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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, [email protected]).

    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, [email protected]).

    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, [email protected]).

    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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        Arthroscopic Anterior Ankle Decompression Is Successful in National Football League Players
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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

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        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, [email protected]).

        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, [email protected]).

        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, [email protected]).

        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.

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        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

        Article Type
        Changed
        Thu, 09/19/2019 - 13:19

        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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        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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        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.

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        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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        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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        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
        The American Journal of Orthopedics - 46(6)
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        The American Journal of Orthopedics - 46(6)
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        Hypercalcemia, Parathyroid Disease, Vitamin D Deficiency

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        OptumCare Medical Group
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        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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        Management of Isolated Greater Tuberosity Fractures: A Systematic Review

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        Take-Home Points

        • Fractures of the greater tuberosity are often mismanaged.
        • Comprehension of greater tuberosity fractures involves classification into nonoperative and operative treatment, displacement >5mm or <5 mm, and open vs arthroscopic surgery.
        • Nearly a third of patients may suffer concomitant anterior glenohumeral instability.
        • Stiffness is the most common postoperative complication.
        • Surgery is associated with high patient satisfaction and low rates of complications and reoperations.

        Although proximal humerus fractures are common in the elderly, isolated fractures of the greater tuberosity occur less often. Management depends on several factors, including fracture pattern and displacement.1,2 Nondisplaced fractures are often successfully managed with sling immobilization and early range of motion.3,4 Although surgical intervention improves outcomes in displaced greater tuberosity fractures, the ideal surgical treatment is less clear.5

        Displaced greater tuberosity fractures may require surgery for prevention of subacromial impingement and range-of-motion deficits.2 Superior fracture displacement results in decreased shoulder abduction, and posterior displacement can limit external rotation.6 Although the greater tuberosity can displace in any direction, posterosuperior displacement has the worst outcomes.1 The exact surgery-warranting displacement amount ranges from 3 mm to 10 mm but is yet to be clearly elucidated.5,6 Less displacement is tolerated by young overhead athletes, and more displacement by older less active patients.5,7,8 Surgical options for isolated greater tuberosity fractures include fragment excision, open reduction and internal fixation (ORIF), closed reduction with percutaneous fixation, and arthroscopically assisted reduction with internal fixation.3,9,10

        We conducted a study to determine the management patterns for isolated greater tuberosity fractures. We hypothesized that greater tuberosity fractures displaced <5 mm may be managed nonoperatively and that greater tuberosity fractures displaced >5 mm require surgical fixation.

        Methods

        Search Strategy

        We performed this systematic review according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist11 and registered it (CRD42014010691) with the PROSPERO international prospective register of systematic reviews. Literature searches using the PubMed/Medline database and the Cochrane Central Register of Clinical Trials were completed in August 2014. There were no date or year restrictions. Key words were used to capture all English- language studies with level I to IV evidence (Oxford Centre for Evidence-Based Medicine) and reported clinical or radiographic outcomes. Initial exclusion criteria were cadaveric, biomechanical, histologic, and kinematic results. An electronic search algorithm with key words and a series of NOT phrases was designed to match our exclusion criteria: 

        ((((((((((((((((((((((((((((((((((((((((((((((((((greater[Title/Abstract]) AND tuberosity [Title/Abstract] OR tubercle [Title/Abstract]) AND fracture[Title/Abstract]) AND proximal[Title/Abstract] AND (English[lang]))) NOT intramedullary[Title] AND (English[lang]))) NOT nonunion[Title] AND (English[lang]))) NOT malunion[Title] AND (English[lang]))) NOT biomechanical[Title/Abstract] AND (English[lang]))) NOT cadaveric[Title/Abstract] AND (English[lang]))) NOT cadaver[Title/Abstract] AND (English[lang]))) NOT ((basic[Title/Abstract]) AND science[Title/Abstract] AND (English[lang])) AND (English[lang]))) NOT revision[Title] AND (English[lang]))) NOT pediatric[Title] AND (English[lang]))) NOT physeal[Title] AND (English[lang]))) NOT children[Title] AND (English[lang]))) NOT instability[Title] AND (English[lang]))) NOT imaging[Title])) NOT salter[Title])) NOT physis[Title])) NOT shaft[Title])) NOT distal[Title])) NOT clavicle[Title])) NOT scapula[Title])) NOT ((diaphysis[Title]) AND diaphyseal[Title]))) NOT infection[Title])) NOT laboratory[Title/Abstract])) NOT metastatic[Title/Abstract])) NOT (((((((malignancy[Title/Abstract]) OR malignant[Title/Abstract]) OR tumor[Title/Abstract]) OR oncologic[Title/Abstract]) OR cyst[Title/Abstract]) OR aneurysmal[Title/Abstract]) OR unicameral[Title/Abstract]).

        Study Selection

        Figure.
        Table 1.
        We obtained 135 search results and reviewed them for further differentiation. All the references in these studies were cross-referenced for inclusion (if missed by the initial search), which added another 15 studies. Technical notes, letters to the editor, and level V evidence reviews were excluded. Double-counting of patients was avoided by comparing each study’s authors, data collection period, and ethnic population with those of the other studies. In cases of overlapping authorship, period, or place, only the study with the longer follow-up, more patients, or more comprehensive data was included. For studies separating outcomes by diagnosis, only outcomes of isolated greater tuberosity fractures were included. Data on 3- or 4-part proximal humerus fractures and isolated lesser tuberosity fractures were excluded. Studies that could not be deconstructed as such or that were devoted solely to one of our exclusion criteria were excluded. Minimum follow-up was 2 years. After all inclusion and exclusion criteria were accounted for, 13 studies with 429 patients (429 shoulders) were selected for inclusion (Figure, Table 1).2,5,12-22

         

         

        Data Extraction

        We extracted data from the 13 studies that met the eligibility criteria. Details of study design, sample size, and patient demographics, including age, sex, and hand dominance, were recorded, as were mechanism of injury and concomitant anterior shoulder instability. To capture the most patients, we noted radiographic fracture displacement categorically rather than continuously; patients were divided into 2 displacement groups (<5 mm, >5 mm). Most studies did not define degree of comminution or specific direction of displacement per fracture, so these variables were not included in the data analysis. Nonoperative management and operative management were studied. We abstracted surgical factors, such as approach, method, fixation type (screws or sutures), and technique (suture anchors or transosseous tunnels). Clinical outcomes included physical examination findings, functional assessment results (patient satisfaction; Constant and University of California Los Angeles [UCLA] shoulder scores), and the number of revisions. Radiologic outcomes, retrieved from radiographs or computed tomography scans, focused on loss of reduction (as determined by the respective authors), malunion, nonunion, and heterotopic ossification. Each study’s methodologic quality and bias were evaluated with the 15-item Modified Coleman Methodology Score (MCMS), which was described by Cowan and colleagues.23 The MCMS has been used to assess randomized and nonrandomized patient trials.24,25 Its scaled potential score ranges from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor).

        Statistical Analysis

        We report our data as weighted means (SDs). A mean was calculated for each study that reported a respective data point, and each mean was then weighed according to its study sample size. This calculation was performed by multiplying a study’s individual mean by the number of patients enrolled in that study and dividing the sum of these weighted data points by the number of eligible patients in all relevant studies. The result was that the nonweighted means from studies with smaller sample sizes did not carry as much weight as the nonweighted means from larger studies. We compared 3 paired groups: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic). Regarding all patient, surgery, and outcomes data, unpaired Student t tests were used for continuous variables and 2-tailed Fisher exact tests for categorical variables with α = 0.05 (SPSS Version 18; IBM).

        Results

        Table 2.
        Demographic information and treatment strategies are listed in Table 2. Fifty-eight percent of patients were male, 59.0% of dominant shoulders were affected, and 59.2% of fractures were displaced <5 mm. Concomitant shoulder instability was reported in 28.1% of patients. Mechanism of injury was not reported in all studies but most commonly (n = 75; 49.3%) involved a fall on an outstretched hand; 31 patients (20.4%) had a sports-related injury, and another 37 (24.3%) were injured in a motor vehicle collision. Of the 429 patients, 217 (50.6%) were treated nonoperatively, and 212 (49.4%) underwent surgery. Open, arthroscopic, and percutaneous approaches were reported. No studies presented outcomes of fragment excision.

        Postoperative physical examination findings were underreported so that surgical groups could be compared. Of all the surgical studies, 4 reported postoperative forward elevation (mean, 160°; SD, 9.8°) and external rotation (mean, 46.4°; SD 26.3°).14,15,18,22 No malunions and only 1 nonunion were reported in all 13 studies. No deaths or other serious medical complications were reported. Patients with anterior instability more often underwent surgery than were treated nonoperatively (39.2% vs 12.0%; P < .01) and more often had fractures displaced >5 mm than <5 mm (44.3% vs 14.5%; P < .01).

         

         

        Table 3.
        Comparisons of treatment type are listed in Table 3. Compared with nonoperative patients, operative patients had significantly fewer radiographic losses of reduction (P < .01) and better patient satisfaction (P < .01). Operative patients had a significantly higher rate of shoulder stiffness (P < .01). Eight operative patients (3.8%) and no nonoperative patients required reoperation during clinical follow-up (P < .01). All 12 reported cases of stiffness were in the operative group, and 3 required revision surgery. One patient required revision ORIF. There were 2 cases of postoperative superficial infection (0.9%) and 4 neurologic injuries (1.9%).

        Table 4.
        Comparisons of displacement amount are listed in Table 4. Compared with fractures displaced >5 mm, those displaced <5 mm had more radiographic losses of reduction (P < .01) but fewer instances of heterotopic ossification (P < .01). Fractures displaced >5 mm were significantly more likely than not to be managed with surgery (P < .01) and significantly more likely to develop stiffness after treatment (P = .01). One patient (0.4%) with a fracture displaced <5 mm eventually underwent surgery for stiffness, and 6 patients (3.6%) with fractures displaced >5 mm required reoperation (P = .02).

        Table 5.
        Comparisons of surgery type are listed in Table 5. All open procedures were performed with a deltoid-splitting approach. Screw fixation was used in 4 cases: 2 percutaneous5,21 and 2 open.2,5 The other open and arthroscopic studies described suture fixation, half with anchors (77/156 patients; 49.4%) and half with transosseous tunnels (79/156; 50.6%). There were no statistically significant differences between open/percutaneous and arthroscopic techniques in terms of stiffness, superficial infection, neurologic injury, or reoperation rate.

        Fisher exact tests were used to perform isolated comparisons of screws and sutures as well as suture anchors and transosseous tunnels. Patients with screw fixation were significantly (P = .051) less likely to require reoperation (0/56; 0%) than patients with suture fixation (8/100; 8.0%). Screw fixation also led to significantly less stiffness (0% vs 12.0%; P < .01) but trended toward a higher rate of superficial infection (3.6% vs 0%; P = .13). There was no statistical difference in nerve injury rates between screws and sutures (1.8% vs 3.0%; P = 1.0). There were no significant differences in reoperations, stiffness, superficial infections, or nerve injuries between suture anchor and transosseous tunnel constructs.

         

         

        For all 13 studies, mean (SD) MCMS was 41.1 (8.6).

        Discussion

        Five percent of all fractures involve the proximal humerus, and 20% of proximal humerus fractures are isolated greater tuberosity fractures.26,27 In his classic 1970 article, Neer6 formulated the 4-part proximal humerus fracture classification and defined greater tuberosity fracture “parts” using the same criteria as for other fracture “parts.” Neer6 recommended nonoperative management for isolated greater tuberosity fractures displaced <1 cm but did not present evidence corroborating his recommendation. More recent cutoffs for nonoperative management include 5 mm (general population) and 3 mm (athletes).7,17

        In the present systematic review of greater tuberosity fractures, 3 separate comparisons were made: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic).

        Treatment Type. Only 4 studies reported data on nonoperative treatment outcomes.5,12,16,17 Of these 4 studies, 2 found successful outcomes for fractures displaced <5 mm.12,17 Platzer and colleagues17 found good or excellent results in 97% of 135 shoulders after 4 years. Good results were defined with shoulder scores of ≥80 (Constant), <8 (Vienna), and >28 (UCLA), and excellent results were defined with maximum scores on 2 of the 3 systems. Platzer and colleagues17 also found nonsignificantly worse shoulder scores with superior displacement of 3 mm to 5 mm and recommended surgery for overhead athletes in this group. Rath and colleagues12 described a successful 3-phase rehabilitation protocol of sling immobilization for 3 weeks, pendulum exercises for 3 weeks, and active exercises thereafter. By an average of 31 months, patient satisfaction scores improved to 9.5 from 4.2 (10-point scale), though the authors cautioned that pain and decreased motion lasted 8 months on average. Conservative treatment was far less successful in the 2 studies of fractures displaced >5 mm.5,16 Keene and colleagues16 reported unsatisfactory results in all 4 patients with fractures displaced >1.5 cm. In a study separate from their 2005 analysis,17 Platzer and colleagues5 in 2008 evaluated displaced fractures and found function and patient satisfaction were inferior after nonoperative treatment than after surgery. The studies by Keene and colleagues16 and Platzer and colleagues5 support the finding of an overall lower patient satisfaction rate in nonoperative patients.

        Fracture Displacement Amount. Only 2 arthroscopic studies and no open studies addressed surgery for fractures displaced <5 mm. Fewer than 16% of these fractures were managed operatively, and <1% required reoperation. By contrast, almost all fractures displaced >5 mm were managed operatively, and 3.6% required reoperation. Radiographic loss of reduction was more common in fractures displaced <5 mm, primarily because they were managed without fixation. Radiographic loss of reduction was reported in only 9 operatively treated patients, none of whom was symptomatic enough to require another surgery.5 Reoperations were most commonly performed for stiffness, which itself was significantly more common in fractures displaced >5 mm. Bhatia and colleagues14 reported the highest reoperation rate (14.3%; 3/21), but they studied more complex, comminuted fractures of the greater tuberosity. Two of their 3 reoperations were biceps tenodeses for inflamed, stiff tenosynovitis, and the third patient had a foreign body giant cell reaction to suture material. Fewer than 1% of patients with operatively managed displaced fractures required revision ORIF, and <2% developed a superficial infection or postoperative nerve palsy.19,22 For displaced greater tuberosity fractures, surgery is highly successful overall, complication rates are very low, and 90% of patients report being satisfied.

