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Primary Total Knee Arthroplasty for Distal Femur Fractures: A Systematic Review of Indications, Implants, Techniques, and Results

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Primary Total Knee Arthroplasty for Distal Femur Fractures: A Systematic Review of Indications, Implants, Techniques, and Results

Take-Home Points

  • Arthroplasty is a rarely utilized and, therefore, a rarely reported treatment for distal femur fractures.
  • Arthroplasty carries certain advantages over fixation, including earlier weight-bearing, a benefit for elderly individuals.
  • Arthroplasty is more often described in situations of comminution, often necessitating constrained prostheses.
  • It is not unreasonable to utilize arthroplasty in extra-articular fractures in poor-quality bone, which can take the form of unconstrained prosthesis and supplemental fixation.
  • The true complication rate is unclear, given that the few papers reporting high complication rates were in sicker populations.

Distal femur fractures (DFFs) in the elderly historically were difficult to treat because of osteoporotic bone, comminution, and intra-articular involvement. DFFs in minimally ambulatory patients were once treated nonoperatively, with traction or immobilization,1,2 but surgery is now considered for displaced and unstable fractures, even in myelopathic and nonambulatory patients, to provide pain relief, ease mobility, and decrease the risks associated with prolonged bed rest.1 Options are constantly evolving, but poor knee function, malunion, nonunion, prolonged immobilization, implant failure, and high morbidity and mortality rates have been reported in several studies regardless of fixation method.

Arthritis after DFF has been reported at rates of 36% to 50% by long-term follow-up.3-5 However, total knee arthroplasty (TKA) for posttraumatic arthritis is more complex because of scarring, arthrofibrosis, malunion, nonunion, and the frequent need for hardware removal. These cases have a higher incidence of infection, aseptic loosening, stiffness,6 and skin necrosis.Primary TKA is a rarely used treatment for acute DFF. Several authors have recommended primary TKA for patients with intra-articular DFFs and preexisting osteoarthritis or rheumatoid arthritis, severe comminution, or poor bone stock.7-22 Compared with open reduction and internal fixation (ORIF), primary TKA may allow for earlier mobility and weight-bearing and thereby reduce the rates of complications (eg, respiratory failure, deep vein thrombosis, pulmonary embolism) associated with prolonged immobilization.23As the literature on TKA for acute DFF is scant, and to our knowledge there are no clear indications or guidelines, we performed a systematic review to determine whether TKA has been successful in relieving pain and restoring knee function. In this article, we discuss the indications, implant options, technical considerations, complications, and results (eg, range of motion [ROM], ambulatory status) associated with these procedures.

Methods

On December 1, 2015, we searched the major databases Medline, EMBASE (Excerpta Medica dataBASE), and the Cochrane Library for articles published since 1950. In our searches, we used the conjoint term knee arthroplasty with femur fracture, and knee replacement with femur fracture. Specifically, we queried: ((“knee replacement” OR “knee arthroplasty”) AND (intercondylar OR supracondylar OR femoral OR femur) AND fracture) NOT arthrodesis NOT periprosthetic NOT “posttraumatic arthritis” NOT osteotomy. We also hand-searched the current website of JBJS [Journal of Bone and Joint Surgery] Case Connector, a major case-report repository that was launched in 2011 but is not currently indexed by Medline.

All citations were imported to RefWorks for management and for removal of duplicates. Each article underwent screening and review by Dr. Chen and Dr. Li. Articles were included if titles were relevant to arthroplasty as treatment for acute (within 1 month) DFF. Articles and cases were excluded if they were reviews, published in languages other than English, animal studies, studies regarding nonacute (>3 months or nonunion) DFFs or periprosthetic fractures, or studies that considered only treatments other than TKA (ie, plate osteosynthesis).

Full-text publications were obtained and independently reviewed by Dr. Chen and Dr. Li for relevance and satisfaction of inclusion criteria. Disagreements were resolved by discussion. Given the rarity of publications on the treatment, all study designs from level I to level IV were included.

The same 2 reviewers extracted the data into prearranged summary tables. Data included study size, patient demographics, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) fracture type either reported or assessed by description and imaging (33A, extra-articular; 33B, partial articular with 1 intact condyle; 33C, complete articular with both condyles involved), baseline comorbidity, implant used and fracture treatment (if separate from arthroplasty), postoperative regimen, respective outcomes, and complication rates.

Results

We identified 728 articles: 389 through Medline, 294 through EMBASE, and 45 through the Cochrane Library (Figure 1).

Figure 1.
After duplicates were removed, 476 articles remained. After titles and abstracts were reviewed, 22 articles met the screening criteria. Five series included patients with TKA-treated acute DFF but did not report their specific outcomes (these were described separately).
Table 1.

The current evidence regarding primary TKA for acute DFF is primarily level IV (Table 1). Only 1 level III study16 compared TKA with ORIF. Three case series11,19,24 met our inclusion criteria (Table 1, Table 2). In addition, 5 case series involved patients who met our criteria, but these studies did not separately report results for DFFs and proximal tibia fractures,9,20-22 or separately for acute fractures and nonunions or ORIF failures.8

Table 2.
These studies were considered level IV and were tabulated separately (Table 3). Specific patient characteristics and management strategies varied significantly between studies, though many studies augmented 33A fractures with internal fixation, whereas 33C fractures more often underwent resection and placement of highly constrained implants. Of 117 acute DFFs reviewed, 20% were 33A fractures, 7% were 33B fractures, and 73% were 33C fractures (Table 1). Of the studies that specified, there were 8 cases of rheumatoid arthritis and 18 cases of osteoarthritis (Table 2).
Table 3.


Modular, hinged, and tumor-type arthroplasty designs accounted for 83% of the treatments included in this review. Trade names are listed in Table 4. Authors who used these implants took a more aggressive approach, often resecting the entire femoral epiphyseal-metaphyseal area, menisci, and collateral ligaments.9,13,15,16,18 The majority of patients who underwent resection had 33C fractures (Tables 1, 3).
Table 4.
Figures 2A-2D show an aggressive resection example.Authors who used less constrained arthroplasty designs focused on bone preservation, augmentation with graft, and internal fixation.7,20 In and colleagues25 thought that if the cruciate and collateral ligaments are found to be intact, then resecting these ligaments and performing the deep cuts necessary for linked prostheses are too aggressive. Their internal fixation methods included use of cannulated screws, Dall-Miles cabling (Stryker), and plate osteosynthesis. Choi and colleagues19 took a similar approach but also used stem extensions in 6 of 8 fractures assessed to be unstable (Figures 3A-3H).
Figure 2.
Yoshino and colleagues7 used posterior-stabilized implants with femoral stem extensions (Figures 4A-4C).
Figure 3.
Intraoperative use of an external fixator to align and stabilize a comminuted fracture before insertion of an intramedullary guide and during femoral cutting has also been described.19 All 33B and many 33A fractures were treated in this fashion.

The majority of authors who treated fractures with resection and modular implants allowed their patients full weight-bearing soon after surgery (Table 1),11,12,15-18,24 whereas authors who treated their patients partly with fracture fixation often had to delay weight-bearing (Table 1).
Figure 4.
Overall, results were encouraging, with most studies finding between 90° and 135° of flexion to near full extension after each type of treatment. At follow-up, most survivors achieved full weight-bearing and were capable of walking up and down stairs.

Cement use was universally described in the literature. Some authors avoided placing cement in the fracture site (to reduce the risk of nonunion),7,19 whereas others used bone cement to fill metaphyseal defects that remained after fracture resection and implantation.11,24Complication rates were modest, and there were no reports specifically on implant loosening or fracture nonunion.7,10,12-19 The majority of complications were recorded in 2 studies that used megaprostheses in sicker populations: Bell and colleagues11 noted debilitating illnesses in all their patients, and Appleton and colleagues24 included 9 nonambulatory patients and 36 patients who required 2 assistants to ambulate. All deaths were attributed to medical comorbidities and disseminated malignancy. Contrarily, studies by Pearse and colleagues16 and Choi and colleagues19 included previously ambulatory patients and reported no deaths or complications (Table 2). Likewise, in studies that combined results of DFFs and proximal tibia fractures, death and complication rates varied from 7% to 31% (Table 3).

 

 

Discussion

DFFs in the elderly historically were difficult to treat. Reported outcomes are largely favorable, but, even with newer plate designs, catastrophic failures still occur in the absence of bony union.26,27 After ORIF, patients’ weight-bearing is often restricted for 12 weeks or longer28—a protocol that is undesirable in elderly patients, especially given that the rate of mortality 1 year after these fractures has been found to be as high as 25%.29

Arthroplasty for DFFs—performed either with ORIF, or independently with a constrained implant—is a documented treatment modality, but the evidence is poor, and results have been mixed. Patients who received hinged TKA with major fracture resection had higher complication rates.8,11,22,24 However, the problems were mostly medical, not associated with surgical technique. Appleton and colleagues24 found a higher than expected 1-year mortality rate, 41%, but used an unhealthy baseline population (44% cognitive impairment, 17% nonambulatory before injury).Although Boureau and colleagues22 found a 1-year mortality rate of 30%, only 1 in 10 deaths was attributable to a perioperative complication. Among the remaining cases involving resection and megaprostheses for previously ambulatory patients, only 1 perioperative death was recorded (Table 2).11,12,16,18 Therefore, the risks associated with patients’ baseline health and ambulatory status must be weighed against the benefits of aggressive arthroplasty.

An overwhelming majority of 33C fractures were treated with megaprostheses—a finding perhaps attributable to the higher likelihood that patients with osteoporosis have intra-articular, comminuted injuries. In addition, surgeons may have been more likely to indicate 33C fractures for joint replacement, whereas 33A and 33B patterns were more amenable to fracture fixation.17,18 Interestingly, few type B fractures (0 in primary analysis and only 9 of 67 cases in Table 3) were treated with megaprostheses. In these situations, 1 condyle and ligamentous constraint remain intact, reducing the need for a constrained implant.

There were no reports of atraumatic or aseptic loosening, though use of rotating platforms with linked prostheses helps minimize this complication. Also surprising is the lack of nonunions in any of the reviewed studies, as nonunion is one of the most devastating complications of ORIF. Only 1 superficial and 2 deep infections were reported in all of the literature—representing 1.8% of all cases, which is comparable to the rate for elective primary TKA.30In elderly patients with significant comorbidities, the main surgical goals are to minimize operative time and reduce time to mobility. It is therefore imperative to keep in mind that arthroplasty is elective. However, functional results of primary TKA for DFF may be more encouraging for healthier patients, as many can achieve satisfactory ROM and early weight-bearing. Therefore, TKA for DFF may benefit healthy and ambulatory patients in the setting of intra-articular comminution. Whether this treatment affects mortality rates remains to be seen.

There were several limitations to this study. First, the literature on the topic is scant. Second, exclusion criteria were kept lax to allow for inclusion of all treatments. This came at a cost to internal validity, given the heterogeneous population and differences in comorbidities between studies. Fracture classification was inconsistent as well: Although AO/OTA classification was dominant, descriptive classifications were used in several cases7,10,12 (these descriptions, however, were sufficient for assigning equivalent AO/OTA classes). Details on preoperative functional status and comorbidity status and on postoperative protocols were also limited, though ROM and ambulatory status were provided in most studies. Last, most of these studies were single case reports or case series, so there may be reporting bias in the body of the literature, as reflected in the discrepancies between encouraging case reports and concerning case series with longer follow-up. Such bias can be avoided with larger, controlled sampling and adequate follow-up.

TKA should be considered for acute DFF in patients who have knee arthritis and are able to tolerate the physiological load of the surgery. In the choice of implant design, several factors should be considered, including bone quality, articular involvement, degree of comminution, and ligamentous injury. Unconstrained knee designs should be considered in cases in which the fracture pattern appears stable and the collateral ligaments are intact (eg, 33A and 33BB fractures). Megaprostheses, which may allow for immediate weight-bearing but require considerable bone resection, would be beneficial in 33C fractures and in fractures with ligamentous compromise. However, their complication rates are unclear, and comparative studies are needed to investigate whether the rates are higher for these patients than for patients treated more traditionally.

Am J Orthop. 2017;46(3):E163-E171. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Cass J, Sems SA. Operative versus nonoperative management of distal femur fracture in myelopathic, nonambulatory patients. Orthopedics. 2008;31(11):1091.

2. Eichenholtz SN. Management of long-bone fracture in paraplegic patients. J Bone Joint Surg Am. 1963;45(2):299-310.

3. Thomson AB, Driver R, Kregor PJ, Obremskey WT. Long-term functional outcomes after intra-articular distal femur fractures: ORIF versus retrograde intramedullary nailing. Orthopedics. 2008;31(8):748-750.

4. Rademakers MV, Kerkhoffs GM, Sierevelt IN, Raaymakers EL, Marti RK. Intra-articular fractures of the distal femur: a long-term follow-up study of surgically treated patients. J Orthop Trauma. 2004;18(4):213-219.

5. Schenker ML, Mauck RL, Ahn J, Mehta S. Pathogenesis and prevention of posttraumatic osteoarthritis after intra-articular fracture. J Am Acad Orthop Surg. 2014;22(1):20-28.

6. Papadopoulos EC, Parvizi J, Lai CH, Lewallen DG. Total knee arthroplasty following prior distal femoral fracture. Knee. 2002;9(4):267-274.

7. Yoshino N, Takai S, Watanabe Y, Fujiwara H, Ohshima Y, Hirasawa Y. Primary total knee arthroplasty for supracondylar/condylar femoral fracture in osteoarthritic knees. J Arthroplasty. 2001;16(4):471-475.

8. Rosen AL, Strauss E. Primary total knee arthroplasty for complex distal femur fractures in elderly patients. Clin Orthop Relat Res. 2004;(425):101-105.

9. Malviya A, Reed MR, Partington PF. Acute primary total knee arthroplasty for peri-articular knee fractures in patients over 65 years of age. Injury. 2011;42(11):1368-1371.

10. Wolfgang GL. Primary total knee arthroplasty for intercondylar fracture of the femur in a rheumatoid arthritic patient. A case report. Clin Orthop Relat Res. 1982;(171):80-82.

11. Bell KM, Johnstone AJ, Court-Brown CM, Hughes SP. Primary knee arthroplasty for distal femoral fractures in elderly patients. J Bone Joint Surg Br. 1992;74(3):400-402.

12. Shah A, Asirvatham R, Sudlow RA. Primary resection total knee arthroplasty for complicated fracture of the distal femur with an arthritic knee joint. Contemp Orthop. 1993;26(5):463-467.

13. Freedman EL, Hak DJ, Johnson EE, Eckardt JJ. Total knee replacement including a modular distal femoral component in elderly patients with acute fracture or nonunion. J Orthop Trauma. 1995;9(3):231-237.

14. Patterson RH, Earll M. Repair of supracondylar femur fracture and unilateral knee replacement at the same surgery. J Orthop Trauma. 1999;13(5):388-390.

15. Nau T, Pflegerl E, Erhart J, Vecsei V. Primary total knee arthroplasty for periarticular fractures. J Arthroplasty. 2003;18(8):968-971.

16. Pearse EO, Klass B, Bendall SP, Railton GT. Stanmore total knee replacement versus internal fixation for supracondylar fractures of the distal femur in elderly patients. Injury. 2005;36(1):163-168.

17. Mounasamy V, Ma SY, Schoderbek RJ, Mihalko WM, Saleh KJ, Brown TE. Primary total knee arthroplasty with condylar allograft and MCL reconstruction for a comminuted medial condyle fracture in an arthritic knee—a case report. Knee. 2006;13(5):400-403.

18. Mounasamy V, Cui Q, Brown TE, Saleh KJ, Mihalko WM. Primary total knee arthroplasty for a complex distal femur fracture in the elderly: a case report. Eur J Orthop Surg Traumatol. 2007;17(5):491-494.

19. Choi NY, Sohn JM, Cho SG, Kim SC, In Y. Primary total knee arthroplasty for simple distal femoral fractures in elderly patients with knee osteoarthritis. Knee Surg Relat Res. 2013;25(3):141-146.

20. Parratte S, Bonnevialle P, Pietu G, Saragaglia D, Cherrier B, Lafosse JM. Primary total knee arthroplasty in the management of epiphyseal fracture around the knee. Orthop Traumatol Surg Res. 2011;97(6 suppl):S87-S94.

21. Benazzo F, Rossi SM, Ghiara M, Zanardi A, Perticarini L, Combi A. Total knee replacement in acute and chronic traumatic events. Injury. 2014;45(suppl 6):S98-S104.

22. Boureau F, Benad K, Putman S, Dereudre G, Kern G, Chantelot C. Does primary total knee arthroplasty for acute knee joint fracture maintain autonomy in the elderly? A retrospective study of 21 cases. Orthop Traumatol Surg Res. 2015;101(8):947-951.

23. Bishop JA, Suarez P, Diponio L, Ota D, Curtin CM. Surgical versus nonsurgical treatment of femur fractures in people with spinal cord injury: an administrative analysis of risks. Arch Phys Med Rehabil. 2013;94(12):2357-2364.

24. Appleton P, Moran M, Houshian S, Robinson CM. Distal femoral fractures treated by hinged total knee replacement in elderly patients. J Bone Joint Surg Br. 2006;88(8):1065-1070.

25. In Y, Koh HS, Kim SJ. Cruciate-retaining stemmed total knee arthroplasty for supracondylar-intercondylar femoral fractures in elderly patients: a report of three cases. J Arthroplasty. 2006;21(7):1074-1079.

26. Kregor PJ, Stannard JA, Zlowodzki M, Cole PA. Treatment of distal femur fractures using the less invasive stabilization system: surgical experience and early clinical results in 103 fractures. J Orthop Trauma. 2004;18(8):509-520.

27. Vallier HA, Hennessey TA, Sontich JK, Patterson BM. Failure of LCP condylar plate fixation in the distal part of the femur. A report of six cases. J Bone Joint Surg Am. 2006;88(4):846-853.

28. Gwathmey FW Jr, Jones-Quaidoo SM, Kahler D, Hurwitz S, Cui Q. Distal femoral fractures: current concepts. J Am Acad Orthop Surg. 2010;18(10):597-607.

29. Streubel PN, Ricci WM, Wong A, Gardner MJ. Mortality after distal femur fractures in elderly patients. Clin Orthop Relat Res. 2011;469(4):1188-1196.

30. Peersman G, Laskin R, Davis J, Peterson M. Infection in total knee replacement: a retrospective review of 6489 total knee replacements. Clin Orthop Relat Res. 2001;(392):15-23.

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Take-Home Points

  • Arthroplasty is a rarely utilized and, therefore, a rarely reported treatment for distal femur fractures.
  • Arthroplasty carries certain advantages over fixation, including earlier weight-bearing, a benefit for elderly individuals.
  • Arthroplasty is more often described in situations of comminution, often necessitating constrained prostheses.
  • It is not unreasonable to utilize arthroplasty in extra-articular fractures in poor-quality bone, which can take the form of unconstrained prosthesis and supplemental fixation.
  • The true complication rate is unclear, given that the few papers reporting high complication rates were in sicker populations.

Distal femur fractures (DFFs) in the elderly historically were difficult to treat because of osteoporotic bone, comminution, and intra-articular involvement. DFFs in minimally ambulatory patients were once treated nonoperatively, with traction or immobilization,1,2 but surgery is now considered for displaced and unstable fractures, even in myelopathic and nonambulatory patients, to provide pain relief, ease mobility, and decrease the risks associated with prolonged bed rest.1 Options are constantly evolving, but poor knee function, malunion, nonunion, prolonged immobilization, implant failure, and high morbidity and mortality rates have been reported in several studies regardless of fixation method.

Arthritis after DFF has been reported at rates of 36% to 50% by long-term follow-up.3-5 However, total knee arthroplasty (TKA) for posttraumatic arthritis is more complex because of scarring, arthrofibrosis, malunion, nonunion, and the frequent need for hardware removal. These cases have a higher incidence of infection, aseptic loosening, stiffness,6 and skin necrosis.Primary TKA is a rarely used treatment for acute DFF. Several authors have recommended primary TKA for patients with intra-articular DFFs and preexisting osteoarthritis or rheumatoid arthritis, severe comminution, or poor bone stock.7-22 Compared with open reduction and internal fixation (ORIF), primary TKA may allow for earlier mobility and weight-bearing and thereby reduce the rates of complications (eg, respiratory failure, deep vein thrombosis, pulmonary embolism) associated with prolonged immobilization.23As the literature on TKA for acute DFF is scant, and to our knowledge there are no clear indications or guidelines, we performed a systematic review to determine whether TKA has been successful in relieving pain and restoring knee function. In this article, we discuss the indications, implant options, technical considerations, complications, and results (eg, range of motion [ROM], ambulatory status) associated with these procedures.

Methods

On December 1, 2015, we searched the major databases Medline, EMBASE (Excerpta Medica dataBASE), and the Cochrane Library for articles published since 1950. In our searches, we used the conjoint term knee arthroplasty with femur fracture, and knee replacement with femur fracture. Specifically, we queried: ((“knee replacement” OR “knee arthroplasty”) AND (intercondylar OR supracondylar OR femoral OR femur) AND fracture) NOT arthrodesis NOT periprosthetic NOT “posttraumatic arthritis” NOT osteotomy. We also hand-searched the current website of JBJS [Journal of Bone and Joint Surgery] Case Connector, a major case-report repository that was launched in 2011 but is not currently indexed by Medline.

All citations were imported to RefWorks for management and for removal of duplicates. Each article underwent screening and review by Dr. Chen and Dr. Li. Articles were included if titles were relevant to arthroplasty as treatment for acute (within 1 month) DFF. Articles and cases were excluded if they were reviews, published in languages other than English, animal studies, studies regarding nonacute (>3 months or nonunion) DFFs or periprosthetic fractures, or studies that considered only treatments other than TKA (ie, plate osteosynthesis).

Full-text publications were obtained and independently reviewed by Dr. Chen and Dr. Li for relevance and satisfaction of inclusion criteria. Disagreements were resolved by discussion. Given the rarity of publications on the treatment, all study designs from level I to level IV were included.

The same 2 reviewers extracted the data into prearranged summary tables. Data included study size, patient demographics, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) fracture type either reported or assessed by description and imaging (33A, extra-articular; 33B, partial articular with 1 intact condyle; 33C, complete articular with both condyles involved), baseline comorbidity, implant used and fracture treatment (if separate from arthroplasty), postoperative regimen, respective outcomes, and complication rates.

Results

We identified 728 articles: 389 through Medline, 294 through EMBASE, and 45 through the Cochrane Library (Figure 1).

Figure 1.
After duplicates were removed, 476 articles remained. After titles and abstracts were reviewed, 22 articles met the screening criteria. Five series included patients with TKA-treated acute DFF but did not report their specific outcomes (these were described separately).
Table 1.

The current evidence regarding primary TKA for acute DFF is primarily level IV (Table 1). Only 1 level III study16 compared TKA with ORIF. Three case series11,19,24 met our inclusion criteria (Table 1, Table 2). In addition, 5 case series involved patients who met our criteria, but these studies did not separately report results for DFFs and proximal tibia fractures,9,20-22 or separately for acute fractures and nonunions or ORIF failures.8

Table 2.
These studies were considered level IV and were tabulated separately (Table 3). Specific patient characteristics and management strategies varied significantly between studies, though many studies augmented 33A fractures with internal fixation, whereas 33C fractures more often underwent resection and placement of highly constrained implants. Of 117 acute DFFs reviewed, 20% were 33A fractures, 7% were 33B fractures, and 73% were 33C fractures (Table 1). Of the studies that specified, there were 8 cases of rheumatoid arthritis and 18 cases of osteoarthritis (Table 2).
Table 3.


Modular, hinged, and tumor-type arthroplasty designs accounted for 83% of the treatments included in this review. Trade names are listed in Table 4. Authors who used these implants took a more aggressive approach, often resecting the entire femoral epiphyseal-metaphyseal area, menisci, and collateral ligaments.9,13,15,16,18 The majority of patients who underwent resection had 33C fractures (Tables 1, 3).
Table 4.
Figures 2A-2D show an aggressive resection example.Authors who used less constrained arthroplasty designs focused on bone preservation, augmentation with graft, and internal fixation.7,20 In and colleagues25 thought that if the cruciate and collateral ligaments are found to be intact, then resecting these ligaments and performing the deep cuts necessary for linked prostheses are too aggressive. Their internal fixation methods included use of cannulated screws, Dall-Miles cabling (Stryker), and plate osteosynthesis. Choi and colleagues19 took a similar approach but also used stem extensions in 6 of 8 fractures assessed to be unstable (Figures 3A-3H).
Figure 2.
Yoshino and colleagues7 used posterior-stabilized implants with femoral stem extensions (Figures 4A-4C).
Figure 3.
Intraoperative use of an external fixator to align and stabilize a comminuted fracture before insertion of an intramedullary guide and during femoral cutting has also been described.19 All 33B and many 33A fractures were treated in this fashion.

The majority of authors who treated fractures with resection and modular implants allowed their patients full weight-bearing soon after surgery (Table 1),11,12,15-18,24 whereas authors who treated their patients partly with fracture fixation often had to delay weight-bearing (Table 1).
Figure 4.
Overall, results were encouraging, with most studies finding between 90° and 135° of flexion to near full extension after each type of treatment. At follow-up, most survivors achieved full weight-bearing and were capable of walking up and down stairs.

Cement use was universally described in the literature. Some authors avoided placing cement in the fracture site (to reduce the risk of nonunion),7,19 whereas others used bone cement to fill metaphyseal defects that remained after fracture resection and implantation.11,24Complication rates were modest, and there were no reports specifically on implant loosening or fracture nonunion.7,10,12-19 The majority of complications were recorded in 2 studies that used megaprostheses in sicker populations: Bell and colleagues11 noted debilitating illnesses in all their patients, and Appleton and colleagues24 included 9 nonambulatory patients and 36 patients who required 2 assistants to ambulate. All deaths were attributed to medical comorbidities and disseminated malignancy. Contrarily, studies by Pearse and colleagues16 and Choi and colleagues19 included previously ambulatory patients and reported no deaths or complications (Table 2). Likewise, in studies that combined results of DFFs and proximal tibia fractures, death and complication rates varied from 7% to 31% (Table 3).

 

 

Discussion

DFFs in the elderly historically were difficult to treat. Reported outcomes are largely favorable, but, even with newer plate designs, catastrophic failures still occur in the absence of bony union.26,27 After ORIF, patients’ weight-bearing is often restricted for 12 weeks or longer28—a protocol that is undesirable in elderly patients, especially given that the rate of mortality 1 year after these fractures has been found to be as high as 25%.29

Arthroplasty for DFFs—performed either with ORIF, or independently with a constrained implant—is a documented treatment modality, but the evidence is poor, and results have been mixed. Patients who received hinged TKA with major fracture resection had higher complication rates.8,11,22,24 However, the problems were mostly medical, not associated with surgical technique. Appleton and colleagues24 found a higher than expected 1-year mortality rate, 41%, but used an unhealthy baseline population (44% cognitive impairment, 17% nonambulatory before injury).Although Boureau and colleagues22 found a 1-year mortality rate of 30%, only 1 in 10 deaths was attributable to a perioperative complication. Among the remaining cases involving resection and megaprostheses for previously ambulatory patients, only 1 perioperative death was recorded (Table 2).11,12,16,18 Therefore, the risks associated with patients’ baseline health and ambulatory status must be weighed against the benefits of aggressive arthroplasty.

