older.
        • Hospitalization and blood transfusion rates were higher for THA.
        • Hospital size affected the rate of HAs, while hospital location affected the rate of THAs.
        • A larger proportion of THA patients had private insurance.

        Femoral neck fractures (FNFs) are a common source of morbidity and mortality worldwide. The increasing number of FNFs in the United States is attributed to increases in number of US residents >65 years old, the average life span, and the incidence of osteoporosis.1 Three hundred forty thousand hip fractures occurred in the United States in 1996, and the number is expected to double by 2050.2 By that year, an estimated 6.3 million hip fractures will occur worldwide.3 Given the 1-year mortality rate of 14% to 36%, optimizing the management of these fractures is an important public health issue that must be addressed.4

        Treatment is based on preoperative ambulatory status, cognitive function, comorbidities, fracture type and displacement, and other factors. In physiologically elderly patients with displaced fractures, surgical treatment usually involves either hemiarthroplasty (HA) or total hip arthroplasty (THA). There is controversy regarding which modality is the preferred treatment.

        Proponents of HA point to a higher rate of dislocation for FNFs treated with THAs,5,6 attributed to increased range of motion.7 Proponents of THA point to superior short-term clinical results and fewer complications, especially in mobile, independent patients.8

        We conducted a study to assess recent US national trends in performing THA and HA for FNFs and to evaluate perioperative outcomes for each treatment group. 

        Materials and Methods

        Data for this study were obtained from the National Center for Health Statistics (NCHS) National Hospital Discharge Survey (NHDS) and were imported into Microsoft Office Excel 2010.9 The NHDS examines patient discharges from various hospitals across the US, including federal, military, and Veterans Administration hospitals.9 Only short-stay hospitals (mean stay, <30 days) and hospitals with a general specialty are included in the survey. Each year, about 1% of all hospital admissions from across the US are abstracted and weighted to provide nationwide estimates. The information collected from each hospital record includes age, sex, race, marital status, discharge month, discharge status, days of care, hospital location, hospital size (number of beds), hospital type (proprietary or for-profit, government, nonprofit/church), and up to 15 discharge diagnoses and 8 procedures performed during admission.9

        International Classification of Diseases, Ninth Revision (ICD-9) procedure codes were used to search the NHDS for patients admitted after FNF for each year from 2001 through 2010. These codes were then used to identify patients within this group who underwent THA or HA. We also collected data on patient demographics, hospitalization duration, discharge disposition, in-hospital adverse events (deep vein thrombosis [DVT], pulmonary embolism [PE], blood transfusion, mortality), form of primary medical insurance, number of hospital beds (0-99, 100-199, 200-299, 300-499, ≥500), hospital type (proprietary, government, nonprofit/church), and hospital region (Northeast, Midwest, South, West). 

         

         

        Trends were evaluated by linear regression with the Pearson correlation coefficient (r). Statistical comparisons were made using the Student t test for continuous data, and both the Fisher exact test and the χ2 test for categorical variables. Significance level was set at P < .05. All analyses were performed with IBM SPSS Statistics 22. 

        Results

        Figure 1.
        Of the 12,757 patients identified as having FNFs (Figure 1), 582 (4.6%) underwent THA, 6697 (52.5%) underwent HA, 3453 (27.1%) received internal fixation, and 1809 (14.2%) did not have their surgery documented. There were 164 men (28.2%) in the THA group and 1744 (26.0%) in the HA group (P = .27). Mean age was significantly (P < .01) higher for HA patients (81.1 years; range, 18-99 years) than for THA patients (76.9 years; range, 19-99 years), and there were significantly (P < .01) more medical comorbidities for HA patients (6.4 diagnoses; range, 1-7+ diagnoses) than for THA patients (6.1 diagnoses; range, 1-7 diagnoses).