        Surgery Type. Patients were divided into 2 groups. In the nonarthroscopic group, open and percutaneous approaches were used. All studies that described a percutaneous approach used screw fixation5,21; in addition, 32 patients were treated with screws through an open approach.2,5 The other open and arthroscopic studies used suture fixation. Interestingly, no studies reported on clinical outcomes of fragment excision. There were no statistically significant differences in rates of reoperation, stiffness, infection, or neurologic injury between the arthroscopic and nonarthroscopic groups. Patient satisfaction scores were slightly higher in the nonarthroscopic group (91.0% vs 87.8%), but the difference was not statistically significant.

         

         

        With surgical techniques isolated, there were no significant differences between suture anchors and transosseous tunnel constructs, but screws performed significantly better than suture techniques. Compared with suture fixation, screw fixation led to significantly fewer cases of stiffness and reoperation, which suggests surgeons need to give screws more consideration in the operative management of these fractures. However, the number of patients treated with screws was smaller than the number treated with suture fixation; it is possible the differences between these cohorts would be eliminated if there were more patients in the screw cohort. In addition, screw fixation was universally performed with an open or percutaneous approach and trended toward a higher infection rate. As screw and suture techniques have low rates of complications and reoperations, we recommend leaving fixation choice to the surgeon.

        Anterior shoulder instability has been associated with greater tuberosity fractures.1,8,19 The supraspinatus, infraspinatus, and teres minor muscles all insert into the greater tuberosity and resist anterior translation of the proximal humerus. Loss of this dynamic muscle stabilization is amplified by tuberosity fracture displacement: Anterior shoulder instability was significantly more common in fractures displaced >5 mm (44.3%) vs <5 mm (14.5%). In turn, glenohumeral instability was more common in patients treated with surgery, specifically open surgery, because displaced fractures may not be as easily accessed with arthroscopic techniques. No studies reported concomitant labral repair or capsular plication techniques.

        This systematic review was limited by the studies analyzed. All but 1 study5 had level IV evidence. Mean (SD) MCMS was 41.8 (8.6). Any MCMS score <54 indicates a poor methodology level, but this scoring system is designed for randomized controlled trials,23 and there were none in this study. Physical examination findings, such as range of motion, were underreported. In addition, radiographic parameters were not consistently described but rather were determined by the respective authors’ subjective interpretations of malunion, nonunion, and loss of reduction. Publication bias is present in that we excluded non- English language studies and medical conference abstracts and may have omitted potentially eligible studies not discoverable with our search methodology. Performance bias is a factor in any systematic review with multiple surgeons and wide variation in surgical technique.

        Conclusion

        Greater tuberosity fractures displaced <5 mm may be safely managed nonoperatively, as there are no reports of nonoperatively managed fractures that subsequently required surgery. Nonoperative treatment was initially associated with low patient satisfaction, but only because displaced fractures were conservatively managed in early studies.5,16 Fractures displaced >5 mm respond well to operative fixation with screws, suture anchors, or transosseous suture tunnels. Stiffness is the most common postoperative complication (<6%), followed by heterotopic ossification, transient neurapraxias, and superficial infection. There are no discernible differences in outcome between open and arthroscopic techniques, but screw fixation may lead to significantly fewer cases of stiffness and reoperation in comparison with suture constructs.

        References

        1. Verdano MA, Aliani D, Pellegrini A, Baudi P, Pedrazzi G, Ceccarelli F. Isolated fractures of the greater tuberosity in proximal humerus: does the direction of displacement influence functional outcome? An analysis of displacement in greater tuberosity fractures. Acta Biomed. 2013;84(3):219-228.

        2. Yin B, Moen TC, Thompson SA, Bigliani LU, Ahmad CS, Levine WN. Operative treatment of isolated greater tuberosity fractures: retrospective review of clinical and functional outcomes. Orthopedics. 2012;35(6):e807-e814.

        3. Green A, Izzi J. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.

        4. Norouzi M, Naderi MN, Komasi MH, Sharifzadeh SR, Shahrezaei M, Eajazi A. Clinical results of using the proximal humeral internal locking system plate for internal fixation of displaced proximal humeral fractures. Am J Orthop. 2012;41(5):E64-E68.

        5. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.

        6. Neer CS. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.

        7. Park TS, Choi IY, Kim YH, Park MR, Shon JH, Kim SI. A new suggestion for the treatment of minimally displaced fractures of the greater tuberosity of the proximal humerus. Bull Hosp Jt Dis. 1997;56(3):171-176.

        8. McLaughlin HL. Dislocation of the shoulder with tuberosity fracture. Surg Clin North Am. 1963;43:1615-1620.

        9. DeBottis D, Anavian J, Green A. Surgical management of isolated greater tuberosity fractures of the proximal humerus. Orthop Clin North Am. 2014;45(2):207-218.

        10. Monga P, Verma R, Sharma VK. Closed reduction and external fixation for displaced proximal humeral fractures. J Orthop Surg (Hong Kong). 2009;17(2):142-145.

        11. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. J Clin Epidemiol. 2009;62(10):1006-1012.

        12. Rath E, Alkrinawi N, Levy O, Debbi R, Amar E, Atoun E. Minimally displaced fractures of the greater tuberosity: outcome of non-operative treatment. J Shoulder Elbow Surg. 2013;22(10):e8-e11.

        13. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.

        14. Bhatia DN, van Rooyen KS, Toit du DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.

        15. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.

        16. Keene JS, Huizenga RE, Engber WD, Rogers SC. Proximal humeral fractures: a correlation of residual deformity with long-term function. Orthopedics. 1983;6(2):173-178.

        17. Platzer P, Kutscha-Lissberg F, Lehr S, Vecsei V, Gaebler C. The influence of displacement on shoulder function in patients with minimally displaced fractures of the greater tuberosity. Injury. 2005;36(10):1185-1189.

        18. Park SE, Ji JH, Shafi M, Jung JJ, Gil HJ, Lee HH. Arthroscopic management of occult greater tuberosity fracture of the shoulder. Eur J Orthop Surg Traumatol. 2014;24(4):475-482.

        19. Dimakopoulos P, Panagopoulos A, Kasimatis G, Syggelos SA, Lambiris E. Anterior traumatic shoulder dislocation associated with displaced greater tuberosity fracture: the necessity of operative treatment. J Orthop Trauma. 2007;21(2):104-112.

        20. Kim SH, Ha KI. Arthroscopic treatment of symptomatic shoulders with minimally displaced greater tuberosity fracture. Arthroscopy. 2000;16(7):695-700.

        21. Chen CY, Chao EK, Tu YK, Ueng SW, Shih CH. Closed management and percutaneous fixation of unstable proximal humerus fractures. J Trauma. 1998;45(6):1039-1045.

        22. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.

        23. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

        24. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

        25. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

        26. Chun JM, Groh GI, Rockwood CA. Two-part fractures of the proximal humerus. J Shoulder Elbow Surg. 1994;3(5):273-287.

        27. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.

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        Authors’ Disclosure Statement: Dr. Harris reports that he serves as a board or committee member for the American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy, Arthroscopy Association of North America, and Frontiers in Surgery; he has received research support from DePuy Synthes and Smith & Nephew, royalties from SLACK Incorporated, and is paid by NIA Magellan, Ossur, and Smith & Nephew. Dr. Bach reports that he has received research support from Arthrex, Inc., CONMED Linvatec, DJ Orthopaedics, Ossur, Smith & Nephew, and Tornier as well as royalties from SLACK Incorporated. Dr. Verma reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Arthroscopy Association Learning Center Committee, Journal of Knee Surgery, and SLACK Incorporated; he has received research support from Arthrex, Inc., Arthrosurface, DJ Orthopaedics, Smith & Nephew, Athletico, ConMed Linvatec, Miomed, and Mitek; he has received publishing royalties, financial, or material support from Arthroscopy and Vindico Medical-Orthopedics Hyperguide; he has received stock or stock options from Cymedica, Minivasive, and Omeros and serves as a paid consultant for Orthospace and Smith & Nephew. Dr. Romeo reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Orthopedics, Orthopedics Today, SAGE, and Wolters Kluwer Health—Lippincott Williams & Wilkins; he has received research support from Aesculap/B.Braun, Arthrex, Inc., Histogenics, Medipost, NuTech, Orthospace, Smith & Nephew, and Zimmer Biomet; he has received other financial or material support from AANA, Arthrex, Inc., and Major League Baseball; he has received publishing royalties, financial and/or material support from Saunders/Mosby-Elsevier and SLACK Incorporated. The other authors report no actual or potential conflict of interest in relation to this article. 

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        Authors’ Disclosure Statement: Dr. Harris reports that he serves as a board or committee member for the American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy, Arthroscopy Association of North America, and Frontiers in Surgery; he has received research support from DePuy Synthes and Smith & Nephew, royalties from SLACK Incorporated, and is paid by NIA Magellan, Ossur, and Smith & Nephew. Dr. Bach reports that he has received research support from Arthrex, Inc., CONMED Linvatec, DJ Orthopaedics, Ossur, Smith & Nephew, and Tornier as well as royalties from SLACK Incorporated. Dr. Verma reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Arthroscopy Association Learning Center Committee, Journal of Knee Surgery, and SLACK Incorporated; he has received research support from Arthrex, Inc., Arthrosurface, DJ Orthopaedics, Smith & Nephew, Athletico, ConMed Linvatec, Miomed, and Mitek; he has received publishing royalties, financial, or material support from Arthroscopy and Vindico Medical-Orthopedics Hyperguide; he has received stock or stock options from Cymedica, Minivasive, and Omeros and serves as a paid consultant for Orthospace and Smith & Nephew. Dr. Romeo reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Orthopedics, Orthopedics Today, SAGE, and Wolters Kluwer Health—Lippincott Williams & Wilkins; he has received research support from Aesculap/B.Braun, Arthrex, Inc., Histogenics, Medipost, NuTech, Orthospace, Smith & Nephew, and Zimmer Biomet; he has received other financial or material support from AANA, Arthrex, Inc., and Major League Baseball; he has received publishing royalties, financial and/or material support from Saunders/Mosby-Elsevier and SLACK Incorporated. The other authors report no actual or potential conflict of interest in relation to this article. 

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        Authors’ Disclosure Statement: Dr. Harris reports that he serves as a board or committee member for the American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy, Arthroscopy Association of North America, and Frontiers in Surgery; he has received research support from DePuy Synthes and Smith & Nephew, royalties from SLACK Incorporated, and is paid by NIA Magellan, Ossur, and Smith & Nephew. Dr. Bach reports that he has received research support from Arthrex, Inc., CONMED Linvatec, DJ Orthopaedics, Ossur, Smith & Nephew, and Tornier as well as royalties from SLACK Incorporated. Dr. Verma reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Arthroscopy Association Learning Center Committee, Journal of Knee Surgery, and SLACK Incorporated; he has received research support from Arthrex, Inc., Arthrosurface, DJ Orthopaedics, Smith & Nephew, Athletico, ConMed Linvatec, Miomed, and Mitek; he has received publishing royalties, financial, or material support from Arthroscopy and Vindico Medical-Orthopedics Hyperguide; he has received stock or stock options from Cymedica, Minivasive, and Omeros and serves as a paid consultant for Orthospace and Smith & Nephew. Dr. Romeo reports that he serves as a board or committee member for the American Orthopaedic Society for Sports Medicine, American Shoulder and Elbow Surgeons, Orthopedics, Orthopedics Today, SAGE, and Wolters Kluwer Health—Lippincott Williams & Wilkins; he has received research support from Aesculap/B.Braun, Arthrex, Inc., Histogenics, Medipost, NuTech, Orthospace, Smith & Nephew, and Zimmer Biomet; he has received other financial or material support from AANA, Arthrex, Inc., and Major League Baseball; he has received publishing royalties, financial and/or material support from Saunders/Mosby-Elsevier and SLACK Incorporated. The other authors report no actual or potential conflict of interest in relation to this article. 

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        Take-Home Points

        • Fractures of the greater tuberosity are often mismanaged.
        • Comprehension of greater tuberosity fractures involves classification into nonoperative and operative treatment, displacement >5mm or <5 mm, and open vs arthroscopic surgery.
        • Nearly a third of patients may suffer concomitant anterior glenohumeral instability.
        • Stiffness is the most common postoperative complication.
        • Surgery is associated with high patient satisfaction and low rates of complications and reoperations.

        Although proximal humerus fractures are common in the elderly, isolated fractures of the greater tuberosity occur less often. Management depends on several factors, including fracture pattern and displacement.1,2 Nondisplaced fractures are often successfully managed with sling immobilization and early range of motion.3,4 Although surgical intervention improves outcomes in displaced greater tuberosity fractures, the ideal surgical treatment is less clear.5

        Displaced greater tuberosity fractures may require surgery for prevention of subacromial impingement and range-of-motion deficits.2 Superior fracture displacement results in decreased shoulder abduction, and posterior displacement can limit external rotation.6 Although the greater tuberosity can displace in any direction, posterosuperior displacement has the worst outcomes.1 The exact surgery-warranting displacement amount ranges from 3 mm to 10 mm but is yet to be clearly elucidated.5,6 Less displacement is tolerated by young overhead athletes, and more displacement by older less active patients.5,7,8 Surgical options for isolated greater tuberosity fractures include fragment excision, open reduction and internal fixation (ORIF), closed reduction with percutaneous fixation, and arthroscopically assisted reduction with internal fixation.3,9,10

        We conducted a study to determine the management patterns for isolated greater tuberosity fractures. We hypothesized that greater tuberosity fractures displaced <5 mm may be managed nonoperatively and that greater tuberosity fractures displaced >5 mm require surgical fixation.