An overwhelming majority of 33C fractures were treated with megaprostheses—a finding perhaps attributable to the higher likelihood that patients with osteoporosis have intra-articular, comminuted injuries. In addition, surgeons may have been more likely to indicate 33C fractures for joint replacement, whereas 33A and 33B patterns were more amenable to fracture fixation.17,18 Interestingly, few type B fractures (0 in primary analysis and only 9 of 67 cases in Table 3) were treated with megaprostheses. In these situations, 1 condyle and ligamentous constraint remain intact, reducing the need for a constrained implant.

There were no reports of atraumatic or aseptic loosening, though use of rotating platforms with linked prostheses helps minimize this complication. Also surprising is the lack of nonunions in any of the reviewed studies, as nonunion is one of the most devastating complications of ORIF. Only 1 superficial and 2 deep infections were reported in all of the literature—representing 1.8% of all cases, which is comparable to the rate for elective primary TKA.30In elderly patients with significant comorbidities, the main surgical goals are to minimize operative time and reduce time to mobility. It is therefore imperative to keep in mind that arthroplasty is elective. However, functional results of primary TKA for DFF may be more encouraging for healthier patients, as many can achieve satisfactory ROM and early weight-bearing. Therefore, TKA for DFF may benefit healthy and ambulatory patients in the setting of intra-articular comminution. Whether this treatment affects mortality rates remains to be seen.

There were several limitations to this study. First, the literature on the topic is scant. Second, exclusion criteria were kept lax to allow for inclusion of all treatments. This came at a cost to internal validity, given the heterogeneous population and differences in comorbidities between studies. Fracture classification was inconsistent as well: Although AO/OTA classification was dominant, descriptive classifications were used in several cases7,10,12 (these descriptions, however, were sufficient for assigning equivalent AO/OTA classes). Details on preoperative functional status and comorbidity status and on postoperative protocols were also limited, though ROM and ambulatory status were provided in most studies. Last, most of these studies were single case reports or case series, so there may be reporting bias in the body of the literature, as reflected in the discrepancies between encouraging case reports and concerning case series with longer follow-up. Such bias can be avoided with larger, controlled sampling and adequate follow-up.

TKA should be considered for acute DFF in patients who have knee arthritis and are able to tolerate the physiological load of the surgery. In the choice of implant design, several factors should be considered, including bone quality, articular involvement, degree of comminution, and ligamentous injury. Unconstrained knee designs should be considered in cases in which the fracture pattern appears stable and the collateral ligaments are intact (eg, 33A and 33BB fractures). Megaprostheses, which may allow for immediate weight-bearing but require considerable bone resection, would be beneficial in 33C fractures and in fractures with ligamentous compromise. However, their complication rates are unclear, and comparative studies are needed to investigate whether the rates are higher for these patients than for patients treated more traditionally.

Am J Orthop. 2017;46(3):E163-E171. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

Take-Home Points

  • Arthroplasty is a rarely utilized and, therefore, a rarely reported treatment for distal femur fractures.
  • Arthroplasty carries certain advantages over fixation, including earlier weight-bearing, a benefit for elderly individuals.
  • Arthroplasty is more often described in situations of comminution, often necessitating constrained prostheses.
  • It is not unreasonable to utilize arthroplasty in extra-articular fractures in poor-quality bone, which can take the form of unconstrained prosthesis and supplemental fixation.
  • The true complication rate is unclear, given that the few papers reporting high complication rates were in sicker populations.

Distal femur fractures (DFFs) in the elderly historically were difficult to treat because of osteoporotic bone, comminution, and intra-articular involvement. DFFs in minimally ambulatory patients were once treated nonoperatively, with traction or immobilization,1,2 but surgery is now considered for displaced and unstable fractures, even in myelopathic and nonambulatory patients, to provide pain relief, ease mobility, and decrease the risks associated with prolonged bed rest.1 Options are constantly evolving, but poor knee function, malunion, nonunion, prolonged immobilization, implant failure, and high morbidity and mortality rates have been reported in several studies regardless of fixation method.

Arthritis after DFF has been reported at rates of 36% to 50% by long-term follow-up.3-5 However, total knee arthroplasty (TKA) for posttraumatic arthritis is more complex because of scarring, arthrofibrosis, malunion, nonunion, and the frequent need for hardware removal. These cases have a higher incidence of infection, aseptic loosening, stiffness,6 and skin necrosis.Primary TKA is a rarely used treatment for acute DFF. Several authors have recommended primary TKA for patients with intra-articular DFFs and preexisting osteoarthritis or rheumatoid arthritis, severe comminution, or poor bone stock.7-22 Compared with open reduction and internal fixation (ORIF), primary TKA may allow for earlier mobility and weight-bearing and thereby reduce the rates of complications (eg, respiratory failure, deep vein thrombosis, pulmonary embolism) associated with prolonged immobilization.23As the literature on TKA for acute DFF is scant, and to our knowledge there are no clear indications or guidelines, we performed a systematic review to determine whether TKA has been successful in relieving pain and restoring knee function. In this article, we discuss the indications, implant options, technical considerations, complications, and results (eg, range of motion [ROM], ambulatory status) associated with these procedures.

Methods

On December 1, 2015, we searched the major databases Medline, EMBASE (Excerpta Medica dataBASE), and the Cochrane Library for articles published since 1950. In our searches, we used the conjoint term knee arthroplasty with femur fracture, and knee replacement with femur fracture. Specifically, we queried: ((“knee replacement” OR “knee arthroplasty”) AND (intercondylar OR supracondylar OR femoral OR femur) AND fracture) NOT arthrodesis NOT periprosthetic NOT “posttraumatic arthritis” NOT osteotomy. We also hand-searched the current website of JBJS [Journal of Bone and Joint Surgery] Case Connector, a major case-report repository that was launched in 2011 but is not currently indexed by Medline.

All citations were imported to RefWorks for management and for removal of duplicates. Each article underwent screening and review by Dr. Chen and Dr. Li. Articles were included if titles were relevant to arthroplasty as treatment for acute (within 1 month) DFF. Articles and cases were excluded if they were reviews, published in languages other than English, animal studies, studies regarding nonacute (>3 months or nonunion) DFFs or periprosthetic fractures, or studies that considered only treatments other than TKA (ie, plate osteosynthesis).

Full-text publications were obtained and independently reviewed by Dr. Chen and Dr. Li for relevance and satisfaction of inclusion criteria. Disagreements were resolved by discussion. Given the rarity of publications on the treatment, all study designs from level I to level IV were included.

The same 2 reviewers extracted the data into prearranged summary tables. Data included study size, patient demographics, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) fracture type either reported or assessed by description and imaging (33A, extra-articular; 33B, partial articular with 1 intact condyle; 33C, complete articular with both condyles involved), baseline comorbidity, implant used and fracture treatment (if separate from arthroplasty), postoperative regimen, respective outcomes, and complication rates.

Results

We identified 728 articles: 389 through Medline, 294 through EMBASE, and 45 through the Cochrane Library (Figure 1).

Figure 1.
After duplicates were removed, 476 articles remained. After titles and abstracts were reviewed, 22 articles met the screening criteria. Five series included patients with TKA-treated acute DFF but did not report their specific outcomes (these were described separately).
Table 1.

The current evidence regarding primary TKA for acute DFF is primarily level IV (Table 1). Only 1 level III study16 compared TKA with ORIF. Three case series11,19,24 met our inclusion criteria (Table 1, Table 2). In addition, 5 case series involved patients who met our criteria, but these studies did not separately report results for DFFs and proximal tibia fractures,9,20-22 or separately for acute fractures and nonunions or ORIF failures.8

Table 2.
These studies were considered level IV and were tabulated separately (Table 3). Specific patient characteristics and management strategies varied significantly between studies, though many studies augmented 33A fractures with internal fixation, whereas 33C fractures more often underwent resection and placement of highly constrained implants. Of 117 acute DFFs reviewed, 20% were 33A fractures, 7% were 33B fractures, and 73% were 33C fractures (Table 1). Of the studies that specified, there were 8 cases of rheumatoid arthritis and 18 cases of osteoarthritis (Table 2).
Table 3.


Modular, hinged, and tumor-type arthroplasty designs accounted for 83% of the treatments included in this review. Trade names are listed in Table 4. Authors who used these implants took a more aggressive approach, often resecting the entire femoral epiphyseal-metaphyseal area, menisci, and collateral ligaments.9,13,15,16,18 The majority of patients who underwent resection had 33C fractures (Tables 1, 3).
Table 4.
Figures 2A-2D show an aggressive resection example.Authors who used less constrained arthroplasty designs focused on bone preservation, augmentation with graft, and internal fixation.7,20 In and colleagues25 thought that if the cruciate and collateral ligaments are found to be intact, then resecting these ligaments and performing the deep cuts necessary for linked prostheses are too aggressive. Their internal fixation methods included use of cannulated screws, Dall-Miles cabling (Stryker), and plate osteosynthesis. Choi and colleagues19 took a similar approach but also used stem extensions in 6 of 8 fractures assessed to be unstable (Figures 3A-3H).
Figure 2.
Yoshino and colleagues7 used posterior-stabilized implants with femoral stem extensions (Figures 4A-4C).
Figure 3.
Intraoperative use of an external fixator to align and stabilize a comminuted fracture before insertion of an intramedullary guide and during femoral cutting has also been described.19 All 33B and many 33A fractures were treated in this fashion.

The majority of authors who treated fractures with resection and modular implants allowed their patients full weight-bearing soon after surgery (Table 1),11,12,15-18,24 whereas authors who treated their patients partly with fracture fixation often had to delay weight-bearing (Table 1).
Figure 4.
Overall, results were encouraging, with most studies finding between 90° and 135° of flexion to near full extension after each type of treatment. At follow-up, most survivors achieved full weight-bearing and were capable of walking up and down stairs.

Cement use was universally described in the literature. Some authors avoided placing cement in the fracture site (to reduce the risk of nonunion),7,19 whereas others used bone cement to fill metaphyseal defects that remained after fracture resection and implantation.11,24Complication rates were modest, and there were no reports specifically on implant loosening or fracture nonunion.7,10,12-19 The majority of complications were recorded in 2 studies that used megaprostheses in sicker populations: Bell and colleagues11 noted debilitating illnesses in all their patients, and Appleton and colleagues24 included 9 nonambulatory patients and 36 patients who required 2 assistants to ambulate. All deaths were attributed to medical comorbidities and disseminated malignancy. Contrarily, studies by Pearse and colleagues16 and Choi and colleagues19 included previously ambulatory patients and reported no deaths or complications (Table 2). Likewise, in studies that combined results of DFFs and proximal tibia fractures, death and complication rates varied from 7% to 31% (Table 3).

 

 

Discussion

DFFs in the elderly historically were difficult to treat. Reported outcomes are largely favorable, but, even with newer plate designs, catastrophic failures still occur in the absence of bony union.26,27 After ORIF, patients’ weight-bearing is often restricted for 12 weeks or longer28—a protocol that is undesirable in elderly patients, especially given that the rate of mortality 1 year after these fractures has been found to be as high as 25%.29

Arthroplasty for DFFs—performed either with ORIF, or independently with a constrained implant—is a documented treatment modality, but the evidence is poor, and results have been mixed. Patients who received hinged TKA with major fracture resection had higher complication rates.8,11,22,24 However, the problems were mostly medical, not associated with surgical technique. Appleton and colleagues24 found a higher than expected 1-year mortality rate, 41%, but used an unhealthy baseline population (44% cognitive impairment, 17% nonambulatory before injury).Although Boureau and colleagues22 found a 1-year mortality rate of 30%, only 1 in 10 deaths was attributable to a perioperative complication. Among the remaining cases involving resection and megaprostheses for previously ambulatory patients, only 1 perioperative death was recorded (Table 2).11,12,16,18 Therefore, the risks associated with patients’ baseline health and ambulatory status must be weighed against the benefits of aggressive arthroplasty.

An overwhelming majority of 33C fractures were treated with megaprostheses—a finding perhaps attributable to the higher likelihood that patients with osteoporosis have intra-articular, comminuted injuries. In addition, surgeons may have been more likely to indicate 33C fractures for joint replacement, whereas 33A and 33B patterns were more amenable to fracture fixation.17,18 Interestingly, few type B fractures (0 in primary analysis and only 9 of 67 cases in Table 3) were treated with megaprostheses. In these situations, 1 condyle and ligamentous constraint remain intact, reducing the need for a constrained implant.

There were no reports of atraumatic or aseptic loosening, though use of rotating platforms with linked prostheses helps minimize this complication. Also surprising is the lack of nonunions in any of the reviewed studies, as nonunion is one of the most devastating complications of ORIF. Only 1 superficial and 2 deep infections were reported in all of the literature—representing 1.8% of all cases, which is comparable to the rate for elective primary TKA.30In elderly patients with significant comorbidities, the main surgical goals are to minimize operative time and reduce time to mobility. It is therefore imperative to keep in mind that arthroplasty is elective. However, functional results of primary TKA for DFF may be more encouraging for healthier patients, as many can achieve satisfactory ROM and early weight-bearing. Therefore, TKA for DFF may benefit healthy and ambulatory patients in the setting of intra-articular comminution. Whether this treatment affects mortality rates remains to be seen.

There were several limitations to this study. First, the literature on the topic is scant. Second, exclusion criteria were kept lax to allow for inclusion of all treatments. This came at a cost to internal validity, given the heterogeneous population and differences in comorbidities between studies. Fracture classification was inconsistent as well: Although AO/OTA classification was dominant, descriptive classifications were used in several cases7,10,12 (these descriptions, however, were sufficient for assigning equivalent AO/OTA classes). Details on preoperative functional status and comorbidity status and on postoperative protocols were also limited, though ROM and ambulatory status were provided in most studies. Last, most of these studies were single case reports or case series, so there may be reporting bias in the body of the literature, as reflected in the discrepancies between encouraging case reports and concerning case series with longer follow-up. Such bias can be avoided with larger, controlled sampling and adequate follow-up.

TKA should be considered for acute DFF in patients who have knee arthritis and are able to tolerate the physiological load of the surgery. In the choice of implant design, several factors should be considered, including bone quality, articular involvement, degree of comminution, and ligamentous injury. Unconstrained knee designs should be considered in cases in which the fracture pattern appears stable and the collateral ligaments are intact (eg, 33A and 33BB fractures). Megaprostheses, which may allow for immediate weight-bearing but require considerable bone resection, would be beneficial in 33C fractures and in fractures with ligamentous compromise. However, their complication rates are unclear, and comparative studies are needed to investigate whether the rates are higher for these patients than for patients treated more traditionally.

Am J Orthop. 2017;46(3):E163-E171. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Cass J, Sems SA. Operative versus nonoperative management of distal femur fracture in myelopathic, nonambulatory patients. Orthopedics. 2008;31(11):1091.

2. Eichenholtz SN. Management of long-bone fracture in paraplegic patients. J Bone Joint Surg Am. 1963;45(2):299-310.

3. Thomson AB, Driver R, Kregor PJ, Obremskey WT. Long-term functional outcomes after intra-articular distal femur fractures: ORIF versus retrograde intramedullary nailing. Orthopedics. 2008;31(8):748-750.

4. Rademakers MV, Kerkhoffs GM, Sierevelt IN, Raaymakers EL, Marti RK. Intra-articular fractures of the distal femur: a long-term follow-up study of surgically treated patients. J Orthop Trauma. 2004;18(4):213-219.

5. Schenker ML, Mauck RL, Ahn J, Mehta S. Pathogenesis and prevention of posttraumatic osteoarthritis after intra-articular fracture. J Am Acad Orthop Surg. 2014;22(1):20-28.

6. Papadopoulos EC, Parvizi J, Lai CH, Lewallen DG. Total knee arthroplasty following prior distal femoral fracture. Knee. 2002;9(4):267-274.

7. Yoshino N, Takai S, Watanabe Y, Fujiwara H, Ohshima Y, Hirasawa Y. Primary total knee arthroplasty for supracondylar/condylar femoral fracture in osteoarthritic knees. J Arthroplasty. 2001;16(4):471-475.

8. Rosen AL, Strauss E. Primary total knee arthroplasty for complex distal femur fractures in elderly patients. Clin Orthop Relat Res. 2004;(425):101-105.

9. Malviya A, Reed MR, Partington PF. Acute primary total knee arthroplasty for peri-articular knee fractures in patients over 65 years of age. Injury. 2011;42(11):1368-1371.

10. Wolfgang GL. Primary total knee arthroplasty for intercondylar fracture of the femur in a rheumatoid arthritic patient. A case report. Clin Orthop Relat Res. 1982;(171):80-82.

11. Bell KM, Johnstone AJ, Court-Brown CM, Hughes SP. Primary knee arthroplasty for distal femoral fractures in elderly patients. J Bone Joint Surg Br. 1992;74(3):400-402.

12. Shah A, Asirvatham R, Sudlow RA. Primary resection total knee arthroplasty for complicated fracture of the distal femur with an arthritic knee joint. Contemp Orthop. 1993;26(5):463-467.

13. Freedman EL, Hak DJ, Johnson EE, Eckardt JJ. Total knee replacement including a modular distal femoral component in elderly patients with acute fracture or nonunion. J Orthop Trauma. 1995;9(3):231-237.

14. Patterson RH, Earll M. Repair of supracondylar femur fracture and unilateral knee replacement at the same surgery. J Orthop Trauma. 1999;13(5):388-390.

15. Nau T, Pflegerl E, Erhart J, Vecsei V. Primary total knee arthroplasty for periarticular fractures. J Arthroplasty. 2003;18(8):968-971.

16. Pearse EO, Klass B, Bendall SP, Railton GT. Stanmore total knee replacement versus internal fixation for supracondylar fractures of the distal femur in elderly patients. Injury. 2005;36(1):163-168.

17. Mounasamy V, Ma SY, Schoderbek RJ, Mihalko WM, Saleh KJ, Brown TE. Primary total knee arthroplasty with condylar allograft and MCL reconstruction for a comminuted medial condyle fracture in an arthritic knee—a case report. Knee. 2006;13(5):400-403.

18. Mounasamy V, Cui Q, Brown TE, Saleh KJ, Mihalko WM. Primary total knee arthroplasty for a complex distal femur fracture in the elderly: a case report. Eur J Orthop Surg Traumatol. 2007;17(5):491-494.

19. Choi NY, Sohn JM, Cho SG, Kim SC, In Y. Primary total knee arthroplasty for simple distal femoral fractures in elderly patients with knee osteoarthritis. Knee Surg Relat Res. 2013;25(3):141-146.

20. Parratte S, Bonnevialle P, Pietu G, Saragaglia D, Cherrier B, Lafosse JM. Primary total knee arthroplasty in the management of epiphyseal fracture around the knee. Orthop Traumatol Surg Res. 2011;97(6 suppl):S87-S94.

21. Benazzo F, Rossi SM, Ghiara M, Zanardi A, Perticarini L, Combi A. Total knee replacement in acute and chronic traumatic events. Injury. 2014;45(suppl 6):S98-S104.

22. Boureau F, Benad K, Putman S, Dereudre G, Kern G, Chantelot C. Does primary total knee arthroplasty for acute knee joint fracture maintain autonomy in the elderly? A retrospective study of 21 cases. Orthop Traumatol Surg Res. 2015;101(8):947-951.

23. Bishop JA, Suarez P, Diponio L, Ota D, Curtin CM. Surgical versus nonsurgical treatment of femur fractures in people with spinal cord injury: an administrative analysis of risks. Arch Phys Med Rehabil. 2013;94(12):2357-2364.

24. Appleton P, Moran M, Houshian S, Robinson CM. Distal femoral fractures treated by hinged total knee replacement in elderly patients. J Bone Joint Surg Br. 2006;88(8):1065-1070.

25. In Y, Koh HS, Kim SJ. Cruciate-retaining stemmed total knee arthroplasty for supracondylar-intercondylar femoral fractures in elderly patients: a report of three cases. J Arthroplasty. 2006;21(7):1074-1079.

26. Kregor PJ, Stannard JA, Zlowodzki M, Cole PA. Treatment of distal femur fractures using the less invasive stabilization system: surgical experience and early clinical results in 103 fractures. J Orthop Trauma. 2004;18(8):509-520.

27. Vallier HA, Hennessey TA, Sontich JK, Patterson BM. Failure of LCP condylar plate fixation in the distal part of the femur. A report of six cases. J Bone Joint Surg Am. 2006;88(4):846-853.

28. Gwathmey FW Jr, Jones-Quaidoo SM, Kahler D, Hurwitz S, Cui Q. Distal femoral fractures: current concepts. J Am Acad Orthop Surg. 2010;18(10):597-607.

29. Streubel PN, Ricci WM, Wong A, Gardner MJ. Mortality after distal femur fractures in elderly patients. Clin Orthop Relat Res. 2011;469(4):1188-1196.

30. Peersman G, Laskin R, Davis J, Peterson M. Infection in total knee replacement: a retrospective review of 6489 total knee replacements. Clin Orthop Relat Res. 2001;(392):15-23.

References

1. Cass J, Sems SA. Operative versus nonoperative management of distal femur fracture in myelopathic, nonambulatory patients. Orthopedics. 2008;31(11):1091.

2. Eichenholtz SN. Management of long-bone fracture in paraplegic patients. J Bone Joint Surg Am. 1963;45(2):299-310.

3. Thomson AB, Driver R, Kregor PJ, Obremskey WT. Long-term functional outcomes after intra-articular distal femur fractures: ORIF versus retrograde intramedullary nailing. Orthopedics. 2008;31(8):748-750.

4. Rademakers MV, Kerkhoffs GM, Sierevelt IN, Raaymakers EL, Marti RK. Intra-articular fractures of the distal femur: a long-term follow-up study of surgically treated patients. J Orthop Trauma. 2004;18(4):213-219.

5. Schenker ML, Mauck RL, Ahn J, Mehta S. Pathogenesis and prevention of posttraumatic osteoarthritis after intra-articular fracture. J Am Acad Orthop Surg. 2014;22(1):20-28.

6. Papadopoulos EC, Parvizi J, Lai CH, Lewallen DG. Total knee arthroplasty following prior distal femoral fracture. Knee. 2002;9(4):267-274.

7. Yoshino N, Takai S, Watanabe Y, Fujiwara H, Ohshima Y, Hirasawa Y. Primary total knee arthroplasty for supracondylar/condylar femoral fracture in osteoarthritic knees. J Arthroplasty. 2001;16(4):471-475.

8. Rosen AL, Strauss E. Primary total knee arthroplasty for complex distal femur fractures in elderly patients. Clin Orthop Relat Res. 2004;(425):101-105.

9. Malviya A, Reed MR, Partington PF. Acute primary total knee arthroplasty for peri-articular knee fractures in patients over 65 years of age. Injury. 2011;42(11):1368-1371.

10. Wolfgang GL. Primary total knee arthroplasty for intercondylar fracture of the femur in a rheumatoid arthritic patient. A case report. Clin Orthop Relat Res. 1982;(171):80-82.

11. Bell KM, Johnstone AJ, Court-Brown CM, Hughes SP. Primary knee arthroplasty for distal femoral fractures in elderly patients. J Bone Joint Surg Br. 1992;74(3):400-402.

12. Shah A, Asirvatham R, Sudlow RA. Primary resection total knee arthroplasty for complicated fracture of the distal femur with an arthritic knee joint. Contemp Orthop. 1993;26(5):463-467.

13. Freedman EL, Hak DJ, Johnson EE, Eckardt JJ. Total knee replacement including a modular distal femoral component in elderly patients with acute fracture or nonunion. J Orthop Trauma. 1995;9(3):231-237.

14. Patterson RH, Earll M. Repair of supracondylar femur fracture and unilateral knee replacement at the same surgery. J Orthop Trauma. 1999;13(5):388-390.

15. Nau T, Pflegerl E, Erhart J, Vecsei V. Primary total knee arthroplasty for periarticular fractures. J Arthroplasty. 2003;18(8):968-971.

16. Pearse EO, Klass B, Bendall SP, Railton GT. Stanmore total knee replacement versus internal fixation for supracondylar fractures of the distal femur in elderly patients. Injury. 2005;36(1):163-168.

17. Mounasamy V, Ma SY, Schoderbek RJ, Mihalko WM, Saleh KJ, Brown TE. Primary total knee arthroplasty with condylar allograft and MCL reconstruction for a comminuted medial condyle fracture in an arthritic knee—a case report. Knee. 2006;13(5):400-403.

18. Mounasamy V, Cui Q, Brown TE, Saleh KJ, Mihalko WM. Primary total knee arthroplasty for a complex distal femur fracture in the elderly: a case report. Eur J Orthop Surg Traumatol. 2007;17(5):491-494.

19. Choi NY, Sohn JM, Cho SG, Kim SC, In Y. Primary total knee arthroplasty for simple distal femoral fractures in elderly patients with knee osteoarthritis. Knee Surg Relat Res. 2013;25(3):141-146.

20. Parratte S, Bonnevialle P, Pietu G, Saragaglia D, Cherrier B, Lafosse JM. Primary total knee arthroplasty in the management of epiphyseal fracture around the knee. Orthop Traumatol Surg Res. 2011;97(6 suppl):S87-S94.

21. Benazzo F, Rossi SM, Ghiara M, Zanardi A, Perticarini L, Combi A. Total knee replacement in acute and chronic traumatic events. Injury. 2014;45(suppl 6):S98-S104.

22. Boureau F, Benad K, Putman S, Dereudre G, Kern G, Chantelot C. Does primary total knee arthroplasty for acute knee joint fracture maintain autonomy in the elderly? A retrospective study of 21 cases. Orthop Traumatol Surg Res. 2015;101(8):947-951.

23. Bishop JA, Suarez P, Diponio L, Ota D, Curtin CM. Surgical versus nonsurgical treatment of femur fractures in people with spinal cord injury: an administrative analysis of risks. Arch Phys Med Rehabil. 2013;94(12):2357-2364.

24. Appleton P, Moran M, Houshian S, Robinson CM. Distal femoral fractures treated by hinged total knee replacement in elderly patients. J Bone Joint Surg Br. 2006;88(8):1065-1070.

25. In Y, Koh HS, Kim SJ. Cruciate-retaining stemmed total knee arthroplasty for supracondylar-intercondylar femoral fractures in elderly patients: a report of three cases. J Arthroplasty. 2006;21(7):1074-1079.

26. Kregor PJ, Stannard JA, Zlowodzki M, Cole PA. Treatment of distal femur fractures using the less invasive stabilization system: surgical experience and early clinical results in 103 fractures. J Orthop Trauma. 2004;18(8):509-520.

27. Vallier HA, Hennessey TA, Sontich JK, Patterson BM. Failure of LCP condylar plate fixation in the distal part of the femur. A report of six cases. J Bone Joint Surg Am. 2006;88(4):846-853.

28. Gwathmey FW Jr, Jones-Quaidoo SM, Kahler D, Hurwitz S, Cui Q. Distal femoral fractures: current concepts. J Am Acad Orthop Surg. 2010;18(10):597-607.

29. Streubel PN, Ricci WM, Wong A, Gardner MJ. Mortality after distal femur fractures in elderly patients. Clin Orthop Relat Res. 2011;469(4):1188-1196.

