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Preoperative Corticosteroid Use for Medical Conditions is Associated with Increased Postoperative Infectious Complications and Readmissions After Total Hip Arthroplasty: A Propensity-Matched Study
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
28. Shrader MW, Schall D, Parvizi J, McCarthy JT, Lewallen DG. Total hip arthroplasty in patients with renal failure: a comparison between transplant and dialysis patients. J Arthroplasty. 2006;21(3):324-329. doi: 10.1016/j.arth.2005.07.008.
29. Nowicki P, Chaudhary H. Total hip replacement in renal transplant patients. J Bone Joint Surg Br. 2007;89(12):1561-1566.
30. Johannesdottir SA, Horváth-Puhó E, Dekkers OM, Cannegieter SC, Jørgensen JO, Ehrenstein V, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. doi: 10.1001/jamainternmed.2013.122.
31. Hartman J, Khanna V, Habib A, Farrokhyar F, Memon M, Adili A. Perioperative systemic glucocorticoids in total hip and knee arthroplasty: a systematic review of outcomes. J Orthop. 2017;14(2):294-301. doi: 10.1016/j.jor.2017.03.012.
32. Sculco PK, McLawhorn AS, Desai N, Su EP, Padgett DE, Jules-Elysee K. The effect of perioperative corticosteroids in total hip arthroplasty: a prospective double-blind placebo controlled pilot study. J Arthroplasty. 2016;31(6):1208-1212. doi: 10.1016/j.arth.2015.11.011.
33. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470. doi: 10.1007/s11999-013-3121-5.
34. US Department of Health and Human Services. Comprehensive Care for Joint Replacement Model. Centers for Medicare & Medicaid Services. https://innovation.cms.gov/initiatives/cjr. Accessed June 15, 2017.
35. Bozic KJ, Ward L, Vail TP, Maze M. Bundled payments in total joint arthroplasty: targeting opportunities for quality improvement and cost reduction. Clin Orthop Relat Res. 2014;472(1):188-193. doi: 10.1007/s11999-013-3034-3.
36. Bosco JA, 3rd, Karkenny AJ, Hutzler LH, Slover JD, Iorio R. Cost burden of 30-day readmissions following Medicare total hip and knee arthroplasty. J Arthroplasty. 2014;29(5): 903-905. doi: 10.1016/j.arth.2013.11.006.
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
28. Shrader MW, Schall D, Parvizi J, McCarthy JT, Lewallen DG. Total hip arthroplasty in patients with renal failure: a comparison between transplant and dialysis patients. J Arthroplasty. 2006;21(3):324-329. doi: 10.1016/j.arth.2005.07.008.
29. Nowicki P, Chaudhary H. Total hip replacement in renal transplant patients. J Bone Joint Surg Br. 2007;89(12):1561-1566.
30. Johannesdottir SA, Horváth-Puhó E, Dekkers OM, Cannegieter SC, Jørgensen JO, Ehrenstein V, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. doi: 10.1001/jamainternmed.2013.122.
31. Hartman J, Khanna V, Habib A, Farrokhyar F, Memon M, Adili A. Perioperative systemic glucocorticoids in total hip and knee arthroplasty: a systematic review of outcomes. J Orthop. 2017;14(2):294-301. doi: 10.1016/j.jor.2017.03.012.
32. Sculco PK, McLawhorn AS, Desai N, Su EP, Padgett DE, Jules-Elysee K. The effect of perioperative corticosteroids in total hip arthroplasty: a prospective double-blind placebo controlled pilot study. J Arthroplasty. 2016;31(6):1208-1212. doi: 10.1016/j.arth.2015.11.011.
33. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470. doi: 10.1007/s11999-013-3121-5.
34. US Department of Health and Human Services. Comprehensive Care for Joint Replacement Model. Centers for Medicare & Medicaid Services. https://innovation.cms.gov/initiatives/cjr. Accessed June 15, 2017.
35. Bozic KJ, Ward L, Vail TP, Maze M. Bundled payments in total joint arthroplasty: targeting opportunities for quality improvement and cost reduction. Clin Orthop Relat Res. 2014;472(1):188-193. doi: 10.1007/s11999-013-3034-3.
36. Bosco JA, 3rd, Karkenny AJ, Hutzler LH, Slover JD, Iorio R. Cost burden of 30-day readmissions following Medicare total hip and knee arthroplasty. J Arthroplasty. 2014;29(5): 903-905. doi: 10.1016/j.arth.2013.11.006.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
28. Shrader MW, Schall D, Parvizi J, McCarthy JT, Lewallen DG. Total hip arthroplasty in patients with renal failure: a comparison between transplant and dialysis patients. J Arthroplasty. 2006;21(3):324-329. doi: 10.1016/j.arth.2005.07.008.
29. Nowicki P, Chaudhary H. Total hip replacement in renal transplant patients. J Bone Joint Surg Br. 2007;89(12):1561-1566.
30. Johannesdottir SA, Horváth-Puhó E, Dekkers OM, Cannegieter SC, Jørgensen JO, Ehrenstein V, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. doi: 10.1001/jamainternmed.2013.122.
31. Hartman J, Khanna V, Habib A, Farrokhyar F, Memon M, Adili A. Perioperative systemic glucocorticoids in total hip and knee arthroplasty: a systematic review of outcomes. J Orthop. 2017;14(2):294-301. doi: 10.1016/j.jor.2017.03.012.
32. Sculco PK, McLawhorn AS, Desai N, Su EP, Padgett DE, Jules-Elysee K. The effect of perioperative corticosteroids in total hip arthroplasty: a prospective double-blind placebo controlled pilot study. J Arthroplasty. 2016;31(6):1208-1212. doi: 10.1016/j.arth.2015.11.011.
33. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470. doi: 10.1007/s11999-013-3121-5.
34. US Department of Health and Human Services. Comprehensive Care for Joint Replacement Model. Centers for Medicare & Medicaid Services. https://innovation.cms.gov/initiatives/cjr. Accessed June 15, 2017.
35. Bozic KJ, Ward L, Vail TP, Maze M. Bundled payments in total joint arthroplasty: targeting opportunities for quality improvement and cost reduction. Clin Orthop Relat Res. 2014;472(1):188-193. doi: 10.1007/s11999-013-3034-3.
36. Bosco JA, 3rd, Karkenny AJ, Hutzler LH, Slover JD, Iorio R. Cost burden of 30-day readmissions following Medicare total hip and knee arthroplasty. J Arthroplasty. 2014;29(5): 903-905. doi: 10.1016/j.arth.2013.11.006.
TAKE-HOME POINTS
- The rate of preoperative corticosteroid usage is low (3.7%).
- Patients using preoperative corticosteroids had increased rates of total 30-day complications.
- Adverse outcomes that are increased include infectious complications (eg, sepsis, urinary tract infection, surgical site infection).
- Hospital readmissions are also increased in patients taking preoperative corticosteroids, with the most common reason being infection.
- Increased postoperative counseling and surveillance may be warranted in this patient population.
Trends in Utilization of Total Hip Arthroplasty for Femoral Neck Fractures in the United States
ABSTRACT
The ideal mode of fixation for patients with femoral neck fractures is not well defined in the current literature. This study describes the recent trends in surgical management of femoral neck fractures with an analysis on perioperative outcomes.
The National Hospital Discharge Survey was used to identify femoral neck fractures in the United States between 1990 and 2007 (n = 1,155,960) treated with open reduction and internal fixation (ORIF), total hip arthroplasty (THA), or hemiarthroplasty (HA). Trends were examined over the following 3 time periods: 1990 to 1995 (group 1), 1996 to 2001 (group 2), and 2002 to 2007 (group 3). Elixhauser Comorbidity Index and perioperative complications were calculated.
Use of HA increased (74.4% to 84.6%), whereas that of THA (7.3% to 4.9%) and ORIF (18.3% to 10.6%) decreased, from group 1 to group 3 in the age group of >80 years. The use of ORIF increased (63.9% to 81.4%), whereas the use of both HA and THA decreased, from group 1 to group 3 in the age group of <50 years. The rate of adverse events increased across all fixation types but was greatest among THA (32.2% to 48.3%).
The femoral neck patient population is now older and has more medical comorbidities. We observed a trend toward performing HA in older patients and ORIF in younger patients. Despite superior functional outcomes reported in THA, this study found a decreased utilization of THA in all age groups along with an increase in adverse events and nonroutine discharges for patients with femoral neck fractures treated with THA.
Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Continue to: Femoral neck fractures...
Femoral neck fractures are a common occurrence in the United States. A recent study estimated an incidence of >63 per 100,000 population.1-8 Although the incidence appears to have decreased over recent decades, there is a projected exponential increase in the incidence of hip fractures over the next 30 years in the baby boomer population.8,9 Given that these fractures have a significant impact on patient morbidity, mortality, and quality of life, research efforts have been directed toward optimizing the treatment of affected patients and improving the outcomes.4,9-24
The treatment of choice for femoral neck fractures and the use of total hip arthroplasty (THA)11 have been a topic of debate.4,9,10,15-17,22,25 Total hip arthroplasty has been advocated for younger, more active patients, whereas hemiarthroplasty (HA) has been reserved for patients who are older and less active. Although several studies have demonstrated that arthroplasty outperforms open reduction and internal fixation (ORIF) in the elderly population with displaced femoral neck fractures, ORIF is still commonly performed in the United States for nondisplaced fractures and in patients aged <50 years.26-29
In an attempt to quantify the use of THA in the treatment of femoral neck fractures and demonstrate the national trends, Miller and colleagues5 pooled the American Board of Orthopaedic Surgery (ABOS) database and analyzed the treatment trends of surgeons taking part II of the ABOS examination from 1999 to 2011. The authors found an increased utilization of THA by recently graduated orthopedic surgeons. In contrast, Jain and colleagues30 found different national trends when they analyzed data from the National Inpatient Sample containing data between 1990 and 2001 and further found decreased utilization of THA procedures by orthopedic surgeons of all levels of training nationwide. However, neither of these studies reported about the trends in demographics, comorbidities, risk factors, or outcomes in this patient population following surgery.