        Figure 2.
        There was no clear trend in prevalence of FNFs between 2001 and 2010 (r = 0.25; Figure 2). During this period, fracture prevalence ranged from 406 to 477 per 100,000 admissions. However, there was increased frequency in use of both surgical techniques for FNFs over time: THA (r = 0.82; Figure 3) and HA (r = 0.80; Figure 4).
        Figure 3.
        Figure 4.
        The rate of THAs for FNFs increased from 4.2% for 2001 to 2005 to 5.0% for 2006 to 2010 (P = .04); similarly, the rate of HAs for FNFs increased from 51.0% for 2001 to 2005 to 54.7% for 2006 to 2010 (P < .01).

        Hospital stay was longer (P < .01) for THA patients (7.7 days; range, 1-312 days) than for HA patients (6.7 days; range, 1-118 days), and blood transfusion rate was higher (P = .02) for THA patients (30.4%) than for HA patients (25.7%), but the groups did not differ in their rates of DVT (THA, 1.2%; HA, 0.80%, P = .50), PE (THA, 0.52%; HA, 0.72%, P = .52), or mortality (THA, 1.8%; HA, 2.9%; P = .16). Discharge disposition varied with surgical status (P < .01): 23.2% of THA patients and 11.6% of HA patients were discharged directly home after their inpatient stay, and 76.8% of THA patients and 88.4% of HA patients were discharged or transferred to a short- or long-term care facility.

        Table.
        Figure 5.
        Hospital size (number of beds) affected the number of HAs performed (P < .01) but not the number of THAs performed (P = .10; Table). Hospital location (Northeast, Midwest, South, West) affected THA frequency (P = .01), but not HA frequency (P = .07; Figure 5). In contrast, hospital type (proprietary, government, nonprofit/church) affected the HA rate (P < .01) but not the THA rate (P = .12; Table). 

        Private medical insurance provided coverage for 14.3% of THAs and 9.1% of HAs, and Medicare provided coverage for 80.9% of THAs and 86.0% of HAs (P < .01).

         

         

        Discussion

        The NHDS data showed a preference for HA over THA in the treatment of FNFs and suggested THA was favored for younger, healthier patients while HA was reserved for older patients with more comorbidities. Despite being younger and healthier, the THA group had higher transfusion rates and longer hospitalizations, possibly because of the increased complexity of THA procedures, which generally involve more operative time and increased blood loss. The resultant higher transfusion rate for THAs likely contributed to longer hospitalizations for FNFs. However, the THA and HA groups did not differ in their rates of DVT, PE, or mortality.

        Multiple studies have noted no differences in mortality, infection, or general complications between THA and HA for FNF.8,10,11 THA patients have better functional outcomes, including Harris and Oxford hip scores and walking distance, but higher dislocation rates,8,10-12 and HA patients are at higher risk for reoperation because of progressive acetabular erosion.8,10,11

        We noted an increase in use of both THA and HA for FNF over the study period (2001-2010). In a review of operative treatment for FNF by surgeons applying for the American Board of Orthopaedic Surgery certification between 1999 and 2011, Miller and colleagues13 found a similar increase in the THA rate over time, but decreases in the HA and internal fixation rates, with candidates in the “adult reconstruction” subspecialty showing a particularly strong trend toward THA use.

        These findings reflect a general propensity toward femoral head replacement rather than preservation through open reduction and internal fixation (ORIF). Recent studies have found that ORIF carries a 39% to 43% rate of fixation failure and need for secondary revision, as well as risks of avascular necrosis, malunion, and nonunion.1,14-16 This need for secondary surgery makes ORIF ultimately less cost-effective than either THA or HA.16,17 Most authors would recommend arthroplasty for FNF in elderly patients with normal mental function1,16,18 and would reserve ORIF for young patients with good bone stock, joint space preservation, and reducible noncomminuted fractures.1,19

        Our study results suggest that smaller hospitals (<100 beds) tend to have lower rates of HA (P < .01, significant) and THA (P = .10, not significant; Table), possibly because FNF patients who present to these hospitals may be referred elsewhere because of regional differences in the availability of orthopedic traumatologists and arthroplasty subspecialists. Surgeon volume affects postoperative outcomes and may play a role in referral patterns.20 Ames and colleagues20 found that HA performed for FNF by surgeons with high-volume THA experience (vs non-hip-arthroplasty surgeons) had lower rates of dislocation, superficial infection, and mortality.