30. Peersman G, Laskin R, Davis J, Peterson M. Infection in total knee replacement: a retrospective review of 6489 total knee replacements. Clin Orthop Relat Res. 2001;(392):15-23.

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Primary Total Knee Arthroplasty for Distal Femur Fractures: A Systematic Review of Indications, Implants, Techniques, and Results
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Acute Intraprosthetic Dissociation of a Dual-Mobility Hip in the United States

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Acute Intraprosthetic Dissociation of a Dual-Mobility Hip in the United States

Take-Home Points

  • AIPD of DM-THA is defined by dissociation within 1 year of implantation resulting from component impingement or closed reduction maneuvers.
  • This is a distinct entity from “late” IPD (>1 year) from implantation as this is associated most often with polyethylene wear, component loosening, and arthrofibrosis.
  • A history of DM dislocation followed by subjective “clunking,” instability, and a series of more frequent dislocations should raise concern for AIPD.
  • Classic radiographic findings of AIPD include eccentric hip reduction and soft tissue radiolucency (ie, halo sign) from dissociated polyethylene component.
  • Treating practitioners of AIPD should consider closed reduction with general anesthesia and sedation in the operating room to limit risk of dissociation.

Dual-mobility (DM) components were invented in the 1970s and have been used in primary and revision total hip arthroplasty (THA) in Europe ever since.1 However, DM components are most commonly used in the treatment of recurrent hip instability, and early results have been promising.2 In DM-THAs, a smaller (22-mm or 28-mm) metal femoral head snap-fits into a larger polyethylene ball (inner articulation), which articulates with a highly polished metal shell (outer articulation), which is either implanted directly in the acetabulum or placed in an uncemented acetabular cup. The 2 articulations used in these devices theoretically increase hip range of motion (ROM) and increase the inferior head displacement distance (jump distance) required for dislocation.3

However, this DM articulation with increased ROM may also cause chronic impingement of the femoral component neck or Morse taper against the outer polyethylene bearing, resulting in polyethylene wear and late intraprosthetic dissociation (IPD) (separation of inner articulation between femoral head and polyethylene liner). In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation during the period 1989 to 1997. In 2013, Philippot and colleagues5 reported that 81 of 1960 primary THAs developed IPD a mean of 9 years after implantation. These IPD cases were attributed to polyethylene wear or outer articulation blockage caused by arthrofibrosis or heterotopic ossification. Reports of acute IPD (AIPD), however, are rare. In 2011, Stigbrand and Ullmark6 reported 3 cases in which the DM prosthesis dislocated within 1 year after implantation. It was suggested that the inner metal head dissociated from the larger polyethylene component after attempted closed reduction for dislocation (separation of larger polyethylene component from acetabulum or acetabular liner).

DM components were unavailable to surgeons in the United States until 2011. The first US Food and Drug Administration (FDA)-approved DM device was the MDM (Modular Dual Mobility, Stryker). To our knowledge, 2 cases of AIPD with this prosthesis have been reported.7, 8 As with the cases in Europe, closed reduction was the suspected cause, but there was no explanation for the initial dislocation event.

In this article, we present the case of a nondemented man who developed AIPD of a THA with the MDM component and a 28-mm femoral head with a skirted neck (StelKast). His operative findings suggest a poor head-to-neck ratio caused by a larger diameter femoral neck or a skirted prosthesis, or a forceful reduction maneuver, may predispose DM components to AIPD. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

In 2012, a 63-year-old man with a history of drug abuse underwent left primary THA. Seven posterior dislocations and 3 years later, the acetabular component was revised to the MDM prosthesis; the well-fixed StelKast femoral component was retained (Figure 1).

Figure 1.

Within 3 months after revision surgery, the left hip dislocated 3 times in 1 week, when the patient bent over to retrieve an object on the ground. The first 2 dislocations were treated with closed reduction under conscious sedation at an outside emergency department.

Figure 2.
Shortly after, the patient, with complaints of left hip pain and clunking, was seen by a physician assistant, but the treating team did not notice the eccentric reduction on radiographs. The third dislocation was treated with closed reduction under conscious sedation in the emergency department at our institution (Figure 2). Postreduction radiographs still showed the eccentric reduction, and a radiolucent halo was visible superior to the greater trochanter (Figure 3).
Figure 3.


With the patient’s erythrocyte sedimentation rate and C-reactive protein level both normal, a second revision was performed. During surgery, the polyethylene head was found beneath the gluteus maximus (Figure 4).
Figure 4.
Gross inspection revealed a small amount of eccentric polyethylene wear and metal debris of the inner articulation (Figure 5). As the abductor muscles were intact, it was decided to proceed with revision to a larger DM component and to downsize the femoral head to a skirtless component (Table, Figure 6).

 

 

Discussion

Recurrent dislocation and instability accounts for 22.5% of THA revisions in the United States.9 Until 2011, options for managing recurrent dislocation in the United States included modular component exchange, component revision for malposition, and use of constrained components.10

Figure 5.
However, the decreased motion of constrained components may produce excess stress that eventually results in failure.11-13

In 1974, Bousquet first reported use of the DM prosthesis in primary THA; the prosthesis allowed increased stability without sacrificing motion or fixation.1 However, longer-term studies of DM components disclosed a new complication, IPD. In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation of the Bousquet prosthesis.

Table.
Philippot and colleagues5 reported that 81 of 1960 primary THAs with DM components developed IPD a mean of 9 years after implantation. They described 3 types of IPD based on mechanism of injury: type I, caused by wear of the inner articulation without arthrofibrosis or cup loosening (n = 26); type II, resulting from blocked outer articulation motion, caused by arthrofibrosis, nonunion, calcification, or heterotopic ossification (n = 41); and type III, associated with acetabular component loosening (n = 14). IPD occurred an average of 11 years (type I), 8 years (type II), and 9 years (type III) after implantation.

AIPD, which occurs within 1 year after implantation, has been reported much less often than late IPD. Stigbrand and Ullmark6 reported 3 cases of AIPD that developed within 7 months after implantation of Amplitude and Advantage (Zimmer Biomet) DM prostheses.
Figure 6.
The authors proposed that AIPD is related to incomplete coupling of the metal head and the inner polyethylene liner or to shearing of the large polyethylene component on the acetabular rim during a closed reduction maneuver. According to their description, the femoral head in the acetabulum had an “eccentric” radiographic appearance. The authors recommended administering muscle relaxants during closed reduction to avoid dissociation of the liner during the reduction.

This unusual complication apparently is not confined to a specific implant or region. Since the MDM component was introduced in the United States, 2 more cases of AIPD have been identified (Table). Banzhof and colleagues7 reported the case of a 68-year-old woman who, 2 months after the MDM was placed for recurrent instability, dislocated the component while rising from a seated position. Her IPD most likely resulted from a closed reduction. The affected hip eventually required closed reduction in the operating room. Postreduction radiographs showed the characteristic eccentric appearance; a halo, also visible in the soft tissues, corresponded with the dissociated radiolucent polyethylene liner. The authors attributed the early failure to an eccentrically seated metal liner that separated the locking mechanism. The MDM component was revised to a conventional THA, with the femoral head upsized and length added.

Ward and colleagues8 reported the case of an 87-year-old woman who had a conventional THA revised to an MDM component for recurrent instability. Two months after surgery, this patient, who had dementia, experienced 2 posterior dislocations while rising from a chair. Closed reduction in the emergency department seemed successful, but later she presented to the surgeon’s office with symptoms of instability and clunking, complaints similar to our patient’s. Radiographs showed an eccentric reduction caused by IPD, and the MDM component was revised to a constrained liner. Adding a MDM component to a retained DePuy (DePuy Synthes) femoral stem and head is considered “off-label use,” which, the authors proposed, may have been related to the AIPD in their patient’s case. However, one manufacturer’s femoral component and head are often mated with another manufacturer’s acetabular component to allow for a less complex revision. Our recommendation for surgeons is that, before proceeding with this treatment option, they investigate each component’s exact dimensions to ensure there are no subtle size differences that could cause problems. For example, a 28-mm head diameter that is actually 28.2 mm may affect mating properties, with the inner polyethylene articulation causing AIPD to develop.

Other cases of earlier IPD have been described, but they do not fit the APID definition given in this article. Riviere and colleagues14 reported the case of a 42-year-old man who, because of a previous adverse reaction to metal debris, underwent revision to a DM polyethylene ball in a retained BHR (Birmingham Hip Resurfacing) acetabular shell (Birmingham Hip, Smith & Nephew). Unfortunately, IPD occurred 14 months after surgery. Banka and colleagues15 reported the case of a 70-year-old woman who underwent revision to a DM cup for recurrent instability, but they did not specify the length of time between implantation and IPD and did not offer an explanation for the complication. Finally, Odland and Sierra16 reported the case of a 77-year-old man, with previous intertrochanteric and pelvic fractures, who underwent revision to a DM cup with retention of a Waldemar femoral component (Waldemar Link). He spontaneously developed IPD with ambulation 2 years after surgery.

Certainly, our patient’s presentation course is similar to other patients’. Within 3 months after revision to the MDM component, his left hip dislocated 3 times in 1 week. We contend his AIPD resulted from closed reduction, with the polyethylene dislodged from the femoral head with contact on the acetabulum. A larger or skirted neck may increase impingement during normal activity and thereby widen the polyethylene opening excessively and/or reduce the polyethylene ball ROM to impinge during the relocation maneuver. In this case, dissociation was noted only after the third dislocation. Pathognomonic eccentric positioning of the head in the acetabulum and, less commonly, the halo sign were evident on postreduction radiographs. Optimal treatment for AIPD of a DM component is controversial. Choices are limited to a constrained liner or, if possible, repeat DM with larger components. For recurrent dislocation, our patient underwent revision to an MDM component, but a femoral head with a skirted neck was used in an attempt to increase soft-tissue tension. During the second revision, minor eccentric wear of the inner articulation of the polyethylene component (consistent with impingement) was noted, and wear was visible on inspection of the outer articulation. We think his AIPD resulted from femoral neck impingement of the skirted head against the polyethylene ball.

AIPD is a discrete entity, with sudden failure of a DM component within 1 year after implantation. AIPD is characterized by dissociation of the femoral head from the inner articulation, resulting from impingement or closed reduction. More studies are needed to determine which patients with DM components are at highest risk and which treatment is most appropriate. We recommend taking extra care when reducing hips with this articulation and adopting a low threshold for general anesthesia use in the presence of paralysis.

Am J Orthop. 2017;46(3):E154-E159. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Farizon F, de Lavison R, Azoulai JJ, Bousquet G. Results with a cementless alumina-coated cup with dual mobility. A twelve-year follow-up study. Int Orthop. 1998;22(4):219-224.

2. Lachiewicz PF, Watters TS. The use of dual-mobility components in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(8):481-486.

3. De Martino I, Triantafyllopoulos GK, Sculco PK, Sculco TP. Dual mobility cups in total hip arthroplasty. World J Orthop. 2014;5(3):180-187.

4. Lecuire F, Benareau I, Rubini J, Basso M. Intra-prosthetic dislocation of the Bousquet dual mobility socket [in French]. Rev Chir Orthop Reparatrice Appar Mot. 2004;90(3):249-255.

5. Philippot R, Boyer B, Farizon F. Intraprosthetic dislocation: a specific complication of the dual-mobility system. Clin Orthop Relat Res. 2013;471(3):965-970.

6. Stigbrand H, Ullmark G. Component dissociation after closed reduction of dual mobility sockets—a report of three cases. Hip Int. 2011;21(2):263-266.

7. Banzhof JA, Robbins CE, Ven AV, Talmo CT, Bono JV. Femoral head dislodgement complicating use of a dual mobility prosthesis for recurrent instability. J Arthroplasty. 2013;28(3):543.e1-e3.

8. Ward JP, McCardel BR, Hallstrom BR. Complete dissociation of the polyethylene component in a newly available dual-mobility bearing used in total hip arthroplasty: a case report. JBJS Case Connect. 2013;3(3):e94.

9. Bozic KJ, Kurtz SM, Lau E, Ong K, Vail TP, Berry DJ. The epidemiology of revision total hip arthroplasty in the United States. J Bone Joint Surg Am. 2009;91(1):128-133.

10. Parvizi J, Picinic E, Sharkey PF. Revision total hip arthroplasty for instability: surgical techniques and principles. J Bone Joint Surg Am. 2008;90(5):1134-1142.

11. Guyen O, Lewallen DG, Cabanela ME. Modes of failure of Osteonics constrained tripolar implants: a retrospective analysis of forty-three failed implants. J Bone Joint Surg Am. 2008;90(7):1553-1560.

12. Lachiewicz PF, Kelley SS. The use of constrained components in total hip arthroplasty. J Am Acad Orthop Surg. 2002;10(4):233-238.

13. Williams JT Jr, Ragland PS, Clarke S. Constrained components for the unstable hip following total hip arthroplasty: a literature review. Int Orthop. 2007;31(3):273-277.

14. Riviere C, Lavigne M, Alghamdi A, Vendittoli PA. Early failure of metal-on-metal large-diameter head total hip arthroplasty revised with a dual-mobility bearing: a case report. JBJS Case Connect. 2013;3(3):e95.

15. Banka TR, Ast MP, Parks ML. Early intraprosthetic dislocation in a revision dual-mobility hip prosthesis. Orthopedics. 2014;37(4):e395-e397.

16. Odland AN, Sierra RJ. Intraprosthetic dislocation of a contemporary dual-mobility design used during conversion THA. Orthopedics. 2014;37(12):e1124-e1128.

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Take-Home Points

  • AIPD of DM-THA is defined by dissociation within 1 year of implantation resulting from component impingement or closed reduction maneuvers.
  • This is a distinct entity from “late” IPD (>1 year) from implantation as this is associated most often with polyethylene wear, component loosening, and arthrofibrosis.
  • A history of DM dislocation followed by subjective “clunking,” instability, and a series of more frequent dislocations should raise concern for AIPD.
  • Classic radiographic findings of AIPD include eccentric hip reduction and soft tissue radiolucency (ie, halo sign) from dissociated polyethylene component.
  • Treating practitioners of AIPD should consider closed reduction with general anesthesia and sedation in the operating room to limit risk of dissociation.

Dual-mobility (DM) components were invented in the 1970s and have been used in primary and revision total hip arthroplasty (THA) in Europe ever since.1 However, DM components are most commonly used in the treatment of recurrent hip instability, and early results have been promising.2 In DM-THAs, a smaller (22-mm or 28-mm) metal femoral head snap-fits into a larger polyethylene ball (inner articulation), which articulates with a highly polished metal shell (outer articulation), which is either implanted directly in the acetabulum or placed in an uncemented acetabular cup. The 2 articulations used in these devices theoretically increase hip range of motion (ROM) and increase the inferior head displacement distance (jump distance) required for dislocation.3

However, this DM articulation with increased ROM may also cause chronic impingement of the femoral component neck or Morse taper against the outer polyethylene bearing, resulting in polyethylene wear and late intraprosthetic dissociation (IPD) (separation of inner articulation between femoral head and polyethylene liner). In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation during the period 1989 to 1997. In 2013, Philippot and colleagues5 reported that 81 of 1960 primary THAs developed IPD a mean of 9 years after implantation. These IPD cases were attributed to polyethylene wear or outer articulation blockage caused by arthrofibrosis or heterotopic ossification. Reports of acute IPD (AIPD), however, are rare. In 2011, Stigbrand and Ullmark6 reported 3 cases in which the DM prosthesis dislocated within 1 year after implantation. It was suggested that the inner metal head dissociated from the larger polyethylene component after attempted closed reduction for dislocation (separation of larger polyethylene component from acetabulum or acetabular liner).

DM components were unavailable to surgeons in the United States until 2011. The first US Food and Drug Administration (FDA)-approved DM device was the MDM (Modular Dual Mobility, Stryker). To our knowledge, 2 cases of AIPD with this prosthesis have been reported.7, 8 As with the cases in Europe, closed reduction was the suspected cause, but there was no explanation for the initial dislocation event.

In this article, we present the case of a nondemented man who developed AIPD of a THA with the MDM component and a 28-mm femoral head with a skirted neck (StelKast). His operative findings suggest a poor head-to-neck ratio caused by a larger diameter femoral neck or a skirted prosthesis, or a forceful reduction maneuver, may predispose DM components to AIPD. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

In 2012, a 63-year-old man with a history of drug abuse underwent left primary THA. Seven posterior dislocations and 3 years later, the acetabular component was revised to the MDM prosthesis; the well-fixed StelKast femoral component was retained (Figure 1).

Figure 1.

Within 3 months after revision surgery, the left hip dislocated 3 times in 1 week, when the patient bent over to retrieve an object on the ground. The first 2 dislocations were treated with closed reduction under conscious sedation at an outside emergency department.

Figure 2.
Shortly after, the patient, with complaints of left hip pain and clunking, was seen by a physician assistant, but the treating team did not notice the eccentric reduction on radiographs. The third dislocation was treated with closed reduction under conscious sedation in the emergency department at our institution (Figure 2). Postreduction radiographs still showed the eccentric reduction, and a radiolucent halo was visible superior to the greater trochanter (Figure 3).
Figure 3.


With the patient’s erythrocyte sedimentation rate and C-reactive protein level both normal, a second revision was performed. During surgery, the polyethylene head was found beneath the gluteus maximus (Figure 4).
Figure 4.
Gross inspection revealed a small amount of eccentric polyethylene wear and metal debris of the inner articulation (Figure 5). As the abductor muscles were intact, it was decided to proceed with revision to a larger DM component and to downsize the femoral head to a skirtless component (Table, Figure 6).

 

 

Discussion

Recurrent dislocation and instability accounts for 22.5% of THA revisions in the United States.9 Until 2011, options for managing recurrent dislocation in the United States included modular component exchange, component revision for malposition, and use of constrained components.10

Figure 5.
However, the decreased motion of constrained components may produce excess stress that eventually results in failure.11-13

In 1974, Bousquet first reported use of the DM prosthesis in primary THA; the prosthesis allowed increased stability without sacrificing motion or fixation.1 However, longer-term studies of DM components disclosed a new complication, IPD. In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation of the Bousquet prosthesis.

Table.
Philippot and colleagues5 reported that 81 of 1960 primary THAs with DM components developed IPD a mean of 9 years after implantation. They described 3 types of IPD based on mechanism of injury: type I, caused by wear of the inner articulation without arthrofibrosis or cup loosening (n = 26); type II, resulting from blocked outer articulation motion, caused by arthrofibrosis, nonunion, calcification, or heterotopic ossification (n = 41); and type III, associated with acetabular component loosening (n = 14). IPD occurred an average of 11 years (type I), 8 years (type II), and 9 years (type III) after implantation.

AIPD, which occurs within 1 year after implantation, has been reported much less often than late IPD. Stigbrand and Ullmark6 reported 3 cases of AIPD that developed within 7 months after implantation of Amplitude and Advantage (Zimmer Biomet) DM prostheses.
Figure 6.
The authors proposed that AIPD is related to incomplete coupling of the metal head and the inner polyethylene liner or to shearing of the large polyethylene component on the acetabular rim during a closed reduction maneuver. According to their description, the femoral head in the acetabulum had an “eccentric” radiographic appearance. The authors recommended administering muscle relaxants during closed reduction to avoid dissociation of the liner during the reduction.

This unusual complication apparently is not confined to a specific implant or region. Since the MDM component was introduced in the United States, 2 more cases of AIPD have been identified (Table). Banzhof and colleagues7 reported the case of a 68-year-old woman who, 2 months after the MDM was placed for recurrent instability, dislocated the component while rising from a seated position. Her IPD most likely resulted from a closed reduction. The affected hip eventually required closed reduction in the operating room. Postreduction radiographs showed the characteristic eccentric appearance; a halo, also visible in the soft tissues, corresponded with the dissociated radiolucent polyethylene liner. The authors attributed the early failure to an eccentrically seated metal liner that separated the locking mechanism. The MDM component was revised to a conventional THA, with the femoral head upsized and length added.

Ward and colleagues8 reported the case of an 87-year-old woman who had a conventional THA revised to an MDM component for recurrent instability. Two months after surgery, this patient, who had dementia, experienced 2 posterior dislocations while rising from a chair. Closed reduction in the emergency department seemed successful, but later she presented to the surgeon’s office with symptoms of instability and clunking, complaints similar to our patient’s. Radiographs showed an eccentric reduction caused by IPD, and the MDM component was revised to a constrained liner. Adding a MDM component to a retained DePuy (DePuy Synthes) femoral stem and head is considered “off-label use,” which, the authors proposed, may have been related to the AIPD in their patient’s case. However, one manufacturer’s femoral component and head are often mated with another manufacturer’s acetabular component to allow for a less complex revision. Our recommendation for surgeons is that, before proceeding with this treatment option, they investigate each component’s exact dimensions to ensure there are no subtle size differences that could cause problems. For example, a 28-mm head diameter that is actually 28.2 mm may affect mating properties, with the inner polyethylene articulation causing AIPD to develop.

Other cases of earlier IPD have been described, but they do not fit the APID definition given in this article. Riviere and colleagues14 reported the case of a 42-year-old man who, because of a previous adverse reaction to metal debris, underwent revision to a DM polyethylene ball in a retained BHR (Birmingham Hip Resurfacing) acetabular shell (Birmingham Hip, Smith & Nephew). Unfortunately, IPD occurred 14 months after surgery. Banka and colleagues15 reported the case of a 70-year-old woman who underwent revision to a DM cup for recurrent instability, but they did not specify the length of time between implantation and IPD and did not offer an explanation for the complication. Finally, Odland and Sierra16 reported the case of a 77-year-old man, with previous intertrochanteric and pelvic fractures, who underwent revision to a DM cup with retention of a Waldemar femoral component (Waldemar Link). He spontaneously developed IPD with ambulation 2 years after surgery.

Certainly, our patient’s presentation course is similar to other patients’. Within 3 months after revision to the MDM component, his left hip dislocated 3 times in 1 week. We contend his AIPD resulted from closed reduction, with the polyethylene dislodged from the femoral head with contact on the acetabulum. A larger or skirted neck may increase impingement during normal activity and thereby widen the polyethylene opening excessively and/or reduce the polyethylene ball ROM to impinge during the relocation maneuver. In this case, dissociation was noted only after the third dislocation. Pathognomonic eccentric positioning of the head in the acetabulum and, less commonly, the halo sign were evident on postreduction radiographs. Optimal treatment for AIPD of a DM component is controversial. Choices are limited to a constrained liner or, if possible, repeat DM with larger components. For recurrent dislocation, our patient underwent revision to an MDM component, but a femoral head with a skirted neck was used in an attempt to increase soft-tissue tension. During the second revision, minor eccentric wear of the inner articulation of the polyethylene component (consistent with impingement) was noted, and wear was visible on inspection of the outer articulation. We think his AIPD resulted from femoral neck impingement of the skirted head against the polyethylene ball.

AIPD is a discrete entity, with sudden failure of a DM component within 1 year after implantation. AIPD is characterized by dissociation of the femoral head from the inner articulation, resulting from impingement or closed reduction. More studies are needed to determine which patients with DM components are at highest risk and which treatment is most appropriate. We recommend taking extra care when reducing hips with this articulation and adopting a low threshold for general anesthesia use in the presence of paralysis.

Am J Orthop. 2017;46(3):E154-E159. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

Take-Home Points

  • AIPD of DM-THA is defined by dissociation within 1 year of implantation resulting from component impingement or closed reduction maneuvers.
  • This is a distinct entity from “late” IPD (>1 year) from implantation as this is associated most often with polyethylene wear, component loosening, and arthrofibrosis.
  • A history of DM dislocation followed by subjective “clunking,” instability, and a series of more frequent dislocations should raise concern for AIPD.
  • Classic radiographic findings of AIPD include eccentric hip reduction and soft tissue radiolucency (ie, halo sign) from dissociated polyethylene component.
  • Treating practitioners of AIPD should consider closed reduction with general anesthesia and sedation in the operating room to limit risk of dissociation.

Dual-mobility (DM) components were invented in the 1970s and have been used in primary and revision total hip arthroplasty (THA) in Europe ever since.1 However, DM components are most commonly used in the treatment of recurrent hip instability, and early results have been promising.2 In DM-THAs, a smaller (22-mm or 28-mm) metal femoral head snap-fits into a larger polyethylene ball (inner articulation), which articulates with a highly polished metal shell (outer articulation), which is either implanted directly in the acetabulum or placed in an uncemented acetabular cup. The 2 articulations used in these devices theoretically increase hip range of motion (ROM) and increase the inferior head displacement distance (jump distance) required for dislocation.3

However, this DM articulation with increased ROM may also cause chronic impingement of the femoral component neck or Morse taper against the outer polyethylene bearing, resulting in polyethylene wear and late intraprosthetic dissociation (IPD) (separation of inner articulation between femoral head and polyethylene liner). In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation during the period 1989 to 1997. In 2013, Philippot and colleagues5 reported that 81 of 1960 primary THAs developed IPD a mean of 9 years after implantation. These IPD cases were attributed to polyethylene wear or outer articulation blockage caused by arthrofibrosis or heterotopic ossification. Reports of acute IPD (AIPD), however, are rare. In 2011, Stigbrand and Ullmark6 reported 3 cases in which the DM prosthesis dislocated within 1 year after implantation. It was suggested that the inner metal head dissociated from the larger polyethylene component after attempted closed reduction for dislocation (separation of larger polyethylene component from acetabulum or acetabular liner).

DM components were unavailable to surgeons in the United States until 2011. The first US Food and Drug Administration (FDA)-approved DM device was the MDM (Modular Dual Mobility, Stryker). To our knowledge, 2 cases of AIPD with this prosthesis have been reported.7, 8 As with the cases in Europe, closed reduction was the suspected cause, but there was no explanation for the initial dislocation event.

In this article, we present the case of a nondemented man who developed AIPD of a THA with the MDM component and a 28-mm femoral head with a skirted neck (StelKast). His operative findings suggest a poor head-to-neck ratio caused by a larger diameter femoral neck or a skirted prosthesis, or a forceful reduction maneuver, may predispose DM components to AIPD. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

In 2012, a 63-year-old man with a history of drug abuse underwent left primary THA. Seven posterior dislocations and 3 years later, the acetabular component was revised to the MDM prosthesis; the well-fixed StelKast femoral component was retained (Figure 1).

Figure 1.

Within 3 months after revision surgery, the left hip dislocated 3 times in 1 week, when the patient bent over to retrieve an object on the ground. The first 2 dislocations were treated with closed reduction under conscious sedation at an outside emergency department.

Figure 2.
Shortly after, the patient, with complaints of left hip pain and clunking, was seen by a physician assistant, but the treating team did not notice the eccentric reduction on radiographs. The third dislocation was treated with closed reduction under conscious sedation in the emergency department at our institution (Figure 2). Postreduction radiographs still showed the eccentric reduction, and a radiolucent halo was visible superior to the greater trochanter (Figure 3).
Figure 3.


With the patient’s erythrocyte sedimentation rate and C-reactive protein level both normal, a second revision was performed. During surgery, the polyethylene head was found beneath the gluteus maximus (Figure 4).
Figure 4.
Gross inspection revealed a small amount of eccentric polyethylene wear and metal debris of the inner articulation (Figure 5). As the abductor muscles were intact, it was decided to proceed with revision to a larger DM component and to downsize the femoral head to a skirtless component (Table, Figure 6).