The purpose of this study was to help clarify the findings of these authors using the largest dataset to date and also report on the perioperative complications associated with each mode of fixation in patients who undergo operative treatment for femoral neck fractures in the United States. Our hypotheses were that the femoral neck fracture patient population has become older and has more medical comorbidities. We also hypothesized that there has been a trend toward performing fewer THA procedures in the United States and that THA is associated with increased perioperative complications compared to those with HA and ORIF.
MATERIALS AND METHODS
We conducted a retrospective epidemiological study using the National Hospital Discharge Survey (NHDS) on surgical trends in the management of femoral neck fractures. The NHDS is a publicly available survey that is conducted annually to provide data of nonfederal, short-stay hospitals to the public. The sample data are weighted to provide nationwide estimates of annual inpatient care. The NHDS includes up to 7 medical diagnoses and 4 procedural codes per case, which are categorized using the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes, that were collected along with patient demographic information, length of stay (LOS), and discharge disposition. The diagnostic and procedural codes used for this study are presented in the Appendix. The year 2007 was chosen as the endpoint of this study due to the fact that the relative standard error of the NHDS doubled in 2008 as a result of a decrease in its survey size. As this is a publicly available database, our study was exempt from institutional review board approval.
Continue to: All pateints admitted...
All patients admitted with a primary diagnosis of closed transcervical fracture of the femoral neck (ICD-9-CM 820.0x) were selected. This resulted in 1,674,160 fractures. All patients with fractures with a concurrent primary procedural code of ORIF (79.35), HA (81.52), or THA (81.51) were identified, resulting in a total sample size of 1,155,960 surgical fractures. Analysis of the fractures based on additional specificity,ie subcapital versus midcervical versus basicervical, was not carried out because >90% of femoral neck fractures in the database were coded as “unspecified” or “other” (ICD9 CM 820.00 and 820.09, respectively).
Comorbidity burden was quantified using Elixhauser coding algorithms as previously described.31 The Elixhauser comorbidity measure is a model consisting of 31 conditions and has recently been identified as a better predictor of mortality in patients undergoing orthopedic procedures when compared with the Charlson Comorbidity Index.31 Dichotomous variables for each Elixhauser comorbidity were created, and χ2 tests were utilized to assess the association between each comorbidity and mortality. The weighted Elixhauser score for each statistically significant comorbidity was calculated as described by van Walraven and colleagues.32 The Elixhauser comorbidity score was then calculated for each patient by summing the individual weights of all comorbidities. Postoperative adverse events were determined using the complication-screening-package as previously described.33
All adverse events were categorized into 3 categories, including general medical complications, mechanical complications, and surgical complications. All adverse events recorded in the NHDS database are events that occurred during a single hospitalization. Therefore, it does not take into account adverse events that occurred after discharge, and, for example, mortality refers to postoperative mortality that occurs prior to discharge. The study period comprised data captured from 1990 to 2007, and 3 groups were generated from this time period to better characterize patients throughout the large study time frame. Group 1 comprised patients who underwent surgical management of femoral neck fractures from 1990 to 1995, group 2 consisted of patients treated from 1996 to 2001, and group 3 included patients treated from 2002 to 2007.
Categorical data were analyzed using the χ2 test, and continuous data were analyzed by the independent-samples t test and ANOVA. Multivariable binary logistic regression analyses were performed to assess the contributions of individual comorbidities to mortality, adverse events, and nonroutine discharge. Elixhauser comorbidities with a P value of < .10 in the bivariate analysis and presenting in at least 0.2% of the population were included in the logistic regression.31 Odds ratios and confidence intervals were calculated to assess the association between comorbidities and our dichotomous variables. A P value of < .001 defined statistical significance.33 Statistical analysis was conducted using SPSS version 21 (IBM).
RESULTS
Patient Demographics
Our query demonstrated a total of 1,155,960 patients who underwent surgical fixation of femoral neck fractures (Table 1). The most commonly used treatment modality was HA (75%), followed by ORIF (18%) and later by THA (7%). The majority of patients were females in each treatment group. Patients’ age varied according to treatment group, with patients undergoing HA having a mean age of 81.0 ± 9.0 years, patients undergoing ORIF having a mean age of 75.0 ± 17.0 years, and those undergoing THA having a mean age of 79.0 ± 10.0 years (P < .001). The majority of patients were ≥80 years in all treatment groups, but the ORIF group had the greatest proportion of patients <65 years (P < .001). Among patients undergoing HA, 62.4% were ≥80 years, while the ORIF and HA groups consisted of 48.6% and 51.5% of patients in that same age group, respectively.
Continue to: TRENDS ANALYSIS
TRENDS ANALYSIS
There was a significant change in the distributions of the procedures performed according to age group over time. Patients >80 years continued to undergo primarily HA, with an increase from 74.4% during 1990 to 1995 up to 84.6% during the 2002 to 2007 period and a concomitant decrease in ORIF from 18.3% to 10.6% during the same time period in this age group. Surgical trends in patients 65 to 79 years demonstrated a significant decrease in management with ORIF from 19.1% in 1990 to 1995 to 16.8% in the 2002 to 2007 cohort (P < .001 for all, Table 2). There was an increase in the use of HA from 71.9% during the 1990 to 1995 period to 75.5% during the final study period (Table 2, Figure 1). The use of THA for all age groups decreased between 1990 and 2007, except for the 50- to 64-year-old group where THA utilization remained constant.
Management patterns in patients 50 to 64 years varied throughout the analysis and demonstrated the following trend: treatment with HA remained the most common technique used but varied slightly from 59.7% during 1990 to 1995 to 60.3% during 2002 to2007 (P < .001, Table 2). The second most common treatment used was ORIF, which decreased from 32.2% to 31.5% (P < .001, Table 2). The use of THA varied significantly from 8.2% among those managed during 1990 to 1995 to 11.7% during 1996 to 2001 but later declined to the initial 8.2% (P < .001, Table 2).
Analysis of patients ≤49 years demonstrated that ORIF was the preferred technique, which experienced a growth from 63.9% during 1990 to 1995 to 81.4% during the 2002 to 2007 period (P < .001, Table 2). A decreased use in THA was observed from 2.0% in the initial period to 0.6% in the final period (P < .001, Table 2). Use of HA decreased from 34.0% in 1990 to 1995 to 18.0% in 2002 to 2007 (P < .001, Table 2).
LENGTH OF STAY
Mean number of in-hospital days decreased throughout the study period for all treatment techniques. During the 1990 to 1995 study period, patients who underwent ORIF had a mean LOS of 8 ± 7 days, which decreased (P < .001, Table 2) to 6 ± 3 days in 1996 to 2001 and remained constant during 2002 to 2007 (mean 6 ± 4 days). This decrease in LOS was also observed in patients who underwent THA (P < .001, Table 2), who initially had a mean LOS of 11 ± 7 days during 1990 to 1995, which later decreased to 7 ± 5 days for the remainder of the study. The LOS for patients who underwent HA also decreased (P < .001, Table 2), which initially was reported to be 11 ± 11 days during 1990 to 1995, decreasing to 7 ±7 days in 1996–2001 and later to 6 ± 4 days in 2002 to 2007.
COMORBIDITIY ANALYSIS
The Elixhauser Comorbidity Index varied significantly among groups over time (P < .001, Table 2). Overall mean Elixhauser Comorbidity Index score per procedure type is provided in Table 1, with HA patients having the highest score (-0.15 ± 13.09, p<.001).
Continue to: Analysis of the preoperative comorbidities...
Analysis of the preoperative comorbidities demonstrated significant differences among each surgical treatment group (P < .001 for all, Table 3). The most common comorbidities in patients who underwent HA were uncomplicated hypertension (33.2%), fluid/electrolyte disorders (17.4%), chronic pulmonary disease (14.9%), and congestive heart failure (13.7%). The most common comorbidities in the ORIF group were uncomplicated hypertension (30.8%), fluid/electrolyte disorders (14.5%), chronic pulmonary disease (14.0%), and uncomplicated diabetes (10.9%). Patients treated with THA had most commonly uncomplicated hypertension (30.1%), fluid/electrolyte disorders (17.2%), uncomplicated diabetes (15.5%), and chronic pulmonary disease (14.4%). The prevalence of comorbidities is displayed in Table 3.
DISCHARGE STATUS
Mortality varied significantly, being lowest in those who underwent ORIF (0.8%), followed those who underwent THA (1.8%), and HA (2.6%) (P < .001, Table 1).
The majority of patients in each group were discharged to long-term rehabilitation facilities, including 53.0% of those treated with HA, 40.4% of those treated with ORIF, and 44.3% of patients treated with THA. The second most common discharge location was home, which included 14.8% of patients who underwent HA, 32.2% of patients treated with ORIF, and 20.8% of those who underwent THA. Table 3 demonstrates the details of the discharge settings.
Mortality analysis over time demonstrated a significant decrease in each treatment group (P < .001). Mortality in the ORIF group decreased from 1.2% during 1990 to 1995 to 0.8% in 2002 to 2007. Mortality in the THA group also decreased significantly from 0.8% during 1990 to 1995 to 0.5% during the 2002 to 2007 time period. Patients who underwent HA also exhibited a decrease in mortality rate from 3.3% during 1990 to 1995 to 2.2% during 2002 to 2007 (P < .001, Table 4, Figure 2).
GENERAL ADVERSE EVENTS
There was a significant difference (P < .001) in the percentage of adverse events experienced, the maximum being observed in the THA group (41.0%), followed by the HA group (37.9%) and trailed by the ORIF group (20.3%, (P < .001, Table 1). The prevalence of adverse events is detailed in Table 5.
Continue to: Patients who underwent THA...
Patients who underwent THA had the highest rate of any adverse event, LOS, and transfusion rate (Table 1 and Table 5).