        Methods

        Search Strategy

        We performed this systematic review according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist11 and registered it (CRD42014010691) with the PROSPERO international prospective register of systematic reviews. Literature searches using the PubMed/Medline database and the Cochrane Central Register of Clinical Trials were completed in August 2014. There were no date or year restrictions. Key words were used to capture all English- language studies with level I to IV evidence (Oxford Centre for Evidence-Based Medicine) and reported clinical or radiographic outcomes. Initial exclusion criteria were cadaveric, biomechanical, histologic, and kinematic results. An electronic search algorithm with key words and a series of NOT phrases was designed to match our exclusion criteria: 

        ((((((((((((((((((((((((((((((((((((((((((((((((((greater[Title/Abstract]) AND tuberosity [Title/Abstract] OR tubercle [Title/Abstract]) AND fracture[Title/Abstract]) AND proximal[Title/Abstract] AND (English[lang]))) NOT intramedullary[Title] AND (English[lang]))) NOT nonunion[Title] AND (English[lang]))) NOT malunion[Title] AND (English[lang]))) NOT biomechanical[Title/Abstract] AND (English[lang]))) NOT cadaveric[Title/Abstract] AND (English[lang]))) NOT cadaver[Title/Abstract] AND (English[lang]))) NOT ((basic[Title/Abstract]) AND science[Title/Abstract] AND (English[lang])) AND (English[lang]))) NOT revision[Title] AND (English[lang]))) NOT pediatric[Title] AND (English[lang]))) NOT physeal[Title] AND (English[lang]))) NOT children[Title] AND (English[lang]))) NOT instability[Title] AND (English[lang]))) NOT imaging[Title])) NOT salter[Title])) NOT physis[Title])) NOT shaft[Title])) NOT distal[Title])) NOT clavicle[Title])) NOT scapula[Title])) NOT ((diaphysis[Title]) AND diaphyseal[Title]))) NOT infection[Title])) NOT laboratory[Title/Abstract])) NOT metastatic[Title/Abstract])) NOT (((((((malignancy[Title/Abstract]) OR malignant[Title/Abstract]) OR tumor[Title/Abstract]) OR oncologic[Title/Abstract]) OR cyst[Title/Abstract]) OR aneurysmal[Title/Abstract]) OR unicameral[Title/Abstract]).

        Study Selection

        Figure.
        Table 1.
        We obtained 135 search results and reviewed them for further differentiation. All the references in these studies were cross-referenced for inclusion (if missed by the initial search), which added another 15 studies. Technical notes, letters to the editor, and level V evidence reviews were excluded. Double-counting of patients was avoided by comparing each study’s authors, data collection period, and ethnic population with those of the other studies. In cases of overlapping authorship, period, or place, only the study with the longer follow-up, more patients, or more comprehensive data was included. For studies separating outcomes by diagnosis, only outcomes of isolated greater tuberosity fractures were included. Data on 3- or 4-part proximal humerus fractures and isolated lesser tuberosity fractures were excluded. Studies that could not be deconstructed as such or that were devoted solely to one of our exclusion criteria were excluded. Minimum follow-up was 2 years. After all inclusion and exclusion criteria were accounted for, 13 studies with 429 patients (429 shoulders) were selected for inclusion (Figure, Table 1).2,5,12-22

         

         

        Data Extraction

        We extracted data from the 13 studies that met the eligibility criteria. Details of study design, sample size, and patient demographics, including age, sex, and hand dominance, were recorded, as were mechanism of injury and concomitant anterior shoulder instability. To capture the most patients, we noted radiographic fracture displacement categorically rather than continuously; patients were divided into 2 displacement groups (<5 mm, >5 mm). Most studies did not define degree of comminution or specific direction of displacement per fracture, so these variables were not included in the data analysis. Nonoperative management and operative management were studied. We abstracted surgical factors, such as approach, method, fixation type (screws or sutures), and technique (suture anchors or transosseous tunnels). Clinical outcomes included physical examination findings, functional assessment results (patient satisfaction; Constant and University of California Los Angeles [UCLA] shoulder scores), and the number of revisions. Radiologic outcomes, retrieved from radiographs or computed tomography scans, focused on loss of reduction (as determined by the respective authors), malunion, nonunion, and heterotopic ossification. Each study’s methodologic quality and bias were evaluated with the 15-item Modified Coleman Methodology Score (MCMS), which was described by Cowan and colleagues.23 The MCMS has been used to assess randomized and nonrandomized patient trials.24,25 Its scaled potential score ranges from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor).

        Statistical Analysis

        We report our data as weighted means (SDs). A mean was calculated for each study that reported a respective data point, and each mean was then weighed according to its study sample size. This calculation was performed by multiplying a study’s individual mean by the number of patients enrolled in that study and dividing the sum of these weighted data points by the number of eligible patients in all relevant studies. The result was that the nonweighted means from studies with smaller sample sizes did not carry as much weight as the nonweighted means from larger studies. We compared 3 paired groups: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic). Regarding all patient, surgery, and outcomes data, unpaired Student t tests were used for continuous variables and 2-tailed Fisher exact tests for categorical variables with α = 0.05 (SPSS Version 18; IBM).

        Results

        Table 2.
        Demographic information and treatment strategies are listed in Table 2. Fifty-eight percent of patients were male, 59.0% of dominant shoulders were affected, and 59.2% of fractures were displaced <5 mm. Concomitant shoulder instability was reported in 28.1% of patients. Mechanism of injury was not reported in all studies but most commonly (n = 75; 49.3%) involved a fall on an outstretched hand; 31 patients (20.4%) had a sports-related injury, and another 37 (24.3%) were injured in a motor vehicle collision. Of the 429 patients, 217 (50.6%) were treated nonoperatively, and 212 (49.4%) underwent surgery. Open, arthroscopic, and percutaneous approaches were reported. No studies presented outcomes of fragment excision.

        Postoperative physical examination findings were underreported so that surgical groups could be compared. Of all the surgical studies, 4 reported postoperative forward elevation (mean, 160°; SD, 9.8°) and external rotation (mean, 46.4°; SD 26.3°).14,15,18,22 No malunions and only 1 nonunion were reported in all 13 studies. No deaths or other serious medical complications were reported. Patients with anterior instability more often underwent surgery than were treated nonoperatively (39.2% vs 12.0%; P < .01) and more often had fractures displaced >5 mm than <5 mm (44.3% vs 14.5%; P < .01).

         

         

        Table 3.
        Comparisons of treatment type are listed in Table 3. Compared with nonoperative patients, operative patients had significantly fewer radiographic losses of reduction (P < .01) and better patient satisfaction (P < .01). Operative patients had a significantly higher rate of shoulder stiffness (P < .01). Eight operative patients (3.8%) and no nonoperative patients required reoperation during clinical follow-up (P < .01). All 12 reported cases of stiffness were in the operative group, and 3 required revision surgery. One patient required revision ORIF. There were 2 cases of postoperative superficial infection (0.9%) and 4 neurologic injuries (1.9%).

        Table 4.
        Comparisons of displacement amount are listed in Table 4. Compared with fractures displaced >5 mm, those displaced <5 mm had more radiographic losses of reduction (P < .01) but fewer instances of heterotopic ossification (P < .01). Fractures displaced >5 mm were significantly more likely than not to be managed with surgery (P < .01) and significantly more likely to develop stiffness after treatment (P = .01). One patient (0.4%) with a fracture displaced <5 mm eventually underwent surgery for stiffness, and 6 patients (3.6%) with fractures displaced >5 mm required reoperation (P = .02).

        Table 5.
        Comparisons of surgery type are listed in Table 5. All open procedures were performed with a deltoid-splitting approach. Screw fixation was used in 4 cases: 2 percutaneous5,21 and 2 open.2,5 The other open and arthroscopic studies described suture fixation, half with anchors (77/156 patients; 49.4%) and half with transosseous tunnels (79/156; 50.6%). There were no statistically significant differences between open/percutaneous and arthroscopic techniques in terms of stiffness, superficial infection, neurologic injury, or reoperation rate.

        Fisher exact tests were used to perform isolated comparisons of screws and sutures as well as suture anchors and transosseous tunnels. Patients with screw fixation were significantly (P = .051) less likely to require reoperation (0/56; 0%) than patients with suture fixation (8/100; 8.0%). Screw fixation also led to significantly less stiffness (0% vs 12.0%; P < .01) but trended toward a higher rate of superficial infection (3.6% vs 0%; P = .13). There was no statistical difference in nerve injury rates between screws and sutures (1.8% vs 3.0%; P = 1.0). There were no significant differences in reoperations, stiffness, superficial infections, or nerve injuries between suture anchor and transosseous tunnel constructs.

         

         

        For all 13 studies, mean (SD) MCMS was 41.1 (8.6).

        Discussion

        Five percent of all fractures involve the proximal humerus, and 20% of proximal humerus fractures are isolated greater tuberosity fractures.26,27 In his classic 1970 article, Neer6 formulated the 4-part proximal humerus fracture classification and defined greater tuberosity fracture “parts” using the same criteria as for other fracture “parts.” Neer6 recommended nonoperative management for isolated greater tuberosity fractures displaced <1 cm but did not present evidence corroborating his recommendation. More recent cutoffs for nonoperative management include 5 mm (general population) and 3 mm (athletes).7,17

        In the present systematic review of greater tuberosity fractures, 3 separate comparisons were made: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic).

        Treatment Type. Only 4 studies reported data on nonoperative treatment outcomes.5,12,16,17 Of these 4 studies, 2 found successful outcomes for fractures displaced <5 mm.12,17 Platzer and colleagues17 found good or excellent results in 97% of 135 shoulders after 4 years. Good results were defined with shoulder scores of ≥80 (Constant), <8 (Vienna), and >28 (UCLA), and excellent results were defined with maximum scores on 2 of the 3 systems. Platzer and colleagues17 also found nonsignificantly worse shoulder scores with superior displacement of 3 mm to 5 mm and recommended surgery for overhead athletes in this group. Rath and colleagues12 described a successful 3-phase rehabilitation protocol of sling immobilization for 3 weeks, pendulum exercises for 3 weeks, and active exercises thereafter. By an average of 31 months, patient satisfaction scores improved to 9.5 from 4.2 (10-point scale), though the authors cautioned that pain and decreased motion lasted 8 months on average. Conservative treatment was far less successful in the 2 studies of fractures displaced >5 mm.5,16 Keene and colleagues16 reported unsatisfactory results in all 4 patients with fractures displaced >1.5 cm. In a study separate from their 2005 analysis,17 Platzer and colleagues5 in 2008 evaluated displaced fractures and found function and patient satisfaction were inferior after nonoperative treatment than after surgery. The studies by Keene and colleagues16 and Platzer and colleagues5 support the finding of an overall lower patient satisfaction rate in nonoperative patients.

        Fracture Displacement Amount. Only 2 arthroscopic studies and no open studies addressed surgery for fractures displaced <5 mm. Fewer than 16% of these fractures were managed operatively, and <1% required reoperation. By contrast, almost all fractures displaced >5 mm were managed operatively, and 3.6% required reoperation. Radiographic loss of reduction was more common in fractures displaced <5 mm, primarily because they were managed without fixation. Radiographic loss of reduction was reported in only 9 operatively treated patients, none of whom was symptomatic enough to require another surgery.5 Reoperations were most commonly performed for stiffness, which itself was significantly more common in fractures displaced >5 mm. Bhatia and colleagues14 reported the highest reoperation rate (14.3%; 3/21), but they studied more complex, comminuted fractures of the greater tuberosity. Two of their 3 reoperations were biceps tenodeses for inflamed, stiff tenosynovitis, and the third patient had a foreign body giant cell reaction to suture material. Fewer than 1% of patients with operatively managed displaced fractures required revision ORIF, and <2% developed a superficial infection or postoperative nerve palsy.19,22 For displaced greater tuberosity fractures, surgery is highly successful overall, complication rates are very low, and 90% of patients report being satisfied.

        Surgery Type. Patients were divided into 2 groups. In the nonarthroscopic group, open and percutaneous approaches were used. All studies that described a percutaneous approach used screw fixation5,21; in addition, 32 patients were treated with screws through an open approach.2,5 The other open and arthroscopic studies used suture fixation. Interestingly, no studies reported on clinical outcomes of fragment excision. There were no statistically significant differences in rates of reoperation, stiffness, infection, or neurologic injury between the arthroscopic and nonarthroscopic groups. Patient satisfaction scores were slightly higher in the nonarthroscopic group (91.0% vs 87.8%), but the difference was not statistically significant.

         

         

        With surgical techniques isolated, there were no significant differences between suture anchors and transosseous tunnel constructs, but screws performed significantly better than suture techniques. Compared with suture fixation, screw fixation led to significantly fewer cases of stiffness and reoperation, which suggests surgeons need to give screws more consideration in the operative management of these fractures. However, the number of patients treated with screws was smaller than the number treated with suture fixation; it is possible the differences between these cohorts would be eliminated if there were more patients in the screw cohort. In addition, screw fixation was universally performed with an open or percutaneous approach and trended toward a higher infection rate. As screw and suture techniques have low rates of complications and reoperations, we recommend leaving fixation choice to the surgeon.

        Anterior shoulder instability has been associated with greater tuberosity fractures.1,8,19 The supraspinatus, infraspinatus, and teres minor muscles all insert into the greater tuberosity and resist anterior translation of the proximal humerus. Loss of this dynamic muscle stabilization is amplified by tuberosity fracture displacement: Anterior shoulder instability was significantly more common in fractures displaced >5 mm (44.3%) vs <5 mm (14.5%). In turn, glenohumeral instability was more common in patients treated with surgery, specifically open surgery, because displaced fractures may not be as easily accessed with arthroscopic techniques. No studies reported concomitant labral repair or capsular plication techniques.

        This systematic review was limited by the studies analyzed. All but 1 study5 had level IV evidence. Mean (SD) MCMS was 41.8 (8.6). Any MCMS score <54 indicates a poor methodology level, but this scoring system is designed for randomized controlled trials,23 and there were none in this study. Physical examination findings, such as range of motion, were underreported. In addition, radiographic parameters were not consistently described but rather were determined by the respective authors’ subjective interpretations of malunion, nonunion, and loss of reduction. Publication bias is present in that we excluded non- English language studies and medical conference abstracts and may have omitted potentially eligible studies not discoverable with our search methodology. Performance bias is a factor in any systematic review with multiple surgeons and wide variation in surgical technique.

        Conclusion

        Greater tuberosity fractures displaced <5 mm may be safely managed nonoperatively, as there are no reports of nonoperatively managed fractures that subsequently required surgery. Nonoperative treatment was initially associated with low patient satisfaction, but only because displaced fractures were conservatively managed in early studies.5,16 Fractures displaced >5 mm respond well to operative fixation with screws, suture anchors, or transosseous suture tunnels. Stiffness is the most common postoperative complication (<6%), followed by heterotopic ossification, transient neurapraxias, and superficial infection. There are no discernible differences in outcome between open and arthroscopic techniques, but screw fixation may lead to significantly fewer cases of stiffness and reoperation in comparison with suture constructs.