 

 

Discussion

Recurrent dislocation and instability accounts for 22.5% of THA revisions in the United States.9 Until 2011, options for managing recurrent dislocation in the United States included modular component exchange, component revision for malposition, and use of constrained components.10

Figure 5.
However, the decreased motion of constrained components may produce excess stress that eventually results in failure.11-13

In 1974, Bousquet first reported use of the DM prosthesis in primary THA; the prosthesis allowed increased stability without sacrificing motion or fixation.1 However, longer-term studies of DM components disclosed a new complication, IPD. In 2004, Lecuire and colleagues4 reported 7 cases of IPD occurring a mean of 10 years after implantation of the Bousquet prosthesis.

Table.
Philippot and colleagues5 reported that 81 of 1960 primary THAs with DM components developed IPD a mean of 9 years after implantation. They described 3 types of IPD based on mechanism of injury: type I, caused by wear of the inner articulation without arthrofibrosis or cup loosening (n = 26); type II, resulting from blocked outer articulation motion, caused by arthrofibrosis, nonunion, calcification, or heterotopic ossification (n = 41); and type III, associated with acetabular component loosening (n = 14). IPD occurred an average of 11 years (type I), 8 years (type II), and 9 years (type III) after implantation.

AIPD, which occurs within 1 year after implantation, has been reported much less often than late IPD. Stigbrand and Ullmark6 reported 3 cases of AIPD that developed within 7 months after implantation of Amplitude and Advantage (Zimmer Biomet) DM prostheses.
Figure 6.
The authors proposed that AIPD is related to incomplete coupling of the metal head and the inner polyethylene liner or to shearing of the large polyethylene component on the acetabular rim during a closed reduction maneuver. According to their description, the femoral head in the acetabulum had an “eccentric” radiographic appearance. The authors recommended administering muscle relaxants during closed reduction to avoid dissociation of the liner during the reduction.

This unusual complication apparently is not confined to a specific implant or region. Since the MDM component was introduced in the United States, 2 more cases of AIPD have been identified (Table). Banzhof and colleagues7 reported the case of a 68-year-old woman who, 2 months after the MDM was placed for recurrent instability, dislocated the component while rising from a seated position. Her IPD most likely resulted from a closed reduction. The affected hip eventually required closed reduction in the operating room. Postreduction radiographs showed the characteristic eccentric appearance; a halo, also visible in the soft tissues, corresponded with the dissociated radiolucent polyethylene liner. The authors attributed the early failure to an eccentrically seated metal liner that separated the locking mechanism. The MDM component was revised to a conventional THA, with the femoral head upsized and length added.

Ward and colleagues8 reported the case of an 87-year-old woman who had a conventional THA revised to an MDM component for recurrent instability. Two months after surgery, this patient, who had dementia, experienced 2 posterior dislocations while rising from a chair. Closed reduction in the emergency department seemed successful, but later she presented to the surgeon’s office with symptoms of instability and clunking, complaints similar to our patient’s. Radiographs showed an eccentric reduction caused by IPD, and the MDM component was revised to a constrained liner. Adding a MDM component to a retained DePuy (DePuy Synthes) femoral stem and head is considered “off-label use,” which, the authors proposed, may have been related to the AIPD in their patient’s case. However, one manufacturer’s femoral component and head are often mated with another manufacturer’s acetabular component to allow for a less complex revision. Our recommendation for surgeons is that, before proceeding with this treatment option, they investigate each component’s exact dimensions to ensure there are no subtle size differences that could cause problems. For example, a 28-mm head diameter that is actually 28.2 mm may affect mating properties, with the inner polyethylene articulation causing AIPD to develop.

Other cases of earlier IPD have been described, but they do not fit the APID definition given in this article. Riviere and colleagues14 reported the case of a 42-year-old man who, because of a previous adverse reaction to metal debris, underwent revision to a DM polyethylene ball in a retained BHR (Birmingham Hip Resurfacing) acetabular shell (Birmingham Hip, Smith & Nephew). Unfortunately, IPD occurred 14 months after surgery. Banka and colleagues15 reported the case of a 70-year-old woman who underwent revision to a DM cup for recurrent instability, but they did not specify the length of time between implantation and IPD and did not offer an explanation for the complication. Finally, Odland and Sierra16 reported the case of a 77-year-old man, with previous intertrochanteric and pelvic fractures, who underwent revision to a DM cup with retention of a Waldemar femoral component (Waldemar Link). He spontaneously developed IPD with ambulation 2 years after surgery.

Certainly, our patient’s presentation course is similar to other patients’. Within 3 months after revision to the MDM component, his left hip dislocated 3 times in 1 week. We contend his AIPD resulted from closed reduction, with the polyethylene dislodged from the femoral head with contact on the acetabulum. A larger or skirted neck may increase impingement during normal activity and thereby widen the polyethylene opening excessively and/or reduce the polyethylene ball ROM to impinge during the relocation maneuver. In this case, dissociation was noted only after the third dislocation. Pathognomonic eccentric positioning of the head in the acetabulum and, less commonly, the halo sign were evident on postreduction radiographs. Optimal treatment for AIPD of a DM component is controversial. Choices are limited to a constrained liner or, if possible, repeat DM with larger components. For recurrent dislocation, our patient underwent revision to an MDM component, but a femoral head with a skirted neck was used in an attempt to increase soft-tissue tension. During the second revision, minor eccentric wear of the inner articulation of the polyethylene component (consistent with impingement) was noted, and wear was visible on inspection of the outer articulation. We think his AIPD resulted from femoral neck impingement of the skirted head against the polyethylene ball.

AIPD is a discrete entity, with sudden failure of a DM component within 1 year after implantation. AIPD is characterized by dissociation of the femoral head from the inner articulation, resulting from impingement or closed reduction. More studies are needed to determine which patients with DM components are at highest risk and which treatment is most appropriate. We recommend taking extra care when reducing hips with this articulation and adopting a low threshold for general anesthesia use in the presence of paralysis.

Am J Orthop. 2017;46(3):E154-E159. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

 

 

References

1. Farizon F, de Lavison R, Azoulai JJ, Bousquet G. Results with a cementless alumina-coated cup with dual mobility. A twelve-year follow-up study. Int Orthop. 1998;22(4):219-224.

2. Lachiewicz PF, Watters TS. The use of dual-mobility components in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(8):481-486.

3. De Martino I, Triantafyllopoulos GK, Sculco PK, Sculco TP. Dual mobility cups in total hip arthroplasty. World J Orthop. 2014;5(3):180-187.

4. Lecuire F, Benareau I, Rubini J, Basso M. Intra-prosthetic dislocation of the Bousquet dual mobility socket [in French]. Rev Chir Orthop Reparatrice Appar Mot. 2004;90(3):249-255.

5. Philippot R, Boyer B, Farizon F. Intraprosthetic dislocation: a specific complication of the dual-mobility system. Clin Orthop Relat Res. 2013;471(3):965-970.

6. Stigbrand H, Ullmark G. Component dissociation after closed reduction of dual mobility sockets—a report of three cases. Hip Int. 2011;21(2):263-266.

7. Banzhof JA, Robbins CE, Ven AV, Talmo CT, Bono JV. Femoral head dislodgement complicating use of a dual mobility prosthesis for recurrent instability. J Arthroplasty. 2013;28(3):543.e1-e3.

8. Ward JP, McCardel BR, Hallstrom BR. Complete dissociation of the polyethylene component in a newly available dual-mobility bearing used in total hip arthroplasty: a case report. JBJS Case Connect. 2013;3(3):e94.

9. Bozic KJ, Kurtz SM, Lau E, Ong K, Vail TP, Berry DJ. The epidemiology of revision total hip arthroplasty in the United States. J Bone Joint Surg Am. 2009;91(1):128-133.

10. Parvizi J, Picinic E, Sharkey PF. Revision total hip arthroplasty for instability: surgical techniques and principles. J Bone Joint Surg Am. 2008;90(5):1134-1142.

11. Guyen O, Lewallen DG, Cabanela ME. Modes of failure of Osteonics constrained tripolar implants: a retrospective analysis of forty-three failed implants. J Bone Joint Surg Am. 2008;90(7):1553-1560.

12. Lachiewicz PF, Kelley SS. The use of constrained components in total hip arthroplasty. J Am Acad Orthop Surg. 2002;10(4):233-238.

13. Williams JT Jr, Ragland PS, Clarke S. Constrained components for the unstable hip following total hip arthroplasty: a literature review. Int Orthop. 2007;31(3):273-277.

14. Riviere C, Lavigne M, Alghamdi A, Vendittoli PA. Early failure of metal-on-metal large-diameter head total hip arthroplasty revised with a dual-mobility bearing: a case report. JBJS Case Connect. 2013;3(3):e95.

15. Banka TR, Ast MP, Parks ML. Early intraprosthetic dislocation in a revision dual-mobility hip prosthesis. Orthopedics. 2014;37(4):e395-e397.

16. Odland AN, Sierra RJ. Intraprosthetic dislocation of a contemporary dual-mobility design used during conversion THA. Orthopedics. 2014;37(12):e1124-e1128.

References

1. Farizon F, de Lavison R, Azoulai JJ, Bousquet G. Results with a cementless alumina-coated cup with dual mobility. A twelve-year follow-up study. Int Orthop. 1998;22(4):219-224.

2. Lachiewicz PF, Watters TS. The use of dual-mobility components in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(8):481-486.

3. De Martino I, Triantafyllopoulos GK, Sculco PK, Sculco TP. Dual mobility cups in total hip arthroplasty. World J Orthop. 2014;5(3):180-187.

4. Lecuire F, Benareau I, Rubini J, Basso M. Intra-prosthetic dislocation of the Bousquet dual mobility socket [in French]. Rev Chir Orthop Reparatrice Appar Mot. 2004;90(3):249-255.

5. Philippot R, Boyer B, Farizon F. Intraprosthetic dislocation: a specific complication of the dual-mobility system. Clin Orthop Relat Res. 2013;471(3):965-970.

6. Stigbrand H, Ullmark G. Component dissociation after closed reduction of dual mobility sockets—a report of three cases. Hip Int. 2011;21(2):263-266.

7. Banzhof JA, Robbins CE, Ven AV, Talmo CT, Bono JV. Femoral head dislodgement complicating use of a dual mobility prosthesis for recurrent instability. J Arthroplasty. 2013;28(3):543.e1-e3.

8. Ward JP, McCardel BR, Hallstrom BR. Complete dissociation of the polyethylene component in a newly available dual-mobility bearing used in total hip arthroplasty: a case report. JBJS Case Connect. 2013;3(3):e94.

9. Bozic KJ, Kurtz SM, Lau E, Ong K, Vail TP, Berry DJ. The epidemiology of revision total hip arthroplasty in the United States. J Bone Joint Surg Am. 2009;91(1):128-133.

10. Parvizi J, Picinic E, Sharkey PF. Revision total hip arthroplasty for instability: surgical techniques and principles. J Bone Joint Surg Am. 2008;90(5):1134-1142.

11. Guyen O, Lewallen DG, Cabanela ME. Modes of failure of Osteonics constrained tripolar implants: a retrospective analysis of forty-three failed implants. J Bone Joint Surg Am. 2008;90(7):1553-1560.

12. Lachiewicz PF, Kelley SS. The use of constrained components in total hip arthroplasty. J Am Acad Orthop Surg. 2002;10(4):233-238.

13. Williams JT Jr, Ragland PS, Clarke S. Constrained components for the unstable hip following total hip arthroplasty: a literature review. Int Orthop. 2007;31(3):273-277.

14. Riviere C, Lavigne M, Alghamdi A, Vendittoli PA. Early failure of metal-on-metal large-diameter head total hip arthroplasty revised with a dual-mobility bearing: a case report. JBJS Case Connect. 2013;3(3):e95.

15. Banka TR, Ast MP, Parks ML. Early intraprosthetic dislocation in a revision dual-mobility hip prosthesis. Orthopedics. 2014;37(4):e395-e397.

16. Odland AN, Sierra RJ. Intraprosthetic dislocation of a contemporary dual-mobility design used during conversion THA. Orthopedics. 2014;37(12):e1124-e1128.

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Think twice before recommending partial meniscectomy

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– Patients with knee osteoarthritis (OA) and a meniscal tear who underwent arthroscopic partial meniscectomy (APM) subsequently experienced accelerated structural progression of their OA, compared with those randomized to physical therapy alone in the randomized METEOR trial.

“In discussing treatment options for symptomatic meniscal tear, patients and providers must weigh the potential benefits and risks of arthroscopic partial meniscectomy, including this increased risk of structural progression,” Jamie E. Collins, PhD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News
Dr. Jamie E. Collins
The METEOR (Meniscal Tear in Osteoarthritis Research; NCT00597012) findings are clinically relevant because an estimated 14 million Americans have knee OA, and three-quarters of them also have MRI evidence of a meniscal tear, observed Dr. Collins, a senior statistician at the Orthopaedic and Arthritis Center for Outcomes Research at Brigham and Women’s Hospital, Boston.

A thorough physician-patient discussion also needs to mention that several large randomized trials have suggested that patients with meniscal tear and osteoarthritic changes experience similar pain relief with APM plus physical therapy (PT) as compared with PT alone, she added at the congress sponsored by the Osteoarthritis Research Society International.

The METEOR trial was a seven-center U.S. randomized trial of APM plus PT or PT alone in patients with MRI or radiographic evidence of OA changes, a meniscal tear on MRI, and mechanical knee symptoms. Dr. Collins reported on 176 randomized patients with baseline and 18-month follow-up MRIs read by a specialist musculoskeletal radiologist. This analysis excluded the 37 patients in the PT group who crossed over to APM within 6 months after randomization.

In an analysis adjusted for baseline Kellgren-Lawrence grade of radiographic knee changes and other potential confounders, the surgically treated group was 2.6 times more likely to demonstrate an increase in the number of knee subregions affected by osteophytes on their MRIs at 18 months. They were also 2.4 times more likely to have any worsening in osteophyte score and 5.1 times more likely to have worsening of their effusion-synovitis score on the MRI OA Knee Score. In addition, the APM group also demonstrated both worsening cartilage thickness and surface area.

There was no significant difference between the two treatment groups in changes in bone marrow lesions or Hoffa-synovitis.

A secondary analysis that incorporated the 37 crossovers from PT to APM within 6 months showed similarly accelerated OA progression after arthroscopic surgery.

“Future work should focus on determining whether this accelerated structural progression is associated with changes in symptoms and ultimately with a higher risk of total knee replacement. In other words, is 2+ structural worsening something that’s noticeable or important for patients?” Dr. Collins concluded.

She reported having no financial conflicts regarding her study, which was sponsored by Brigham and Women’s Hospital.

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– Patients with knee osteoarthritis (OA) and a meniscal tear who underwent arthroscopic partial meniscectomy (APM) subsequently experienced accelerated structural progression of their OA, compared with those randomized to physical therapy alone in the randomized METEOR trial.

“In discussing treatment options for symptomatic meniscal tear, patients and providers must weigh the potential benefits and risks of arthroscopic partial meniscectomy, including this increased risk of structural progression,” Jamie E. Collins, PhD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News
Dr. Jamie E. Collins
The METEOR (Meniscal Tear in Osteoarthritis Research; NCT00597012) findings are clinically relevant because an estimated 14 million Americans have knee OA, and three-quarters of them also have MRI evidence of a meniscal tear, observed Dr. Collins, a senior statistician at the Orthopaedic and Arthritis Center for Outcomes Research at Brigham and Women’s Hospital, Boston.

A thorough physician-patient discussion also needs to mention that several large randomized trials have suggested that patients with meniscal tear and osteoarthritic changes experience similar pain relief with APM plus physical therapy (PT) as compared with PT alone, she added at the congress sponsored by the Osteoarthritis Research Society International.

The METEOR trial was a seven-center U.S. randomized trial of APM plus PT or PT alone in patients with MRI or radiographic evidence of OA changes, a meniscal tear on MRI, and mechanical knee symptoms. Dr. Collins reported on 176 randomized patients with baseline and 18-month follow-up MRIs read by a specialist musculoskeletal radiologist. This analysis excluded the 37 patients in the PT group who crossed over to APM within 6 months after randomization.

In an analysis adjusted for baseline Kellgren-Lawrence grade of radiographic knee changes and other potential confounders, the surgically treated group was 2.6 times more likely to demonstrate an increase in the number of knee subregions affected by osteophytes on their MRIs at 18 months. They were also 2.4 times more likely to have any worsening in osteophyte score and 5.1 times more likely to have worsening of their effusion-synovitis score on the MRI OA Knee Score. In addition, the APM group also demonstrated both worsening cartilage thickness and surface area.

There was no significant difference between the two treatment groups in changes in bone marrow lesions or Hoffa-synovitis.

A secondary analysis that incorporated the 37 crossovers from PT to APM within 6 months showed similarly accelerated OA progression after arthroscopic surgery.

“Future work should focus on determining whether this accelerated structural progression is associated with changes in symptoms and ultimately with a higher risk of total knee replacement. In other words, is 2+ structural worsening something that’s noticeable or important for patients?” Dr. Collins concluded.

She reported having no financial conflicts regarding her study, which was sponsored by Brigham and Women’s Hospital.

 

– Patients with knee osteoarthritis (OA) and a meniscal tear who underwent arthroscopic partial meniscectomy (APM) subsequently experienced accelerated structural progression of their OA, compared with those randomized to physical therapy alone in the randomized METEOR trial.

“In discussing treatment options for symptomatic meniscal tear, patients and providers must weigh the potential benefits and risks of arthroscopic partial meniscectomy, including this increased risk of structural progression,” Jamie E. Collins, PhD, said at the World Congress on Osteoarthritis.

Bruce Jancin/Frontline Medical News
Dr. Jamie E. Collins
The METEOR (Meniscal Tear in Osteoarthritis Research; NCT00597012) findings are clinically relevant because an estimated 14 million Americans have knee OA, and three-quarters of them also have MRI evidence of a meniscal tear, observed Dr. Collins, a senior statistician at the Orthopaedic and Arthritis Center for Outcomes Research at Brigham and Women’s Hospital, Boston.

A thorough physician-patient discussion also needs to mention that several large randomized trials have suggested that patients with meniscal tear and osteoarthritic changes experience similar pain relief with APM plus physical therapy (PT) as compared with PT alone, she added at the congress sponsored by the Osteoarthritis Research Society International.

The METEOR trial was a seven-center U.S. randomized trial of APM plus PT or PT alone in patients with MRI or radiographic evidence of OA changes, a meniscal tear on MRI, and mechanical knee symptoms. Dr. Collins reported on 176 randomized patients with baseline and 18-month follow-up MRIs read by a specialist musculoskeletal radiologist. This analysis excluded the 37 patients in the PT group who crossed over to APM within 6 months after randomization.

In an analysis adjusted for baseline Kellgren-Lawrence grade of radiographic knee changes and other potential confounders, the surgically treated group was 2.6 times more likely to demonstrate an increase in the number of knee subregions affected by osteophytes on their MRIs at 18 months. They were also 2.4 times more likely to have any worsening in osteophyte score and 5.1 times more likely to have worsening of their effusion-synovitis score on the MRI OA Knee Score. In addition, the APM group also demonstrated both worsening cartilage thickness and surface area.

There was no significant difference between the two treatment groups in changes in bone marrow lesions or Hoffa-synovitis.

A secondary analysis that incorporated the 37 crossovers from PT to APM within 6 months showed similarly accelerated OA progression after arthroscopic surgery.

“Future work should focus on determining whether this accelerated structural progression is associated with changes in symptoms and ultimately with a higher risk of total knee replacement. In other words, is 2+ structural worsening something that’s noticeable or important for patients?” Dr. Collins concluded.

She reported having no financial conflicts regarding her study, which was sponsored by Brigham and Women’s Hospital.

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Key clinical point: Patients with knee osteoarthritis and a meniscal tear treated via arthroscopic partial meniscectomy subsequently experienced accelerated structural progression of their osteoarthritis.

Major finding: Surgically treated patients were 2.6 times more likely to demonstrate MRI evidence of structural disease progression at 18 months than those who received physical therapy alone.

Data source: This analysis from the multicenter METEOR trial included 176 patients with a symptomatic meniscal tear.

Disclosures: The presenter reported having no financial conflicts regarding her study, which was sponsored by Brigham and Women’s Hospital.

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When Can Exercise Supplant Surgery for Degenerative Meniscal Tears?

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When Can Exercise Supplant Surgery for Degenerative Meniscal Tears?

 

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the past 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus but does have medial joint line tenderness of his right knee. An MRI shows a partial medial meniscal tear. Do you refer him to physical therapy (PT) or to orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or as a result of degeneration over time. Traumatic meniscal tears typically occur in those younger than 30 during sports (eg, basketball, soccer), whereas degenerative meniscal tears generally occur in patients ages 40 to 60.2,3 The annual incidence of all meniscal tears is 79 per 100,000.4 While some clinicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are more challenging and typically warrant an MRI for confirmation.3

Meniscal tears can be treated either conservatively, with supportive care and exercise, or surgically. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study, 95 of 117 patients (81.2%) were generally satisfied with surgical treatment at four-year follow-up; satisfaction was higher among those with a traumatic meniscal tear than in those with a degenerative tear.5

Two systematic reviews of surgery versus nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.6,7 However, both studies were of only moderate quality, because of the number of patients in the nonoperative groups who ultimately underwent surgery. Neither of the studies directly compared surgery to nonoperative management.6,7Another investigation—a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients—compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.8

Clinical practice recommendations devised from a vast systematic review of the literature recommend that the decision for surgery be based on patient-specific factors, such as symptoms, age, mechanism of tear, extent of damage, and occupational/social/activity needs.9

STUDY SUMMARY

Exercise is as good as surgery

The current superiority RCT compared exercise therapy to arthroscopic partial meniscectomy. Subjects (ages 35 to 60) presented to the orthopedic department of two hospitals in Norway with unilateral knee pain of more than two months’ duration and an MRI-delineated medial meniscal tear. They were included in the study only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤ 2). Exclusion criteria included acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous two years.

The primary outcomes were change in patient-reported knee function (as determined by overall Knee injury and Osteoarthritis Outcome Score [KOOS] after two years) and thigh muscle strength at three months (as measured by physiotherapists). The researchers used four of the five KOOS subscales for this analysis: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). The average score of each subscale was used.

Secondary outcomes included the five individual KOOS subscales (the four previously mentioned, plus activities of daily living [ADLs]), as well as thigh muscle strength and lower-extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy; upon discharge, those in the latter group received written and oral encouragement to perform simple exercises at home, two to four times daily, to regain range of motion and reduce swelling.

Results. At two years, the overall mean improvement in KOOS4 score from baseline was similar between the exercise group and the meniscectomy group (25.3 pts vs 24.4 pts, respectively; mean difference [MD], 0.9). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both three and 12 months showed significant objective improvements favoring exercise therapy.

In the secondary analysis of the KOOS subscale scores, change from baseline was nonsignificant for four of the five (pain, ADL, sports/recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 pts); this was likely clinically insignificant on a grading scale of 0 to 100.

Of the patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the two-year study period.

 

 

 

WHAT’S NEW

Head-to-head comparison adds evidence

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a two-year follow-up period and was superior in the short term for thigh muscle strength.1

The results of this study build on those from the aforementioned smaller study conducted in Finland.8 In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

What about more severe osteoarthritis?

This trial included patients with no to mild osteoarthritis in addition to their meniscal tear.1 It is unclear if the results would be maintained in those with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

Cost and effort of PT

The cost of PT can be a barrier for patients who have adequate insurance coverage for surgery but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing time and effort, which may deter those with busy lifestyles. Patients and clinicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2017. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2017;66[4]:250-252).

References

1. Kise NJ, Risberg MA, Stensrud S, et al. Exercise therapy versus arthroscopic partial meniscectomy for degenerative meniscal tear in middle aged patients: randomised controlled trial with two year follow-up. BMJ. 2016;354:i3740.
2. Beals CT, Magnussen RA, Graham WC, et al. The prevalence of meniscal pathology in asymptomatic athletes. Sports Med. 2016;46:1517-1524.
3. Maffulli N, Longo UG, Campi S, et al. Meniscal tears. Open Access J Sports Med. 2010;1:45-54.
4. Peat G, Bergknut C, Frobell R, et al. Population-wide incidence estimates for soft tissue knee injuries presenting to healthcare in southern Sweden: data from the Skåne Healthcare Register. Arthritis Res Ther. 2014;16:R162.
5. Ghislain NA, Wei JN, Li YG. Study of the clinical outcome between traumatic and degenerative (non-traumatic) meniscal tears after arthroscopic surgery: a 4-years follow-up study. J Clin Diagn Res. 2016;10:RC01-RC04.
6. Khan M, Evaniew N, Bedi A, et al. Arthroscopic surgery for degenerative tears of the meniscus: a systematic review and meta-analysis. CMAJ. 2014;186:1057-1064.
7. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery: a systematic review of the evidence for operative management of meniscal tears. Am J Sports Med. 2017;45:965-973.
8. Sihvonen R, Paavola M, Malmivaara A, et al; Finnish Degenerative Meniscal Lesion Study (FIDELITY) Group. Arthroscopic partial meniscectomy versus sham surgery for a degenerative meniscal tear. N Engl J Med. 2013;369:2515-2524.
9. Beaufils P, Hulet C, Dhénain M, et al. Clinical practice guidelines for the management of meniscal lesions and isolated lesions of the anterior cruciate ligament of the knee in adults. Orthop Traumatol Surg Res. 2009;95:437-442.

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Related Articles

 

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the past 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus but does have medial joint line tenderness of his right knee. An MRI shows a partial medial meniscal tear. Do you refer him to physical therapy (PT) or to orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or as a result of degeneration over time. Traumatic meniscal tears typically occur in those younger than 30 during sports (eg, basketball, soccer), whereas degenerative meniscal tears generally occur in patients ages 40 to 60.2,3 The annual incidence of all meniscal tears is 79 per 100,000.4 While some clinicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are more challenging and typically warrant an MRI for confirmation.3

Meniscal tears can be treated either conservatively, with supportive care and exercise, or surgically. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study, 95 of 117 patients (81.2%) were generally satisfied with surgical treatment at four-year follow-up; satisfaction was higher among those with a traumatic meniscal tear than in those with a degenerative tear.5

Two systematic reviews of surgery versus nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.6,7 However, both studies were of only moderate quality, because of the number of patients in the nonoperative groups who ultimately underwent surgery. Neither of the studies directly compared surgery to nonoperative management.6,7Another investigation—a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients—compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.8

Clinical practice recommendations devised from a vast systematic review of the literature recommend that the decision for surgery be based on patient-specific factors, such as symptoms, age, mechanism of tear, extent of damage, and occupational/social/activity needs.9

STUDY SUMMARY

Exercise is as good as surgery

The current superiority RCT compared exercise therapy to arthroscopic partial meniscectomy. Subjects (ages 35 to 60) presented to the orthopedic department of two hospitals in Norway with unilateral knee pain of more than two months’ duration and an MRI-delineated medial meniscal tear. They were included in the study only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤ 2). Exclusion criteria included acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous two years.

The primary outcomes were change in patient-reported knee function (as determined by overall Knee injury and Osteoarthritis Outcome Score [KOOS] after two years) and thigh muscle strength at three months (as measured by physiotherapists). The researchers used four of the five KOOS subscales for this analysis: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). The average score of each subscale was used.