        Regional differences were significant for THA alone, with the highest THA rates in the South (5.2%) and the lowest in the West (3.3%; Figure 5). There were no clear regional trends for HA. Possible explanations include a propensity toward a more aggressive approach in these regions, increased regional prevalence of acetabular disease, regional surgeon preferences, and regional differences in patient characteristics (eg, increased prevalence of obesity in the South).21

         

         

        HA rates were highest for nonprofit/church hospitals and lowest for proprietary hospitals, whereas THA rates did not differ by hospital type. Possible explanations include an older, less mobile nonprofit/church patient cohort that is more amenable to HA, and surgeon preference. 

        THA patients were more likely to be covered by private medical insurance than by Medicare—a finding in agreement with Hochfelder and colleagues,22 who found that, compared with federal insurance and self-pay patients, private insurance patients were 41% more likely to undergo THA than HA or internal fixation for FNF. We think that the age difference between our THA and HA groups contributed to the insurance variability in our study.

        Our study had several limitations. It was conducted to examine the rates of THA and HA after FNF, not to survey treatment types, including ORIF and nonoperative management. The NHDS database does not provide information on HA implant type (unipolar, bipolar), use or nonuse of cement with HA, or surgical approach. Surgical approach could influence the rate of postoperative dislocation, an outcome measure that was not examined in this study. Last, the NHDS database tracks admissions and discharges, not patients. When a patient is discharged, collection of information on the patient’s postoperative course stops; a patient who returns even only 1 day later is recorded as a new or unique patient. Therefore, intermediate or long-term outcome information is unavailable, which likely led to an underrepresentation of DVT, PE, and mortality after these THA and HA procedures.

        There was a trend toward femoral head replacement rather than ORIF in the treatment of FNF. Cognitively functional and independent elderly patients, and patients with osteoarthritis or rheumatoid arthritis, may benefit from THA, whereas HA may be better suited to cognitively dysfunctional patients.23,24 The NHDS reflects an increasing trend toward arthroplasty over ORIF, but the exact treatment choice is affected by hospital type, size,  location and surgeon preference, training, and subspecialization.

        References

        1. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287-293.

        2. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596-607.

        3. Kannus P, Parkkari J, Sievänen H, Heinonen A, Vuori I, Järvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 suppl):57S-63S.

        4. Zuckerman JD. Hip fracture. N Engl J Med. 1996;334(23):1519-1525.

        5. Papandrea RF, Froimson MI. Total hip arthroplasty after acute displaced femoral neck fractures. Am J Orthop. 1996;25(2):85-88.

        6. Burgers PT, Van Geene AR, Van den Bekerom MP, et al. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures in the healthy elderly: a meta-analysis and systematic review of randomized trials. Int Orthop. 2012;36(8):1549-1560.

        7. Skinner P, Riley D, Ellery J, Beaumont A, Coumine R, Shafighian B. Displaced subcapital fractures of the femur: a prospective randomized comparison of internal fixation, hemiarthroplasty and total hip replacement. Injury. 1989;20(5):291-293.

        8. Baker RP, Squires B, Gargan MF, Bannister GC. Total hip arthroplasty and hemiarthroplasty in mobile, independent patients with a displaced intracapsular fracture of the femoral neck. A randomized, controlled trial. J Bone Joint Surg Am. 2006;88(12):2583-2589.

        9. Centers for Disease Control and Prevention, National Center for Health Statistics. National Hospital Discharge Survey. http://www.cdc.gov/nchs/nhds/about_nhds.htm. Last updated December 6, 2011. Accessed December 10, 2013.

        10. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplasty. 2012;27(4):583-590.