        Take-Home Points

        • Fractures of the greater tuberosity are often mismanaged.
        • Comprehension of greater tuberosity fractures involves classification into nonoperative and operative treatment, displacement >5mm or <5 mm, and open vs arthroscopic surgery.
        • Nearly a third of patients may suffer concomitant anterior glenohumeral instability.
        • Stiffness is the most common postoperative complication.
        • Surgery is associated with high patient satisfaction and low rates of complications and reoperations.

        Although proximal humerus fractures are common in the elderly, isolated fractures of the greater tuberosity occur less often. Management depends on several factors, including fracture pattern and displacement.1,2 Nondisplaced fractures are often successfully managed with sling immobilization and early range of motion.3,4 Although surgical intervention improves outcomes in displaced greater tuberosity fractures, the ideal surgical treatment is less clear.5

        Displaced greater tuberosity fractures may require surgery for prevention of subacromial impingement and range-of-motion deficits.2 Superior fracture displacement results in decreased shoulder abduction, and posterior displacement can limit external rotation.6 Although the greater tuberosity can displace in any direction, posterosuperior displacement has the worst outcomes.1 The exact surgery-warranting displacement amount ranges from 3 mm to 10 mm but is yet to be clearly elucidated.5,6 Less displacement is tolerated by young overhead athletes, and more displacement by older less active patients.5,7,8 Surgical options for isolated greater tuberosity fractures include fragment excision, open reduction and internal fixation (ORIF), closed reduction with percutaneous fixation, and arthroscopically assisted reduction with internal fixation.3,9,10

        We conducted a study to determine the management patterns for isolated greater tuberosity fractures. We hypothesized that greater tuberosity fractures displaced <5 mm may be managed nonoperatively and that greater tuberosity fractures displaced >5 mm require surgical fixation.

        Methods

        Search Strategy

        We performed this systematic review according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) checklist11 and registered it (CRD42014010691) with the PROSPERO international prospective register of systematic reviews. Literature searches using the PubMed/Medline database and the Cochrane Central Register of Clinical Trials were completed in August 2014. There were no date or year restrictions. Key words were used to capture all English- language studies with level I to IV evidence (Oxford Centre for Evidence-Based Medicine) and reported clinical or radiographic outcomes. Initial exclusion criteria were cadaveric, biomechanical, histologic, and kinematic results. An electronic search algorithm with key words and a series of NOT phrases was designed to match our exclusion criteria: 

        ((((((((((((((((((((((((((((((((((((((((((((((((((greater[Title/Abstract]) AND tuberosity [Title/Abstract] OR tubercle [Title/Abstract]) AND fracture[Title/Abstract]) AND proximal[Title/Abstract] AND (English[lang]))) NOT intramedullary[Title] AND (English[lang]))) NOT nonunion[Title] AND (English[lang]))) NOT malunion[Title] AND (English[lang]))) NOT biomechanical[Title/Abstract] AND (English[lang]))) NOT cadaveric[Title/Abstract] AND (English[lang]))) NOT cadaver[Title/Abstract] AND (English[lang]))) NOT ((basic[Title/Abstract]) AND science[Title/Abstract] AND (English[lang])) AND (English[lang]))) NOT revision[Title] AND (English[lang]))) NOT pediatric[Title] AND (English[lang]))) NOT physeal[Title] AND (English[lang]))) NOT children[Title] AND (English[lang]))) NOT instability[Title] AND (English[lang]))) NOT imaging[Title])) NOT salter[Title])) NOT physis[Title])) NOT shaft[Title])) NOT distal[Title])) NOT clavicle[Title])) NOT scapula[Title])) NOT ((diaphysis[Title]) AND diaphyseal[Title]))) NOT infection[Title])) NOT laboratory[Title/Abstract])) NOT metastatic[Title/Abstract])) NOT (((((((malignancy[Title/Abstract]) OR malignant[Title/Abstract]) OR tumor[Title/Abstract]) OR oncologic[Title/Abstract]) OR cyst[Title/Abstract]) OR aneurysmal[Title/Abstract]) OR unicameral[Title/Abstract]).

        Study Selection

        Figure.
        Table 1.
        We obtained 135 search results and reviewed them for further differentiation. All the references in these studies were cross-referenced for inclusion (if missed by the initial search), which added another 15 studies. Technical notes, letters to the editor, and level V evidence reviews were excluded. Double-counting of patients was avoided by comparing each study’s authors, data collection period, and ethnic population with those of the other studies. In cases of overlapping authorship, period, or place, only the study with the longer follow-up, more patients, or more comprehensive data was included. For studies separating outcomes by diagnosis, only outcomes of isolated greater tuberosity fractures were included. Data on 3- or 4-part proximal humerus fractures and isolated lesser tuberosity fractures were excluded. Studies that could not be deconstructed as such or that were devoted solely to one of our exclusion criteria were excluded. Minimum follow-up was 2 years. After all inclusion and exclusion criteria were accounted for, 13 studies with 429 patients (429 shoulders) were selected for inclusion (Figure, Table 1).2,5,12-22

         

         

        Data Extraction

        We extracted data from the 13 studies that met the eligibility criteria. Details of study design, sample size, and patient demographics, including age, sex, and hand dominance, were recorded, as were mechanism of injury and concomitant anterior shoulder instability. To capture the most patients, we noted radiographic fracture displacement categorically rather than continuously; patients were divided into 2 displacement groups (<5 mm, >5 mm). Most studies did not define degree of comminution or specific direction of displacement per fracture, so these variables were not included in the data analysis. Nonoperative management and operative management were studied. We abstracted surgical factors, such as approach, method, fixation type (screws or sutures), and technique (suture anchors or transosseous tunnels). Clinical outcomes included physical examination findings, functional assessment results (patient satisfaction; Constant and University of California Los Angeles [UCLA] shoulder scores), and the number of revisions. Radiologic outcomes, retrieved from radiographs or computed tomography scans, focused on loss of reduction (as determined by the respective authors), malunion, nonunion, and heterotopic ossification. Each study’s methodologic quality and bias were evaluated with the 15-item Modified Coleman Methodology Score (MCMS), which was described by Cowan and colleagues.23 The MCMS has been used to assess randomized and nonrandomized patient trials.24,25 Its scaled potential score ranges from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor).

        Statistical Analysis

        We report our data as weighted means (SDs). A mean was calculated for each study that reported a respective data point, and each mean was then weighed according to its study sample size. This calculation was performed by multiplying a study’s individual mean by the number of patients enrolled in that study and dividing the sum of these weighted data points by the number of eligible patients in all relevant studies. The result was that the nonweighted means from studies with smaller sample sizes did not carry as much weight as the nonweighted means from larger studies. We compared 3 paired groups: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic). Regarding all patient, surgery, and outcomes data, unpaired Student t tests were used for continuous variables and 2-tailed Fisher exact tests for categorical variables with α = 0.05 (SPSS Version 18; IBM).

        Results

        Table 2.
        Demographic information and treatment strategies are listed in Table 2. Fifty-eight percent of patients were male, 59.0% of dominant shoulders were affected, and 59.2% of fractures were displaced <5 mm. Concomitant shoulder instability was reported in 28.1% of patients. Mechanism of injury was not reported in all studies but most commonly (n = 75; 49.3%) involved a fall on an outstretched hand; 31 patients (20.4%) had a sports-related injury, and another 37 (24.3%) were injured in a motor vehicle collision. Of the 429 patients, 217 (50.6%) were treated nonoperatively, and 212 (49.4%) underwent surgery. Open, arthroscopic, and percutaneous approaches were reported. No studies presented outcomes of fragment excision.

        Postoperative physical examination findings were underreported so that surgical groups could be compared. Of all the surgical studies, 4 reported postoperative forward elevation (mean, 160°; SD, 9.8°) and external rotation (mean, 46.4°; SD 26.3°).14,15,18,22 No malunions and only 1 nonunion were reported in all 13 studies. No deaths or other serious medical complications were reported. Patients with anterior instability more often underwent surgery than were treated nonoperatively (39.2% vs 12.0%; P < .01) and more often had fractures displaced >5 mm than <5 mm (44.3% vs 14.5%; P < .01).

         

         

        Table 3.
        Comparisons of treatment type are listed in Table 3. Compared with nonoperative patients, operative patients had significantly fewer radiographic losses of reduction (P < .01) and better patient satisfaction (P < .01). Operative patients had a significantly higher rate of shoulder stiffness (P < .01). Eight operative patients (3.8%) and no nonoperative patients required reoperation during clinical follow-up (P < .01). All 12 reported cases of stiffness were in the operative group, and 3 required revision surgery. One patient required revision ORIF. There were 2 cases of postoperative superficial infection (0.9%) and 4 neurologic injuries (1.9%).

        Table 4.
        Comparisons of displacement amount are listed in Table 4. Compared with fractures displaced >5 mm, those displaced <5 mm had more radiographic losses of reduction (P < .01) but fewer instances of heterotopic ossification (P < .01). Fractures displaced >5 mm were significantly more likely than not to be managed with surgery (P < .01) and significantly more likely to develop stiffness after treatment (P = .01). One patient (0.4%) with a fracture displaced <5 mm eventually underwent surgery for stiffness, and 6 patients (3.6%) with fractures displaced >5 mm required reoperation (P = .02).

        Table 5.
        Comparisons of surgery type are listed in Table 5. All open procedures were performed with a deltoid-splitting approach. Screw fixation was used in 4 cases: 2 percutaneous5,21 and 2 open.2,5 The other open and arthroscopic studies described suture fixation, half with anchors (77/156 patients; 49.4%) and half with transosseous tunnels (79/156; 50.6%). There were no statistically significant differences between open/percutaneous and arthroscopic techniques in terms of stiffness, superficial infection, neurologic injury, or reoperation rate.

        Fisher exact tests were used to perform isolated comparisons of screws and sutures as well as suture anchors and transosseous tunnels. Patients with screw fixation were significantly (P = .051) less likely to require reoperation (0/56; 0%) than patients with suture fixation (8/100; 8.0%). Screw fixation also led to significantly less stiffness (0% vs 12.0%; P < .01) but trended toward a higher rate of superficial infection (3.6% vs 0%; P = .13). There was no statistical difference in nerve injury rates between screws and sutures (1.8% vs 3.0%; P = 1.0). There were no significant differences in reoperations, stiffness, superficial infections, or nerve injuries between suture anchor and transosseous tunnel constructs.

         

         

        For all 13 studies, mean (SD) MCMS was 41.1 (8.6).

        Discussion

        Five percent of all fractures involve the proximal humerus, and 20% of proximal humerus fractures are isolated greater tuberosity fractures.26,27 In his classic 1970 article, Neer6 formulated the 4-part proximal humerus fracture classification and defined greater tuberosity fracture “parts” using the same criteria as for other fracture “parts.” Neer6 recommended nonoperative management for isolated greater tuberosity fractures displaced <1 cm but did not present evidence corroborating his recommendation. More recent cutoffs for nonoperative management include 5 mm (general population) and 3 mm (athletes).7,17

        In the present systematic review of greater tuberosity fractures, 3 separate comparisons were made: treatment type (nonoperative vs operative), fracture displacement amount (<5 mm vs >5 mm), and surgery type (open vs arthroscopic).

        Treatment Type. Only 4 studies reported data on nonoperative treatment outcomes.5,12,16,17 Of these 4 studies, 2 found successful outcomes for fractures displaced <5 mm.12,17 Platzer and colleagues17 found good or excellent results in 97% of 135 shoulders after 4 years. Good results were defined with shoulder scores of ≥80 (Constant), <8 (Vienna), and >28 (UCLA), and excellent results were defined with maximum scores on 2 of the 3 systems. Platzer and colleagues17 also found nonsignificantly worse shoulder scores with superior displacement of 3 mm to 5 mm and recommended surgery for overhead athletes in this group. Rath and colleagues12 described a successful 3-phase rehabilitation protocol of sling immobilization for 3 weeks, pendulum exercises for 3 weeks, and active exercises thereafter. By an average of 31 months, patient satisfaction scores improved to 9.5 from 4.2 (10-point scale), though the authors cautioned that pain and decreased motion lasted 8 months on average. Conservative treatment was far less successful in the 2 studies of fractures displaced >5 mm.5,16 Keene and colleagues16 reported unsatisfactory results in all 4 patients with fractures displaced >1.5 cm. In a study separate from their 2005 analysis,17 Platzer and colleagues5 in 2008 evaluated displaced fractures and found function and patient satisfaction were inferior after nonoperative treatment than after surgery. The studies by Keene and colleagues16 and Platzer and colleagues5 support the finding of an overall lower patient satisfaction rate in nonoperative patients.

        Fracture Displacement Amount. Only 2 arthroscopic studies and no open studies addressed surgery for fractures displaced <5 mm. Fewer than 16% of these fractures were managed operatively, and <1% required reoperation. By contrast, almost all fractures displaced >5 mm were managed operatively, and 3.6% required reoperation. Radiographic loss of reduction was more common in fractures displaced <5 mm, primarily because they were managed without fixation. Radiographic loss of reduction was reported in only 9 operatively treated patients, none of whom was symptomatic enough to require another surgery.5 Reoperations were most commonly performed for stiffness, which itself was significantly more common in fractures displaced >5 mm. Bhatia and colleagues14 reported the highest reoperation rate (14.3%; 3/21), but they studied more complex, comminuted fractures of the greater tuberosity. Two of their 3 reoperations were biceps tenodeses for inflamed, stiff tenosynovitis, and the third patient had a foreign body giant cell reaction to suture material. Fewer than 1% of patients with operatively managed displaced fractures required revision ORIF, and <2% developed a superficial infection or postoperative nerve palsy.19,22 For displaced greater tuberosity fractures, surgery is highly successful overall, complication rates are very low, and 90% of patients report being satisfied.

        Surgery Type. Patients were divided into 2 groups. In the nonarthroscopic group, open and percutaneous approaches were used. All studies that described a percutaneous approach used screw fixation5,21; in addition, 32 patients were treated with screws through an open approach.2,5 The other open and arthroscopic studies used suture fixation. Interestingly, no studies reported on clinical outcomes of fragment excision. There were no statistically significant differences in rates of reoperation, stiffness, infection, or neurologic injury between the arthroscopic and nonarthroscopic groups. Patient satisfaction scores were slightly higher in the nonarthroscopic group (91.0% vs 87.8%), but the difference was not statistically significant.