Secondary outcomes included the five individual KOOS subscales (the four previously mentioned, plus activities of daily living [ADLs]), as well as thigh muscle strength and lower-extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy; upon discharge, those in the latter group received written and oral encouragement to perform simple exercises at home, two to four times daily, to regain range of motion and reduce swelling.

Results. At two years, the overall mean improvement in KOOS4 score from baseline was similar between the exercise group and the meniscectomy group (25.3 pts vs 24.4 pts, respectively; mean difference [MD], 0.9). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both three and 12 months showed significant objective improvements favoring exercise therapy.

In the secondary analysis of the KOOS subscale scores, change from baseline was nonsignificant for four of the five (pain, ADL, sports/recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 pts); this was likely clinically insignificant on a grading scale of 0 to 100.

Of the patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the two-year study period.

 

 

 

WHAT’S NEW

Head-to-head comparison adds evidence

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a two-year follow-up period and was superior in the short term for thigh muscle strength.1

The results of this study build on those from the aforementioned smaller study conducted in Finland.8 In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

What about more severe osteoarthritis?

This trial included patients with no to mild osteoarthritis in addition to their meniscal tear.1 It is unclear if the results would be maintained in those with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

Cost and effort of PT

The cost of PT can be a barrier for patients who have adequate insurance coverage for surgery but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing time and effort, which may deter those with busy lifestyles. Patients and clinicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2017. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2017;66[4]:250-252).

 

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the past 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus but does have medial joint line tenderness of his right knee. An MRI shows a partial medial meniscal tear. Do you refer him to physical therapy (PT) or to orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or as a result of degeneration over time. Traumatic meniscal tears typically occur in those younger than 30 during sports (eg, basketball, soccer), whereas degenerative meniscal tears generally occur in patients ages 40 to 60.2,3 The annual incidence of all meniscal tears is 79 per 100,000.4 While some clinicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are more challenging and typically warrant an MRI for confirmation.3

Meniscal tears can be treated either conservatively, with supportive care and exercise, or surgically. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study, 95 of 117 patients (81.2%) were generally satisfied with surgical treatment at four-year follow-up; satisfaction was higher among those with a traumatic meniscal tear than in those with a degenerative tear.5

Two systematic reviews of surgery versus nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.6,7 However, both studies were of only moderate quality, because of the number of patients in the nonoperative groups who ultimately underwent surgery. Neither of the studies directly compared surgery to nonoperative management.6,7Another investigation—a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients—compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.8

Clinical practice recommendations devised from a vast systematic review of the literature recommend that the decision for surgery be based on patient-specific factors, such as symptoms, age, mechanism of tear, extent of damage, and occupational/social/activity needs.9

STUDY SUMMARY

Exercise is as good as surgery

The current superiority RCT compared exercise therapy to arthroscopic partial meniscectomy. Subjects (ages 35 to 60) presented to the orthopedic department of two hospitals in Norway with unilateral knee pain of more than two months’ duration and an MRI-delineated medial meniscal tear. They were included in the study only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤ 2). Exclusion criteria included acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous two years.

The primary outcomes were change in patient-reported knee function (as determined by overall Knee injury and Osteoarthritis Outcome Score [KOOS] after two years) and thigh muscle strength at three months (as measured by physiotherapists). The researchers used four of the five KOOS subscales for this analysis: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). The average score of each subscale was used.

Secondary outcomes included the five individual KOOS subscales (the four previously mentioned, plus activities of daily living [ADLs]), as well as thigh muscle strength and lower-extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy; upon discharge, those in the latter group received written and oral encouragement to perform simple exercises at home, two to four times daily, to regain range of motion and reduce swelling.

Results. At two years, the overall mean improvement in KOOS4 score from baseline was similar between the exercise group and the meniscectomy group (25.3 pts vs 24.4 pts, respectively; mean difference [MD], 0.9). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both three and 12 months showed significant objective improvements favoring exercise therapy.

In the secondary analysis of the KOOS subscale scores, change from baseline was nonsignificant for four of the five (pain, ADL, sports/recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 pts); this was likely clinically insignificant on a grading scale of 0 to 100.

Of the patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the two-year study period.

 

 

 

WHAT’S NEW

Head-to-head comparison adds evidence

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a two-year follow-up period and was superior in the short term for thigh muscle strength.1

The results of this study build on those from the aforementioned smaller study conducted in Finland.8 In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

What about more severe osteoarthritis?

This trial included patients with no to mild osteoarthritis in addition to their meniscal tear.1 It is unclear if the results would be maintained in those with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

Cost and effort of PT

The cost of PT can be a barrier for patients who have adequate insurance coverage for surgery but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing time and effort, which may deter those with busy lifestyles. Patients and clinicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2017. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2017;66[4]:250-252).

References

1. Kise NJ, Risberg MA, Stensrud S, et al. Exercise therapy versus arthroscopic partial meniscectomy for degenerative meniscal tear in middle aged patients: randomised controlled trial with two year follow-up. BMJ. 2016;354:i3740.
2. Beals CT, Magnussen RA, Graham WC, et al. The prevalence of meniscal pathology in asymptomatic athletes. Sports Med. 2016;46:1517-1524.
3. Maffulli N, Longo UG, Campi S, et al. Meniscal tears. Open Access J Sports Med. 2010;1:45-54.
4. Peat G, Bergknut C, Frobell R, et al. Population-wide incidence estimates for soft tissue knee injuries presenting to healthcare in southern Sweden: data from the Skåne Healthcare Register. Arthritis Res Ther. 2014;16:R162.
5. Ghislain NA, Wei JN, Li YG. Study of the clinical outcome between traumatic and degenerative (non-traumatic) meniscal tears after arthroscopic surgery: a 4-years follow-up study. J Clin Diagn Res. 2016;10:RC01-RC04.
6. Khan M, Evaniew N, Bedi A, et al. Arthroscopic surgery for degenerative tears of the meniscus: a systematic review and meta-analysis. CMAJ. 2014;186:1057-1064.
7. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery: a systematic review of the evidence for operative management of meniscal tears. Am J Sports Med. 2017;45:965-973.
8. Sihvonen R, Paavola M, Malmivaara A, et al; Finnish Degenerative Meniscal Lesion Study (FIDELITY) Group. Arthroscopic partial meniscectomy versus sham surgery for a degenerative meniscal tear. N Engl J Med. 2013;369:2515-2524.
9. Beaufils P, Hulet C, Dhénain M, et al. Clinical practice guidelines for the management of meniscal lesions and isolated lesions of the anterior cruciate ligament of the knee in adults. Orthop Traumatol Surg Res. 2009;95:437-442.

References

1. Kise NJ, Risberg MA, Stensrud S, et al. Exercise therapy versus arthroscopic partial meniscectomy for degenerative meniscal tear in middle aged patients: randomised controlled trial with two year follow-up. BMJ. 2016;354:i3740.
2. Beals CT, Magnussen RA, Graham WC, et al. The prevalence of meniscal pathology in asymptomatic athletes. Sports Med. 2016;46:1517-1524.
3. Maffulli N, Longo UG, Campi S, et al. Meniscal tears. Open Access J Sports Med. 2010;1:45-54.
4. Peat G, Bergknut C, Frobell R, et al. Population-wide incidence estimates for soft tissue knee injuries presenting to healthcare in southern Sweden: data from the Skåne Healthcare Register. Arthritis Res Ther. 2014;16:R162.
5. Ghislain NA, Wei JN, Li YG. Study of the clinical outcome between traumatic and degenerative (non-traumatic) meniscal tears after arthroscopic surgery: a 4-years follow-up study. J Clin Diagn Res. 2016;10:RC01-RC04.
6. Khan M, Evaniew N, Bedi A, et al. Arthroscopic surgery for degenerative tears of the meniscus: a systematic review and meta-analysis. CMAJ. 2014;186:1057-1064.
7. Monk P, Garfjeld Roberts P, Palmer AJ, et al. The urgent need for evidence in arthroscopic meniscal surgery: a systematic review of the evidence for operative management of meniscal tears. Am J Sports Med. 2017;45:965-973.
8. Sihvonen R, Paavola M, Malmivaara A, et al; Finnish Degenerative Meniscal Lesion Study (FIDELITY) Group. Arthroscopic partial meniscectomy versus sham surgery for a degenerative meniscal tear. N Engl J Med. 2013;369:2515-2524.
9. Beaufils P, Hulet C, Dhénain M, et al. Clinical practice guidelines for the management of meniscal lesions and isolated lesions of the anterior cruciate ligament of the knee in adults. Orthop Traumatol Surg Res. 2009;95:437-442.

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Blood Loss and Need for Blood Transfusions in Total Knee and Total Hip Arthroplasty

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Use of tranexamic acid during total knee and total hip arthroplasty procedures may safely and effectively reduce blood loss and the need for transfusions in patients.

The number of patients who undergo total knee arthroplasty (TKA) and total hip arthroplasty (THA) procedures has significantly increased over the past 2 to 3 decades. As life expectancy in the U.S. increases and medical advances allow patients with preexisting conditions to successfully undergo joint replacements, the demand for these procedures is expected to grow.1 In 2010, the CDC estimated that 719,000 patients underwent TKA procedures and 332,000 patients underwent THA procedures in the U.S.2 Kurtz and colleagues have projected that by 2030 the annual number of TKA procedures will increase to 3.5 million and the number of THA procedures will increase to 572,000.1

Although becoming more prevalent, these procedures are still associated with considerable intra- and postoperative blood loss that may lead to complications and blood transfusions.3 Previous studies have shown that perioperative anemia and red blood cell transfusions are associated with negative outcomes, including increased health care resource utilization; length of hospitalization; pulmonary, septic, wound, or thromboembolic complications; and mortality.4,5

In order to prevent excessive blood loss during TKA and THA procedures, antifibrinolytic agents, such as tranexamic acid, have been used. Tranexamic acid is a synthetic form of lysine that binds to the lysine-binding sites on plasminogen and slows the conversion of plasminogen to plasmin. This interaction inhibits fibrinolysis and theoretically decreases bleeding.6 Because tranexamic acid is an antifibrinolytic, its mechanism of action has raised concerns that it could increase the risk of clotting complications, such as venous thromboembolism and myocardial infarction.7

Several published meta-analyses and systematic reviews have shown that tranexamic acid reduces blood loss in patients undergoing orthopedic surgery. Despite positive results, many study authors have acknowledged limitations in their analyses, such as heterogeneity of study results, small trial size, and varied dosing strategies.3,7-12 There is no FDA-approved tranexamic acid dosing strategy for orthopedic procedures; therefore, its use in TKA and THA procedures is off label. This lack of guidance results in the medication being used at varied doses, timing of doses, and routes of administration with no clear dosing strategy showing the best outcomes.

Tranexamic acid was first used in TKA and THA surgical procedures at the Sioux Falls VA Health Care System (SFVAHCS) in South Dakota in October 2012. The dose used during these procedures was 1 g IV at first surgical incision and 1 g IV at incision closure. The objective of this study was to determine whether this tranexamic acid dosing strategy utilized at SFVAHCS safely improved outcomes related to blood loss.

Methods

A single-center retrospective chart review was performed on all patients who underwent TKA and THA procedures by 4 orthopedic surgeons between January 2010 and August 2015 at SFVAHCS. This study received approval by the local institutional review board and research and development committee in September 2015.

Patients were included in the study if they were aged ≥ 18 years and underwent primary unilateral TKA or THA procedures during the study time frame. Patients were excluded if they underwent bilateral or revision TKA or THA procedures, did not have recorded blood loss measurements during and/or after the procedure, or did not receive tranexamic acid between October 2012 and August 2015 at the standard dosing strategy utilized at SFVAHCS.

Patients who underwent surgery between January 2010 and October 2012 and did not receive tranexamic acid were included in the control groups. The treatment groups contained patients who underwent surgery between October 2012 and August 2015 and received tranexamic acid at the standard SFVAHCS dosing strategy. Patients in the control and treatment groups were divided and compared with patients who underwent the same type of surgery.

The primary endpoint of this study was total blood loss, which included intraoperative and postoperative blood loss. Intraoperative blood loss was measured by a suctioning device that the surgical physician’s assistant used to keep the surgical site clear of bodily fluids. The suctioning device collected blood as well as irrigation fluids used throughout the surgical procedure. The volume of irrigation fluids used during the procedure was subtracted from the total volume collected by the suctioning device to estimate the total blood volume lost during surgery. Sponges and other surgical materials that may have collected blood were not included in the intraoperative blood loss calculation. Postoperative blood loss was collected by a drain that was placed in the surgical site prior to incision closure. The drain collected postoperative blood loss until it was removed 1 day after surgery.

The secondary endpoints for the study were changes in hemoglobin (Hgb) and hematocrit (Hct) from before surgery to after surgery. These changes were calculated by subtracting the lowest measured postoperative Hgb or Hct level within 21 days postsurgery from the closest measured Hgb or Hct level obtained presurgery.

Follow-up appointments were routinely conducted 2 weeks after surgery, so the 21-day time frame would include any laboratory results drawn at these appointments. Other secondary endpoints included the number of patients receiving at least 1 blood transfusion during hospitalization and the number of patients experiencing clotting complications within 30 days of surgery. Postoperative and progress notes were reviewed by a single study investigator in order to record blood transfusions and clotting complications.

All patients who underwent TKA or THA procedures were instructed to stop taking antiplatelet agents 7 days prior to surgery and warfarin 5 days prior to surgery. If patients were determined to be at high risk for thromboembolic complications following warfarin discontinuation, therapeutic doses of low-molecular weight heparin or unfractionated heparin were used as a bridging therapy pre- and postsurgery. Enoxaparin 30 mg twice daily was started the day after surgery in all patients not previously on warfarin therapy prior to surgery to prevent clotting complications. If a patient was on warfarin therapy prior to the procedure but not considered to be at high risk of thromboembolic complications by the surgeon, warfarin was restarted after surgery, and enoxaparin 30 mg twice daily was used until therapeutic international normalized ratio values were obtained. If the patient had ongoing bleeding after the procedure or was determined to be at high risk for bleeding complications, the provider may have delayed anticoagulant use.

Some patients who underwent TKA or THA procedures during the study time frame received periarticular pain injections during surgery. These pain injections included a combination of ropivacaine 200 mg, ketorolac 30 mg, epinephrine 0.5 mg, and clonidine 0.08 mg and were compounded in a sterile mixture with normal saline. Several injections of this mixture were administered into the surgical site to reduce postoperative pain. These periarticular pain injections were first implemented into TKA and THA procedures in August 2012 and were used in patients at the surgeon’s discretion.

Baseline characteristics were analyzed using a chi-square test for categoric variables and an unpaired t test for continuous variables to determine whether any differences were present. Total blood loss, change in Hgb, and change in Hct were analyzed using an unpaired t test. Patients receiving at least 1 blood transfusion during hospitalization and patients experiencing a clotting complication were analyzed using a chi-square test. P values < .05 were considered to indicate statistical significance. Descriptive statistics were calculated using Microsoft Excel (Redmond, WA), and GraphPad Prism (La Jolla, CA) was used for all statistical analyses.

 

 

Results

Initially, a total of 443 TKA patients and 111 THA patients were reviewed. Of these patients, 418 TKA patients and 100 THA patients met the inclusion criteria. Due to the retrospective design of this study, not all of the baseline characteristics were equal between groups (Table 1). Most notably, the number of patients who received the periarticular pain injection and the distribution of surgeons performing the procedures were different between groups in both the TKA and THA procedures.

Baseline Hgb levels were not found to be different between groups in either type of procedure; however, the baseline Hct levels of patients undergoing TKA who received tranexamic acid were found to be statistically higher when compared with those who did not receive tranexamic acid. Other baseline characteristics with statistically higher values included average weight and BMI in patients who received tranexamic acid and underwent THA and serum creatinine in patients who did not receive tranexamic acid and underwent TKA.

In the primary analysis (Tables 2 and 3), the mean estimated total blood loss in TKA patients was lower in patients who received tranexamic acid than it was in the control group (339.4 mL vs 457.4 mL, P < .001). Patients who underwent THA receiving tranexamic acid similarly had significantly less total blood loss than that of the control group (419.7 mL vs 585.7 mL, P < .001). Consistent with previous studies, patients undergoing TKA procedures in the treatment group when compared to the control group, respectively, were likely to have more blood loss postoperatively (275.9 mL vs 399.7 mL) than intraoperatively (63.5 mL vs 57.7 mL) regardless of tranexamic acid administration.6 On the other hand, patients who had undergone THA were more likely to experience more intraoperative blood loss (281.6 mL in treatment group vs 328.9 mL in control group) than postoperative blood loss (138.1 mL in treatment group vs 256.8 mL in control group) regardless of tranexamic acid administration.

In the secondary analysis, the change between preoperative and postoperative Hgb and Hct had results consistent with the total blood loss results. Patients receiving tranexamic acid in TKA procedures had a lower decrease in Hgb compared with the control group (3.3 mg/dL vs 4.0 mg/dL, P < .001). Similarly, patients undergoing TKA who received tranexamic acid had a smaller decrease in Hct than that of the control group (9.4% vs 11.1%, P < .001). Consistent with the TKA procedure results, patients undergoing THA who received tranexamic acid had a smaller decrease in Hgb (3.6 mg/dL vs 4.7 mg/dL, P < .001) and Hct (10.5% vs 13.0%, P = .0012) than that of the control group.

Patients who did not receive tranexamic acid were more likely to require at least 1 blood transfusion than were patients who received tranexamic acid in TKA (14 patients vs 0 patients, P = .0005) and THA procedures (8 patients vs 2 patients, P = .019). Despite the theoretically increased likelihood of clotting complications with tranexamic acid, no significant differences were observed between the treatment and control groups in either TKA (0 vs 4, P = .065) or THA (1 vs 0, P = .363) procedures.

Discussion

Patients undergoing total joint arthroplasty are at risk for significant blood loss with a potential need for postoperative blood transfusions.6,13 The use of tranexamic acid during these procedures offers a possible solution to decrease blood loss and minimize blood transfusions. This study retrospectively evaluated whether tranexamic acid safely decreased blood loss and the need for blood transfusions at SFVAHCS with the dosing strategy of 1 g IV at first incision and 1 g IV at incision closure.

Patients who received tranexamic acid in TKA and THA procedures had significantly less blood loss than did patients who did not receive tranexamic acid. Patients receiving tranexamic acid also had a significantly lower change from preoperative to postoperative Hgb and Hct levels than did patients who did not receive tranexamic acid in TKA and THA procedures. In addition to decreasing blood loss, the tranexamic acid groups had significantly fewer patients who required blood transfusions than that of the control groups.

This reduction in blood transfusions should be considered clinically significant. Blood transfusions require substantial health care resource utilization and may cause complications in recipients.3 There was no clear association between tranexamic acid and clotting complications in this study, which may suggest that this risk is theoretical. However, larger prospective studies would be needed to further examine this potential risk.

Even though baseline Hct levels were found to be significantly different between the tranexamic acid group and the control group for patients who underwent TKA, medical record documentation indicated that the determination whether postoperative blood transfusions were needed was based primarily on Hgb levels. Baseline Hgb levels were found not to be significantly different between the tranexamic acid and control groups for either TKA or THA procedures. This suggests that at baseline the tranexamic acid and control groups had the same risk of reaching the Hgb threshold where blood transfusions would be required.

There was a significant difference in the proportion of patients receiving the periarticular pain injection of ropivacaine, ketorolac, epinephrine, and clonidine between the groups who received tranexamic acid and those who did not. Originally, this baseline characteristic was theorized to be a major confounder in the primary and secondary analyses because epinephrine is a vasoconstrictor and ketorolac is a reversible antiplatelet agent. However, Vendittoli and colleagues showed that patients receiving these periarticular pain injections during surgery actually had greater total blood loss than did patients who did not receive the injections, although this comparison did not reach statistical significance.14 The Vendittoli and colleagues results suggest that the pain injections did not confound the primary and secondary analyses by aiding in the process of reducing blood loss in these procedures.

 

 

Limitations

There are several limitations for extrapolating the results from this study to the general population. Due to the retrospective study design, there was no way to actively control potentially confounding variables during the TKA and THA procedures. Surgeons and surgery teams likely had slightly different techniques and protocols during and after surgery. Several baseline characteristics were not equal between patients who received tranexamic acid and those who did not. Therefore, it is unknown whether these baseline characteristics affected the results of this study. Postoperative anticoagulant use was not recorded and may have differed between study groups, depending on the patient’s risk of thromboembolic complications; however, the drains that collected blood loss were removed prior to the first dose of enoxaparin, which was administered the day after surgery.

Another limitation is that the method of measuring blood loss during and after the procedure was imprecise. Blood not suctioned through the suctioning device during surgery or not collected in the drain after surgery was not measured and may have increased the total blood loss. Hemoglobin and Hct levels also are sensitive to intravascular volume changes. If a patient required more IV fluids during or after a procedure, the fluids may have lowered the Hgb and/or Hct levels by dilution.

Conclusion

This study suggests that using tranexamic acid at a dose of 1 g IV at first incision and 1 g IV at incision closure safely and effectively reduced blood loss and the need for transfusions in patients undergoing TKA and THA procedures at SFVAHCS. Further prospective studies are needed to compare different tranexamic dosing strategies to minimize blood loss during these procedures. ˜

Acknowledgments
This study is the result of work supported with resources and the use of facilities at the Sioux Falls VA Health Care System in South Dakota.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

2. Centers for Disease Control and Prevention. Number of all-listed procedures for discharges from short-stay hospitals, by procedure category and age: United States, 2010. https://www.cdc.gov/nchs/data/nhds/4procedures/2010pro4_numberprocedureage.pdf. Published 2010. Accessed March 15, 2017.

3. Wei Z, Liu M. The effectiveness and safety of tranexamic acid in total hip or knee arthroplasty: a meta-analysis of 2720 cases. Transfus Med. 2015;25(3):151-162.

4. Glance LG, Dick AW, Mukamel DB, et al. Association between intraoperative blood transfusion and mortality and morbidity in patients undergoing noncardiac surgery. Anesthesiology. 2011;114(2):283-292.

5. Wu WC, Smith TS, Henderson WG, et al. Operative blood loss, blood transfusion, and 30-day mortality in older patients after major noncardiac surgery. Ann Surg. 2010;252(1):283-292.

6. Sehat KR, Evans RL, Newman JH. Hidden blood loss following hip and knee arthroplasty. Correct management of blood loss should take hidden loss into account. J Bone Joint Surg Br. 2004;86(4):561-565.

7. Gandhi R, Evans HMK, Mahomed SR, Mahomed NN. Tranexamic acid and the reduction of blood loss in total knee and hip arthroplasty: a meta-analysis. BMC Res Notes. 2013;6:184.

8. Alshryda S, Sarda P, Sukeik M, Nargol A, Blenkinsopp J, Mason JM. Tranexamic acid in total knee replacement: a systematic review and meta-analysis. J Bone Joint Surg Br. 2011;93(12):1577-1585.

9. Yang ZG, Chen WP, Wu LE. Effectiveness and safety of tranexamic acid in reducing blood loss in total knee arthroplasty: a meta-analysis. J Bone Joint Surg Am. 2012;94(13):1153-1159.

10. Tan J, Chen H, Liu Q, Chen C, Huang W. A meta-analysis of the effectiveness and safety of using tranexamic acid in primary unilateral total knee arthroplasty. J Surg Res. 2013;184(2):880-887.

11. Sukeik M, Alshryda S, Haddad FS, Mason JM. Systematic review and meta-analysis of the use of tranexamic acid in total hip replacement. J Bone Joint Surg Br. 2011;93(1):39-46.

12. Zhou XD, Tao LJ, Li J, Wu LD. Do we really need tranexamic acid in total hip arthroplasty? A meta-analysis of nineteen randomized controlled trials. Arch Orthop Trauma Surg. 2013;133(7):1017-1027.

13. Bierbaum BE, Callaghan JJ, Galante JO, Rubash HE, Tooms RE, Welch RB. An analysis of blood management in patients having a total hip or knee arthroplasty. J Bone Joint Surg Am. 1999;81(1):2-10.

14. Vendittoli PA, Makinen P, Drolet P, et al. A multimodal analgesia protocol for total knee arthroplasty: a randomized, controlled study. J Bone Joint Surg Am. 2006;88(2):282-289.

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Dr. Larson is an inpatient clinical pharmacist, Dr. Hoitsma is an inpatient pharmacy supervisor, Dr. Metzger is the chief of pharmacy, Dr. Oehlke is the associate chief of pharmacy, and Dr. Bebensee is a home-based primary care clinical pharmacist; all at Sioux Falls VA Health Care System in South Dakota. At the time the article was written Dr. Larson was a PGY1 pharmacy resident.

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The opinions expressed herein are those of the authors and do not necessarily reflect those of
Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

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The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of
Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Author and Disclosure Information

Dr. Larson is an inpatient clinical pharmacist, Dr. Hoitsma is an inpatient pharmacy supervisor, Dr. Metzger is the chief of pharmacy, Dr. Oehlke is the associate chief of pharmacy, and Dr. Bebensee is a home-based primary care clinical pharmacist; all at Sioux Falls VA Health Care System in South Dakota. At the time the article was written Dr. Larson was a PGY1 pharmacy resident.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of
Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

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Use of tranexamic acid during total knee and total hip arthroplasty procedures may safely and effectively reduce blood loss and the need for transfusions in patients.
Use of tranexamic acid during total knee and total hip arthroplasty procedures may safely and effectively reduce blood loss and the need for transfusions in patients.

The number of patients who undergo total knee arthroplasty (TKA) and total hip arthroplasty (THA) procedures has significantly increased over the past 2 to 3 decades. As life expectancy in the U.S. increases and medical advances allow patients with preexisting conditions to successfully undergo joint replacements, the demand for these procedures is expected to grow.1 In 2010, the CDC estimated that 719,000 patients underwent TKA procedures and 332,000 patients underwent THA procedures in the U.S.2 Kurtz and colleagues have projected that by 2030 the annual number of TKA procedures will increase to 3.5 million and the number of THA procedures will increase to 572,000.1

Although becoming more prevalent, these procedures are still associated with considerable intra- and postoperative blood loss that may lead to complications and blood transfusions.3 Previous studies have shown that perioperative anemia and red blood cell transfusions are associated with negative outcomes, including increased health care resource utilization; length of hospitalization; pulmonary, septic, wound, or thromboembolic complications; and mortality.4,5

In order to prevent excessive blood loss during TKA and THA procedures, antifibrinolytic agents, such as tranexamic acid, have been used. Tranexamic acid is a synthetic form of lysine that binds to the lysine-binding sites on plasminogen and slows the conversion of plasminogen to plasmin. This interaction inhibits fibrinolysis and theoretically decreases bleeding.6 Because tranexamic acid is an antifibrinolytic, its mechanism of action has raised concerns that it could increase the risk of clotting complications, such as venous thromboembolism and myocardial infarction.7

Several published meta-analyses and systematic reviews have shown that tranexamic acid reduces blood loss in patients undergoing orthopedic surgery. Despite positive results, many study authors have acknowledged limitations in their analyses, such as heterogeneity of study results, small trial size, and varied dosing strategies.3,7-12 There is no FDA-approved tranexamic acid dosing strategy for orthopedic procedures; therefore, its use in TKA and THA procedures is off label. This lack of guidance results in the medication being used at varied doses, timing of doses, and routes of administration with no clear dosing strategy showing the best outcomes.