The prevalence of postoperative pneumonia was highest in the HA group (3.4%), followed by the ORIF group (2.9%), and the THA group (2.6%) (P < .001, Table 5). There was also a significant difference in rates of intubation, pulmonary insufficiency, acute renal failure, pulmonary embolism, acute myocardial infarction, induced mental disorder, and deep venous thrombosis (P < .001 for all, Table 5).
SURGERY-RELATED ADVERSE EVENTS
Surgery-related outcomes over the entire study period were significantly different according to the type of procedure performed (P < .001, Table 5). Patients who underwent HA had the highest rate of acute postoperative anemia (20.2%), followed by those who underwent THA (19.7%), and ORIF (10.2%). Postoperative bleeding rates also varied significantly, with 1.2% in the HA group, followed by 1.0% in the ORIF group and 0.4% in the THA group (P < .001, Table 5). Acute postoperative infection rates also varied significantly, with the highest rate being observed in the HA group (0.6%) compared to that in the THA and ORIF groups (both 0.3%) (P < .001, Table 5).
Table 6, Table 7, and Table 8 detail the results of regression analyses in patients with femoral neck fractures for individual risk factors associated with mortality, any adverse event, and nonroutine discharge to a short- or long-term rehabilitation facility, respectively. Increasing age (50–64 years, OR: 0.238; 65–79 years, OR: 1.762; and ≥80 years, OR: 2.700), THA (OR: 1.743), and HA (OR: 2.574) were found to be independent risk factors for mortality in the perioperative period (P < .001 for each, Table 6). Increasing age (50–64 years, OR: 1.888; 65–79 years, OR: 2.983; and ≥80 years, OR: 3.722), THA (OR: 2.489), and HA (OR: 2.098) were also found to be independent risk factors for any adverse event in the perioperative period (P < .001, Table 7). Age (50–64 years, OR: 1.662; 65–79 years, OR: 4.320; and ≥80 years, OR: 7.102) was the best predictor for nonroutine discharge to a short- or long-term rehabilitation facility (P < .001, Table 8).
DISCUSSION
Femoral neck fractures in the elderly population present a significant financial burden to the healthcare system.1-3,24,25 Consistent with previous epidemiological studies, our results show that the femoral neck fracture population has become older and has more medical comorbidities over the last 3 decades.27,28. Similarly, we also found that the rate of medical, surgical, and mechanical perioperative complications has increased in the same time period. Interestingly, the mortality rate has remained relatively similar.
Continue to: Although patients undergoing HA...
Although patients undergoing HA for femoral neck fractures are older and have more medical comorbidities, we found that the rate of adverse events in the perioperative period for patients undergoing THA was higher than that in the HA group. Consistent with prior studies, patients who underwent THA had higher rates of blood transfusion, pulmonary embolism, and induced mental disorders.34 Multivariable regression analysis demonstrated that after controlling for age, medical comorbidity, and type of surgery performed, THA emerged as an independent risk factor for any adverse event in the perioperative period. Increased anesthesia time, reaming of the acetabulum, and increased complexity of surgery probably account for these changes.
Our study results are consistent with those of Jain and colleagues,30 which showed a decrease in utilization of THA for femoral neck fractures between 1990 and 2001. Since THA is generally indicated for younger, more active patients in relatively good health, this would explain why changes in baseline health in this cohort over the last 20 years would lead to fewer THA procedures being performed. Surgeons in the US may be finding there are fewer patients who are candidates for THA. Miller and colleagues5 reported conflicting results and showed an increase in THA utilization in this patient population. However, their study evaluated treatment trends based on data from the ABOS part II of recently graduated orthopedic surgeons and may not be an accurate representation of national practice trends in the US. The trend toward increased subspecialization may explain their findings. As the authors noted, although they found an increase in the use of THA for femoral neck fractures by new adult reconstruction surgeons, the percentage of new surgeons treating femoral neck fractures has declined.5
Our analysis showed very concrete trends in treatment management at the extremes of the age ranges. There were substantial increases in the use of ORIF for patients <50 years (from 63.9% in 1990–1995 to 81.4% in 2002–2007, P < .001) and in the use of HA for patients >80 years (from 74.4% in 1990–1995 to 84.6% in 2002–2007, P < .001). This trend parallels recent studies that purport better outcomes for young patients undergoing ORIF and elderly patients undergoing HA.30 Our analysis did not demonstrate a large shift in surgeon preference for treatment of patients between 50 and 80 years, although there was a statistically significant decrease in ORIF and THA usage and a reflective increase in HA usage in this population as well. The fact that there has not been as substantial a shift in treatment trends for this large age group is potentially due to the wide variations in comorbid conditions and the functionality that abounds in this age group.1
The limitations of the current study are those inherent with a retrospective database analysis. The reliance on accurate coding brings up a potential for error; however, it is unlikely that comorbidities and outcomes are undercoded as hospitals are incentivized to input values that increase the acuity and thus reimbursement for each hospital stay.35 The database also relies on the ICD-9 procedural and diagnostic codes, which are not as specific as the currently adopted ICD-10 codes; hence, we are unable to distinguish between different forms of internal fixation, for example intramedullary nailing versus dynamic hip screw. This also precludes us from including other critical data such as degree of fracture displacement, cemented versus uncemented implantation, surgical approach for arthroplasty, and functional outcomes of individual patients. Moreover, the database used, although the largest inpatient sample available for analysis, represents only approximately 20% of hospitals nationwide. In addition, as patients cannot be tracked over time within the database, we are limited to outcomes in the perioperative period captured in a single hospital stay and cannot identify readmissions. Finally, our analysis is limited to the years 1990 to 2007 because of an increase in the relative standard error of the database in more recent years. Although this results in data that are not the most current, we believe that this study provides valuable insight regarding the trends in surgical treatment and acute postoperative outcomes of these injuries that have hitherto not been reported. To limit the inherent biases and the limitations within this study, prospective, randomized studies with long-term follow-up comparing outcomes across modes of treatment are needed to definitively determine the optimum form of treatment for this fracture type.
CONCLUSION
This is the largest study to date reporting on national trends in the surgical treatment and outcomes of the femoral neck fracture population. Orthopedic surgeons performing THA should be aware that the femoral neck fracture population is changing and at higher risk for perioperative complications. The advent of bisphosphonate therapy has been suggested as a possible reason for the decrease in fragility fractures and why a larger proportion of the femoral neck fracture population is now >80 years.36,37 With an aging population at a higher risk for perioperative complications, clinicians must take special care in choosing the appropriate surgical intervention that will give their patients the best functional outcome while minimizing the risk of surgical complications. Orthopedic surgeons should weigh the added risk associated with THA in this population.
1. Bishop J, Yang A, Githens M, Sox AH. Evaluation of contemporary trends in femoral neck fracture management reveals discrepancies in treatment. Geriatr Orthop Surg Rehabil. 2016;7(3):135. doi:10.1177/2151458516658328.
2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res Off J Am Soc Bone Miner Res. 2007;22(3):465. doi:10.1359/jbmr.061113.
3. Kannus P, Parkkari J, Sievanen H, Heinonen A, Vuori I, Jarvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 Suppl.):57s. doi:10.1016/8756-3282(95)00381-9.
4. Koval KJ, Zuckerman JD. Hip fractures: I. Overview and evaluation and treatment of femoral-neck fractures. J Am Acad Orthop Surg. 1994;2(3):141. doi:10.5435/00124635-199405000-00002.
5. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg. (American) 2014;96(17):e149. doi:10.2106/JBJS.M.01122.
6. Miller BJ, Lu X, Cram P. The trends in treatment of femoral neck fractures in the Medicare population from 1991 to 2008. J Bone Joint Surg. (American) 2013;95(18):e132. doi:10.2106/JBJS.L.01163.
7. Nwachukwu BU, McCormick F, Provencher MT, Roche M, Rubash HE. A comprehensive analysis of Medicare trends in utilization and hospital economics for total knee and hip arthroplasty from 2005 to 2011. J Arthroplast. 2015;30(1):15. doi:10.1016/j.arth.2014.08.025.
8. Su EP, Su SL. Femoral neck fractures: a changing paradigm. Bone Joint J. 2014;96-b(11) Supple A):43. doi:10.1302/0301-620X.96B11.34334.
9. Ahn J, Man LX, Park S, Sodl JF, Esterhai JL. Systematic review of cemented and uncemented hemiarthroplasty outcomes for femoral neck fractures. Clin Orthop Relat Res. 2008;466(10):2513. doi:10.1007/s11999-008-0368-3.
10. Alolabi B, Bajammal S, Shirali J, Karanicolas PJ, Gafni A, Bhandari M. Treatment of displaced femoral neck fractures in the elderly: a cost-benefit analysis. J Orthop Trauma. 2009;23(6):442. doi:10.1097/BOT.0b013e31817614dd.
11. Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290. doi:10.1093/aje/kwp266.
12. Brox WT, Chan PH, Cafri G, Inacio MC. Similar mortality with general or regional anesthesia in elderly hip fracture patients. Acta Orthop. 2016;87(2):152. doi:10.3109/17453674.2015.1128781.
13. Catal B, Sener M. Treatment and displacement affect the reoperation rate for femoral neck fracture. Clin Orthop Relat Res. 2013;471(12):4096. doi:10.1007/s11999-013-3295-x.
14. Dailiana Z, Papakostidou I, Varitimidis S, Michalitsis S, Veloni A, Malizos K. Surgical treatment of hip fractures: factors influencing mortality. Hippokratia. 2013;17(3):252.
15. Deangelis JP, Ademi A, Staff I, Lewis CG. Cemented versus uncemented hemiarthroplasty for displaced femoral neck fractures: a prospective randomized trial with early follow-up. J Orthop Trauma. 2012;26(3):135. doi:10.1097/BOT.0b013e318238b7a5.