         

         

        With surgical techniques isolated, there were no significant differences between suture anchors and transosseous tunnel constructs, but screws performed significantly better than suture techniques. Compared with suture fixation, screw fixation led to significantly fewer cases of stiffness and reoperation, which suggests surgeons need to give screws more consideration in the operative management of these fractures. However, the number of patients treated with screws was smaller than the number treated with suture fixation; it is possible the differences between these cohorts would be eliminated if there were more patients in the screw cohort. In addition, screw fixation was universally performed with an open or percutaneous approach and trended toward a higher infection rate. As screw and suture techniques have low rates of complications and reoperations, we recommend leaving fixation choice to the surgeon.

        Anterior shoulder instability has been associated with greater tuberosity fractures.1,8,19 The supraspinatus, infraspinatus, and teres minor muscles all insert into the greater tuberosity and resist anterior translation of the proximal humerus. Loss of this dynamic muscle stabilization is amplified by tuberosity fracture displacement: Anterior shoulder instability was significantly more common in fractures displaced >5 mm (44.3%) vs <5 mm (14.5%). In turn, glenohumeral instability was more common in patients treated with surgery, specifically open surgery, because displaced fractures may not be as easily accessed with arthroscopic techniques. No studies reported concomitant labral repair or capsular plication techniques.

        This systematic review was limited by the studies analyzed. All but 1 study5 had level IV evidence. Mean (SD) MCMS was 41.8 (8.6). Any MCMS score <54 indicates a poor methodology level, but this scoring system is designed for randomized controlled trials,23 and there were none in this study. Physical examination findings, such as range of motion, were underreported. In addition, radiographic parameters were not consistently described but rather were determined by the respective authors’ subjective interpretations of malunion, nonunion, and loss of reduction. Publication bias is present in that we excluded non- English language studies and medical conference abstracts and may have omitted potentially eligible studies not discoverable with our search methodology. Performance bias is a factor in any systematic review with multiple surgeons and wide variation in surgical technique.

        Conclusion

        Greater tuberosity fractures displaced <5 mm may be safely managed nonoperatively, as there are no reports of nonoperatively managed fractures that subsequently required surgery. Nonoperative treatment was initially associated with low patient satisfaction, but only because displaced fractures were conservatively managed in early studies.5,16 Fractures displaced >5 mm respond well to operative fixation with screws, suture anchors, or transosseous suture tunnels. Stiffness is the most common postoperative complication (<6%), followed by heterotopic ossification, transient neurapraxias, and superficial infection. There are no discernible differences in outcome between open and arthroscopic techniques, but screw fixation may lead to significantly fewer cases of stiffness and reoperation in comparison with suture constructs.

        References

        1. Verdano MA, Aliani D, Pellegrini A, Baudi P, Pedrazzi G, Ceccarelli F. Isolated fractures of the greater tuberosity in proximal humerus: does the direction of displacement influence functional outcome? An analysis of displacement in greater tuberosity fractures. Acta Biomed. 2013;84(3):219-228.

        2. Yin B, Moen TC, Thompson SA, Bigliani LU, Ahmad CS, Levine WN. Operative treatment of isolated greater tuberosity fractures: retrospective review of clinical and functional outcomes. Orthopedics. 2012;35(6):e807-e814.

        3. Green A, Izzi J. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.

        4. Norouzi M, Naderi MN, Komasi MH, Sharifzadeh SR, Shahrezaei M, Eajazi A. Clinical results of using the proximal humeral internal locking system plate for internal fixation of displaced proximal humeral fractures. Am J Orthop. 2012;41(5):E64-E68.

        5. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.

        6. Neer CS. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.

        7. Park TS, Choi IY, Kim YH, Park MR, Shon JH, Kim SI. A new suggestion for the treatment of minimally displaced fractures of the greater tuberosity of the proximal humerus. Bull Hosp Jt Dis. 1997;56(3):171-176.

        8. McLaughlin HL. Dislocation of the shoulder with tuberosity fracture. Surg Clin North Am. 1963;43:1615-1620.

        9. DeBottis D, Anavian J, Green A. Surgical management of isolated greater tuberosity fractures of the proximal humerus. Orthop Clin North Am. 2014;45(2):207-218.

        10. Monga P, Verma R, Sharma VK. Closed reduction and external fixation for displaced proximal humeral fractures. J Orthop Surg (Hong Kong). 2009;17(2):142-145.

        11. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. J Clin Epidemiol. 2009;62(10):1006-1012.

        12. Rath E, Alkrinawi N, Levy O, Debbi R, Amar E, Atoun E. Minimally displaced fractures of the greater tuberosity: outcome of non-operative treatment. J Shoulder Elbow Surg. 2013;22(10):e8-e11.

        13. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.

        14. Bhatia DN, van Rooyen KS, Toit du DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.

        15. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.

        16. Keene JS, Huizenga RE, Engber WD, Rogers SC. Proximal humeral fractures: a correlation of residual deformity with long-term function. Orthopedics. 1983;6(2):173-178.

        17. Platzer P, Kutscha-Lissberg F, Lehr S, Vecsei V, Gaebler C. The influence of displacement on shoulder function in patients with minimally displaced fractures of the greater tuberosity. Injury. 2005;36(10):1185-1189.

        18. Park SE, Ji JH, Shafi M, Jung JJ, Gil HJ, Lee HH. Arthroscopic management of occult greater tuberosity fracture of the shoulder. Eur J Orthop Surg Traumatol. 2014;24(4):475-482.

        19. Dimakopoulos P, Panagopoulos A, Kasimatis G, Syggelos SA, Lambiris E. Anterior traumatic shoulder dislocation associated with displaced greater tuberosity fracture: the necessity of operative treatment. J Orthop Trauma. 2007;21(2):104-112.

        20. Kim SH, Ha KI. Arthroscopic treatment of symptomatic shoulders with minimally displaced greater tuberosity fracture. Arthroscopy. 2000;16(7):695-700.

        21. Chen CY, Chao EK, Tu YK, Ueng SW, Shih CH. Closed management and percutaneous fixation of unstable proximal humerus fractures. J Trauma. 1998;45(6):1039-1045.

        22. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.

        23. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

        24. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

        25. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

        26. Chun JM, Groh GI, Rockwood CA. Two-part fractures of the proximal humerus. J Shoulder Elbow Surg. 1994;3(5):273-287.

        27. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.

        References

        1. Verdano MA, Aliani D, Pellegrini A, Baudi P, Pedrazzi G, Ceccarelli F. Isolated fractures of the greater tuberosity in proximal humerus: does the direction of displacement influence functional outcome? An analysis of displacement in greater tuberosity fractures. Acta Biomed. 2013;84(3):219-228.

        2. Yin B, Moen TC, Thompson SA, Bigliani LU, Ahmad CS, Levine WN. Operative treatment of isolated greater tuberosity fractures: retrospective review of clinical and functional outcomes. Orthopedics. 2012;35(6):e807-e814.

        3. Green A, Izzi J. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elbow Surg. 2003;12(6):641-649.

        4. Norouzi M, Naderi MN, Komasi MH, Sharifzadeh SR, Shahrezaei M, Eajazi A. Clinical results of using the proximal humeral internal locking system plate for internal fixation of displaced proximal humeral fractures. Am J Orthop. 2012;41(5):E64-E68.

        5. Platzer P, Thalhammer G, Oberleitner G, et al. Displaced fractures of the greater tuberosity: a comparison of operative and nonoperative treatment. J Trauma. 2008;65(4):843-848.

        6. Neer CS. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am. 1970;52(6):1077-1089.

        7. Park TS, Choi IY, Kim YH, Park MR, Shon JH, Kim SI. A new suggestion for the treatment of minimally displaced fractures of the greater tuberosity of the proximal humerus. Bull Hosp Jt Dis. 1997;56(3):171-176.

        8. McLaughlin HL. Dislocation of the shoulder with tuberosity fracture. Surg Clin North Am. 1963;43:1615-1620.

        9. DeBottis D, Anavian J, Green A. Surgical management of isolated greater tuberosity fractures of the proximal humerus. Orthop Clin North Am. 2014;45(2):207-218.

        10. Monga P, Verma R, Sharma VK. Closed reduction and external fixation for displaced proximal humeral fractures. J Orthop Surg (Hong Kong). 2009;17(2):142-145.

        11. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. J Clin Epidemiol. 2009;62(10):1006-1012.

        12. Rath E, Alkrinawi N, Levy O, Debbi R, Amar E, Atoun E. Minimally displaced fractures of the greater tuberosity: outcome of non-operative treatment. J Shoulder Elbow Surg. 2013;22(10):e8-e11.

        13. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am. 2007;89(8):1700-1709.

        14. Bhatia DN, van Rooyen KS, Toit du DF, de Beer JF. Surgical treatment of comminuted, displaced fractures of the greater tuberosity of the proximal humerus: a new technique of double-row suture-anchor fixation and long-term results. Injury. 2006;37(10):946-952.

        15. Flatow EL, Cuomo F, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of two-part displaced fractures of the greater tuberosity of the proximal part of the humerus. J Bone Joint Surg Am. 1991;73(8):1213-1218.

        16. Keene JS, Huizenga RE, Engber WD, Rogers SC. Proximal humeral fractures: a correlation of residual deformity with long-term function. Orthopedics. 1983;6(2):173-178.

        17. Platzer P, Kutscha-Lissberg F, Lehr S, Vecsei V, Gaebler C. The influence of displacement on shoulder function in patients with minimally displaced fractures of the greater tuberosity. Injury. 2005;36(10):1185-1189.

        18. Park SE, Ji JH, Shafi M, Jung JJ, Gil HJ, Lee HH. Arthroscopic management of occult greater tuberosity fracture of the shoulder. Eur J Orthop Surg Traumatol. 2014;24(4):475-482.

        19. Dimakopoulos P, Panagopoulos A, Kasimatis G, Syggelos SA, Lambiris E. Anterior traumatic shoulder dislocation associated with displaced greater tuberosity fracture: the necessity of operative treatment. J Orthop Trauma. 2007;21(2):104-112.

        20. Kim SH, Ha KI. Arthroscopic treatment of symptomatic shoulders with minimally displaced greater tuberosity fracture. Arthroscopy. 2000;16(7):695-700.

        21. Chen CY, Chao EK, Tu YK, Ueng SW, Shih CH. Closed management and percutaneous fixation of unstable proximal humerus fractures. J Trauma. 1998;45(6):1039-1045.

        22. Ji JH, Shafi M, Song IS, Kim YY, McFarland EG, Moon CY. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600-609.

        23. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

        24. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

        25. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

        26. Chun JM, Groh GI, Rockwood CA. Two-part fractures of the proximal humerus. J Shoulder Elbow Surg. 1994;3(5):273-287.

        27. Gruson KI, Ruchelsman DE, Tejwani NC. Isolated tuberosity fractures of the proximal humeral: current concepts. Injury. 2008;39(3):284-298.

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        Gorham Disease

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        Take-Home Points

        • Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
        • There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
        • Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
        • Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
        • There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

        Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.4,6

        Jackson and colleagues first described idiopathic osteolysis in 1838,1,2 and Gorham and Stout3 introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.7,8

        Clinical Presentation

        Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.7 Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.6 Pelvic bones seem to be involved least often.6,7

        Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.1,2

        Imaging

        Figure 1.
        Plain radiographs show permeative osteolysis involving the subcortical and intramedullary regions and typically affecting regional, contiguous bones, without adjacent sclerosis, and somewhat resembling heterogeneous osteoporosis (Figure 1).8-10

        Computed tomography (CT) better defines the severity and extent of these changes.

        Figure 2.
        Progression can result in osseous tapering, or “pointing” at lytic margins, forming cone-shaped spicules. In progressive cases, there is an “extraosseous” stage characterized by frank cortical destruction and true “disappearance” of bone, with extensive soft-tissue edema8-10 (Figures 2A, 2B).

        Magnetic resonance imaging shows an infiltrative and irregular T2 hyperintense signal throughout regions of bone affected by osteolysis, but this finding is not characteristic. There is heterogeneous enhancement on postcontrast sequences, and, though masslike enhancement is absent, signal abnormalities may extend into adjacent soft tissues.
        Figure 3.
        These changes indicate inflammation and hemorrhage of various degrees interspersed with scant fibrous tissue8-10 (Figures 3A, 3B).

        Bone scintigraphy using technetium-99m is similarly nonspecific, typically revealing radiotracer uptake that is consistent with bony reaction to an underlying osteolytic process (Figure 4) but turning negative with ongoing resorption.
        Figure 4.
        In some cases of Gorham disease, bone scintigraphy did not reveal a significant increase in activity, such as would be expected in a vascular malformation or purely angiomatous neoplasm. Similar findings could be attributed to a variety of pathologies, including primary bone tumor, metastasis, or even osteomyelitis.8-10

        Positron emission tomography/CT typically shows foci of increased metabolic activity in the areas of osteolysis.10

         

         

        Diagnosis

        There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

        Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

        Figure 5.
        Biopsies typically show a progressive osteolysis that is consistently associated with a benign but abnormal vascular proliferation that in many cases has characteristics of lymphatic endothelium. The apparent bony destruction is largely attributed to this process (Figures 5A-5D).11,12

        The differential diagnosis includes infection (osteomyelitis, Brodie abscess), benign tumors (eosinophilic granuloma/Langerhans cell histiocytosis), malignant tumors (Ewing sarcoma and angiosarcoma), inflammatory conditions (eg, apatite- associated destructive arthritis), endocrine disorders (eg, osteolytic hyperparathyroidism), benign non-neoplastic conditions (venous or venolymphatic malformation), and other syndromes that present with osteolysis.1,2 Nevertheless, progressive and unusually substantial bone destruction without evidence of repair is almost pathognomonic for Gorham disease.9

        Treatment

        Table.
        Although no single or combined treatment modality is considered the gold standard (Table),1,2,4,13-23 management of Gorham disease generally centers on radiation therapy for local control of large and painful lesions and on surgical intervention for pathologic progression that would otherwise result in substantial functional limitations.2 Also described for treatment are antiosteoclastic medications (bisphosphonates), which are often used in conjunction with radiation and/or surgical intervention.2,4 The newer literature cites some benefit of using various experimental modalities, including a combination of interferon alfa-2b and low-molecular-weight heparin,13 and even propranolol.14

        Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.1,2,4,20

        References

        1. Saify FY, Gosavi SR. Gorham’s disease: a diagnostic challenge. J Oral Maxillofac Pathol. 2014;18(3):411-414.

        2. Patel DV. Gorham’s disease or massive osteolysis. Clin Med Res. 2005;3(2):65-74.

        3. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone); its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.