Tranexamic acid was first used in TKA and THA surgical procedures at the Sioux Falls VA Health Care System (SFVAHCS) in South Dakota in October 2012. The dose used during these procedures was 1 g IV at first surgical incision and 1 g IV at incision closure. The objective of this study was to determine whether this tranexamic acid dosing strategy utilized at SFVAHCS safely improved outcomes related to blood loss.

Methods

A single-center retrospective chart review was performed on all patients who underwent TKA and THA procedures by 4 orthopedic surgeons between January 2010 and August 2015 at SFVAHCS. This study received approval by the local institutional review board and research and development committee in September 2015.

Patients were included in the study if they were aged ≥ 18 years and underwent primary unilateral TKA or THA procedures during the study time frame. Patients were excluded if they underwent bilateral or revision TKA or THA procedures, did not have recorded blood loss measurements during and/or after the procedure, or did not receive tranexamic acid between October 2012 and August 2015 at the standard dosing strategy utilized at SFVAHCS.

Patients who underwent surgery between January 2010 and October 2012 and did not receive tranexamic acid were included in the control groups. The treatment groups contained patients who underwent surgery between October 2012 and August 2015 and received tranexamic acid at the standard SFVAHCS dosing strategy. Patients in the control and treatment groups were divided and compared with patients who underwent the same type of surgery.

The primary endpoint of this study was total blood loss, which included intraoperative and postoperative blood loss. Intraoperative blood loss was measured by a suctioning device that the surgical physician’s assistant used to keep the surgical site clear of bodily fluids. The suctioning device collected blood as well as irrigation fluids used throughout the surgical procedure. The volume of irrigation fluids used during the procedure was subtracted from the total volume collected by the suctioning device to estimate the total blood volume lost during surgery. Sponges and other surgical materials that may have collected blood were not included in the intraoperative blood loss calculation. Postoperative blood loss was collected by a drain that was placed in the surgical site prior to incision closure. The drain collected postoperative blood loss until it was removed 1 day after surgery.

The secondary endpoints for the study were changes in hemoglobin (Hgb) and hematocrit (Hct) from before surgery to after surgery. These changes were calculated by subtracting the lowest measured postoperative Hgb or Hct level within 21 days postsurgery from the closest measured Hgb or Hct level obtained presurgery.

Follow-up appointments were routinely conducted 2 weeks after surgery, so the 21-day time frame would include any laboratory results drawn at these appointments. Other secondary endpoints included the number of patients receiving at least 1 blood transfusion during hospitalization and the number of patients experiencing clotting complications within 30 days of surgery. Postoperative and progress notes were reviewed by a single study investigator in order to record blood transfusions and clotting complications.

All patients who underwent TKA or THA procedures were instructed to stop taking antiplatelet agents 7 days prior to surgery and warfarin 5 days prior to surgery. If patients were determined to be at high risk for thromboembolic complications following warfarin discontinuation, therapeutic doses of low-molecular weight heparin or unfractionated heparin were used as a bridging therapy pre- and postsurgery. Enoxaparin 30 mg twice daily was started the day after surgery in all patients not previously on warfarin therapy prior to surgery to prevent clotting complications. If a patient was on warfarin therapy prior to the procedure but not considered to be at high risk of thromboembolic complications by the surgeon, warfarin was restarted after surgery, and enoxaparin 30 mg twice daily was used until therapeutic international normalized ratio values were obtained. If the patient had ongoing bleeding after the procedure or was determined to be at high risk for bleeding complications, the provider may have delayed anticoagulant use.

Some patients who underwent TKA or THA procedures during the study time frame received periarticular pain injections during surgery. These pain injections included a combination of ropivacaine 200 mg, ketorolac 30 mg, epinephrine 0.5 mg, and clonidine 0.08 mg and were compounded in a sterile mixture with normal saline. Several injections of this mixture were administered into the surgical site to reduce postoperative pain. These periarticular pain injections were first implemented into TKA and THA procedures in August 2012 and were used in patients at the surgeon’s discretion.

Baseline characteristics were analyzed using a chi-square test for categoric variables and an unpaired t test for continuous variables to determine whether any differences were present. Total blood loss, change in Hgb, and change in Hct were analyzed using an unpaired t test. Patients receiving at least 1 blood transfusion during hospitalization and patients experiencing a clotting complication were analyzed using a chi-square test. P values < .05 were considered to indicate statistical significance. Descriptive statistics were calculated using Microsoft Excel (Redmond, WA), and GraphPad Prism (La Jolla, CA) was used for all statistical analyses.

 

 

Results

Initially, a total of 443 TKA patients and 111 THA patients were reviewed. Of these patients, 418 TKA patients and 100 THA patients met the inclusion criteria. Due to the retrospective design of this study, not all of the baseline characteristics were equal between groups (Table 1). Most notably, the number of patients who received the periarticular pain injection and the distribution of surgeons performing the procedures were different between groups in both the TKA and THA procedures.

Baseline Hgb levels were not found to be different between groups in either type of procedure; however, the baseline Hct levels of patients undergoing TKA who received tranexamic acid were found to be statistically higher when compared with those who did not receive tranexamic acid. Other baseline characteristics with statistically higher values included average weight and BMI in patients who received tranexamic acid and underwent THA and serum creatinine in patients who did not receive tranexamic acid and underwent TKA.

In the primary analysis (Tables 2 and 3), the mean estimated total blood loss in TKA patients was lower in patients who received tranexamic acid than it was in the control group (339.4 mL vs 457.4 mL, P < .001). Patients who underwent THA receiving tranexamic acid similarly had significantly less total blood loss than that of the control group (419.7 mL vs 585.7 mL, P < .001). Consistent with previous studies, patients undergoing TKA procedures in the treatment group when compared to the control group, respectively, were likely to have more blood loss postoperatively (275.9 mL vs 399.7 mL) than intraoperatively (63.5 mL vs 57.7 mL) regardless of tranexamic acid administration.6 On the other hand, patients who had undergone THA were more likely to experience more intraoperative blood loss (281.6 mL in treatment group vs 328.9 mL in control group) than postoperative blood loss (138.1 mL in treatment group vs 256.8 mL in control group) regardless of tranexamic acid administration.

In the secondary analysis, the change between preoperative and postoperative Hgb and Hct had results consistent with the total blood loss results. Patients receiving tranexamic acid in TKA procedures had a lower decrease in Hgb compared with the control group (3.3 mg/dL vs 4.0 mg/dL, P < .001). Similarly, patients undergoing TKA who received tranexamic acid had a smaller decrease in Hct than that of the control group (9.4% vs 11.1%, P < .001). Consistent with the TKA procedure results, patients undergoing THA who received tranexamic acid had a smaller decrease in Hgb (3.6 mg/dL vs 4.7 mg/dL, P < .001) and Hct (10.5% vs 13.0%, P = .0012) than that of the control group.

Patients who did not receive tranexamic acid were more likely to require at least 1 blood transfusion than were patients who received tranexamic acid in TKA (14 patients vs 0 patients, P = .0005) and THA procedures (8 patients vs 2 patients, P = .019). Despite the theoretically increased likelihood of clotting complications with tranexamic acid, no significant differences were observed between the treatment and control groups in either TKA (0 vs 4, P = .065) or THA (1 vs 0, P = .363) procedures.

Discussion

Patients undergoing total joint arthroplasty are at risk for significant blood loss with a potential need for postoperative blood transfusions.6,13 The use of tranexamic acid during these procedures offers a possible solution to decrease blood loss and minimize blood transfusions. This study retrospectively evaluated whether tranexamic acid safely decreased blood loss and the need for blood transfusions at SFVAHCS with the dosing strategy of 1 g IV at first incision and 1 g IV at incision closure.

Patients who received tranexamic acid in TKA and THA procedures had significantly less blood loss than did patients who did not receive tranexamic acid. Patients receiving tranexamic acid also had a significantly lower change from preoperative to postoperative Hgb and Hct levels than did patients who did not receive tranexamic acid in TKA and THA procedures. In addition to decreasing blood loss, the tranexamic acid groups had significantly fewer patients who required blood transfusions than that of the control groups.

This reduction in blood transfusions should be considered clinically significant. Blood transfusions require substantial health care resource utilization and may cause complications in recipients.3 There was no clear association between tranexamic acid and clotting complications in this study, which may suggest that this risk is theoretical. However, larger prospective studies would be needed to further examine this potential risk.

Even though baseline Hct levels were found to be significantly different between the tranexamic acid group and the control group for patients who underwent TKA, medical record documentation indicated that the determination whether postoperative blood transfusions were needed was based primarily on Hgb levels. Baseline Hgb levels were found not to be significantly different between the tranexamic acid and control groups for either TKA or THA procedures. This suggests that at baseline the tranexamic acid and control groups had the same risk of reaching the Hgb threshold where blood transfusions would be required.

There was a significant difference in the proportion of patients receiving the periarticular pain injection of ropivacaine, ketorolac, epinephrine, and clonidine between the groups who received tranexamic acid and those who did not. Originally, this baseline characteristic was theorized to be a major confounder in the primary and secondary analyses because epinephrine is a vasoconstrictor and ketorolac is a reversible antiplatelet agent. However, Vendittoli and colleagues showed that patients receiving these periarticular pain injections during surgery actually had greater total blood loss than did patients who did not receive the injections, although this comparison did not reach statistical significance.14 The Vendittoli and colleagues results suggest that the pain injections did not confound the primary and secondary analyses by aiding in the process of reducing blood loss in these procedures.

 

 

Limitations

There are several limitations for extrapolating the results from this study to the general population. Due to the retrospective study design, there was no way to actively control potentially confounding variables during the TKA and THA procedures. Surgeons and surgery teams likely had slightly different techniques and protocols during and after surgery. Several baseline characteristics were not equal between patients who received tranexamic acid and those who did not. Therefore, it is unknown whether these baseline characteristics affected the results of this study. Postoperative anticoagulant use was not recorded and may have differed between study groups, depending on the patient’s risk of thromboembolic complications; however, the drains that collected blood loss were removed prior to the first dose of enoxaparin, which was administered the day after surgery.

Another limitation is that the method of measuring blood loss during and after the procedure was imprecise. Blood not suctioned through the suctioning device during surgery or not collected in the drain after surgery was not measured and may have increased the total blood loss. Hemoglobin and Hct levels also are sensitive to intravascular volume changes. If a patient required more IV fluids during or after a procedure, the fluids may have lowered the Hgb and/or Hct levels by dilution.

Conclusion

This study suggests that using tranexamic acid at a dose of 1 g IV at first incision and 1 g IV at incision closure safely and effectively reduced blood loss and the need for transfusions in patients undergoing TKA and THA procedures at SFVAHCS. Further prospective studies are needed to compare different tranexamic dosing strategies to minimize blood loss during these procedures. ˜

Acknowledgments
This study is the result of work supported with resources and the use of facilities at the Sioux Falls VA Health Care System in South Dakota.

The number of patients who undergo total knee arthroplasty (TKA) and total hip arthroplasty (THA) procedures has significantly increased over the past 2 to 3 decades. As life expectancy in the U.S. increases and medical advances allow patients with preexisting conditions to successfully undergo joint replacements, the demand for these procedures is expected to grow.1 In 2010, the CDC estimated that 719,000 patients underwent TKA procedures and 332,000 patients underwent THA procedures in the U.S.2 Kurtz and colleagues have projected that by 2030 the annual number of TKA procedures will increase to 3.5 million and the number of THA procedures will increase to 572,000.1

Although becoming more prevalent, these procedures are still associated with considerable intra- and postoperative blood loss that may lead to complications and blood transfusions.3 Previous studies have shown that perioperative anemia and red blood cell transfusions are associated with negative outcomes, including increased health care resource utilization; length of hospitalization; pulmonary, septic, wound, or thromboembolic complications; and mortality.4,5

In order to prevent excessive blood loss during TKA and THA procedures, antifibrinolytic agents, such as tranexamic acid, have been used. Tranexamic acid is a synthetic form of lysine that binds to the lysine-binding sites on plasminogen and slows the conversion of plasminogen to plasmin. This interaction inhibits fibrinolysis and theoretically decreases bleeding.6 Because tranexamic acid is an antifibrinolytic, its mechanism of action has raised concerns that it could increase the risk of clotting complications, such as venous thromboembolism and myocardial infarction.7

Several published meta-analyses and systematic reviews have shown that tranexamic acid reduces blood loss in patients undergoing orthopedic surgery. Despite positive results, many study authors have acknowledged limitations in their analyses, such as heterogeneity of study results, small trial size, and varied dosing strategies.3,7-12 There is no FDA-approved tranexamic acid dosing strategy for orthopedic procedures; therefore, its use in TKA and THA procedures is off label. This lack of guidance results in the medication being used at varied doses, timing of doses, and routes of administration with no clear dosing strategy showing the best outcomes.

Tranexamic acid was first used in TKA and THA surgical procedures at the Sioux Falls VA Health Care System (SFVAHCS) in South Dakota in October 2012. The dose used during these procedures was 1 g IV at first surgical incision and 1 g IV at incision closure. The objective of this study was to determine whether this tranexamic acid dosing strategy utilized at SFVAHCS safely improved outcomes related to blood loss.

Methods

A single-center retrospective chart review was performed on all patients who underwent TKA and THA procedures by 4 orthopedic surgeons between January 2010 and August 2015 at SFVAHCS. This study received approval by the local institutional review board and research and development committee in September 2015.

Patients were included in the study if they were aged ≥ 18 years and underwent primary unilateral TKA or THA procedures during the study time frame. Patients were excluded if they underwent bilateral or revision TKA or THA procedures, did not have recorded blood loss measurements during and/or after the procedure, or did not receive tranexamic acid between October 2012 and August 2015 at the standard dosing strategy utilized at SFVAHCS.

Patients who underwent surgery between January 2010 and October 2012 and did not receive tranexamic acid were included in the control groups. The treatment groups contained patients who underwent surgery between October 2012 and August 2015 and received tranexamic acid at the standard SFVAHCS dosing strategy. Patients in the control and treatment groups were divided and compared with patients who underwent the same type of surgery.

The primary endpoint of this study was total blood loss, which included intraoperative and postoperative blood loss. Intraoperative blood loss was measured by a suctioning device that the surgical physician’s assistant used to keep the surgical site clear of bodily fluids. The suctioning device collected blood as well as irrigation fluids used throughout the surgical procedure. The volume of irrigation fluids used during the procedure was subtracted from the total volume collected by the suctioning device to estimate the total blood volume lost during surgery. Sponges and other surgical materials that may have collected blood were not included in the intraoperative blood loss calculation. Postoperative blood loss was collected by a drain that was placed in the surgical site prior to incision closure. The drain collected postoperative blood loss until it was removed 1 day after surgery.

The secondary endpoints for the study were changes in hemoglobin (Hgb) and hematocrit (Hct) from before surgery to after surgery. These changes were calculated by subtracting the lowest measured postoperative Hgb or Hct level within 21 days postsurgery from the closest measured Hgb or Hct level obtained presurgery.

Follow-up appointments were routinely conducted 2 weeks after surgery, so the 21-day time frame would include any laboratory results drawn at these appointments. Other secondary endpoints included the number of patients receiving at least 1 blood transfusion during hospitalization and the number of patients experiencing clotting complications within 30 days of surgery. Postoperative and progress notes were reviewed by a single study investigator in order to record blood transfusions and clotting complications.

All patients who underwent TKA or THA procedures were instructed to stop taking antiplatelet agents 7 days prior to surgery and warfarin 5 days prior to surgery. If patients were determined to be at high risk for thromboembolic complications following warfarin discontinuation, therapeutic doses of low-molecular weight heparin or unfractionated heparin were used as a bridging therapy pre- and postsurgery. Enoxaparin 30 mg twice daily was started the day after surgery in all patients not previously on warfarin therapy prior to surgery to prevent clotting complications. If a patient was on warfarin therapy prior to the procedure but not considered to be at high risk of thromboembolic complications by the surgeon, warfarin was restarted after surgery, and enoxaparin 30 mg twice daily was used until therapeutic international normalized ratio values were obtained. If the patient had ongoing bleeding after the procedure or was determined to be at high risk for bleeding complications, the provider may have delayed anticoagulant use.

Some patients who underwent TKA or THA procedures during the study time frame received periarticular pain injections during surgery. These pain injections included a combination of ropivacaine 200 mg, ketorolac 30 mg, epinephrine 0.5 mg, and clonidine 0.08 mg and were compounded in a sterile mixture with normal saline. Several injections of this mixture were administered into the surgical site to reduce postoperative pain. These periarticular pain injections were first implemented into TKA and THA procedures in August 2012 and were used in patients at the surgeon’s discretion.

Baseline characteristics were analyzed using a chi-square test for categoric variables and an unpaired t test for continuous variables to determine whether any differences were present. Total blood loss, change in Hgb, and change in Hct were analyzed using an unpaired t test. Patients receiving at least 1 blood transfusion during hospitalization and patients experiencing a clotting complication were analyzed using a chi-square test. P values < .05 were considered to indicate statistical significance. Descriptive statistics were calculated using Microsoft Excel (Redmond, WA), and GraphPad Prism (La Jolla, CA) was used for all statistical analyses.

 

 

Results

Initially, a total of 443 TKA patients and 111 THA patients were reviewed. Of these patients, 418 TKA patients and 100 THA patients met the inclusion criteria. Due to the retrospective design of this study, not all of the baseline characteristics were equal between groups (Table 1). Most notably, the number of patients who received the periarticular pain injection and the distribution of surgeons performing the procedures were different between groups in both the TKA and THA procedures.

Baseline Hgb levels were not found to be different between groups in either type of procedure; however, the baseline Hct levels of patients undergoing TKA who received tranexamic acid were found to be statistically higher when compared with those who did not receive tranexamic acid. Other baseline characteristics with statistically higher values included average weight and BMI in patients who received tranexamic acid and underwent THA and serum creatinine in patients who did not receive tranexamic acid and underwent TKA.

In the primary analysis (Tables 2 and 3), the mean estimated total blood loss in TKA patients was lower in patients who received tranexamic acid than it was in the control group (339.4 mL vs 457.4 mL, P < .001). Patients who underwent THA receiving tranexamic acid similarly had significantly less total blood loss than that of the control group (419.7 mL vs 585.7 mL, P < .001). Consistent with previous studies, patients undergoing TKA procedures in the treatment group when compared to the control group, respectively, were likely to have more blood loss postoperatively (275.9 mL vs 399.7 mL) than intraoperatively (63.5 mL vs 57.7 mL) regardless of tranexamic acid administration.6 On the other hand, patients who had undergone THA were more likely to experience more intraoperative blood loss (281.6 mL in treatment group vs 328.9 mL in control group) than postoperative blood loss (138.1 mL in treatment group vs 256.8 mL in control group) regardless of tranexamic acid administration.

In the secondary analysis, the change between preoperative and postoperative Hgb and Hct had results consistent with the total blood loss results. Patients receiving tranexamic acid in TKA procedures had a lower decrease in Hgb compared with the control group (3.3 mg/dL vs 4.0 mg/dL, P < .001). Similarly, patients undergoing TKA who received tranexamic acid had a smaller decrease in Hct than that of the control group (9.4% vs 11.1%, P < .001). Consistent with the TKA procedure results, patients undergoing THA who received tranexamic acid had a smaller decrease in Hgb (3.6 mg/dL vs 4.7 mg/dL, P < .001) and Hct (10.5% vs 13.0%, P = .0012) than that of the control group.

Patients who did not receive tranexamic acid were more likely to require at least 1 blood transfusion than were patients who received tranexamic acid in TKA (14 patients vs 0 patients, P = .0005) and THA procedures (8 patients vs 2 patients, P = .019). Despite the theoretically increased likelihood of clotting complications with tranexamic acid, no significant differences were observed between the treatment and control groups in either TKA (0 vs 4, P = .065) or THA (1 vs 0, P = .363) procedures.

Discussion

Patients undergoing total joint arthroplasty are at risk for significant blood loss with a potential need for postoperative blood transfusions.6,13 The use of tranexamic acid during these procedures offers a possible solution to decrease blood loss and minimize blood transfusions. This study retrospectively evaluated whether tranexamic acid safely decreased blood loss and the need for blood transfusions at SFVAHCS with the dosing strategy of 1 g IV at first incision and 1 g IV at incision closure.

Patients who received tranexamic acid in TKA and THA procedures had significantly less blood loss than did patients who did not receive tranexamic acid. Patients receiving tranexamic acid also had a significantly lower change from preoperative to postoperative Hgb and Hct levels than did patients who did not receive tranexamic acid in TKA and THA procedures. In addition to decreasing blood loss, the tranexamic acid groups had significantly fewer patients who required blood transfusions than that of the control groups.

This reduction in blood transfusions should be considered clinically significant. Blood transfusions require substantial health care resource utilization and may cause complications in recipients.3 There was no clear association between tranexamic acid and clotting complications in this study, which may suggest that this risk is theoretical. However, larger prospective studies would be needed to further examine this potential risk.

Even though baseline Hct levels were found to be significantly different between the tranexamic acid group and the control group for patients who underwent TKA, medical record documentation indicated that the determination whether postoperative blood transfusions were needed was based primarily on Hgb levels. Baseline Hgb levels were found not to be significantly different between the tranexamic acid and control groups for either TKA or THA procedures. This suggests that at baseline the tranexamic acid and control groups had the same risk of reaching the Hgb threshold where blood transfusions would be required.

There was a significant difference in the proportion of patients receiving the periarticular pain injection of ropivacaine, ketorolac, epinephrine, and clonidine between the groups who received tranexamic acid and those who did not. Originally, this baseline characteristic was theorized to be a major confounder in the primary and secondary analyses because epinephrine is a vasoconstrictor and ketorolac is a reversible antiplatelet agent. However, Vendittoli and colleagues showed that patients receiving these periarticular pain injections during surgery actually had greater total blood loss than did patients who did not receive the injections, although this comparison did not reach statistical significance.14 The Vendittoli and colleagues results suggest that the pain injections did not confound the primary and secondary analyses by aiding in the process of reducing blood loss in these procedures.

 

 

Limitations

There are several limitations for extrapolating the results from this study to the general population. Due to the retrospective study design, there was no way to actively control potentially confounding variables during the TKA and THA procedures. Surgeons and surgery teams likely had slightly different techniques and protocols during and after surgery. Several baseline characteristics were not equal between patients who received tranexamic acid and those who did not. Therefore, it is unknown whether these baseline characteristics affected the results of this study. Postoperative anticoagulant use was not recorded and may have differed between study groups, depending on the patient’s risk of thromboembolic complications; however, the drains that collected blood loss were removed prior to the first dose of enoxaparin, which was administered the day after surgery.

Another limitation is that the method of measuring blood loss during and after the procedure was imprecise. Blood not suctioned through the suctioning device during surgery or not collected in the drain after surgery was not measured and may have increased the total blood loss. Hemoglobin and Hct levels also are sensitive to intravascular volume changes. If a patient required more IV fluids during or after a procedure, the fluids may have lowered the Hgb and/or Hct levels by dilution.

Conclusion

This study suggests that using tranexamic acid at a dose of 1 g IV at first incision and 1 g IV at incision closure safely and effectively reduced blood loss and the need for transfusions in patients undergoing TKA and THA procedures at SFVAHCS. Further prospective studies are needed to compare different tranexamic dosing strategies to minimize blood loss during these procedures. ˜

Acknowledgments
This study is the result of work supported with resources and the use of facilities at the Sioux Falls VA Health Care System in South Dakota.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

2. Centers for Disease Control and Prevention. Number of all-listed procedures for discharges from short-stay hospitals, by procedure category and age: United States, 2010. https://www.cdc.gov/nchs/data/nhds/4procedures/2010pro4_numberprocedureage.pdf. Published 2010. Accessed March 15, 2017.

3. Wei Z, Liu M. The effectiveness and safety of tranexamic acid in total hip or knee arthroplasty: a meta-analysis of 2720 cases. Transfus Med. 2015;25(3):151-162.

4. Glance LG, Dick AW, Mukamel DB, et al. Association between intraoperative blood transfusion and mortality and morbidity in patients undergoing noncardiac surgery. Anesthesiology. 2011;114(2):283-292.

5. Wu WC, Smith TS, Henderson WG, et al. Operative blood loss, blood transfusion, and 30-day mortality in older patients after major noncardiac surgery. Ann Surg. 2010;252(1):283-292.

6. Sehat KR, Evans RL, Newman JH. Hidden blood loss following hip and knee arthroplasty. Correct management of blood loss should take hidden loss into account. J Bone Joint Surg Br. 2004;86(4):561-565.

7. Gandhi R, Evans HMK, Mahomed SR, Mahomed NN. Tranexamic acid and the reduction of blood loss in total knee and hip arthroplasty: a meta-analysis. BMC Res Notes. 2013;6:184.

8. Alshryda S, Sarda P, Sukeik M, Nargol A, Blenkinsopp J, Mason JM. Tranexamic acid in total knee replacement: a systematic review and meta-analysis. J Bone Joint Surg Br. 2011;93(12):1577-1585.

9. Yang ZG, Chen WP, Wu LE. Effectiveness and safety of tranexamic acid in reducing blood loss in total knee arthroplasty: a meta-analysis. J Bone Joint Surg Am. 2012;94(13):1153-1159.

10. Tan J, Chen H, Liu Q, Chen C, Huang W. A meta-analysis of the effectiveness and safety of using tranexamic acid in primary unilateral total knee arthroplasty. J Surg Res. 2013;184(2):880-887.

11. Sukeik M, Alshryda S, Haddad FS, Mason JM. Systematic review and meta-analysis of the use of tranexamic acid in total hip replacement. J Bone Joint Surg Br. 2011;93(1):39-46.

12. Zhou XD, Tao LJ, Li J, Wu LD. Do we really need tranexamic acid in total hip arthroplasty? A meta-analysis of nineteen randomized controlled trials. Arch Orthop Trauma Surg. 2013;133(7):1017-1027.

13. Bierbaum BE, Callaghan JJ, Galante JO, Rubash HE, Tooms RE, Welch RB. An analysis of blood management in patients having a total hip or knee arthroplasty. J Bone Joint Surg Am. 1999;81(1):2-10.

14. Vendittoli PA, Makinen P, Drolet P, et al. A multimodal analgesia protocol for total knee arthroplasty: a randomized, controlled study. J Bone Joint Surg Am. 2006;88(2):282-289.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

2. Centers for Disease Control and Prevention. Number of all-listed procedures for discharges from short-stay hospitals, by procedure category and age: United States, 2010. https://www.cdc.gov/nchs/data/nhds/4procedures/2010pro4_numberprocedureage.pdf. Published 2010. Accessed March 15, 2017.

3. Wei Z, Liu M. The effectiveness and safety of tranexamic acid in total hip or knee arthroplasty: a meta-analysis of 2720 cases. Transfus Med. 2015;25(3):151-162.

4. Glance LG, Dick AW, Mukamel DB, et al. Association between intraoperative blood transfusion and mortality and morbidity in patients undergoing noncardiac surgery. Anesthesiology. 2011;114(2):283-292.

5. Wu WC, Smith TS, Henderson WG, et al. Operative blood loss, blood transfusion, and 30-day mortality in older patients after major noncardiac surgery. Ann Surg. 2010;252(1):283-292.