16. Hedbeck CJ, Inngul C, Blomfeldt R, Ponzer S, Tornkvist H, Enocson A. Internal fixation versus cemented hemiarthroplasty for displaced femoral neck fractures in patients with severe cognitive dysfunction: a randomized controlled trial. J Orthop Trauma. 2013;27(12):690. doi:10.1097/BOT.0b013e318291f544.
17. Jia Z, Ding F, Wu Y, et al. Unipolar versus bipolar hemiarthroplasty for displaced femoral neck fractures: a systematic review and meta-analysis of randomized controlled trials. J Orthop Surg Res. 2015;10:8. doi:10.1186/s13018-015-0165-0.
18. Lapidus LJ, Charalampidis A, Rundgren J, Enocson A. Internal fixation of garden I and II femoral neck fractures: posterior tilt did not influence the reoperation rate in 382 consecutive hips followed for a minimum of 5 years. J Orthop Trauma. 2013;27(7):386. doi:10.1097/BOT.0b013e318281da6e.
19. Mariconda M, Costa GG, Cerbasi S, et al. Factors predicting mobility and the change in Activities of Daily Living After hip fracture: A 1-year prospective cohort study. J Orthop Trauma. 2016;30(2):71. doi:10.1097/BOT.0000000000000448.
20. Nyholm AM, Gromov K, Palm H, et al. Time to surgery is associated with thirty-day and ninety-day mortality After proximal femoral fracture: A retrospective observational study on prospectively collected data from the Danish Fracture Database Collaborators. J Bone Joint Surg. (American) 2015;97(16):1333. doi:10.2106/JBJS.O.00029.
21. Samuel AM, Russo GS, Lukasiewicz AM, et al. Surgical treatment of femoral neck fractures after 24 hours in patients between the ages of 18 and 49 is associated with poor inpatient outcomes: an analysis of 1361 patients in the National Trauma Data Bank. J Orthop Trauma. 2016;30(2):89. doi:10.1097/BOT.0000000000000456.
22. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235. doi:10.1007/s11999-012-2293-8.
23. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplast. 2012;27(4):583. doi:10.1016/j.arth.2011.07.009.
24. Zielinski SM, Keijsers NL, Praet SF, et al. Functional outcome after successful internal fixation versus salvage arthroplasty of patients with a femoral neck fracture. J Orthop Trauma. 2014;28(12):e273. doi:10.1097/BOT.0000000000000123.
25. Gu Q, Koenig L, Mather RC, 3rd, Tongue J. Surgery for hip fracture yields societal benefits that exceed the direct medical costs. Clin Orthop Relat Res. 2014;472(11):3536. doi:10.1007/s11999-014-3820-6.
26. Forsh DA, Ferguson TA. Contemporary management of femoral neck fractures: the young and the old. Curr Rev Musculoskelet Med. 2012;5(3):214. doi:10.1007/s12178-012-9127-x.
27. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287. doi:10.5435/00124635-200605000-00004.
28. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: Femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596. doi:10.5435/00124635-200810000-00005.
29. Probe R, Ward R. Internal fixation of femoral neck fractures. J Am Acad Orthop Surg. 2006;14(9):565. doi:10.5435/00124635-200609000-00006.
30. Jain NB, Losina E, Ward DM, Harris MB, Katz JN. Trends in surgical management of femoral neck fractures in the United States. Clin Orthop Relat Res. 2008;466(12):3116. doi:10.1007/s11999-008-0392-3.
31. Menendez ME, Neuhaus V, van Dijk CN, Ring D. The Elixhauser comorbidity method outperforms the Charlson index in predicting inpatient death after orthopaedic surgery. Clin Orthop Relat Res. 2014;472(9):2878. doi:10.1007/s11999-014-3686-7.
32. Van Walraven C, Austin PC, Jennings A, Quan H, Forster AJ. A modification of the Elixhauser Comorbidity measures into a point system for hospital death using administrative data. Med Care. 2009;47(6):626-633.
33. Best MJ, Buller LT, Falakassa J, Vecchione D. Risk factors for nonroutine discharge in patients undergoing spinal fusion for intervertebral disc disorders. Iowa Orthop J. 2015;35:147.
34. Schairer WW, Lane JM, Halsey DA, Iorio R, Padgett DE, McLawhorn AS. The Frank Stinchfield award: total hip arthroplasty for femoral neck fracture is not a typical DRG 470: A propensity-matched cohort study. Clin Orthop Relat Res. 2017;475(2):353-360. doi:10.1007/s11999-016-4868-2.
35. Nikkel LE, Fox EJ, Black KP, Davis C, Andersen L, Hollenbeak CS. Impact of comorbidities on hospitalization costs following hip fracture. J Bone Joint Surg Am. 2012;94(1):9. doi:10.2106/JBJS.J.01077.
36. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2 Suppl.):S14. doi:10.1016/j.amjmed.2008.12.003.
37. Siris ES, Pasquale MK, Wang Y, Watts NB. Estimating bisphosphonate use and fracture reduction among US women aged 45 years and older, 2001-2008. J Bone Miner Res Off J Am Soc Bone Miner Res. 2011;26(1):3. doi:10.1002/jbmr.189.
ABSTRACT
The ideal mode of fixation for patients with femoral neck fractures is not well defined in the current literature. This study describes the recent trends in surgical management of femoral neck fractures with an analysis on perioperative outcomes.
The National Hospital Discharge Survey was used to identify femoral neck fractures in the United States between 1990 and 2007 (n = 1,155,960) treated with open reduction and internal fixation (ORIF), total hip arthroplasty (THA), or hemiarthroplasty (HA). Trends were examined over the following 3 time periods: 1990 to 1995 (group 1), 1996 to 2001 (group 2), and 2002 to 2007 (group 3). Elixhauser Comorbidity Index and perioperative complications were calculated.
Use of HA increased (74.4% to 84.6%), whereas that of THA (7.3% to 4.9%) and ORIF (18.3% to 10.6%) decreased, from group 1 to group 3 in the age group of >80 years. The use of ORIF increased (63.9% to 81.4%), whereas the use of both HA and THA decreased, from group 1 to group 3 in the age group of <50 years. The rate of adverse events increased across all fixation types but was greatest among THA (32.2% to 48.3%).
The femoral neck patient population is now older and has more medical comorbidities. We observed a trend toward performing HA in older patients and ORIF in younger patients. Despite superior functional outcomes reported in THA, this study found a decreased utilization of THA in all age groups along with an increase in adverse events and nonroutine discharges for patients with femoral neck fractures treated with THA.
Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Continue to: Femoral neck fractures...
Femoral neck fractures are a common occurrence in the United States. A recent study estimated an incidence of >63 per 100,000 population.1-8 Although the incidence appears to have decreased over recent decades, there is a projected exponential increase in the incidence of hip fractures over the next 30 years in the baby boomer population.8,9 Given that these fractures have a significant impact on patient morbidity, mortality, and quality of life, research efforts have been directed toward optimizing the treatment of affected patients and improving the outcomes.4,9-24
The treatment of choice for femoral neck fractures and the use of total hip arthroplasty (THA)11 have been a topic of debate.4,9,10,15-17,22,25 Total hip arthroplasty has been advocated for younger, more active patients, whereas hemiarthroplasty (HA) has been reserved for patients who are older and less active. Although several studies have demonstrated that arthroplasty outperforms open reduction and internal fixation (ORIF) in the elderly population with displaced femoral neck fractures, ORIF is still commonly performed in the United States for nondisplaced fractures and in patients aged <50 years.26-29
In an attempt to quantify the use of THA in the treatment of femoral neck fractures and demonstrate the national trends, Miller and colleagues5 pooled the American Board of Orthopaedic Surgery (ABOS) database and analyzed the treatment trends of surgeons taking part II of the ABOS examination from 1999 to 2011. The authors found an increased utilization of THA by recently graduated orthopedic surgeons. In contrast, Jain and colleagues30 found different national trends when they analyzed data from the National Inpatient Sample containing data between 1990 and 2001 and further found decreased utilization of THA procedures by orthopedic surgeons of all levels of training nationwide. However, neither of these studies reported about the trends in demographics, comorbidities, risk factors, or outcomes in this patient population following surgery.
The purpose of this study was to help clarify the findings of these authors using the largest dataset to date and also report on the perioperative complications associated with each mode of fixation in patients who undergo operative treatment for femoral neck fractures in the United States. Our hypotheses were that the femoral neck fracture patient population has become older and has more medical comorbidities. We also hypothesized that there has been a trend toward performing fewer THA procedures in the United States and that THA is associated with increased perioperative complications compared to those with HA and ORIF.
MATERIALS AND METHODS
We conducted a retrospective epidemiological study using the National Hospital Discharge Survey (NHDS) on surgical trends in the management of femoral neck fractures. The NHDS is a publicly available survey that is conducted annually to provide data of nonfederal, short-stay hospitals to the public. The sample data are weighted to provide nationwide estimates of annual inpatient care. The NHDS includes up to 7 medical diagnoses and 4 procedural codes per case, which are categorized using the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes, that were collected along with patient demographic information, length of stay (LOS), and discharge disposition. The diagnostic and procedural codes used for this study are presented in the Appendix. The year 2007 was chosen as the endpoint of this study due to the fact that the relative standard error of the NHDS doubled in 2008 as a result of a decrease in its survey size. As this is a publicly available database, our study was exempt from institutional review board approval.
Continue to: All pateints admitted...
All patients admitted with a primary diagnosis of closed transcervical fracture of the femoral neck (ICD-9-CM 820.0x) were selected. This resulted in 1,674,160 fractures. All patients with fractures with a concurrent primary procedural code of ORIF (79.35), HA (81.52), or THA (81.51) were identified, resulting in a total sample size of 1,155,960 surgical fractures. Analysis of the fractures based on additional specificity,ie subcapital versus midcervical versus basicervical, was not carried out because >90% of femoral neck fractures in the database were coded as “unspecified” or “other” (ICD9 CM 820.00 and 820.09, respectively).