        4. Heffez L, Doku HC, Carter BL, Feeney JE. Perspectives on massive osteolysis. Report of a case and review of the literature. Oral Surg Oral Med Oral Pathol. 1983;55(4):331-343.

        5. Gulati U, Mohanty S, Dabas J, Chandra N. “Vanishing bone disease” in maxillofacial region: a review and our experience. J Maxillofac Oral Surg. 2015;14(3):548-557.

        6. Nikolaou VS, Chytas D, Korres D, Efstathopoulos N. Vanishing bone disease (Gorham-Stout syndrome): a review of a rare entity. World J Orthop. 2014;5(5):694-698.

        7. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.

        8. Dominguez R, Washowich TL. Gorham’s disease or vanishing bone disease: plain film, CT, and MRI findings of two cases. Pediatr Radiol. 1994;24(5):316-318.

        9. Kotecha R, Mascarenhas L, Jackson HA, Venkatramani R. Radiological features of Gorham’s disease. Clin Radiol. 2012;67(8):782-788.

        10. Dong A, Bai Y, Wang Y, Zuo C. Bone scan, MRI, and FDG PET/CT findings in composite hemangioendothelioma of the manubrium sterni. Clin Nucl Med. 2014;39(2):e180-e183.

        11. Baulieu F, De Pinieux G, Maruani A, Vaillant L, Lorette G. Serial lymphoscintigraphic findings in a patient with Gorham’s disease with lymphedema. Lymphology. 2014;47(3):118-122.

        12. Manisali M, Ozaksoy D. Gorham disease: correlation of MR findings with histopathologic changes. Eur Radiol. 1998;8(9):1647-1650.

        13. Brodszki N, Länsberg JK, Dictor M, et al. A novel treatment approach for paediatric Gorham-Stout syndrome with chylothorax. Acta Paediatr. 2011;100(11):1448-1453.

        14. Nir V, Guralnik L, Livnat G, et al. Propranolol as a treatment option in Gorham-Stout syndrome: a case report. Pediatr Pulmonol. 2014;49(4):417-419.

        15. Fontanesi J. Radiation therapy in the treatment of Gorham disease. J Pediatr Hematol. 2003;25(10):816-817.

        16. Pfleger A, Schwinger W, Maier A, Tauss J, Popper HH, Zach MS. Gorham-Stout syndrome in a male adolescent—case report and review of the literature. J Pediatr Hematol Oncol. 2006;28(4):231-233.

        17. Patrick JH. Massive osteolysis complicated by chylothorax successfully treated by pleurodesis. J Bone Joint Surg Br. 1976;58(3):347-349.

        18. Hagberg H, Lamberg K, Åström G. α-2b interferon and oral clodronate for Gorham’s disease. Lancet. 1997;350(9094):1822-1823.

        19. Takahashi A, Ogawa C, Kanazawa T, et al. Remission induced by interferon alfa in a patient with massive osteolysis and extension of lymph-hemangiomatosis: a severe case of Gorham-Stout syndrome. J Pediatr Surg. 2005;40(3):E47-E50.

        20. Paley MD, Lloyd CJ, Penfold CN. Total mandibular reconstruction for massive osteolysis of the mandible (Gorham-Stout syndrome). Br J Oral Maxillofac Surg. 2005;43(2):166-168.

        21. Avelar RL, Martins VB, Antunes AA, de Oliveira Neto PJ, de Souza Andrade ES. Use of zoledronic acid in the treatment of Gorham’s disease. Int J Pediatr Otorhinolaryngol. 2010;74(3):319-322.

        22. Holroyd I, Dillon M, Roberts GJ. Gorham’s disease: a case (including dental presentation) of vanishing bone disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89(1):125-129.

        23. Lee S, Finn L, Sze RW, Perkins JA, Sie KC. Gorham Stout syndrome (disappearing bone disease): two additional case reports and a review of the literature. Arch Otolaryngol Head Neck Surg. 2003;129(12):1340-1343.

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        Take-Home Points

        • Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
        • There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
        • Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
        • Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
        • There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

        Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.4,6

        Jackson and colleagues first described idiopathic osteolysis in 1838,1,2 and Gorham and Stout3 introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.7,8

        Clinical Presentation

        Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.7 Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.6 Pelvic bones seem to be involved least often.6,7

        Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.1,2

        Imaging

        Figure 1.
        Plain radiographs show permeative osteolysis involving the subcortical and intramedullary regions and typically affecting regional, contiguous bones, without adjacent sclerosis, and somewhat resembling heterogeneous osteoporosis (Figure 1).8-10

        Computed tomography (CT) better defines the severity and extent of these changes.

        Figure 2.
        Progression can result in osseous tapering, or “pointing” at lytic margins, forming cone-shaped spicules. In progressive cases, there is an “extraosseous” stage characterized by frank cortical destruction and true “disappearance” of bone, with extensive soft-tissue edema8-10 (Figures 2A, 2B).

        Magnetic resonance imaging shows an infiltrative and irregular T2 hyperintense signal throughout regions of bone affected by osteolysis, but this finding is not characteristic. There is heterogeneous enhancement on postcontrast sequences, and, though masslike enhancement is absent, signal abnormalities may extend into adjacent soft tissues.
        Figure 3.
        These changes indicate inflammation and hemorrhage of various degrees interspersed with scant fibrous tissue8-10 (Figures 3A, 3B).

        Bone scintigraphy using technetium-99m is similarly nonspecific, typically revealing radiotracer uptake that is consistent with bony reaction to an underlying osteolytic process (Figure 4) but turning negative with ongoing resorption.
        Figure 4.
        In some cases of Gorham disease, bone scintigraphy did not reveal a significant increase in activity, such as would be expected in a vascular malformation or purely angiomatous neoplasm. Similar findings could be attributed to a variety of pathologies, including primary bone tumor, metastasis, or even osteomyelitis.8-10

        Positron emission tomography/CT typically shows foci of increased metabolic activity in the areas of osteolysis.10

         

         

        Diagnosis

        There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

        Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

        Figure 5.
        Biopsies typically show a progressive osteolysis that is consistently associated with a benign but abnormal vascular proliferation that in many cases has characteristics of lymphatic endothelium. The apparent bony destruction is largely attributed to this process (Figures 5A-5D).11,12

        The differential diagnosis includes infection (osteomyelitis, Brodie abscess), benign tumors (eosinophilic granuloma/Langerhans cell histiocytosis), malignant tumors (Ewing sarcoma and angiosarcoma), inflammatory conditions (eg, apatite- associated destructive arthritis), endocrine disorders (eg, osteolytic hyperparathyroidism), benign non-neoplastic conditions (venous or venolymphatic malformation), and other syndromes that present with osteolysis.1,2 Nevertheless, progressive and unusually substantial bone destruction without evidence of repair is almost pathognomonic for Gorham disease.9

        Treatment

        Table.
        Although no single or combined treatment modality is considered the gold standard (Table),1,2,4,13-23 management of Gorham disease generally centers on radiation therapy for local control of large and painful lesions and on surgical intervention for pathologic progression that would otherwise result in substantial functional limitations.2 Also described for treatment are antiosteoclastic medications (bisphosphonates), which are often used in conjunction with radiation and/or surgical intervention.2,4 The newer literature cites some benefit of using various experimental modalities, including a combination of interferon alfa-2b and low-molecular-weight heparin,13 and even propranolol.14

        Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.1,2,4,20

        Take-Home Points

        • Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
        • There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
        • Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
        • Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
        • There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

        Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.4,6

        Jackson and colleagues first described idiopathic osteolysis in 1838,1,2 and Gorham and Stout3 introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.7,8

        Clinical Presentation

        Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.7 Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.6 Pelvic bones seem to be involved least often.6,7

        Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.1,2

        Imaging

        Figure 1.
        Plain radiographs show permeative osteolysis involving the subcortical and intramedullary regions and typically affecting regional, contiguous bones, without adjacent sclerosis, and somewhat resembling heterogeneous osteoporosis (Figure 1).8-10

        Computed tomography (CT) better defines the severity and extent of these changes.

        Figure 2.
        Progression can result in osseous tapering, or “pointing” at lytic margins, forming cone-shaped spicules. In progressive cases, there is an “extraosseous” stage characterized by frank cortical destruction and true “disappearance” of bone, with extensive soft-tissue edema8-10 (Figures 2A, 2B).

        Magnetic resonance imaging shows an infiltrative and irregular T2 hyperintense signal throughout regions of bone affected by osteolysis, but this finding is not characteristic. There is heterogeneous enhancement on postcontrast sequences, and, though masslike enhancement is absent, signal abnormalities may extend into adjacent soft tissues.
        Figure 3.
        These changes indicate inflammation and hemorrhage of various degrees interspersed with scant fibrous tissue8-10 (Figures 3A, 3B).

        Bone scintigraphy using technetium-99m is similarly nonspecific, typically revealing radiotracer uptake that is consistent with bony reaction to an underlying osteolytic process (Figure 4) but turning negative with ongoing resorption.
        Figure 4.
        In some cases of Gorham disease, bone scintigraphy did not reveal a significant increase in activity, such as would be expected in a vascular malformation or purely angiomatous neoplasm. Similar findings could be attributed to a variety of pathologies, including primary bone tumor, metastasis, or even osteomyelitis.8-10

        Positron emission tomography/CT typically shows foci of increased metabolic activity in the areas of osteolysis.10

         

         

        Diagnosis

        There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

        Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

        Figure 5.
        Biopsies typically show a progressive osteolysis that is consistently associated with a benign but abnormal vascular proliferation that in many cases has characteristics of lymphatic endothelium. The apparent bony destruction is largely attributed to this process (Figures 5A-5D).11,12

        The differential diagnosis includes infection (osteomyelitis, Brodie abscess), benign tumors (eosinophilic granuloma/Langerhans cell histiocytosis), malignant tumors (Ewing sarcoma and angiosarcoma), inflammatory conditions (eg, apatite- associated destructive arthritis), endocrine disorders (eg, osteolytic hyperparathyroidism), benign non-neoplastic conditions (venous or venolymphatic malformation), and other syndromes that present with osteolysis.1,2 Nevertheless, progressive and unusually substantial bone destruction without evidence of repair is almost pathognomonic for Gorham disease.9

        Treatment

        Table.
        Although no single or combined treatment modality is considered the gold standard (Table),1,2,4,13-23 management of Gorham disease generally centers on radiation therapy for local control of large and painful lesions and on surgical intervention for pathologic progression that would otherwise result in substantial functional limitations.2 Also described for treatment are antiosteoclastic medications (bisphosphonates), which are often used in conjunction with radiation and/or surgical intervention.2,4 The newer literature cites some benefit of using various experimental modalities, including a combination of interferon alfa-2b and low-molecular-weight heparin,13 and even propranolol.14

        Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.1,2,4,20

        References

        1. Saify FY, Gosavi SR. Gorham’s disease: a diagnostic challenge. J Oral Maxillofac Pathol. 2014;18(3):411-414.

        2. Patel DV. Gorham’s disease or massive osteolysis. Clin Med Res. 2005;3(2):65-74.

        3. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone); its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.

        4. Heffez L, Doku HC, Carter BL, Feeney JE. Perspectives on massive osteolysis. Report of a case and review of the literature. Oral Surg Oral Med Oral Pathol. 1983;55(4):331-343.

        5. Gulati U, Mohanty S, Dabas J, Chandra N. “Vanishing bone disease” in maxillofacial region: a review and our experience. J Maxillofac Oral Surg. 2015;14(3):548-557.

        6. Nikolaou VS, Chytas D, Korres D, Efstathopoulos N. Vanishing bone disease (Gorham-Stout syndrome): a review of a rare entity. World J Orthop. 2014;5(5):694-698.

        7. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.

        8. Dominguez R, Washowich TL. Gorham’s disease or vanishing bone disease: plain film, CT, and MRI findings of two cases. Pediatr Radiol. 1994;24(5):316-318.

        9. Kotecha R, Mascarenhas L, Jackson HA, Venkatramani R. Radiological features of Gorham’s disease. Clin Radiol. 2012;67(8):782-788.

        10. Dong A, Bai Y, Wang Y, Zuo C. Bone scan, MRI, and FDG PET/CT findings in composite hemangioendothelioma of the manubrium sterni. Clin Nucl Med. 2014;39(2):e180-e183.

        11. Baulieu F, De Pinieux G, Maruani A, Vaillant L, Lorette G. Serial lymphoscintigraphic findings in a patient with Gorham’s disease with lymphedema. Lymphology. 2014;47(3):118-122.

        12. Manisali M, Ozaksoy D. Gorham disease: correlation of MR findings with histopathologic changes. Eur Radiol. 1998;8(9):1647-1650.

        13. Brodszki N, Länsberg JK, Dictor M, et al. A novel treatment approach for paediatric Gorham-Stout syndrome with chylothorax. Acta Paediatr. 2011;100(11):1448-1453.

        14. Nir V, Guralnik L, Livnat G, et al. Propranolol as a treatment option in Gorham-Stout syndrome: a case report. Pediatr Pulmonol. 2014;49(4):417-419.

        15. Fontanesi J. Radiation therapy in the treatment of Gorham disease. J Pediatr Hematol. 2003;25(10):816-817.

        16. Pfleger A, Schwinger W, Maier A, Tauss J, Popper HH, Zach MS. Gorham-Stout syndrome in a male adolescent—case report and review of the literature. J Pediatr Hematol Oncol. 2006;28(4):231-233.

        17. Patrick JH. Massive osteolysis complicated by chylothorax successfully treated by pleurodesis. J Bone Joint Surg Br. 1976;58(3):347-349.

        18. Hagberg H, Lamberg K, Åström G. α-2b interferon and oral clodronate for Gorham’s disease. Lancet. 1997;350(9094):1822-1823.

        19. Takahashi A, Ogawa C, Kanazawa T, et al. Remission induced by interferon alfa in a patient with massive osteolysis and extension of lymph-hemangiomatosis: a severe case of Gorham-Stout syndrome. J Pediatr Surg. 2005;40(3):E47-E50.

        20. Paley MD, Lloyd CJ, Penfold CN. Total mandibular reconstruction for massive osteolysis of the mandible (Gorham-Stout syndrome). Br J Oral Maxillofac Surg. 2005;43(2):166-168.