6. Sehat KR, Evans RL, Newman JH. Hidden blood loss following hip and knee arthroplasty. Correct management of blood loss should take hidden loss into account. J Bone Joint Surg Br. 2004;86(4):561-565.

7. Gandhi R, Evans HMK, Mahomed SR, Mahomed NN. Tranexamic acid and the reduction of blood loss in total knee and hip arthroplasty: a meta-analysis. BMC Res Notes. 2013;6:184.

8. Alshryda S, Sarda P, Sukeik M, Nargol A, Blenkinsopp J, Mason JM. Tranexamic acid in total knee replacement: a systematic review and meta-analysis. J Bone Joint Surg Br. 2011;93(12):1577-1585.

9. Yang ZG, Chen WP, Wu LE. Effectiveness and safety of tranexamic acid in reducing blood loss in total knee arthroplasty: a meta-analysis. J Bone Joint Surg Am. 2012;94(13):1153-1159.

10. Tan J, Chen H, Liu Q, Chen C, Huang W. A meta-analysis of the effectiveness and safety of using tranexamic acid in primary unilateral total knee arthroplasty. J Surg Res. 2013;184(2):880-887.

11. Sukeik M, Alshryda S, Haddad FS, Mason JM. Systematic review and meta-analysis of the use of tranexamic acid in total hip replacement. J Bone Joint Surg Br. 2011;93(1):39-46.

12. Zhou XD, Tao LJ, Li J, Wu LD. Do we really need tranexamic acid in total hip arthroplasty? A meta-analysis of nineteen randomized controlled trials. Arch Orthop Trauma Surg. 2013;133(7):1017-1027.

13. Bierbaum BE, Callaghan JJ, Galante JO, Rubash HE, Tooms RE, Welch RB. An analysis of blood management in patients having a total hip or knee arthroplasty. J Bone Joint Surg Am. 1999;81(1):2-10.

14. Vendittoli PA, Makinen P, Drolet P, et al. A multimodal analgesia protocol for total knee arthroplasty: a randomized, controlled study. J Bone Joint Surg Am. 2006;88(2):282-289.

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For bone and joint infections, oral antibiotics match IV, cost less

Article Type
Changed
Wed, 03/13/2019 - 14:55

 

– Oral antibiotic therapy is just as effective as intravenous treatment in curing bone and joint infections, but costs about $3,500 less.

Treating these infections with oral agents also “improves patient autonomy, as it’s not necessary to have IV lines at home,” and represents a generally wiser use of powerful antibiotics, Matthew Scarborough, MD, said at the European Society of Clinical Microbiology and Infectious Diseases annual congress.

Michele G Sullivan/Frontline Medical News
Dr. Matthew Scarborough
“The OVIVA study is really good news for our patients, for our practice in terms of antibiotic stewardship and reducing the risk of health care–associated infections, and fantastic for the health economy worldwide,” said Dr. Scarborough of Oxford (England) University.

OVIVA (Oral vs. Intravenous Antibiotics for Bone and Joint Infection) was conducted at 26 sites in the United Kingdom. It randomized 1,054 adults with bone or joint infections to 6 weeks of either oral or intravenous treatment.

An important aspect of the trial was that both oral and IV treatment choices were made before randomization, Dr. Scarborough said. However, the decisions on what drug to use were left up to the treating physician and depended on the infection site and pathogen.

The primary outcome was definite treatment failure (bacteriologic, histologic, and clinical). Patients were followed for 1 year.

Patients were a median of 60 years old. All had surgical treatment before antibiotic therapy, including debridement and, in those with implants, removal of infected devices. The lower limb was involved in 81%, including hip, knee, and foot. The infection was in an upper limb in 10% and in the spine in 7%.

Staphylococcus aureus was present in 38% of cases, coagulase-negative staphylococci in 27%, and streptococci in 15%. Gram-negative bacteria were found in 22%.

For those patients randomized to IV therapy, glycopeptides and cephalosporins were most commonly employed (41% and 33%, respectively). For oral therapy, quinolones and penicillins were most common (37% and 16%). Most patients (74%) continued antibiotic treatment for more than 6 weeks. Forty patients were lost to follow-up.

In the primary intent-to-treat analysis, the failure rate was 13% for oral therapy and 14% for IV therapy, not a significant difference. Results were similar in the other analyses, including a modified intent to treat with only patients who had complete 1-year data, and a per-protocol analysis. All of the point prevalence numbers favored oral therapy, but crossed the null. Curves in the time-to-treatment-failure analysis were virtually superimposable, as were curves in time to discontinuation of therapy.

Another subgroup analysis examined treatment failure by infective organism; again, there were no significant treatment differences in any of the pathogen subgroups examined (S. aureus, coagulase-negative staph, streptococci species, and other gram-negative bacteria).

Nor did the type of antibiotic significantly affect failure rate, Dr. Scarborough noted. The median length of stay was 14 days for patients on IV treatment and 11 days for those taking oral medications. The incidence of serious adverse events was very similar – about 86% in each group.

On a visual analog scale that assessed health-related quality of life, patients taking oral treatment reported better mobility, self-care, and activity level, and less pain, discomfort, anxiety, and depression than those taking IV medications.

Cost represented the other significant difference between the groups. Over 1 year, the mean IV treatment cost was the equivalent of $17,152, and the mean oral treatment cost was $13,611 – a significant difference of $3,541.

“This represents a potential savings to the National Health Service of 16-25 million pounds sterling ($20.6 million-$32.3 million) per year,” Dr. Scarborough said. “All coming at no expense of good clinical outcomes.”

OVIVA was sponsored by the U.K. National Institute of Health Research. Dr. Scarborough had no financial disclosures.

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– Oral antibiotic therapy is just as effective as intravenous treatment in curing bone and joint infections, but costs about $3,500 less.

Treating these infections with oral agents also “improves patient autonomy, as it’s not necessary to have IV lines at home,” and represents a generally wiser use of powerful antibiotics, Matthew Scarborough, MD, said at the European Society of Clinical Microbiology and Infectious Diseases annual congress.

Michele G Sullivan/Frontline Medical News
Dr. Matthew Scarborough
“The OVIVA study is really good news for our patients, for our practice in terms of antibiotic stewardship and reducing the risk of health care–associated infections, and fantastic for the health economy worldwide,” said Dr. Scarborough of Oxford (England) University.

OVIVA (Oral vs. Intravenous Antibiotics for Bone and Joint Infection) was conducted at 26 sites in the United Kingdom. It randomized 1,054 adults with bone or joint infections to 6 weeks of either oral or intravenous treatment.

An important aspect of the trial was that both oral and IV treatment choices were made before randomization, Dr. Scarborough said. However, the decisions on what drug to use were left up to the treating physician and depended on the infection site and pathogen.

The primary outcome was definite treatment failure (bacteriologic, histologic, and clinical). Patients were followed for 1 year.

Patients were a median of 60 years old. All had surgical treatment before antibiotic therapy, including debridement and, in those with implants, removal of infected devices. The lower limb was involved in 81%, including hip, knee, and foot. The infection was in an upper limb in 10% and in the spine in 7%.

Staphylococcus aureus was present in 38% of cases, coagulase-negative staphylococci in 27%, and streptococci in 15%. Gram-negative bacteria were found in 22%.

For those patients randomized to IV therapy, glycopeptides and cephalosporins were most commonly employed (41% and 33%, respectively). For oral therapy, quinolones and penicillins were most common (37% and 16%). Most patients (74%) continued antibiotic treatment for more than 6 weeks. Forty patients were lost to follow-up.

In the primary intent-to-treat analysis, the failure rate was 13% for oral therapy and 14% for IV therapy, not a significant difference. Results were similar in the other analyses, including a modified intent to treat with only patients who had complete 1-year data, and a per-protocol analysis. All of the point prevalence numbers favored oral therapy, but crossed the null. Curves in the time-to-treatment-failure analysis were virtually superimposable, as were curves in time to discontinuation of therapy.

Another subgroup analysis examined treatment failure by infective organism; again, there were no significant treatment differences in any of the pathogen subgroups examined (S. aureus, coagulase-negative staph, streptococci species, and other gram-negative bacteria).

Nor did the type of antibiotic significantly affect failure rate, Dr. Scarborough noted. The median length of stay was 14 days for patients on IV treatment and 11 days for those taking oral medications. The incidence of serious adverse events was very similar – about 86% in each group.

On a visual analog scale that assessed health-related quality of life, patients taking oral treatment reported better mobility, self-care, and activity level, and less pain, discomfort, anxiety, and depression than those taking IV medications.

Cost represented the other significant difference between the groups. Over 1 year, the mean IV treatment cost was the equivalent of $17,152, and the mean oral treatment cost was $13,611 – a significant difference of $3,541.

“This represents a potential savings to the National Health Service of 16-25 million pounds sterling ($20.6 million-$32.3 million) per year,” Dr. Scarborough said. “All coming at no expense of good clinical outcomes.”

OVIVA was sponsored by the U.K. National Institute of Health Research. Dr. Scarborough had no financial disclosures.

 

– Oral antibiotic therapy is just as effective as intravenous treatment in curing bone and joint infections, but costs about $3,500 less.

Treating these infections with oral agents also “improves patient autonomy, as it’s not necessary to have IV lines at home,” and represents a generally wiser use of powerful antibiotics, Matthew Scarborough, MD, said at the European Society of Clinical Microbiology and Infectious Diseases annual congress.

Michele G Sullivan/Frontline Medical News
Dr. Matthew Scarborough
“The OVIVA study is really good news for our patients, for our practice in terms of antibiotic stewardship and reducing the risk of health care–associated infections, and fantastic for the health economy worldwide,” said Dr. Scarborough of Oxford (England) University.

OVIVA (Oral vs. Intravenous Antibiotics for Bone and Joint Infection) was conducted at 26 sites in the United Kingdom. It randomized 1,054 adults with bone or joint infections to 6 weeks of either oral or intravenous treatment.

An important aspect of the trial was that both oral and IV treatment choices were made before randomization, Dr. Scarborough said. However, the decisions on what drug to use were left up to the treating physician and depended on the infection site and pathogen.

The primary outcome was definite treatment failure (bacteriologic, histologic, and clinical). Patients were followed for 1 year.

Patients were a median of 60 years old. All had surgical treatment before antibiotic therapy, including debridement and, in those with implants, removal of infected devices. The lower limb was involved in 81%, including hip, knee, and foot. The infection was in an upper limb in 10% and in the spine in 7%.

Staphylococcus aureus was present in 38% of cases, coagulase-negative staphylococci in 27%, and streptococci in 15%. Gram-negative bacteria were found in 22%.

For those patients randomized to IV therapy, glycopeptides and cephalosporins were most commonly employed (41% and 33%, respectively). For oral therapy, quinolones and penicillins were most common (37% and 16%). Most patients (74%) continued antibiotic treatment for more than 6 weeks. Forty patients were lost to follow-up.

In the primary intent-to-treat analysis, the failure rate was 13% for oral therapy and 14% for IV therapy, not a significant difference. Results were similar in the other analyses, including a modified intent to treat with only patients who had complete 1-year data, and a per-protocol analysis. All of the point prevalence numbers favored oral therapy, but crossed the null. Curves in the time-to-treatment-failure analysis were virtually superimposable, as were curves in time to discontinuation of therapy.

Another subgroup analysis examined treatment failure by infective organism; again, there were no significant treatment differences in any of the pathogen subgroups examined (S. aureus, coagulase-negative staph, streptococci species, and other gram-negative bacteria).

Nor did the type of antibiotic significantly affect failure rate, Dr. Scarborough noted. The median length of stay was 14 days for patients on IV treatment and 11 days for those taking oral medications. The incidence of serious adverse events was very similar – about 86% in each group.

On a visual analog scale that assessed health-related quality of life, patients taking oral treatment reported better mobility, self-care, and activity level, and less pain, discomfort, anxiety, and depression than those taking IV medications.

Cost represented the other significant difference between the groups. Over 1 year, the mean IV treatment cost was the equivalent of $17,152, and the mean oral treatment cost was $13,611 – a significant difference of $3,541.

“This represents a potential savings to the National Health Service of 16-25 million pounds sterling ($20.6 million-$32.3 million) per year,” Dr. Scarborough said. “All coming at no expense of good clinical outcomes.”

OVIVA was sponsored by the U.K. National Institute of Health Research. Dr. Scarborough had no financial disclosures.

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Key clinical point: For bone and joint infections, oral antibiotics are as good as IV antibiotics and cost much less.

Major finding: At 1 year, cure rates were identical, but oral treatment cost about $3,500 less than IV treatment.

Data source: The study randomized 1,054 patients.

Disclosures: OVIVA was sponsored by the U.K. National Institute of Health Research. Dr. Scarborough had no financial disclosures.

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The End of a Season

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Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.

In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.

I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.

As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.

A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”

To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.

We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.

I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.

Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.

In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.

I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.

As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.

A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”

To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.

We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.

I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.

Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Spring, it symbolizes a new beginning. The smell of fresh cut grass hangs in the air, and it’s my favorite time of the sports year. A new season has begun in baseball, and the NHL and NBA playoffs are underway. As a new season begins, two more draw to a close. In this fan’s opinion, there is nothing quite as exciting as playoff hockey, and this month AJO hopes to “Capital-ize” on that excitement by presenting the hockey issue.

In “The Ice Hockey Issue”, Popkin and colleagues present a review of upper extremity injuries in hockey, which will serve as a guide for sports medicine physicians covering hockey games. There’s even a segment covering dental and ocular injuries, in case you don’t have a dentist or ophthalmologist handy. While we typically no longer publish case reports, Degen and colleagues present a unique report detailing an unusual injury to a prominent NHL goaltender. AJO presents it to expand your diagnostic differential for neck injuries.

I had another reason in mind when I mentioned the end of a season in this month’s editorial. The new AJO has seen a lot of changes, and it is our Editorial Team’s goal to continuously improve the journal and to provide timely features that are directly relevant to your practice. We’ve updated our website, and we’ve added some features, such as QR codes and take-home points, to improve your reading experience. But our ability to further enhance the journal is limited in print, and our web statistics show that a large percentage of our readers view the articles on their smartphones.

As I’ve written before, these are challenging times for printed media. The digital age has arrived and technology has made traditional publications less appealing. Our younger readers now demand a portable, electronic, media-rich publication that provides information that directly benefits their practices. To provide this, we envision a digital journal that is immersed in a learning environment, with videos, technique guides, and supplementary materials just a click away.

A few months back, AJO tested the digital waters. Our trial met with a positive response, and so, it is with great excitement that we announce that beginning in 2018, AJO will be the first orthopedic journal to go “All Digital.”

To further our goal of creating material that directly impacts your practice, we will present each feature review article as a learning module. The articles will feature extensive photos and videos, PowerPoint presentations for download, test questions, and patient information sheets. We will publish authors’ preference cards and postoperative protocols.

We’re currently developing applications and tools to improve your interactive experience. In the coming months, look for announcements regarding new strategic partnerships and features that will become mainstays of our electronic environment.

I hope you share the excitement of a new beginning in the digital era. I know the transition will provide a greatly enhanced, valuable resource that will change the way we utilize journals in our practice.

Am J Orthop. 2017;46(3):122. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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Head, Neck, and Shoulder Injuries in Ice Hockey: Current Concepts

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Head, Neck, and Shoulder Injuries in Ice Hockey: Current Concepts

Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.

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Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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72. Kuzuhara K, Shimamoto H, Mase Y. Ice hockey injuries in a Japanese elite team: a 3-year prospective study. J Athl Train. 2009;44(2):208-214.

73. Rishiraj N, Lloyd-Smith R, Lorenz T, Niven B, Michel M. University men’s ice hockey: rates and risk of injuries over 6-years. J Sports Med Phys Fitness. 2009;49(2):159-166.

74. Tuominen M, Stuart MJ, Aubry M, Kannus P, Parkkari J. Injuries in men’s international ice hockey: a 7-year study of the International Ice Hockey Federation Adult World Championship Tournaments and Olympic Winter Games. Br J Sports Med. 2015;49(1):30-36.

75. Heckman JD, Bucholz RW. In: Rockwood CA, Green DP, Heckman JD, Bucholz RW, eds. Rockwood and Green’s Fractures in Adults, Volume 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

References

1. Vaughan G. The Puck Starts Here: The Origin of Canada’s Great Winter Game, Ice Hockey. Fredericton, Canada: Goose Lane Editions; 1996.

2. IIHF member national associations. International Ice Hockey Federation website. http://www.iihf.com/iihf-home/the-iihf/members. Accessed April 6, 2017.

3. Flik K, Lyman S, Marx RG. American collegiate men’s ice hockey: an analysis of injuries. Am J Sports Med. 2005;33(2):183-187.

4. Engebretsen L, Steffen K, Alonso JM, et al. Sports injuries and illnesses during the Winter Olympic Games 2010. Br J Sports Med. 2010;44(11):772-780.

5. Deits J, Yard EE, Collins CL, Fields SK, Comstock RD. Patients with ice hockey injuries presenting to US emergency departments, 1990-2006. J Athl Train. 2010;45(5):467-474.

6. Brooks A, Loud KJ, Brenner JS, et al. Reducing injury risk from body checking in boys’ youth ice hockey. Pediatrics. 2014;133(6):1151-1157.

7. Agel J, Harvey EJ. A 7-year review of men’s and women’s ice hockey injuries in the NCAA. Can J Surg. 2010;53(5):319-323.

8. Micieli JA, Zurakowski D, Ahmed, II. Impact of visors on eye and orbital injuries in the National Hockey League. Can J Ophthalmol. 2014;49(3):243-248.

9. Pashby TJ. Ocular injuries in hockey. Int Ophthalmol Clin. 1988;28(3):228-231.

10. Leivo T, Haavisto AK, Sahraravand A. Sports-related eye injuries: the current picture. Acta Ophthalmol. 2015;93(3):224-231.

11. Cohn RM, Alaia MJ, Strauss EJ, Feldman AF. Rink-side management of ice hockey related injuries to the face, neck, and chest. Bull Hosp Jt Dis. 2013;71(4):253-256.

12. Reehal P. Facial injury in sport. Curr Sports Med Rep. 2010;9(1):27-34.

13. Stuart MJ, Smith AM, Malo-Ortiguera SA, Fischer TL, Larson DR. A comparison of facial protection and the incidence of head, neck, and facial injuries in Junior A hockey players. A function of individual playing time. Am J Sports Med. 2002;30(1):39-44.

14. MacEwen CJ, McLatchie GR. Eye injuries in sport. Scott Med J. 2010;55(2):22-24.

15. Stevens ST, Lassonde M, de Beaumont L, Keenan JP. The effect of visors on head and facial injury in National Hockey League players. J Sci Med Sport. 2006;9(3):238-242.

16. Moslener MD, Wadsworth LT. Ice hockey: a team physician’s perspective. Curr Sports Med Rep. 2010;9(3):134-138.

17. LaPrade RF, Burnett QM, Zarzour R, Moss R. The effect of the mandatory use of face masks on facial lacerations and head and neck injuries in ice hockey. A prospective study. Am J Sports Med. 1995;23(6):773-775.

18. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA. 1999;282(24):2328-2332.

19. Lahti H, Sane J, Ylipaavalniemi P. Dental injuries in ice hockey games and training. Med Sci Sports Exerc. 2002;34(3):400-402.

20. Sane J, Ylipaavalniemi P, Leppanen H. Maxillofacial and dental ice hockey injuries. Med Sci Sports Exerc. 1988;20(2):202-207.

21. Emerich K, Kaczmarek J. First aid for dental trauma caused by sports activities: state of knowledge, treatment and prevention. Sports Med. 2010;40(5):361-366.

22. Rosenberg H, Rosenberg H, Hickey M. Emergency management of a traumatic tooth avulsion. Ann Emerg Med. 2011;57(4):375-377.

23. Young EJ, Macias CR, Stephens L. Common dental injury management in athletes. Sports Health. 2015;7(3):250-255.

24. Andersson L, Andreasen JO, Day P, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2012;28(2):88-96.

25. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med. 2009;19(3):185-200.

26. Schneider KJ, Meeuwisse WH, Kang J, Schneider GM, Emery CA. Preseason reports of neck pain, dizziness, and headache as risk factors for concussion in male youth ice hockey players. Clin J Sport Med. 2013;23(4):267-272.

27. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013;47(5):250-258.

28. Delaney JS, Lamfookon C, Bloom GA, Al-Kashmiri A, Correa JA. Why university athletes choose not to reveal their concussion symptoms during a practice or game. Clin J Sport Med. 2015;25(2):113-125.

29. Ventura RE, Balcer LJ, Galetta SL. The concussion toolbox: the role of vision in the assessment of concussion. Semin Neurol. 2015;35(5):599-606.

30. Vartiainen MV, Holm A, Peltonen K, Luoto TM, Iverson GL, Hokkanen L. King-Devick test normative reference values for professional male ice hockey players. Scand J Med Sci Sports. 2015;25(3):e327-e330.

31. Galetta MS, Galetta KM, McCrossin J, et al. Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci. 2013;328(1-2):28-31.

32. Vernau BT, Grady MF, Goodman A, et al. Oculomotor and neurocognitive assessment of youth ice hockey players: baseline associations and observations after concussion. Dev Neuropsychol. 2015;40(1):7-11.

 

 

33. Fry AF, Hale S. Relationships among processing speed, working memory, and fluid intelligence in children. Biol Psychol. 2000;54(1-3):1-34.

34. Felleman DJ, Van Essen DC. Distributed hierarchical processing in the primate cerebral cortex. Cereb Cortex. 1991;1(1):1-47.

35. Guskiewicz KM, Register-Mihalik J, McCrory P, et al. Evidence-based approach to revising the SCAT2: introducing the SCAT3. Br J Sports Med. 2013;47(5):289-293.

36. Smith AM, Stuart MJ, Dodick DW, et al. Ice Hockey Summit II: zero tolerance for head hits and fighting. Curr Sports Med Rep. 2015;14(2):135-144.

37. Mihalik JP, Beard JR, Petschauer MA, Prentice WE, Guskiewicz KM. Effect of ice hockey helmet fit on cervical spine motion during an emergency log roll procedure. Clin J Sport Med. 2008;18(5):394-398.

38. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32(4):1077-1087.

39. Reynen PD, Clancy WG Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med. 1994;22(2):167-170.

40. Tator CH, Provvidenza C, Cassidy JD. Update and overview of spinal injuries in Canadian ice hockey, 1943 to 2011: the continuing need for injury prevention and education. Clin J Sport Med. 2016;26(3):232-238.

41. Tator CH, Edmonds VE, Lapczak L, Tator IB. Spinal injuries in ice hockey players, 1966-1987. Can J Surg. 1991;34(1):63-69.

42. Laprade RF, Schnetzler KA, Broxterman RJ, Wentorf F, Gilbert TJ. Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med. 2000;28(6):800-803.

43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.

44. National Athletic Trainers’ Association. Appropriate prehospital management of the spine-injured athlete: updated from 1998 document. http://www.nata.org/sites/default/files/Executive-Summary-Spine-Injury-updated.pdf. Updated August 5, 2015. Accessed April 6, 2017.

45. Del Rossi G, Heffernan TP, Horodyski M, Rechtine GR. The effectiveness of extrication collars tested during the execution of spine-board transfer techniques. Spine J. 2004;4(6):619-623.

46. Morganti C, Sweeney CA, Albanese SA, Burak C, Hosea T, Connolly PJ. Return to play after cervical spine injury. Spine. 2001;26(10):1131-1136.

47. Huang P, Anissipour A, McGee W, Lemak L. Return-to-play recommendations after cervical, thoracic, and lumbar spine injuries: a comprehensive review. Sports Health. 2016;8(1):19-25.

48. Shindle MK, Marx RG, Kelly BT, Bisson L, Burke CJ 3rd. Hockey injuries: a pediatric sport update. Curr Opin Pediatr. 2010;22(1):54-60.

49. Molsa J, Kujala U, Myllynen P, Torstila I, Airaksinen O. Injuries to the upper extremity in ice hockey: analysis of a series of 760 injuries. Am J Sports Med. 2003;31(5):751-757.

50. Dwyer T, Petrera M, Bleakney R, Theodoropoulos JS. Shoulder instability in ice hockey players: incidence, mechanism, and MRI findings. Clin Sports Med. 2013;32(4):803-813.

51. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. Br J Sports Med. 2009;43(13):1000-1005.

52. Willimon SC, Gaskill TR, Millett PJ. Acromioclavicular joint injuries: anatomy, diagnosis, and treatment. Phys Sportsmed. 2011;39(1):116-122.

53. Martetschlager F, Horan MP, Warth RJ, Millett PJ. Complications after anatomic fixation and reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2013;41(12):2896-2903.

54. Carofino BC, Mazzocca AD. The anatomic coracoclavicular ligament reconstruction: surgical technique and indications. J Shoulder Elbow Surg. 2010;19(2 suppl):37-46.

55. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. Br J Sports Med. 2014;48(1):4-10.

56. Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. A multicenter, randomized clinical trial. J Bone Joint Surg Am. 2007;89(1):1-10.

57. Lee JT, Nasreddine AY, Black EM, Bae DS, Kocher MS. Posterior sternoclavicular joint injuries in skeletally immature patients. J Pediatr Orthop. 2014;34(4):369-375.

58. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med. 1978;6(6):373-377.

59. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433.

60. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60.

61. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.

62. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953.

63. Griffin JW, Brockmeier SF. Shoulder instability with concomitant bone loss in the athlete. Orthop Clin North Am. 2015;46(1):89-103.

64. Cohen SB, Towers JD, Bradley JP. Rotator cuff contusions of the shoulder in professional football players: epidemiology and magnetic resonance imaging findings. Am J Sports Med. 2007;35(3):442-447.

65. Lorentzon R, Wedrèn H, Pietilä T. Incidence, nature, and causes of ice hockey injuries. A three-year prospective study of a Swedish elite ice hockey team. Am J Sports Med. 1988;16(4):392-396.

66. Stuart MJ, Smith A. Injuries in Junior A ice hockey. A three-year prospective study. Am J Sports Med. 1995;23(4):458-461.

67. Voaklander DC, Saunders LD, Quinney HA, Macnab RB. Epidemiology of recreational and old-timer ice hockey injuries. Clin J Sport Med. 1996;6(1):15-21.

68. Mölsä J, Airaksinen O, Näsman O, Torstila I. Ice hockey injuries in Finland. A prospective epidemiologic study. Am J Sports Med. 1997;25(4):495-499.

69. Ferrara MS, Schurr KT. Intercollegiate ice hockey injuries: a casual analysis. Clin J Sport Med. 1999;9(1):30-33.

70. Pinto M, Kuhn JE, Greenfield ML, Hawkins RJ. Prospective analysis of ice hockey injuries at the Junior A level over the course of one season. Clin J Sport Med. 1999;9(2):70-74.

71. Emery CA, Meeuwisse WH. Injury rates, risk factors, and mechanisms of injury in minor hockey. Am J Sports Med. 2006;34(12):1960-1969.

72. Kuzuhara K, Shimamoto H, Mase Y. Ice hockey injuries in a Japanese elite team: a 3-year prospective study. J Athl Train. 2009;44(2):208-214.

73. Rishiraj N, Lloyd-Smith R, Lorenz T, Niven B, Michel M. University men’s ice hockey: rates and risk of injuries over 6-years. J Sports Med Phys Fitness. 2009;49(2):159-166.