Comorbidity burden was quantified using Elixhauser coding algorithms as previously described.31 The Elixhauser comorbidity measure is a model consisting of 31 conditions and has recently been identified as a better predictor of mortality in patients undergoing orthopedic procedures when compared with the Charlson Comorbidity Index.31 Dichotomous variables for each Elixhauser comorbidity were created, and χ2 tests were utilized to assess the association between each comorbidity and mortality. The weighted Elixhauser score for each statistically significant comorbidity was calculated as described by van Walraven and colleagues.32 The Elixhauser comorbidity score was then calculated for each patient by summing the individual weights of all comorbidities. Postoperative adverse events were determined using the complication-screening-package as previously described.33
All adverse events were categorized into 3 categories, including general medical complications, mechanical complications, and surgical complications. All adverse events recorded in the NHDS database are events that occurred during a single hospitalization. Therefore, it does not take into account adverse events that occurred after discharge, and, for example, mortality refers to postoperative mortality that occurs prior to discharge. The study period comprised data captured from 1990 to 2007, and 3 groups were generated from this time period to better characterize patients throughout the large study time frame. Group 1 comprised patients who underwent surgical management of femoral neck fractures from 1990 to 1995, group 2 consisted of patients treated from 1996 to 2001, and group 3 included patients treated from 2002 to 2007.
Categorical data were analyzed using the χ2 test, and continuous data were analyzed by the independent-samples t test and ANOVA. Multivariable binary logistic regression analyses were performed to assess the contributions of individual comorbidities to mortality, adverse events, and nonroutine discharge. Elixhauser comorbidities with a P value of < .10 in the bivariate analysis and presenting in at least 0.2% of the population were included in the logistic regression.31 Odds ratios and confidence intervals were calculated to assess the association between comorbidities and our dichotomous variables. A P value of < .001 defined statistical significance.33 Statistical analysis was conducted using SPSS version 21 (IBM).
RESULTS
Patient Demographics
Our query demonstrated a total of 1,155,960 patients who underwent surgical fixation of femoral neck fractures (Table 1). The most commonly used treatment modality was HA (75%), followed by ORIF (18%) and later by THA (7%). The majority of patients were females in each treatment group. Patients’ age varied according to treatment group, with patients undergoing HA having a mean age of 81.0 ± 9.0 years, patients undergoing ORIF having a mean age of 75.0 ± 17.0 years, and those undergoing THA having a mean age of 79.0 ± 10.0 years (P < .001). The majority of patients were ≥80 years in all treatment groups, but the ORIF group had the greatest proportion of patients <65 years (P < .001). Among patients undergoing HA, 62.4% were ≥80 years, while the ORIF and HA groups consisted of 48.6% and 51.5% of patients in that same age group, respectively.
Continue to: TRENDS ANALYSIS
TRENDS ANALYSIS
There was a significant change in the distributions of the procedures performed according to age group over time. Patients >80 years continued to undergo primarily HA, with an increase from 74.4% during 1990 to 1995 up to 84.6% during the 2002 to 2007 period and a concomitant decrease in ORIF from 18.3% to 10.6% during the same time period in this age group. Surgical trends in patients 65 to 79 years demonstrated a significant decrease in management with ORIF from 19.1% in 1990 to 1995 to 16.8% in the 2002 to 2007 cohort (P < .001 for all, Table 2). There was an increase in the use of HA from 71.9% during the 1990 to 1995 period to 75.5% during the final study period (Table 2, Figure 1). The use of THA for all age groups decreased between 1990 and 2007, except for the 50- to 64-year-old group where THA utilization remained constant.
Management patterns in patients 50 to 64 years varied throughout the analysis and demonstrated the following trend: treatment with HA remained the most common technique used but varied slightly from 59.7% during 1990 to 1995 to 60.3% during 2002 to2007 (P < .001, Table 2). The second most common treatment used was ORIF, which decreased from 32.2% to 31.5% (P < .001, Table 2). The use of THA varied significantly from 8.2% among those managed during 1990 to 1995 to 11.7% during 1996 to 2001 but later declined to the initial 8.2% (P < .001, Table 2).
Analysis of patients ≤49 years demonstrated that ORIF was the preferred technique, which experienced a growth from 63.9% during 1990 to 1995 to 81.4% during the 2002 to 2007 period (P < .001, Table 2). A decreased use in THA was observed from 2.0% in the initial period to 0.6% in the final period (P < .001, Table 2). Use of HA decreased from 34.0% in 1990 to 1995 to 18.0% in 2002 to 2007 (P < .001, Table 2).
LENGTH OF STAY
Mean number of in-hospital days decreased throughout the study period for all treatment techniques. During the 1990 to 1995 study period, patients who underwent ORIF had a mean LOS of 8 ± 7 days, which decreased (P < .001, Table 2) to 6 ± 3 days in 1996 to 2001 and remained constant during 2002 to 2007 (mean 6 ± 4 days). This decrease in LOS was also observed in patients who underwent THA (P < .001, Table 2), who initially had a mean LOS of 11 ± 7 days during 1990 to 1995, which later decreased to 7 ± 5 days for the remainder of the study. The LOS for patients who underwent HA also decreased (P < .001, Table 2), which initially was reported to be 11 ± 11 days during 1990 to 1995, decreasing to 7 ±7 days in 1996–2001 and later to 6 ± 4 days in 2002 to 2007.
COMORBIDITIY ANALYSIS
The Elixhauser Comorbidity Index varied significantly among groups over time (P < .001, Table 2). Overall mean Elixhauser Comorbidity Index score per procedure type is provided in Table 1, with HA patients having the highest score (-0.15 ± 13.09, p<.001).
Continue to: Analysis of the preoperative comorbidities...
Analysis of the preoperative comorbidities demonstrated significant differences among each surgical treatment group (P < .001 for all, Table 3). The most common comorbidities in patients who underwent HA were uncomplicated hypertension (33.2%), fluid/electrolyte disorders (17.4%), chronic pulmonary disease (14.9%), and congestive heart failure (13.7%). The most common comorbidities in the ORIF group were uncomplicated hypertension (30.8%), fluid/electrolyte disorders (14.5%), chronic pulmonary disease (14.0%), and uncomplicated diabetes (10.9%). Patients treated with THA had most commonly uncomplicated hypertension (30.1%), fluid/electrolyte disorders (17.2%), uncomplicated diabetes (15.5%), and chronic pulmonary disease (14.4%). The prevalence of comorbidities is displayed in Table 3.
DISCHARGE STATUS
Mortality varied significantly, being lowest in those who underwent ORIF (0.8%), followed those who underwent THA (1.8%), and HA (2.6%) (P < .001, Table 1).
The majority of patients in each group were discharged to long-term rehabilitation facilities, including 53.0% of those treated with HA, 40.4% of those treated with ORIF, and 44.3% of patients treated with THA. The second most common discharge location was home, which included 14.8% of patients who underwent HA, 32.2% of patients treated with ORIF, and 20.8% of those who underwent THA. Table 3 demonstrates the details of the discharge settings.
Mortality analysis over time demonstrated a significant decrease in each treatment group (P < .001). Mortality in the ORIF group decreased from 1.2% during 1990 to 1995 to 0.8% in 2002 to 2007. Mortality in the THA group also decreased significantly from 0.8% during 1990 to 1995 to 0.5% during the 2002 to 2007 time period. Patients who underwent HA also exhibited a decrease in mortality rate from 3.3% during 1990 to 1995 to 2.2% during 2002 to 2007 (P < .001, Table 4, Figure 2).
GENERAL ADVERSE EVENTS
There was a significant difference (P < .001) in the percentage of adverse events experienced, the maximum being observed in the THA group (41.0%), followed by the HA group (37.9%) and trailed by the ORIF group (20.3%, (P < .001, Table 1). The prevalence of adverse events is detailed in Table 5.
Continue to: Patients who underwent THA...
Patients who underwent THA had the highest rate of any adverse event, LOS, and transfusion rate (Table 1 and Table 5).
The prevalence of postoperative pneumonia was highest in the HA group (3.4%), followed by the ORIF group (2.9%), and the THA group (2.6%) (P < .001, Table 5). There was also a significant difference in rates of intubation, pulmonary insufficiency, acute renal failure, pulmonary embolism, acute myocardial infarction, induced mental disorder, and deep venous thrombosis (P < .001 for all, Table 5).
SURGERY-RELATED ADVERSE EVENTS
Surgery-related outcomes over the entire study period were significantly different according to the type of procedure performed (P < .001, Table 5). Patients who underwent HA had the highest rate of acute postoperative anemia (20.2%), followed by those who underwent THA (19.7%), and ORIF (10.2%). Postoperative bleeding rates also varied significantly, with 1.2% in the HA group, followed by 1.0% in the ORIF group and 0.4% in the THA group (P < .001, Table 5). Acute postoperative infection rates also varied significantly, with the highest rate being observed in the HA group (0.6%) compared to that in the THA and ORIF groups (both 0.3%) (P < .001, Table 5).
Table 6, Table 7, and Table 8 detail the results of regression analyses in patients with femoral neck fractures for individual risk factors associated with mortality, any adverse event, and nonroutine discharge to a short- or long-term rehabilitation facility, respectively. Increasing age (50–64 years, OR: 0.238; 65–79 years, OR: 1.762; and ≥80 years, OR: 2.700), THA (OR: 1.743), and HA (OR: 2.574) were found to be independent risk factors for mortality in the perioperative period (P < .001 for each, Table 6). Increasing age (50–64 years, OR: 1.888; 65–79 years, OR: 2.983; and ≥80 years, OR: 3.722), THA (OR: 2.489), and HA (OR: 2.098) were also found to be independent risk factors for any adverse event in the perioperative period (P < .001, Table 7). Age (50–64 years, OR: 1.662; 65–79 years, OR: 4.320; and ≥80 years, OR: 7.102) was the best predictor for nonroutine discharge to a short- or long-term rehabilitation facility (P < .001, Table 8).