        21. Avelar RL, Martins VB, Antunes AA, de Oliveira Neto PJ, de Souza Andrade ES. Use of zoledronic acid in the treatment of Gorham’s disease. Int J Pediatr Otorhinolaryngol. 2010;74(3):319-322.

        22. Holroyd I, Dillon M, Roberts GJ. Gorham’s disease: a case (including dental presentation) of vanishing bone disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89(1):125-129.

        23. Lee S, Finn L, Sze RW, Perkins JA, Sie KC. Gorham Stout syndrome (disappearing bone disease): two additional case reports and a review of the literature. Arch Otolaryngol Head Neck Surg. 2003;129(12):1340-1343.

        References

        1. Saify FY, Gosavi SR. Gorham’s disease: a diagnostic challenge. J Oral Maxillofac Pathol. 2014;18(3):411-414.

        2. Patel DV. Gorham’s disease or massive osteolysis. Clin Med Res. 2005;3(2):65-74.

        3. Gorham LW, Stout AP. Massive osteolysis (acute spontaneous absorption of bone, phantom bone, disappearing bone); its relation to hemangiomatosis. J Bone Joint Surg Am. 1955;37(5):985-1004.

        4. Heffez L, Doku HC, Carter BL, Feeney JE. Perspectives on massive osteolysis. Report of a case and review of the literature. Oral Surg Oral Med Oral Pathol. 1983;55(4):331-343.

        5. Gulati U, Mohanty S, Dabas J, Chandra N. “Vanishing bone disease” in maxillofacial region: a review and our experience. J Maxillofac Oral Surg. 2015;14(3):548-557.

        6. Nikolaou VS, Chytas D, Korres D, Efstathopoulos N. Vanishing bone disease (Gorham-Stout syndrome): a review of a rare entity. World J Orthop. 2014;5(5):694-698.

        7. Möller G, Priemel M, Amling M, Werner M, Kuhlmey AS, Delling G. The Gorham-Stout syndrome (Gorham’s massive osteolysis). A report of six cases with histopathological findings. J Bone Joint Surg Br. 1999;81(3):501-506.

        8. Dominguez R, Washowich TL. Gorham’s disease or vanishing bone disease: plain film, CT, and MRI findings of two cases. Pediatr Radiol. 1994;24(5):316-318.

        9. Kotecha R, Mascarenhas L, Jackson HA, Venkatramani R. Radiological features of Gorham’s disease. Clin Radiol. 2012;67(8):782-788.

        10. Dong A, Bai Y, Wang Y, Zuo C. Bone scan, MRI, and FDG PET/CT findings in composite hemangioendothelioma of the manubrium sterni. Clin Nucl Med. 2014;39(2):e180-e183.

        11. Baulieu F, De Pinieux G, Maruani A, Vaillant L, Lorette G. Serial lymphoscintigraphic findings in a patient with Gorham’s disease with lymphedema. Lymphology. 2014;47(3):118-122.

        12. Manisali M, Ozaksoy D. Gorham disease: correlation of MR findings with histopathologic changes. Eur Radiol. 1998;8(9):1647-1650.

        13. Brodszki N, Länsberg JK, Dictor M, et al. A novel treatment approach for paediatric Gorham-Stout syndrome with chylothorax. Acta Paediatr. 2011;100(11):1448-1453.

        14. Nir V, Guralnik L, Livnat G, et al. Propranolol as a treatment option in Gorham-Stout syndrome: a case report. Pediatr Pulmonol. 2014;49(4):417-419.

        15. Fontanesi J. Radiation therapy in the treatment of Gorham disease. J Pediatr Hematol. 2003;25(10):816-817.

        16. Pfleger A, Schwinger W, Maier A, Tauss J, Popper HH, Zach MS. Gorham-Stout syndrome in a male adolescent—case report and review of the literature. J Pediatr Hematol Oncol. 2006;28(4):231-233.

        17. Patrick JH. Massive osteolysis complicated by chylothorax successfully treated by pleurodesis. J Bone Joint Surg Br. 1976;58(3):347-349.

        18. Hagberg H, Lamberg K, Åström G. α-2b interferon and oral clodronate for Gorham’s disease. Lancet. 1997;350(9094):1822-1823.

        19. Takahashi A, Ogawa C, Kanazawa T, et al. Remission induced by interferon alfa in a patient with massive osteolysis and extension of lymph-hemangiomatosis: a severe case of Gorham-Stout syndrome. J Pediatr Surg. 2005;40(3):E47-E50.

        20. Paley MD, Lloyd CJ, Penfold CN. Total mandibular reconstruction for massive osteolysis of the mandible (Gorham-Stout syndrome). Br J Oral Maxillofac Surg. 2005;43(2):166-168.

        21. Avelar RL, Martins VB, Antunes AA, de Oliveira Neto PJ, de Souza Andrade ES. Use of zoledronic acid in the treatment of Gorham’s disease. Int J Pediatr Otorhinolaryngol. 2010;74(3):319-322.

        22. Holroyd I, Dillon M, Roberts GJ. Gorham’s disease: a case (including dental presentation) of vanishing bone disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89(1):125-129.

        23. Lee S, Finn L, Sze RW, Perkins JA, Sie KC. Gorham Stout syndrome (disappearing bone disease): two additional case reports and a review of the literature. Arch Otolaryngol Head Neck Surg. 2003;129(12):1340-1343.

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        Intraoperative Use of External Fixator Attachments for Reduction of Lower Extremity Fractures and Dislocations

        Article Type
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        Thu, 09/19/2019 - 13:19

        Take-Home Points

        • External fixator attachments are fast and easy to assemble with existing external fixator equipment.
        • They allow for multi-directional force application and use of extrinsic power grip.
        • They limit radiation exposure and provides unobstructred line of sight to zone of injury.
        • The attachments can then be removed once reduction is achieved.

        External fixation has a long history both for initial open or closed management of fractures and for definitive management.1 After the introduction of internal fixation constructs using nails or plates, external fixation largely transitioned from a means of definitive management to a temporizing measure taken before definitive internal fixation.

        The Delta Frame external fixator (DePuy Synthes), which is used for significantly swollen ankle and pilon fractures, features anteromedially placed tibial shaft pins and a transcalcaneal pin. For distal tibia fractures that are not amenable to urgent internal fixation because of the degree of swelling or soft-tissue injury, it provides ligamentotaxis and traction for reduction of fracture fragments and stabilization.2

        Numerous other external fixator configurations, such as knee-spanning or tibia-spanning external fixators, can be used for similar purposes. These stabilization methods are all minimally invasive and thus cause little trauma to the zone of injury3 and give soft-tissue injuries time to heal before definitive internal fixation.

        Several different external fixator configurations can be used for a variety of fracture patterns and locations, but we propose using the external fixator as a starting point and adding proximal and distal attachments. These attachments have the potential to create more reduction force, and they provide more control of proximal and distal fracture fragments, continue to be minimally invasive, offer extrinsic grip power, are easily assembled and disassembled for intraoperative fracture reduction, and reduce the surgeon’s radiation exposure.

        Materials and Methods

        Our institution employs an external fixator system that is often used for high-energy lower extremity pathology. This system facilitates assembly of a Sweet T–Cherry II configuration. For periarticular ankle injuries, a Delta Frame external fixator is applied as described in the AO (Arbeitsgemeinschaft für Osteosynthesefragen) surgical reference. Two diaphyseal Schanz pins are inserted into the tibia anterior to posterior based on the pin-placement guide and confirmed with fluoroscopy. These pins must be positioned close enough to the fracture site to provide stability, but not so close as to enter the zone of injury. A Denham pin is placed in the calcaneus medial to lateral. Care is taken to avoid the posterior tibial neurovascular bundle. Then, with use of pin-carbon fiber rod connectors, rods are attached so the Schanz pins connect with the Denham pin. In Sweet T–Cherry II assembly, a different rod configuration is used; rods are attached to the proximal-most Schanz pin and the Denham pin. In Sweet T assembly, a rod-rod connector is used to attach 2 carbon fiber rods to each other.

        Figure 1.
        These rods are orthogonally connected in a T shape. A pin-rod connector is then used to attach the assembled apparatus to the proximal-most Schanz pin. Figure 1 shows the assembled Sweet T.

        Next, in Cherry II assembly, 2 carbon fiber rods are attached to and locked to the Denham pin, one medial and the other lateral in an orientation orthogonal to the Denham pin extending distally. The Cherry II apparatus is completed with a third rod and is placed parallel to the Denham pin and orthogonal to the first 2 rods.

        Figure 2.
        Figure 3.
        Figure 2 shows the assembled Cherry II, and Figure 3 shows the fully assembled Sweet T–Cherry II external fixator configuration. After the fully assembled external fixator is fitted with the Sweet T and Cherry II attachments, the attachments are used to manually reduce the fracture, the reduction is confirmed with fluoroscopy, and the external fixator connectors are locked to maintain the reduction.

        For knee-spanning external fixators, 2 Sweet T assemblies can be attached to the 2 Schanz pins. Furthermore, if 2 transverse pins are used for tibial external fixation, 2 Cherry II attachments can be used for multidirectional traction. An added benefit is extrinsic grip power, vs the intrinsic grip power provided with use of only the Schanz and Denham pins.

         

         

        Results

        The fully assembled apparatus provides a firm, well-fixed configuration for applying traction in multiple directions. Axial traction can be applied, as can anterior or posterior translation forces, which may be helpful in fracture reduction and joint dislocation. For difficult-to-reduce fractures or dislocations, the surgeon can apply multidirectional traction distally while the assistant applies countertraction proximally. Fracture reduction is confirmed with fluoroscopy, and the external fixator is locked in position to maintain reduction. After reduction is confirmed, Sweet T and Cherry II are easily removed. The end result is a reduced fracture or dislocation that has the typical appearance of the temporizing external fixator.

        Discussion

        The Sweet T–Cherry II configuration is assembled quickly and can aid the orthopedic surgeon and assistant in managing trauma cases involving difficult-to-reduce fractures. The principle is the same as in any other traction-countertraction model, though the materials required for assembly are already available to the surgeon, and additional equipment is not required. Furthermore, the large size of the attachments has the potential to offer more points of manipulation by the surgeon and assistant, when compared with Schanz and Denham pins alone. The configuration allows full extrinsic grip power as well (Figure 4), whereas only intrinsic hand power is allowed with traction applied through Schanz and Denham pins alone.

        Figure 4.
        In addition, one operator applying proximally directed traction and the other applying distally directed traction may generate more force than that obtained with the standard external fixator configuration and may reduce fractures that would otherwise be irreducible by closed means. 

        These attachments also have the potential to reduce surgeon and assistant radiation exposure. By positioning Sweet T and Cherry II proximally and distally, with the fluoroscopy machine over the zone of injury, the operators of the attachments increase their distance from the source of radiation. This strategic positioning decreases radiation exposure and reduces direct and scatter energy from the fluoroscopy machine and the patient.4 In addition, with the operators of the attachments farther from the zone of injury, the surgeon has a clear and direct view of the procedure, which may otherwise be obstructed with use of tensioning devices or conventional external fixator configurations. Sweet T and Cherry II attachments theoretically could be used for any configuration that uses proximal and distal fixation points. There is also the added benefit that these attachments are not restricted to applying traction axially but can also translate fracture fragments anteriorly, posteriorly, medially, or laterally, which has the potential to aid in reducing fractures and dislocations with varying degrees of translation, not only shortening. Although these attachments have mechanical counterparts, such as femoral distractors and other tensioning devices, the counterparts may take longer to assemble, apply, and activate. Sweet T and Cherry II attachments are included in the external fixator equipment and may generate more force and control while achieving reduction and stabilization similar to those achieved with other traction or tensioning devices. In addition, other tensioning devices may be cumbersome and unwieldy relative to Sweet T and Cherry II. For these attachments, research is needed on forces generated, time of assembly, and ease of use.

        Conclusion

        The Sweet T and Cherry II external fixator attachments have the potential to aid in managing difficult-to-reduce complex fractures and dislocations. These attachments are quickly assembled and may generate more force than does reduction with Schanz and Denham pins alone. The shape of these attachments may also provide a more comfortable and easier-to-manipulate base for application of traction in multiple directions. An added benefit is extrinsic grip power. Use of these attachments also has the potential to reduce operator radiation exposure and may provide an unobstructed view of the operative field, as the attachment operators are farther from the zone of injury. In addition, the materials used to assemble these attachments are included in almost all external fixation sets. More research comparing standard external fixator configurations with external fixator configurations using Sweet T and Cherry II attachments is needed.

        References

        1. Tejwani N, Polonet D, Wolinsky PR. External fixation of tibial fractures. J Am Acad Orthop Surg. 2015;23(2):126-130.

        2. Patterson MJ, Cole JD. Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma. 1999;13(2):85-91.

        3. Bible JE, Mir HR. External fixation: principles and applications. J Am Acad Orthop Surg. 2015;23(11):683-690.

        4. Giordano BD, Ryder S, Baumhauer JF, DiGiovanni BF. Exposure to direct and scatter radiation with use of mini-c-arm fluoroscopy. J Bone Joint Surg Am. 2007;89(5):948-952.

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        Take-Home Points

        • External fixator attachments are fast and easy to assemble with existing external fixator equipment.
        • They allow for multi-directional force application and use of extrinsic power grip.
        • They limit radiation exposure and provides unobstructred line of sight to zone of injury.
        • The attachments can then be removed once reduction is achieved.

        External fixation has a long history both for initial open or closed management of fractures and for definitive management.1 After the introduction of internal fixation constructs using nails or plates, external fixation largely transitioned from a means of definitive management to a temporizing measure taken before definitive internal fixation.

        The Delta Frame external fixator (DePuy Synthes), which is used for significantly swollen ankle and pilon fractures, features anteromedially placed tibial shaft pins and a transcalcaneal pin. For distal tibia fractures that are not amenable to urgent internal fixation because of the degree of swelling or soft-tissue injury, it provides ligamentotaxis and traction for reduction of fracture fragments and stabilization.2

        Numerous other external fixator configurations, such as knee-spanning or tibia-spanning external fixators, can be used for similar purposes. These stabilization methods are all minimally invasive and thus cause little trauma to the zone of injury3 and give soft-tissue injuries time to heal before definitive internal fixation.