74. Tuominen M, Stuart MJ, Aubry M, Kannus P, Parkkari J. Injuries in men’s international ice hockey: a 7-year study of the International Ice Hockey Federation Adult World Championship Tournaments and Olympic Winter Games. Br J Sports Med. 2015;49(1):30-36.

75. Heckman JD, Bucholz RW. In: Rockwood CA, Green DP, Heckman JD, Bucholz RW, eds. Rockwood and Green’s Fractures in Adults, Volume 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

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Arthroscopic Excision of Bipartite Patella With Preservation of Lateral Retinaculum in an Adolescent Ice Hockey Player

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Arthroscopic Excision of Bipartite Patella With Preservation of Lateral Retinaculum in an Adolescent Ice Hockey Player

Take-Home Points

  • Bipartite patella is an asymptomatic anatomical variant.
  • Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
  • Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
  • Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.

In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4

The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.

In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.

Case Report

A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.

We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole.

Figure 1.
A magnetic resonance imaging (MRI) series was ordered for further evaluation of the soft tissues (Figure 2).
Figure 2.
There was bony edema in the anteromedial aspect of the distal femur. The visualized patella showed no evidence of fracture, though there was evidence of disruption through the fibrous attachments of the bipartite patella fragment. Physical therapy (range-of-motion exercises, quadriceps sets, and stationary bicycling) was initiated. By 6 weeks, the patient’s discomfort had resolved, and he resumed on-ice activities as tolerated.

Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.

Surgical Technique

The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.

Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B).

Figure 3.
An accessory superolateral arthroscopic portal was created to improve surgical instrument access. Round and oval burrs, straight and curved shavers, pituitary rongeur, curettes, and small osteotome were used to meticulously excise the accessory bipartite patella fragment, leaving the overlying (anterior) retinaculum intact. After the fragment was excised, the region was palpated, and no additional loose fragments were felt (Figures 4A, 4B).
Figure 4.
The remaining patellar articular cartilage was intact. On palpation, the patella did not sublux medially, indicating the lateral retinaculum was well maintained during excision of the patella fragment.

 

 

Postoperative Rehabilitation

Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.

Outcomes

This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.

Discussion

The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.

Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.

Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.

Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.

Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.

Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.

2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.

3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.

4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.

5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.

6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.

7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.

8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.

9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.

10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.

11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.

12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.

13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.

14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.

15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.

16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.

17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.

18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.

19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.

20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.

21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.

22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154

23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.

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Take-Home Points

  • Bipartite patella is an asymptomatic anatomical variant.
  • Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
  • Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
  • Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.

In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4

The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.

In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.

Case Report

A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.

We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole.

Figure 1.
A magnetic resonance imaging (MRI) series was ordered for further evaluation of the soft tissues (Figure 2).
Figure 2.
There was bony edema in the anteromedial aspect of the distal femur. The visualized patella showed no evidence of fracture, though there was evidence of disruption through the fibrous attachments of the bipartite patella fragment. Physical therapy (range-of-motion exercises, quadriceps sets, and stationary bicycling) was initiated. By 6 weeks, the patient’s discomfort had resolved, and he resumed on-ice activities as tolerated.

Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.

Surgical Technique

The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.

Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B).

Figure 3.
An accessory superolateral arthroscopic portal was created to improve surgical instrument access. Round and oval burrs, straight and curved shavers, pituitary rongeur, curettes, and small osteotome were used to meticulously excise the accessory bipartite patella fragment, leaving the overlying (anterior) retinaculum intact. After the fragment was excised, the region was palpated, and no additional loose fragments were felt (Figures 4A, 4B).
Figure 4.
The remaining patellar articular cartilage was intact. On palpation, the patella did not sublux medially, indicating the lateral retinaculum was well maintained during excision of the patella fragment.

 

 

Postoperative Rehabilitation

Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.

Outcomes

This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.

Discussion

The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.

Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.

Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.

Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.

Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.

Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Bipartite patella is an asymptomatic anatomical variant.
  • Occasionally, some adolescent athletes can present with AKP, resulting in decreased participation and performance.
  • Bipartite patella is classified in type I, inferior pole; type II, lateral margin; and type III, superior lateral pole, depending on where the accessory patellar fragment is.
  • Nonoperative treatment is advocated first. If symptoms persist surgical treatment should be attempted.

In 2% to 3% of the general population, the finding of bipartite patella on knee radiographs is often incidental.1,2 During development, the patella normally originates in a primary ossification center. Occasionally, secondary ossification centers emerge around the margins of the primary center and typically join that center. In some cases, the secondary2 center remains separated, leading to patella partita and an accessory patellar fragment.3,4

The bipartite patella is connected to the primary patella by fibrocartilage. The fibrous attachment may become irritated or separated as a result of trauma, overuse, or strenuous activity.1,5-7 Saupe classification of bipartite patella is based on accessory patellar fragment location: type I, inferior pole; type II, lateral margin; and type III, superior lateral pole.8 When an individual with a bipartite patella becomes symptomatic, anterior knee pain (AKP) is the most common complaint—it has been described in adolescent athletes in numerous sports.7,9-11For most patients, first-line treatment is nonoperative management. A typical regimen includes reduced activity, use of nonsteroidal anti-inflammatory drugs, physical therapy, and isometric quadriceps-strengthening exercises.1,12 Other nonoperative approaches described in the literature are immobilization,5,10 steroid and anesthetic injection, and ultrasound therapy.13 If symptoms do not improve, surgical treatment should be considered. Surgical treatment options include open excision of fragment,3,9,12 arthroscopic excision of fragment,7,14,15 tension band wiring,5,16 open reduction and internal fixation,17 open or arthroscopic vastus lateralis release,18-20 and lateral retinacular release.21 However, the optimal surgical option remains controversial.

In this case report, we present a modification of an arthroscopic surgical technique for excising a symptomatic bipartite patella and report midterm clinical outcomes. The patient provided written informed consent for print and electronic publication of this report.

Case Report

A 16-year-old elite male ice hockey player presented to clinic with a 2-week history of left AKP. He could not recall a specific injury that triggered the symptoms. Radiographs were obtained at an outside institution, and knee patellar fracture was diagnosed. The patient, placed in a straight-leg immobilizer, later presented to a referral clinic for a second opinion and further evaluation. Physical examination revealed significant tenderness to palpation of the lateral aspect of the patella. Range of motion was symmetric and fully intact. Patellar mobility was excellent. However, the patient could not perform a straight-leg raise because of the pain.

We obtained anteroposterior and lateral radiographs (Figures 1A, 1B), which showed evidence of a Saupe type III bipartite patella with separation at the superolateral pole.

Figure 1.
A magnetic resonance imaging (MRI) series was ordered for further evaluation of the soft tissues (Figure 2).
Figure 2.
There was bony edema in the anteromedial aspect of the distal femur. The visualized patella showed no evidence of fracture, though there was evidence of disruption through the fibrous attachments of the bipartite patella fragment. Physical therapy (range-of-motion exercises, quadriceps sets, and stationary bicycling) was initiated. By 6 weeks, the patient’s discomfort had resolved, and he resumed on-ice activities as tolerated.

Two years later, the patient returned with left AKP, again localized to the lateral aspect of the patella, over the bipartite fragment. The pain was significant with compression. Given the patient’s history, arthroscopic excision of the bipartite patella was recommended. After discussing all treatment options, the patient elected to proceed with the surgery.

Surgical Technique

The patient was positioned supine on the operating table. Medial and lateral parapatellar arthroscopic portals were created. Menisci, cruciate ligaments, and tibiofemoral articular cartilage were arthroscopically visualized and determined to be normal. The bipartite patella was easily visualized, and notably loose when probed. Grade 2 chondromalacia was present diffusely throughout the bipartite patella and on the far lateral aspect of the patella, at the fragment interface.

Attention was then turned to arthroscopic removal of the accessory patellar fragment (Figures 3A, 3B).

Figure 3.
An accessory superolateral arthroscopic portal was created to improve surgical instrument access. Round and oval burrs, straight and curved shavers, pituitary rongeur, curettes, and small osteotome were used to meticulously excise the accessory bipartite patella fragment, leaving the overlying (anterior) retinaculum intact. After the fragment was excised, the region was palpated, and no additional loose fragments were felt (Figures 4A, 4B).
Figure 4.
The remaining patellar articular cartilage was intact. On palpation, the patella did not sublux medially, indicating the lateral retinaculum was well maintained during excision of the patella fragment.

 

 

Postoperative Rehabilitation

Rehabilitation focused on protection of the healing patella and accelerated rehabilitation for early return to play. Range-of-motion exercises and stationary bicycling were initiated on postoperative day 1. Weight-bearing was allowed as tolerated. Quadriceps sets, straight-leg raises, and ankle pumps were performed 5 times daily for 6 weeks. Six weeks after surgery, the patient was cleared, and he returned to full on-ice activities.

Outcomes

This study was approved by an Institutional Review Board. Preoperative and postoperative outcomes were obtained and stored in a data registry. The patient’s Lysholm score22 improved from 71 before surgery to 100 at 31-month follow-up. In addition, his subjective International Knee Documentation Committee score23 improved from 65.5 before surgery to 72.4 after surgery. At follow-up, patient satisfaction with outcome was 10/10. In addition, the patient had returned to playing hockey at a higher national level without functional limitation.

Discussion

The most important finding in this case is that arthroscopic excision of a bipartite patella with preservation of the lateral retinaculum in an elite adolescent hockey player resulted in improved subjective clinical outcomes scores and early return to competition. Arthroscopic excision was favored over open excision in this patient because of potential quicker recovery,14 less pain, and expedited return to competition. In addition, previous arthroscopic techniques were modified to shorten postoperative rehabilitation. The modified technique included preservation of the lateral retinaculum and total arthroscopic excision of the accessory bipartite patella fragment.

Although results of open techniques have been favorable,3,8,9 these procedures are far more invasive than arthroscopic techniques and may result in loss of quadriceps strength and prolonged rehabilitation.18 Weckström and colleagues12 followed 25 male military recruits for a minimum of 10 years after open excision of symptomatic bipartite patella. Mean Kujala score was 95 (range, 75-100), and median visual analog scale score for knee pain was 1.0 (range, 0.0-6.0). In a study by Bourne and Bianco,3 13 of 16 patients who were followed for an average of 7 years experienced complete pain relief with an average recovery time of 2 months.

Other studies have described the arthroscopic excision technique for symptomatic bipartite patella,7,14,15 but outcomes are underreported, especially for follow-ups longer than 2 years. Felli and colleagues7 described a case of arthroscopic excision and lateral release in a 23-year-old female professional volleyball player; at 1-year follow-up, the patient was symptom-free and back to full athletic participation. Azarbod and colleagues14 also reported on a patient who was symptom-free, 6 weeks after arthroscopic excision of bipartite patella. Carney and colleagues15 indicated that successful excision of bipartite patella was evident on 6-month radiographic follow-up. Our 31-month follow-up is the longest of any study on arthroscopic excision of bipartite patella. Clinical outcomes were excellent both in our patient’s case and in the earlier studies.

Our patient was a high-level hockey player who wanted to return to competition as quickly as possible. Conservative management, including physical therapy, initially resolved his symptoms and allowed him to resume on-ice activities after 6 weeks. In time, however, his symptoms returned and began limiting his on-ice performance. Arthroscopic removal of the bipartite patella accessory fragment allowed him to return to full on-ice activities after 6 weeks. His case provides evidence that arthroscopic management of bipartite patella with preservation of the vastus lateralis and lateral retinaculum may be an excellent treatment option for patients who want to return to athletics as quickly as possible.

Our technique of arthroscopic excision with preservation of lateral retinaculum is an excellent treatment option for symptomatic bipartite patella. This option, combined with an aggressive rehabilitation protocol, allows for pain relief and expedited return to competition.

Am J Orthop. 2017;46(3):135-138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.

2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.

3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.

4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.

5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.

6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.

7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.

8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.

9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.

10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.

11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.

12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.

13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.

14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.

15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.

16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.

17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.

18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.

19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.

20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.

21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.

22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154

23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.

References

1. Atesok K, Doral MN, Lowe J, Finsterbush A. Symptomatic bipartite patella: treatment alternatives. J Am Acad Orthop Surg. 2008;16(8):455-461.

2. Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am. 1982;64(1):147-152.

3. Bourne MH, Bianco AJ Jr. Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10(1):69-73.

4. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1465-1469.

5. Okuno H, Sugita T, Kawamata T, Ohnuma M, Yamada N, Yoshizumi Y. Traumatic separation of a type I bipartite patella: a report of four knees. Clin Orthop Relat Res. 2004;(420):257-260.

6. Yoo JH, Kim EH, Ryu HK. Arthroscopic removal of separated bipartite patella causing snapping knee syndrome. Orthopedics. 2008;31(7):717.

7. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19(3):398-399.

8. Green WT Jr. Painful bipartite patellae. A report of three cases. Clin Orthop Relat Res. 1975;(110):197-200.

9. Ishikawa H, Sakurai A, Hirata S, et al. Painful bipartite patella in young athletes. The diagnostic value of skyline views taken in squatting position and the results of surgical excision. Clin Orthop Relat Res. 1994;(305):223-228.

10. Stocker RL, van Laer L. Injury of a bipartite patella in a young upcoming sportsman. Arch Orthop Trauma Surg. 2011;131(1):75-78.

11. Wong CK. Bipartite patella in a young athlete. J Orthop Sports Phys Ther. 2009;39(7):560.

12. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855.

13. Kumahashi N, Uchio Y, Iwasa J, Kawasaki K, Adachi N, Ochi M. Bone union of painful bipartite patella after treatment with low-intensity pulsed ultrasound: report of two cases. Knee. 2008;15(1):50-53.

14. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy. 2005;21(8):1006.

15. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39(1):40-43.

16. Tauber M, Matis N, Resch H. Traumatic separation of an uncommon bipartite patella type: a case report. Knee Surg Sports Traumatol Arthrosc. 2007;15(1):83-87.

17. Werner S, Durkan M, Jones J, Quilici S, Crawford D. Symptomatic bipartite patella: three subtypes, three representative cases. J Knee Surg. 2013;26(suppl 1):S72-S76.

18. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M. Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18(4):404-411.

19. Maeno S, Hashimoto D, Otani T, Masumoto K, Hui C. The “coiling-up procedure”: a novel technique for extra-articular arthroscopy. Arthroscopy. 2010;26(11):1551-1555.

20. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76(4):573-578.

21. Mori Y, Okumo H, Iketani H, Kuroki Y. Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23(1):13-18.

22. Lysholm J, Gillquist J. Evaluation of knee ligament surgery results with special emphasis on use of a scoring scale. Am J Sports Med. 1982;10(3):150-154

23. Grevnerts HT, Terwee CB, Kvist J. The measurement properties of the IKDC-subjective knee form. Knee Surg Sports Traumatol Arthrosc. 2015;23(12):3698-3706.

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Arthroscopic Excision of Bipartite Patella With Preservation of Lateral Retinaculum in an Adolescent Ice Hockey Player
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Internal Carotid Artery Dissection After Indirect Blunt Cervical Trauma in an Ice Hockey Goaltender

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Internal Carotid Artery Dissection After Indirect Blunt Cervical Trauma in an Ice Hockey Goaltender

Take-Home Points

  • ICA dissections may occur from direct or indirect trauma.
  • Symptoms can be mild, including a persistent headache.
  • High clinical suspicion is required for diagnosis when symptoms are mild.
  • Neuroimaging is required for definitive diagnosis.
  • Conservative management with serial imaging can yield successful outcomes.

Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.

Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.

On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.

Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection.

Figure 1.
There was an associated intimal flap and about 50% luminal narrowing (Figure 1).

Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.

Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation.
Figure 2.
Adjacent to that was an associated pseudoaneurysm (Figure 3). Continued antiplatelet therapy and relative rest were advised. At 4 weeks, imaging showed increased luminal diameter, with the intramural hematoma resolving (Figure 4).
Figure 3.


At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches.
Figure 4.
Neurologic findings were again negative. MRA showed interval improvement with nearly complete resolution of the stenosis, with a small area of resorbing hematoma within the former pseudoaneurysm (Figure 5). Graduated return to activities was recommended, with cessation of activities and repeat assessment if symptoms returned.
Figure 5.
The patient successfully returned to his prior level of competition 8 weeks after injury. The Table summarizes the clinical events.

 

 

Discussion

In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9

Table.
However, CAD is the most common cause of stroke in young and middle-aged patients3; although it accounts for only 2% of all ischemic strokes, it causes 8% to 25% of ischemic strokes among patients under the age of 45 years.3 The ICA is particularly susceptible to injury, as it is mobile within the neck but relatively fixed at the base of the skull, where it pierces the petrous bone, making it susceptible to strain.2,10 Participation in contact sports can result in direct trauma to the anterior neck, or in indirect trauma (acute hyperflexion, hyperextension, lateral flexion, or rotation) that may precipitate these injuries; therefore, CAD should be in the differential diagnosis for athletes who have had such an injury.

As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.

More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.

MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.

 

 

Conclusion

We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.

Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.

2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.

3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.

4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.

5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.

6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.

7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.

8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.

9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.

10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.

11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.

12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.

13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.

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Take-Home Points

  • ICA dissections may occur from direct or indirect trauma.
  • Symptoms can be mild, including a persistent headache.
  • High clinical suspicion is required for diagnosis when symptoms are mild.
  • Neuroimaging is required for definitive diagnosis.
  • Conservative management with serial imaging can yield successful outcomes.

Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.

Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.

On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.

Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection.

Figure 1.
There was an associated intimal flap and about 50% luminal narrowing (Figure 1).

Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.

Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation.
Figure 2.
Adjacent to that was an associated pseudoaneurysm (Figure 3). Continued antiplatelet therapy and relative rest were advised. At 4 weeks, imaging showed increased luminal diameter, with the intramural hematoma resolving (Figure 4).
Figure 3.


At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches.
Figure 4.
Neurologic findings were again negative. MRA showed interval improvement with nearly complete resolution of the stenosis, with a small area of resorbing hematoma within the former pseudoaneurysm (Figure 5). Graduated return to activities was recommended, with cessation of activities and repeat assessment if symptoms returned.
Figure 5.
The patient successfully returned to his prior level of competition 8 weeks after injury. The Table summarizes the clinical events.

 

 

Discussion

In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9

Table.
However, CAD is the most common cause of stroke in young and middle-aged patients3; although it accounts for only 2% of all ischemic strokes, it causes 8% to 25% of ischemic strokes among patients under the age of 45 years.3 The ICA is particularly susceptible to injury, as it is mobile within the neck but relatively fixed at the base of the skull, where it pierces the petrous bone, making it susceptible to strain.2,10 Participation in contact sports can result in direct trauma to the anterior neck, or in indirect trauma (acute hyperflexion, hyperextension, lateral flexion, or rotation) that may precipitate these injuries; therefore, CAD should be in the differential diagnosis for athletes who have had such an injury.

As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.

More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.

MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.

 

 

Conclusion

We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.

Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • ICA dissections may occur from direct or indirect trauma.
  • Symptoms can be mild, including a persistent headache.
  • High clinical suspicion is required for diagnosis when symptoms are mild.
  • Neuroimaging is required for definitive diagnosis.
  • Conservative management with serial imaging can yield successful outcomes.

Cervical artery dissection (CAD) is an uncommon but potentially life-threatening condition that accounts for a high proportion of ischemic strokes in patients under the age of 45 years.1-4 The extracranial internal carotid arteries (ICAs) and vertebral arteries are most commonly involved; dissections can occur after either direct trauma to the neck, or indirect trauma resulting in acute hyperextension or hyperflexion.4-7 ICA dissection can be difficult to diagnose because of the varying symptomatology. Clinical presentation depends on stenosis location, degree of luminal narrowing, and presence or absence of ischemic stroke. Neurologic symptoms may be delayed, and misdiagnosis of an isolated soft-tissue contusion, whiplash, can be made in the setting of indirect cervical trauma.

Although this entity is well described in the literature,2,3,5,8 there are few reported cases of injuries sustained during high-intensity athletic competition. In this case report, we describe the symptoms, physical examination findings, diagnostic imaging results, and treatment of a young male athlete who presented with delayed-onset symptoms of ICA dissection resulting from indirect cervical trauma sustained during an ice hockey game. We discuss the importance of a high level of clinical suspicion in the diagnosis of neck injuries sustained during athletic competition, as well as the need for early vascular imaging for diagnosis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

The patient was a right-handed 32-year-old professional hockey goaltender. Four days before diagnosis, his goaltending mask and attached neck-protector were inadvertently lifted by another player’s stick just as a puck traveling at high speed struck him in the neck, to the right of the larynx, causing acute neck hyperextension. He immediately experienced discomfort and fell to the ice, saying he was “dizzy and light-headed.” Play was stopped, and medical personnel attended to him. His symptoms resolved, and he resumed play without any notable deficits. The next day, he noted discomfort at the impact site, but no additional symptoms, and received a presumptive diagnosis of cervical soft-tissue contusion. Continuing to participate in hockey that day, he did not develop any symptoms other than superficial cervical discomfort. However, the next morning, he presented complaining of severe right frontotemporal headache, which had persisted overnight. Orthopedic examination revealed palpable tenderness over the anterior cervical musculature, including the sternocleidomastoid and strap muscles. There was no appreciable hematoma in the contused area. Cervical range of motion was otherwise preserved. Cervical spine examination, including dermatomal and myotomal examination, was normal, as was cranial nerve examination. However, given the headache intensity and the recency of the injury, the potential for vascular or neurologic injury was considered. A neurology consultation was obtained, and arrangements were made for advanced cross-sectional imaging.

On further evaluation, the patient denied loss of consciousness, seizure, vomiting, amnesia, visual disturbance, language or cognitive impairment, balance or coordination difficulties, or any appreciable face or limb weakness. Review of systems was otherwise negative. Detailed neurologic examination did not reveal any cranial nerve deficits, and pupils were 3 mm, equal, and normally responsive to light and accommodation. Muscular tone and strength were symmetric and full in the upper and lower extremities. Gait, coordination, and response to vibration and temperature sensation were all preserved.

Magnetic resonance imaging of the head and neck was normal, but magnetic resonance angiography (MRA) of the neck showed a 1-cm-long region of the ICA, before piercing the petrous bone, with evidence of dissection.

Figure 1.
There was an associated intimal flap and about 50% luminal narrowing (Figure 1).

Given the normal neurologic examination, and no evidence of brain infarction or other neurovascular complications, the acute ICA dissection was managed with antiplatelet therapy using aspirin (325 mg/d). In addition, the patient was advised to refrain from strenuous physical activity and to present to the hospital immediately if symptoms worsened or any neurologic impairment developed. Follow-up and repeat MRA were planned to monitor healing progression.

Two weeks after injury, the patient returned for follow-up. His headache and neck pain had resolved. Physical examination findings were unchanged, and there were no notable neurologic deficits. Repeat MRA findings were essentially unchanged, except for slightly increased luminal stenosis, exceeding 50% (Figure 2), attributable to intramural hematoma formation.
Figure 2.
Adjacent to that was an associated pseudoaneurysm (Figure 3). Continued antiplatelet therapy and relative rest were advised. At 4 weeks, imaging showed increased luminal diameter, with the intramural hematoma resolving (Figure 4).
Figure 3.


At 6-week follow-up, the patient had no clinical symptoms and no recurrence of headaches.
Figure 4.
Neurologic findings were again negative. MRA showed interval improvement with nearly complete resolution of the stenosis, with a small area of resorbing hematoma within the former pseudoaneurysm (Figure 5). Graduated return to activities was recommended, with cessation of activities and repeat assessment if symptoms returned.
Figure 5.
The patient successfully returned to his prior level of competition 8 weeks after injury. The Table summarizes the clinical events.

 

 

Discussion

In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9

Table.
However, CAD is the most common cause of stroke in young and middle-aged patients3; although it accounts for only 2% of all ischemic strokes, it causes 8% to 25% of ischemic strokes among patients under the age of 45 years.3 The ICA is particularly susceptible to injury, as it is mobile within the neck but relatively fixed at the base of the skull, where it pierces the petrous bone, making it susceptible to strain.2,10 Participation in contact sports can result in direct trauma to the anterior neck, or in indirect trauma (acute hyperflexion, hyperextension, lateral flexion, or rotation) that may precipitate these injuries; therefore, CAD should be in the differential diagnosis for athletes who have had such an injury.

As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.

More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.

MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.

 

 

Conclusion

We have reported the case of a 32-year-old professional hockey goaltender who presented with isolated, persistent, worsening headache of delayed onset after ICA dissection. The ICA dissection resulted from indirect trauma, with reaction to a puck causing acute hyperextension and rotational injury. To our knowledge, this is the first report of a case of ICA dissection in an athlete, lacking neurologic examination findings that could aid in the diagnosis. The index of suspicion for CAD should be high after direct or indirect cervical trauma when patients present with unilateral neck pain or headache, even in the absence of neurologic findings, as stroke is a catastrophic but preventable complication.

Am J Orthop. 2017;46(3):E139-E143. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.

2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.

3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.

4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.

5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.

6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.

7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.

8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.

9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.

10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.

11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.

12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.

13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.

References

1. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274-283.

2. Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012;20(3):145-152.

3. Biller J, Sacco RL, Albuquerque FC, et al; American Heart Association Stroke Council. Cervical arterial dissections and association with cervical manipulative therapy: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(10):3155-3174.

4. Fukunaga N, Hanaoka M, Sato K. Asymptomatic common carotid artery dissection caused by blunt injury. Emerg Med J. 2011;28(1):50.

5. Chen J, Zhou X, Li C, Cheung BM. Risk of stroke due to spontaneous cervical artery dissection. Intern Med. 2013;52(19):2237-2240.

6. Kalantzis G, Georgalas I, Chang BY, Ong C, El-Hindy N. An unusual case of traumatic internal carotid artery dissection during snowboarding. J Sports Sci Med. 2014;13(2):451-453.

7. Lu A, Shen P, Lee P, et al. CrossFit-related cervical internal carotid artery dissection. Emerg Radiol. 2015;22(4):449-452.

8. CADISS Trial Investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.

9. van Wessem KJ, Meijer JM, Leenen LP, van der Worp HB, Moll FL, de Borst GJ. Blunt traumatic carotid artery dissection still a pitfall? The rationale for aggressive screening. Eur J Trauma Emerg Surg. 2011;37(2):147-154.

10. Haneline M, Triano J. Cervical artery dissection. A comparison of highly dynamic mechanisms: manipulation versus motor vehicle collision. J Manipulative Physiol Ther. 2005;28(1):57-63.

11. Thomas LC, Rivett DA, Attia JR, Levi C. Risk factors and clinical presentation of cervical arterial dissection: preliminary results of a prospective case-control study. J Orthop Sports Phys Ther. 2015;45(7):503-511.

12. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;(10):CD000255.

13. Creavin ST, Rice CM, Pollentine A, Cowburn P. Carotid artery dissection presenting with isolated headache and Horner syndrome after minor head injury. Am J Emerg Med. 2012;30(9):2103.e5-e7.

Issue
The American Journal of Orthopedics - 46(3)
Issue
The American Journal of Orthopedics - 46(3)
Page Number
E139-E143
Page Number
E139-E143
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Publications
Topics
Article Type
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Internal Carotid Artery Dissection After Indirect Blunt Cervical Trauma in an Ice Hockey Goaltender
Display Headline
Internal Carotid Artery Dissection After Indirect Blunt Cervical Trauma in an Ice Hockey Goaltender
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