DISCUSSION
Femoral neck fractures in the elderly population present a significant financial burden to the healthcare system.1-3,24,25 Consistent with previous epidemiological studies, our results show that the femoral neck fracture population has become older and has more medical comorbidities over the last 3 decades.27,28. Similarly, we also found that the rate of medical, surgical, and mechanical perioperative complications has increased in the same time period. Interestingly, the mortality rate has remained relatively similar.
Continue to: Although patients undergoing HA...
Although patients undergoing HA for femoral neck fractures are older and have more medical comorbidities, we found that the rate of adverse events in the perioperative period for patients undergoing THA was higher than that in the HA group. Consistent with prior studies, patients who underwent THA had higher rates of blood transfusion, pulmonary embolism, and induced mental disorders.34 Multivariable regression analysis demonstrated that after controlling for age, medical comorbidity, and type of surgery performed, THA emerged as an independent risk factor for any adverse event in the perioperative period. Increased anesthesia time, reaming of the acetabulum, and increased complexity of surgery probably account for these changes.
Our study results are consistent with those of Jain and colleagues,30 which showed a decrease in utilization of THA for femoral neck fractures between 1990 and 2001. Since THA is generally indicated for younger, more active patients in relatively good health, this would explain why changes in baseline health in this cohort over the last 20 years would lead to fewer THA procedures being performed. Surgeons in the US may be finding there are fewer patients who are candidates for THA. Miller and colleagues5 reported conflicting results and showed an increase in THA utilization in this patient population. However, their study evaluated treatment trends based on data from the ABOS part II of recently graduated orthopedic surgeons and may not be an accurate representation of national practice trends in the US. The trend toward increased subspecialization may explain their findings. As the authors noted, although they found an increase in the use of THA for femoral neck fractures by new adult reconstruction surgeons, the percentage of new surgeons treating femoral neck fractures has declined.5
Our analysis showed very concrete trends in treatment management at the extremes of the age ranges. There were substantial increases in the use of ORIF for patients <50 years (from 63.9% in 1990–1995 to 81.4% in 2002–2007, P < .001) and in the use of HA for patients >80 years (from 74.4% in 1990–1995 to 84.6% in 2002–2007, P < .001). This trend parallels recent studies that purport better outcomes for young patients undergoing ORIF and elderly patients undergoing HA.30 Our analysis did not demonstrate a large shift in surgeon preference for treatment of patients between 50 and 80 years, although there was a statistically significant decrease in ORIF and THA usage and a reflective increase in HA usage in this population as well. The fact that there has not been as substantial a shift in treatment trends for this large age group is potentially due to the wide variations in comorbid conditions and the functionality that abounds in this age group.1
The limitations of the current study are those inherent with a retrospective database analysis. The reliance on accurate coding brings up a potential for error; however, it is unlikely that comorbidities and outcomes are undercoded as hospitals are incentivized to input values that increase the acuity and thus reimbursement for each hospital stay.35 The database also relies on the ICD-9 procedural and diagnostic codes, which are not as specific as the currently adopted ICD-10 codes; hence, we are unable to distinguish between different forms of internal fixation, for example intramedullary nailing versus dynamic hip screw. This also precludes us from including other critical data such as degree of fracture displacement, cemented versus uncemented implantation, surgical approach for arthroplasty, and functional outcomes of individual patients. Moreover, the database used, although the largest inpatient sample available for analysis, represents only approximately 20% of hospitals nationwide. In addition, as patients cannot be tracked over time within the database, we are limited to outcomes in the perioperative period captured in a single hospital stay and cannot identify readmissions. Finally, our analysis is limited to the years 1990 to 2007 because of an increase in the relative standard error of the database in more recent years. Although this results in data that are not the most current, we believe that this study provides valuable insight regarding the trends in surgical treatment and acute postoperative outcomes of these injuries that have hitherto not been reported. To limit the inherent biases and the limitations within this study, prospective, randomized studies with long-term follow-up comparing outcomes across modes of treatment are needed to definitively determine the optimum form of treatment for this fracture type.
CONCLUSION
This is the largest study to date reporting on national trends in the surgical treatment and outcomes of the femoral neck fracture population. Orthopedic surgeons performing THA should be aware that the femoral neck fracture population is changing and at higher risk for perioperative complications. The advent of bisphosphonate therapy has been suggested as a possible reason for the decrease in fragility fractures and why a larger proportion of the femoral neck fracture population is now >80 years.36,37 With an aging population at a higher risk for perioperative complications, clinicians must take special care in choosing the appropriate surgical intervention that will give their patients the best functional outcome while minimizing the risk of surgical complications. Orthopedic surgeons should weigh the added risk associated with THA in this population.
ABSTRACT
The ideal mode of fixation for patients with femoral neck fractures is not well defined in the current literature. This study describes the recent trends in surgical management of femoral neck fractures with an analysis on perioperative outcomes.
The National Hospital Discharge Survey was used to identify femoral neck fractures in the United States between 1990 and 2007 (n = 1,155,960) treated with open reduction and internal fixation (ORIF), total hip arthroplasty (THA), or hemiarthroplasty (HA). Trends were examined over the following 3 time periods: 1990 to 1995 (group 1), 1996 to 2001 (group 2), and 2002 to 2007 (group 3). Elixhauser Comorbidity Index and perioperative complications were calculated.
Use of HA increased (74.4% to 84.6%), whereas that of THA (7.3% to 4.9%) and ORIF (18.3% to 10.6%) decreased, from group 1 to group 3 in the age group of >80 years. The use of ORIF increased (63.9% to 81.4%), whereas the use of both HA and THA decreased, from group 1 to group 3 in the age group of <50 years. The rate of adverse events increased across all fixation types but was greatest among THA (32.2% to 48.3%).
The femoral neck patient population is now older and has more medical comorbidities. We observed a trend toward performing HA in older patients and ORIF in younger patients. Despite superior functional outcomes reported in THA, this study found a decreased utilization of THA in all age groups along with an increase in adverse events and nonroutine discharges for patients with femoral neck fractures treated with THA.
Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Continue to: Femoral neck fractures...
Femoral neck fractures are a common occurrence in the United States. A recent study estimated an incidence of >63 per 100,000 population.1-8 Although the incidence appears to have decreased over recent decades, there is a projected exponential increase in the incidence of hip fractures over the next 30 years in the baby boomer population.8,9 Given that these fractures have a significant impact on patient morbidity, mortality, and quality of life, research efforts have been directed toward optimizing the treatment of affected patients and improving the outcomes.4,9-24
The treatment of choice for femoral neck fractures and the use of total hip arthroplasty (THA)11 have been a topic of debate.4,9,10,15-17,22,25 Total hip arthroplasty has been advocated for younger, more active patients, whereas hemiarthroplasty (HA) has been reserved for patients who are older and less active. Although several studies have demonstrated that arthroplasty outperforms open reduction and internal fixation (ORIF) in the elderly population with displaced femoral neck fractures, ORIF is still commonly performed in the United States for nondisplaced fractures and in patients aged <50 years.26-29
In an attempt to quantify the use of THA in the treatment of femoral neck fractures and demonstrate the national trends, Miller and colleagues5 pooled the American Board of Orthopaedic Surgery (ABOS) database and analyzed the treatment trends of surgeons taking part II of the ABOS examination from 1999 to 2011. The authors found an increased utilization of THA by recently graduated orthopedic surgeons. In contrast, Jain and colleagues30 found different national trends when they analyzed data from the National Inpatient Sample containing data between 1990 and 2001 and further found decreased utilization of THA procedures by orthopedic surgeons of all levels of training nationwide. However, neither of these studies reported about the trends in demographics, comorbidities, risk factors, or outcomes in this patient population following surgery.
The purpose of this study was to help clarify the findings of these authors using the largest dataset to date and also report on the perioperative complications associated with each mode of fixation in patients who undergo operative treatment for femoral neck fractures in the United States. Our hypotheses were that the femoral neck fracture patient population has become older and has more medical comorbidities. We also hypothesized that there has been a trend toward performing fewer THA procedures in the United States and that THA is associated with increased perioperative complications compared to those with HA and ORIF.
MATERIALS AND METHODS
We conducted a retrospective epidemiological study using the National Hospital Discharge Survey (NHDS) on surgical trends in the management of femoral neck fractures. The NHDS is a publicly available survey that is conducted annually to provide data of nonfederal, short-stay hospitals to the public. The sample data are weighted to provide nationwide estimates of annual inpatient care. The NHDS includes up to 7 medical diagnoses and 4 procedural codes per case, which are categorized using the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes, that were collected along with patient demographic information, length of stay (LOS), and discharge disposition. The diagnostic and procedural codes used for this study are presented in the Appendix. The year 2007 was chosen as the endpoint of this study due to the fact that the relative standard error of the NHDS doubled in 2008 as a result of a decrease in its survey size. As this is a publicly available database, our study was exempt from institutional review board approval.
Continue to: All pateints admitted...
All patients admitted with a primary diagnosis of closed transcervical fracture of the femoral neck (ICD-9-CM 820.0x) were selected. This resulted in 1,674,160 fractures. All patients with fractures with a concurrent primary procedural code of ORIF (79.35), HA (81.52), or THA (81.51) were identified, resulting in a total sample size of 1,155,960 surgical fractures. Analysis of the fractures based on additional specificity,ie subcapital versus midcervical versus basicervical, was not carried out because >90% of femoral neck fractures in the database were coded as “unspecified” or “other” (ICD9 CM 820.00 and 820.09, respectively).