        11. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235-2243.

        12. Hopley C, Stengel D, Ekkernkamp A, Wich M. Primary total hip arthroplasty versus hemiarthroplasty for displaced intracapsular hip fractures in older patients: systematic review. BMJ. 2010;340:c2332.

        13. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg Am. 2014;96(17):e149.

        14. Rogmark C, Carlsson A, Johnell O, Sernbo I. A prospective randomised trial of internal fixation versus arthroplasty for displaced fractures of the neck of the femur. Functional outcome for 450 patients at two years. J Bone Joint Surg Br. 2002;84(2):183-188.

        15. Bhandari M, Devereaux PJ, Swiontkowski MF, et al. Internal fixation compared with arthroplasty for displaced fractures of the femoral neck. A meta-analysis. J Bone Joint Surg Am. 2003;85(9):1673-1681.

        16. Keating JF, Grant A, Masson M, Scott NW, Forbes JF. Randomized comparison of reduction and fixation, bipolar hemiarthroplasty, and total hip arthroplasty. Treatment of displaced intracapsular hip fractures in healthy older patients. J Bone Joint Surg Am. 2006;88(2):249-260.

        17. Iorio R, Healy WL, Lemos DW, Appleby D, Lucchesi CA, Saleh KJ. Displaced femoral neck fractures in the elderly: outcomes and cost effectiveness. Clin Orthop Relat Res. 2001;(383):229-242.

        18. Johansson T, Jacobsson SA, Ivarsson I, Knutsson A, Wahlström O. Internal fixation versus total hip arthroplasty in the treatment of displaced femoral neck fractures: a prospective randomized study of 100 hips. Acta Orthop Scand. 2000;71(6):597-602.

        19. Shah AK, Eissler J, Radomisli T. Algorithms for the treatment of femoral neck fractures. Clin Orthop Relat Res. 2002;(399):28-34.

        20. Ames JB, Lurie JD, Tomek IM, Zhou W, Koval KJ. Does surgeon volume for total hip arthroplasty affect outcomes after hemiarthroplasty for femoral neck fracture? Am J Orthop. 2010;39(8):E84-E89.

        21. Le A, Judd SE, Allison DB, et al. The geographic distribution of obesity in the US and the potential regional differences in misreporting of obesity. Obesity. 2014;22(1):300-306.

        22. Hochfelder JP, Khatib ON, Glait SA, Slover JD. Femoral neck fractures in New York state. Is the rate of THA increasing, and do race or payer influence decision making? J Orthop Trauma. 2014;28(7):422-426.

        23. Lowe JA, Crist BD, Bhandari M, Ferguson TA. Optimal treatment of femoral neck fractures according to patient’s physiologic age: an evidence-based review. Orthop Clin North Am. 2010;41(2):157-166.

        24. Callaghan JJ, Liu SS, Haidukewych GJ. Subcapital fractures: a changing paradigm. J Bone Joint Surg Br. 2012;94(11 suppl A):19-21.

        References

        1. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287-293.

        2. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596-607.

        3. Kannus P, Parkkari J, Sievänen H, Heinonen A, Vuori I, Järvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 suppl):57S-63S.

        4. Zuckerman JD. Hip fracture. N Engl J Med. 1996;334(23):1519-1525.

        5. Papandrea RF, Froimson MI. Total hip arthroplasty after acute displaced femoral neck fractures. Am J Orthop. 1996;25(2):85-88.

        6. Burgers PT, Van Geene AR, Van den Bekerom MP, et al. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures in the healthy elderly: a meta-analysis and systematic review of randomized trials. Int Orthop. 2012;36(8):1549-1560.

        7. Skinner P, Riley D, Ellery J, Beaumont A, Coumine R, Shafighian B. Displaced subcapital fractures of the femur: a prospective randomized comparison of internal fixation, hemiarthroplasty and total hip replacement. Injury. 1989;20(5):291-293.