        Several different external fixator configurations can be used for a variety of fracture patterns and locations, but we propose using the external fixator as a starting point and adding proximal and distal attachments. These attachments have the potential to create more reduction force, and they provide more control of proximal and distal fracture fragments, continue to be minimally invasive, offer extrinsic grip power, are easily assembled and disassembled for intraoperative fracture reduction, and reduce the surgeon’s radiation exposure.

        Materials and Methods

        Our institution employs an external fixator system that is often used for high-energy lower extremity pathology. This system facilitates assembly of a Sweet T–Cherry II configuration. For periarticular ankle injuries, a Delta Frame external fixator is applied as described in the AO (Arbeitsgemeinschaft für Osteosynthesefragen) surgical reference. Two diaphyseal Schanz pins are inserted into the tibia anterior to posterior based on the pin-placement guide and confirmed with fluoroscopy. These pins must be positioned close enough to the fracture site to provide stability, but not so close as to enter the zone of injury. A Denham pin is placed in the calcaneus medial to lateral. Care is taken to avoid the posterior tibial neurovascular bundle. Then, with use of pin-carbon fiber rod connectors, rods are attached so the Schanz pins connect with the Denham pin. In Sweet T–Cherry II assembly, a different rod configuration is used; rods are attached to the proximal-most Schanz pin and the Denham pin. In Sweet T assembly, a rod-rod connector is used to attach 2 carbon fiber rods to each other.

        Figure 1.
        These rods are orthogonally connected in a T shape. A pin-rod connector is then used to attach the assembled apparatus to the proximal-most Schanz pin. Figure 1 shows the assembled Sweet T.

        Next, in Cherry II assembly, 2 carbon fiber rods are attached to and locked to the Denham pin, one medial and the other lateral in an orientation orthogonal to the Denham pin extending distally. The Cherry II apparatus is completed with a third rod and is placed parallel to the Denham pin and orthogonal to the first 2 rods.

        Figure 2.
        Figure 3.
        Figure 2 shows the assembled Cherry II, and Figure 3 shows the fully assembled Sweet T–Cherry II external fixator configuration. After the fully assembled external fixator is fitted with the Sweet T and Cherry II attachments, the attachments are used to manually reduce the fracture, the reduction is confirmed with fluoroscopy, and the external fixator connectors are locked to maintain the reduction.

        For knee-spanning external fixators, 2 Sweet T assemblies can be attached to the 2 Schanz pins. Furthermore, if 2 transverse pins are used for tibial external fixation, 2 Cherry II attachments can be used for multidirectional traction. An added benefit is extrinsic grip power, vs the intrinsic grip power provided with use of only the Schanz and Denham pins.

         

         

        Results

        The fully assembled apparatus provides a firm, well-fixed configuration for applying traction in multiple directions. Axial traction can be applied, as can anterior or posterior translation forces, which may be helpful in fracture reduction and joint dislocation. For difficult-to-reduce fractures or dislocations, the surgeon can apply multidirectional traction distally while the assistant applies countertraction proximally. Fracture reduction is confirmed with fluoroscopy, and the external fixator is locked in position to maintain reduction. After reduction is confirmed, Sweet T and Cherry II are easily removed. The end result is a reduced fracture or dislocation that has the typical appearance of the temporizing external fixator.

        Discussion

        The Sweet T–Cherry II configuration is assembled quickly and can aid the orthopedic surgeon and assistant in managing trauma cases involving difficult-to-reduce fractures. The principle is the same as in any other traction-countertraction model, though the materials required for assembly are already available to the surgeon, and additional equipment is not required. Furthermore, the large size of the attachments has the potential to offer more points of manipulation by the surgeon and assistant, when compared with Schanz and Denham pins alone. The configuration allows full extrinsic grip power as well (Figure 4), whereas only intrinsic hand power is allowed with traction applied through Schanz and Denham pins alone.

        Figure 4.
        In addition, one operator applying proximally directed traction and the other applying distally directed traction may generate more force than that obtained with the standard external fixator configuration and may reduce fractures that would otherwise be irreducible by closed means. 

        These attachments also have the potential to reduce surgeon and assistant radiation exposure. By positioning Sweet T and Cherry II proximally and distally, with the fluoroscopy machine over the zone of injury, the operators of the attachments increase their distance from the source of radiation. This strategic positioning decreases radiation exposure and reduces direct and scatter energy from the fluoroscopy machine and the patient.4 In addition, with the operators of the attachments farther from the zone of injury, the surgeon has a clear and direct view of the procedure, which may otherwise be obstructed with use of tensioning devices or conventional external fixator configurations. Sweet T and Cherry II attachments theoretically could be used for any configuration that uses proximal and distal fixation points. There is also the added benefit that these attachments are not restricted to applying traction axially but can also translate fracture fragments anteriorly, posteriorly, medially, or laterally, which has the potential to aid in reducing fractures and dislocations with varying degrees of translation, not only shortening. Although these attachments have mechanical counterparts, such as femoral distractors and other tensioning devices, the counterparts may take longer to assemble, apply, and activate. Sweet T and Cherry II attachments are included in the external fixator equipment and may generate more force and control while achieving reduction and stabilization similar to those achieved with other traction or tensioning devices. In addition, other tensioning devices may be cumbersome and unwieldy relative to Sweet T and Cherry II. For these attachments, research is needed on forces generated, time of assembly, and ease of use.

        Conclusion

        The Sweet T and Cherry II external fixator attachments have the potential to aid in managing difficult-to-reduce complex fractures and dislocations. These attachments are quickly assembled and may generate more force than does reduction with Schanz and Denham pins alone. The shape of these attachments may also provide a more comfortable and easier-to-manipulate base for application of traction in multiple directions. An added benefit is extrinsic grip power. Use of these attachments also has the potential to reduce operator radiation exposure and may provide an unobstructed view of the operative field, as the attachment operators are farther from the zone of injury. In addition, the materials used to assemble these attachments are included in almost all external fixation sets. More research comparing standard external fixator configurations with external fixator configurations using Sweet T and Cherry II attachments is needed.

        Take-Home Points

        • External fixator attachments are fast and easy to assemble with existing external fixator equipment.
        • They allow for multi-directional force application and use of extrinsic power grip.
        • They limit radiation exposure and provides unobstructred line of sight to zone of injury.
        • The attachments can then be removed once reduction is achieved.

        External fixation has a long history both for initial open or closed management of fractures and for definitive management.1 After the introduction of internal fixation constructs using nails or plates, external fixation largely transitioned from a means of definitive management to a temporizing measure taken before definitive internal fixation.

        The Delta Frame external fixator (DePuy Synthes), which is used for significantly swollen ankle and pilon fractures, features anteromedially placed tibial shaft pins and a transcalcaneal pin. For distal tibia fractures that are not amenable to urgent internal fixation because of the degree of swelling or soft-tissue injury, it provides ligamentotaxis and traction for reduction of fracture fragments and stabilization.2

        Numerous other external fixator configurations, such as knee-spanning or tibia-spanning external fixators, can be used for similar purposes. These stabilization methods are all minimally invasive and thus cause little trauma to the zone of injury3 and give soft-tissue injuries time to heal before definitive internal fixation.

        Several different external fixator configurations can be used for a variety of fracture patterns and locations, but we propose using the external fixator as a starting point and adding proximal and distal attachments. These attachments have the potential to create more reduction force, and they provide more control of proximal and distal fracture fragments, continue to be minimally invasive, offer extrinsic grip power, are easily assembled and disassembled for intraoperative fracture reduction, and reduce the surgeon’s radiation exposure.

        Materials and Methods

        Our institution employs an external fixator system that is often used for high-energy lower extremity pathology. This system facilitates assembly of a Sweet T–Cherry II configuration. For periarticular ankle injuries, a Delta Frame external fixator is applied as described in the AO (Arbeitsgemeinschaft für Osteosynthesefragen) surgical reference. Two diaphyseal Schanz pins are inserted into the tibia anterior to posterior based on the pin-placement guide and confirmed with fluoroscopy. These pins must be positioned close enough to the fracture site to provide stability, but not so close as to enter the zone of injury. A Denham pin is placed in the calcaneus medial to lateral. Care is taken to avoid the posterior tibial neurovascular bundle. Then, with use of pin-carbon fiber rod connectors, rods are attached so the Schanz pins connect with the Denham pin. In Sweet T–Cherry II assembly, a different rod configuration is used; rods are attached to the proximal-most Schanz pin and the Denham pin. In Sweet T assembly, a rod-rod connector is used to attach 2 carbon fiber rods to each other.

        Figure 1.
        These rods are orthogonally connected in a T shape. A pin-rod connector is then used to attach the assembled apparatus to the proximal-most Schanz pin. Figure 1 shows the assembled Sweet T.

        Next, in Cherry II assembly, 2 carbon fiber rods are attached to and locked to the Denham pin, one medial and the other lateral in an orientation orthogonal to the Denham pin extending distally. The Cherry II apparatus is completed with a third rod and is placed parallel to the Denham pin and orthogonal to the first 2 rods.

        Figure 2.
        Figure 3.
        Figure 2 shows the assembled Cherry II, and Figure 3 shows the fully assembled Sweet T–Cherry II external fixator configuration. After the fully assembled external fixator is fitted with the Sweet T and Cherry II attachments, the attachments are used to manually reduce the fracture, the reduction is confirmed with fluoroscopy, and the external fixator connectors are locked to maintain the reduction.

        For knee-spanning external fixators, 2 Sweet T assemblies can be attached to the 2 Schanz pins. Furthermore, if 2 transverse pins are used for tibial external fixation, 2 Cherry II attachments can be used for multidirectional traction. An added benefit is extrinsic grip power, vs the intrinsic grip power provided with use of only the Schanz and Denham pins.

         

         

        Results

        The fully assembled apparatus provides a firm, well-fixed configuration for applying traction in multiple directions. Axial traction can be applied, as can anterior or posterior translation forces, which may be helpful in fracture reduction and joint dislocation. For difficult-to-reduce fractures or dislocations, the surgeon can apply multidirectional traction distally while the assistant applies countertraction proximally. Fracture reduction is confirmed with fluoroscopy, and the external fixator is locked in position to maintain reduction. After reduction is confirmed, Sweet T and Cherry II are easily removed. The end result is a reduced fracture or dislocation that has the typical appearance of the temporizing external fixator.

        Discussion

        The Sweet T–Cherry II configuration is assembled quickly and can aid the orthopedic surgeon and assistant in managing trauma cases involving difficult-to-reduce fractures. The principle is the same as in any other traction-countertraction model, though the materials required for assembly are already available to the surgeon, and additional equipment is not required. Furthermore, the large size of the attachments has the potential to offer more points of manipulation by the surgeon and assistant, when compared with Schanz and Denham pins alone. The configuration allows full extrinsic grip power as well (Figure 4), whereas only intrinsic hand power is allowed with traction applied through Schanz and Denham pins alone.

        Figure 4.
        In addition, one operator applying proximally directed traction and the other applying distally directed traction may generate more force than that obtained with the standard external fixator configuration and may reduce fractures that would otherwise be irreducible by closed means. 

        These attachments also have the potential to reduce surgeon and assistant radiation exposure. By positioning Sweet T and Cherry II proximally and distally, with the fluoroscopy machine over the zone of injury, the operators of the attachments increase their distance from the source of radiation. This strategic positioning decreases radiation exposure and reduces direct and scatter energy from the fluoroscopy machine and the patient.4 In addition, with the operators of the attachments farther from the zone of injury, the surgeon has a clear and direct view of the procedure, which may otherwise be obstructed with use of tensioning devices or conventional external fixator configurations. Sweet T and Cherry II attachments theoretically could be used for any configuration that uses proximal and distal fixation points. There is also the added benefit that these attachments are not restricted to applying traction axially but can also translate fracture fragments anteriorly, posteriorly, medially, or laterally, which has the potential to aid in reducing fractures and dislocations with varying degrees of translation, not only shortening. Although these attachments have mechanical counterparts, such as femoral distractors and other tensioning devices, the counterparts may take longer to assemble, apply, and activate. Sweet T and Cherry II attachments are included in the external fixator equipment and may generate more force and control while achieving reduction and stabilization similar to those achieved with other traction or tensioning devices. In addition, other tensioning devices may be cumbersome and unwieldy relative to Sweet T and Cherry II. For these attachments, research is needed on forces generated, time of assembly, and ease of use.

        Conclusion

        The Sweet T and Cherry II external fixator attachments have the potential to aid in managing difficult-to-reduce complex fractures and dislocations. These attachments are quickly assembled and may generate more force than does reduction with Schanz and Denham pins alone. The shape of these attachments may also provide a more comfortable and easier-to-manipulate base for application of traction in multiple directions. An added benefit is extrinsic grip power. Use of these attachments also has the potential to reduce operator radiation exposure and may provide an unobstructed view of the operative field, as the attachment operators are farther from the zone of injury. In addition, the materials used to assemble these attachments are included in almost all external fixation sets. More research comparing standard external fixator configurations with external fixator configurations using Sweet T and Cherry II attachments is needed.

        References

        1. Tejwani N, Polonet D, Wolinsky PR. External fixation of tibial fractures. J Am Acad Orthop Surg. 2015;23(2):126-130.

        2. Patterson MJ, Cole JD. Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma. 1999;13(2):85-91.

        3. Bible JE, Mir HR. External fixation: principles and applications. J Am Acad Orthop Surg. 2015;23(11):683-690.

        4. Giordano BD, Ryder S, Baumhauer JF, DiGiovanni BF. Exposure to direct and scatter radiation with use of mini-c-arm fluoroscopy. J Bone Joint Surg Am. 2007;89(5):948-952.

        References

        1. Tejwani N, Polonet D, Wolinsky PR. External fixation of tibial fractures. J Am Acad Orthop Surg. 2015;23(2):126-130.

        2. Patterson MJ, Cole JD. Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma. 1999;13(2):85-91.

        3. Bible JE, Mir HR. External fixation: principles and applications. J Am Acad Orthop Surg. 2015;23(11):683-690.

        4. Giordano BD, Ryder S, Baumhauer JF, DiGiovanni BF. Exposure to direct and scatter radiation with use of mini-c-arm fluoroscopy. J Bone Joint Surg Am. 2007;89(5):948-952.

        Issue
        The American Journal of Orthopedics - 46(6)
        Issue
        The American Journal of Orthopedics - 46(6)
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        E454-E457
        Page Number
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