Comorbidity burden was quantified using Elixhauser coding algorithms as previously described.31 The Elixhauser comorbidity measure is a model consisting of 31 conditions and has recently been identified as a better predictor of mortality in patients undergoing orthopedic procedures when compared with the Charlson Comorbidity Index.31 Dichotomous variables for each Elixhauser comorbidity were created, and χ2 tests were utilized to assess the association between each comorbidity and mortality. The weighted Elixhauser score for each statistically significant comorbidity was calculated as described by van Walraven and colleagues.32 The Elixhauser comorbidity score was then calculated for each patient by summing the individual weights of all comorbidities. Postoperative adverse events were determined using the complication-screening-package as previously described.33
All adverse events were categorized into 3 categories, including general medical complications, mechanical complications, and surgical complications. All adverse events recorded in the NHDS database are events that occurred during a single hospitalization. Therefore, it does not take into account adverse events that occurred after discharge, and, for example, mortality refers to postoperative mortality that occurs prior to discharge. The study period comprised data captured from 1990 to 2007, and 3 groups were generated from this time period to better characterize patients throughout the large study time frame. Group 1 comprised patients who underwent surgical management of femoral neck fractures from 1990 to 1995, group 2 consisted of patients treated from 1996 to 2001, and group 3 included patients treated from 2002 to 2007.
Categorical data were analyzed using the χ2 test, and continuous data were analyzed by the independent-samples t test and ANOVA. Multivariable binary logistic regression analyses were performed to assess the contributions of individual comorbidities to mortality, adverse events, and nonroutine discharge. Elixhauser comorbidities with a P value of < .10 in the bivariate analysis and presenting in at least 0.2% of the population were included in the logistic regression.31 Odds ratios and confidence intervals were calculated to assess the association between comorbidities and our dichotomous variables. A P value of < .001 defined statistical significance.33 Statistical analysis was conducted using SPSS version 21 (IBM).
RESULTS
Patient Demographics
Our query demonstrated a total of 1,155,960 patients who underwent surgical fixation of femoral neck fractures (Table 1). The most commonly used treatment modality was HA (75%), followed by ORIF (18%) and later by THA (7%). The majority of patients were females in each treatment group. Patients’ age varied according to treatment group, with patients undergoing HA having a mean age of 81.0 ± 9.0 years, patients undergoing ORIF having a mean age of 75.0 ± 17.0 years, and those undergoing THA having a mean age of 79.0 ± 10.0 years (P < .001). The majority of patients were ≥80 years in all treatment groups, but the ORIF group had the greatest proportion of patients <65 years (P < .001). Among patients undergoing HA, 62.4% were ≥80 years, while the ORIF and HA groups consisted of 48.6% and 51.5% of patients in that same age group, respectively.
Continue to: TRENDS ANALYSIS
TRENDS ANALYSIS
There was a significant change in the distributions of the procedures performed according to age group over time. Patients >80 years continued to undergo primarily HA, with an increase from 74.4% during 1990 to 1995 up to 84.6% during the 2002 to 2007 period and a concomitant decrease in ORIF from 18.3% to 10.6% during the same time period in this age group. Surgical trends in patients 65 to 79 years demonstrated a significant decrease in management with ORIF from 19.1% in 1990 to 1995 to 16.8% in the 2002 to 2007 cohort (P < .001 for all, Table 2). There was an increase in the use of HA from 71.9% during the 1990 to 1995 period to 75.5% during the final study period (Table 2, Figure 1). The use of THA for all age groups decreased between 1990 and 2007, except for the 50- to 64-year-old group where THA utilization remained constant.
Management patterns in patients 50 to 64 years varied throughout the analysis and demonstrated the following trend: treatment with HA remained the most common technique used but varied slightly from 59.7% during 1990 to 1995 to 60.3% during 2002 to2007 (P < .001, Table 2). The second most common treatment used was ORIF, which decreased from 32.2% to 31.5% (P < .001, Table 2). The use of THA varied significantly from 8.2% among those managed during 1990 to 1995 to 11.7% during 1996 to 2001 but later declined to the initial 8.2% (P < .001, Table 2).
Analysis of patients ≤49 years demonstrated that ORIF was the preferred technique, which experienced a growth from 63.9% during 1990 to 1995 to 81.4% during the 2002 to 2007 period (P < .001, Table 2). A decreased use in THA was observed from 2.0% in the initial period to 0.6% in the final period (P < .001, Table 2). Use of HA decreased from 34.0% in 1990 to 1995 to 18.0% in 2002 to 2007 (P < .001, Table 2).
LENGTH OF STAY
Mean number of in-hospital days decreased throughout the study period for all treatment techniques. During the 1990 to 1995 study period, patients who underwent ORIF had a mean LOS of 8 ± 7 days, which decreased (P < .001, Table 2) to 6 ± 3 days in 1996 to 2001 and remained constant during 2002 to 2007 (mean 6 ± 4 days). This decrease in LOS was also observed in patients who underwent THA (P < .001, Table 2), who initially had a mean LOS of 11 ± 7 days during 1990 to 1995, which later decreased to 7 ± 5 days for the remainder of the study. The LOS for patients who underwent HA also decreased (P < .001, Table 2), which initially was reported to be 11 ± 11 days during 1990 to 1995, decreasing to 7 ±7 days in 1996–2001 and later to 6 ± 4 days in 2002 to 2007.
COMORBIDITIY ANALYSIS
The Elixhauser Comorbidity Index varied significantly among groups over time (P < .001, Table 2). Overall mean Elixhauser Comorbidity Index score per procedure type is provided in Table 1, with HA patients having the highest score (-0.15 ± 13.09, p<.001).
Continue to: Analysis of the preoperative comorbidities...
Analysis of the preoperative comorbidities demonstrated significant differences among each surgical treatment group (P < .001 for all, Table 3). The most common comorbidities in patients who underwent HA were uncomplicated hypertension (33.2%), fluid/electrolyte disorders (17.4%), chronic pulmonary disease (14.9%), and congestive heart failure (13.7%). The most common comorbidities in the ORIF group were uncomplicated hypertension (30.8%), fluid/electrolyte disorders (14.5%), chronic pulmonary disease (14.0%), and uncomplicated diabetes (10.9%). Patients treated with THA had most commonly uncomplicated hypertension (30.1%), fluid/electrolyte disorders (17.2%), uncomplicated diabetes (15.5%), and chronic pulmonary disease (14.4%). The prevalence of comorbidities is displayed in Table 3.
DISCHARGE STATUS
Mortality varied significantly, being lowest in those who underwent ORIF (0.8%), followed those who underwent THA (1.8%), and HA (2.6%) (P < .001, Table 1).
The majority of patients in each group were discharged to long-term rehabilitation facilities, including 53.0% of those treated with HA, 40.4% of those treated with ORIF, and 44.3% of patients treated with THA. The second most common discharge location was home, which included 14.8% of patients who underwent HA, 32.2% of patients treated with ORIF, and 20.8% of those who underwent THA. Table 3 demonstrates the details of the discharge settings.
Mortality analysis over time demonstrated a significant decrease in each treatment group (P < .001). Mortality in the ORIF group decreased from 1.2% during 1990 to 1995 to 0.8% in 2002 to 2007. Mortality in the THA group also decreased significantly from 0.8% during 1990 to 1995 to 0.5% during the 2002 to 2007 time period. Patients who underwent HA also exhibited a decrease in mortality rate from 3.3% during 1990 to 1995 to 2.2% during 2002 to 2007 (P < .001, Table 4, Figure 2).
GENERAL ADVERSE EVENTS
There was a significant difference (P < .001) in the percentage of adverse events experienced, the maximum being observed in the THA group (41.0%), followed by the HA group (37.9%) and trailed by the ORIF group (20.3%, (P < .001, Table 1). The prevalence of adverse events is detailed in Table 5.
Continue to: Patients who underwent THA...
Patients who underwent THA had the highest rate of any adverse event, LOS, and transfusion rate (Table 1 and Table 5).
The prevalence of postoperative pneumonia was highest in the HA group (3.4%), followed by the ORIF group (2.9%), and the THA group (2.6%) (P < .001, Table 5). There was also a significant difference in rates of intubation, pulmonary insufficiency, acute renal failure, pulmonary embolism, acute myocardial infarction, induced mental disorder, and deep venous thrombosis (P < .001 for all, Table 5).
SURGERY-RELATED ADVERSE EVENTS
Surgery-related outcomes over the entire study period were significantly different according to the type of procedure performed (P < .001, Table 5). Patients who underwent HA had the highest rate of acute postoperative anemia (20.2%), followed by those who underwent THA (19.7%), and ORIF (10.2%). Postoperative bleeding rates also varied significantly, with 1.2% in the HA group, followed by 1.0% in the ORIF group and 0.4% in the THA group (P < .001, Table 5). Acute postoperative infection rates also varied significantly, with the highest rate being observed in the HA group (0.6%) compared to that in the THA and ORIF groups (both 0.3%) (P < .001, Table 5).
Table 6, Table 7, and Table 8 detail the results of regression analyses in patients with femoral neck fractures for individual risk factors associated with mortality, any adverse event, and nonroutine discharge to a short- or long-term rehabilitation facility, respectively. Increasing age (50–64 years, OR: 0.238; 65–79 years, OR: 1.762; and ≥80 years, OR: 2.700), THA (OR: 1.743), and HA (OR: 2.574) were found to be independent risk factors for mortality in the perioperative period (P < .001 for each, Table 6). Increasing age (50–64 years, OR: 1.888; 65–79 years, OR: 2.983; and ≥80 years, OR: 3.722), THA (OR: 2.489), and HA (OR: 2.098) were also found to be independent risk factors for any adverse event in the perioperative period (P < .001, Table 7). Age (50–64 years, OR: 1.662; 65–79 years, OR: 4.320; and ≥80 years, OR: 7.102) was the best predictor for nonroutine discharge to a short- or long-term rehabilitation facility (P < .001, Table 8).
DISCUSSION
Femoral neck fractures in the elderly population present a significant financial burden to the healthcare system.1-3,24,25 Consistent with previous epidemiological studies, our results show that the femoral neck fracture population has become older and has more medical comorbidities over the last 3 decades.27,28. Similarly, we also found that the rate of medical, surgical, and mechanical perioperative complications has increased in the same time period. Interestingly, the mortality rate has remained relatively similar.