        8. Baker RP, Squires B, Gargan MF, Bannister GC. Total hip arthroplasty and hemiarthroplasty in mobile, independent patients with a displaced intracapsular fracture of the femoral neck. A randomized, controlled trial. J Bone Joint Surg Am. 2006;88(12):2583-2589.

        9. Centers for Disease Control and Prevention, National Center for Health Statistics. National Hospital Discharge Survey. http://www.cdc.gov/nchs/nhds/about_nhds.htm. Last updated December 6, 2011. Accessed December 10, 2013.

        10. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplasty. 2012;27(4):583-590.

        11. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235-2243.

        12. Hopley C, Stengel D, Ekkernkamp A, Wich M. Primary total hip arthroplasty versus hemiarthroplasty for displaced intracapsular hip fractures in older patients: systematic review. BMJ. 2010;340:c2332.

        13. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg Am. 2014;96(17):e149.

        14. Rogmark C, Carlsson A, Johnell O, Sernbo I. A prospective randomised trial of internal fixation versus arthroplasty for displaced fractures of the neck of the femur. Functional outcome for 450 patients at two years. J Bone Joint Surg Br. 2002;84(2):183-188.

        15. Bhandari M, Devereaux PJ, Swiontkowski MF, et al. Internal fixation compared with arthroplasty for displaced fractures of the femoral neck. A meta-analysis. J Bone Joint Surg Am. 2003;85(9):1673-1681.

        16. Keating JF, Grant A, Masson M, Scott NW, Forbes JF. Randomized comparison of reduction and fixation, bipolar hemiarthroplasty, and total hip arthroplasty. Treatment of displaced intracapsular hip fractures in healthy older patients. J Bone Joint Surg Am. 2006;88(2):249-260.

        17. Iorio R, Healy WL, Lemos DW, Appleby D, Lucchesi CA, Saleh KJ. Displaced femoral neck fractures in the elderly: outcomes and cost effectiveness. Clin Orthop Relat Res. 2001;(383):229-242.

        18. Johansson T, Jacobsson SA, Ivarsson I, Knutsson A, Wahlström O. Internal fixation versus total hip arthroplasty in the treatment of displaced femoral neck fractures: a prospective randomized study of 100 hips. Acta Orthop Scand. 2000;71(6):597-602.

        19. Shah AK, Eissler J, Radomisli T. Algorithms for the treatment of femoral neck fractures. Clin Orthop Relat Res. 2002;(399):28-34.

        20. Ames JB, Lurie JD, Tomek IM, Zhou W, Koval KJ. Does surgeon volume for total hip arthroplasty affect outcomes after hemiarthroplasty for femoral neck fracture? Am J Orthop. 2010;39(8):E84-E89.

        21. Le A, Judd SE, Allison DB, et al. The geographic distribution of obesity in the US and the potential regional differences in misreporting of obesity. Obesity. 2014;22(1):300-306.

        22. Hochfelder JP, Khatib ON, Glait SA, Slover JD. Femoral neck fractures in New York state. Is the rate of THA increasing, and do race or payer influence decision making? J Orthop Trauma. 2014;28(7):422-426.

        23. Lowe JA, Crist BD, Bhandari M, Ferguson TA. Optimal treatment of femoral neck fractures according to patient’s physiologic age: an evidence-based review. Orthop Clin North Am. 2010;41(2):157-166.

        24. Callaghan JJ, Liu SS, Haidukewych GJ. Subcapital fractures: a changing paradigm. J Bone Joint Surg Br. 2012;94(11 suppl A):19-21.

        Issue
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        OptumCare Medical Group
        Laguna Niguel, California
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        American Society of Endocrine PAs
        Adjunct Faculty
        A.T. Still University
        Mesa, AZ

         

        The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

         

        This video was filmed at Metabolic & Endocrine Disease Summit (MEDS). Click here to learn more.

         

        The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

         

        This video was filmed at Metabolic & Endocrine Disease Summit (MEDS). Click here to learn more.

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