Continue to: Although patients undergoing HA...
Although patients undergoing HA for femoral neck fractures are older and have more medical comorbidities, we found that the rate of adverse events in the perioperative period for patients undergoing THA was higher than that in the HA group. Consistent with prior studies, patients who underwent THA had higher rates of blood transfusion, pulmonary embolism, and induced mental disorders.34 Multivariable regression analysis demonstrated that after controlling for age, medical comorbidity, and type of surgery performed, THA emerged as an independent risk factor for any adverse event in the perioperative period. Increased anesthesia time, reaming of the acetabulum, and increased complexity of surgery probably account for these changes.
Our study results are consistent with those of Jain and colleagues,30 which showed a decrease in utilization of THA for femoral neck fractures between 1990 and 2001. Since THA is generally indicated for younger, more active patients in relatively good health, this would explain why changes in baseline health in this cohort over the last 20 years would lead to fewer THA procedures being performed. Surgeons in the US may be finding there are fewer patients who are candidates for THA. Miller and colleagues5 reported conflicting results and showed an increase in THA utilization in this patient population. However, their study evaluated treatment trends based on data from the ABOS part II of recently graduated orthopedic surgeons and may not be an accurate representation of national practice trends in the US. The trend toward increased subspecialization may explain their findings. As the authors noted, although they found an increase in the use of THA for femoral neck fractures by new adult reconstruction surgeons, the percentage of new surgeons treating femoral neck fractures has declined.5
Our analysis showed very concrete trends in treatment management at the extremes of the age ranges. There were substantial increases in the use of ORIF for patients <50 years (from 63.9% in 1990–1995 to 81.4% in 2002–2007, P < .001) and in the use of HA for patients >80 years (from 74.4% in 1990–1995 to 84.6% in 2002–2007, P < .001). This trend parallels recent studies that purport better outcomes for young patients undergoing ORIF and elderly patients undergoing HA.30 Our analysis did not demonstrate a large shift in surgeon preference for treatment of patients between 50 and 80 years, although there was a statistically significant decrease in ORIF and THA usage and a reflective increase in HA usage in this population as well. The fact that there has not been as substantial a shift in treatment trends for this large age group is potentially due to the wide variations in comorbid conditions and the functionality that abounds in this age group.1
The limitations of the current study are those inherent with a retrospective database analysis. The reliance on accurate coding brings up a potential for error; however, it is unlikely that comorbidities and outcomes are undercoded as hospitals are incentivized to input values that increase the acuity and thus reimbursement for each hospital stay.35 The database also relies on the ICD-9 procedural and diagnostic codes, which are not as specific as the currently adopted ICD-10 codes; hence, we are unable to distinguish between different forms of internal fixation, for example intramedullary nailing versus dynamic hip screw. This also precludes us from including other critical data such as degree of fracture displacement, cemented versus uncemented implantation, surgical approach for arthroplasty, and functional outcomes of individual patients. Moreover, the database used, although the largest inpatient sample available for analysis, represents only approximately 20% of hospitals nationwide. In addition, as patients cannot be tracked over time within the database, we are limited to outcomes in the perioperative period captured in a single hospital stay and cannot identify readmissions. Finally, our analysis is limited to the years 1990 to 2007 because of an increase in the relative standard error of the database in more recent years. Although this results in data that are not the most current, we believe that this study provides valuable insight regarding the trends in surgical treatment and acute postoperative outcomes of these injuries that have hitherto not been reported. To limit the inherent biases and the limitations within this study, prospective, randomized studies with long-term follow-up comparing outcomes across modes of treatment are needed to definitively determine the optimum form of treatment for this fracture type.
CONCLUSION
This is the largest study to date reporting on national trends in the surgical treatment and outcomes of the femoral neck fracture population. Orthopedic surgeons performing THA should be aware that the femoral neck fracture population is changing and at higher risk for perioperative complications. The advent of bisphosphonate therapy has been suggested as a possible reason for the decrease in fragility fractures and why a larger proportion of the femoral neck fracture population is now >80 years.36,37 With an aging population at a higher risk for perioperative complications, clinicians must take special care in choosing the appropriate surgical intervention that will give their patients the best functional outcome while minimizing the risk of surgical complications. Orthopedic surgeons should weigh the added risk associated with THA in this population.
1. Bishop J, Yang A, Githens M, Sox AH. Evaluation of contemporary trends in femoral neck fracture management reveals discrepancies in treatment. Geriatr Orthop Surg Rehabil. 2016;7(3):135. doi:10.1177/2151458516658328.
2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res Off J Am Soc Bone Miner Res. 2007;22(3):465. doi:10.1359/jbmr.061113.
3. Kannus P, Parkkari J, Sievanen H, Heinonen A, Vuori I, Jarvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 Suppl.):57s. doi:10.1016/8756-3282(95)00381-9.
4. Koval KJ, Zuckerman JD. Hip fractures: I. Overview and evaluation and treatment of femoral-neck fractures. J Am Acad Orthop Surg. 1994;2(3):141. doi:10.5435/00124635-199405000-00002.
5. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg. (American) 2014;96(17):e149. doi:10.2106/JBJS.M.01122.
6. Miller BJ, Lu X, Cram P. The trends in treatment of femoral neck fractures in the Medicare population from 1991 to 2008. J Bone Joint Surg. (American) 2013;95(18):e132. doi:10.2106/JBJS.L.01163.
7. Nwachukwu BU, McCormick F, Provencher MT, Roche M, Rubash HE. A comprehensive analysis of Medicare trends in utilization and hospital economics for total knee and hip arthroplasty from 2005 to 2011. J Arthroplast. 2015;30(1):15. doi:10.1016/j.arth.2014.08.025.
8. Su EP, Su SL. Femoral neck fractures: a changing paradigm. Bone Joint J. 2014;96-b(11) Supple A):43. doi:10.1302/0301-620X.96B11.34334.
9. Ahn J, Man LX, Park S, Sodl JF, Esterhai JL. Systematic review of cemented and uncemented hemiarthroplasty outcomes for femoral neck fractures. Clin Orthop Relat Res. 2008;466(10):2513. doi:10.1007/s11999-008-0368-3.
10. Alolabi B, Bajammal S, Shirali J, Karanicolas PJ, Gafni A, Bhandari M. Treatment of displaced femoral neck fractures in the elderly: a cost-benefit analysis. J Orthop Trauma. 2009;23(6):442. doi:10.1097/BOT.0b013e31817614dd.
11. Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290. doi:10.1093/aje/kwp266.
12. Brox WT, Chan PH, Cafri G, Inacio MC. Similar mortality with general or regional anesthesia in elderly hip fracture patients. Acta Orthop. 2016;87(2):152. doi:10.3109/17453674.2015.1128781.
13. Catal B, Sener M. Treatment and displacement affect the reoperation rate for femoral neck fracture. Clin Orthop Relat Res. 2013;471(12):4096. doi:10.1007/s11999-013-3295-x.
14. Dailiana Z, Papakostidou I, Varitimidis S, Michalitsis S, Veloni A, Malizos K. Surgical treatment of hip fractures: factors influencing mortality. Hippokratia. 2013;17(3):252.
15. Deangelis JP, Ademi A, Staff I, Lewis CG. Cemented versus uncemented hemiarthroplasty for displaced femoral neck fractures: a prospective randomized trial with early follow-up. J Orthop Trauma. 2012;26(3):135. doi:10.1097/BOT.0b013e318238b7a5.
16. Hedbeck CJ, Inngul C, Blomfeldt R, Ponzer S, Tornkvist H, Enocson A. Internal fixation versus cemented hemiarthroplasty for displaced femoral neck fractures in patients with severe cognitive dysfunction: a randomized controlled trial. J Orthop Trauma. 2013;27(12):690. doi:10.1097/BOT.0b013e318291f544.
17. Jia Z, Ding F, Wu Y, et al. Unipolar versus bipolar hemiarthroplasty for displaced femoral neck fractures: a systematic review and meta-analysis of randomized controlled trials. J Orthop Surg Res. 2015;10:8. doi:10.1186/s13018-015-0165-0.
18. Lapidus LJ, Charalampidis A, Rundgren J, Enocson A. Internal fixation of garden I and II femoral neck fractures: posterior tilt did not influence the reoperation rate in 382 consecutive hips followed for a minimum of 5 years. J Orthop Trauma. 2013;27(7):386. doi:10.1097/BOT.0b013e318281da6e.
19. Mariconda M, Costa GG, Cerbasi S, et al. Factors predicting mobility and the change in Activities of Daily Living After hip fracture: A 1-year prospective cohort study. J Orthop Trauma. 2016;30(2):71. doi:10.1097/BOT.0000000000000448.
20. Nyholm AM, Gromov K, Palm H, et al. Time to surgery is associated with thirty-day and ninety-day mortality After proximal femoral fracture: A retrospective observational study on prospectively collected data from the Danish Fracture Database Collaborators. J Bone Joint Surg. (American) 2015;97(16):1333. doi:10.2106/JBJS.O.00029.
21. Samuel AM, Russo GS, Lukasiewicz AM, et al. Surgical treatment of femoral neck fractures after 24 hours in patients between the ages of 18 and 49 is associated with poor inpatient outcomes: an analysis of 1361 patients in the National Trauma Data Bank. J Orthop Trauma. 2016;30(2):89. doi:10.1097/BOT.0000000000000456.
22. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235. doi:10.1007/s11999-012-2293-8.
23. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplast. 2012;27(4):583. doi:10.1016/j.arth.2011.07.009.
24. Zielinski SM, Keijsers NL, Praet SF, et al. Functional outcome after successful internal fixation versus salvage arthroplasty of patients with a femoral neck fracture. J Orthop Trauma. 2014;28(12):e273. doi:10.1097/BOT.0000000000000123.
25. Gu Q, Koenig L, Mather RC, 3rd, Tongue J. Surgery for hip fracture yields societal benefits that exceed the direct medical costs. Clin Orthop Relat Res. 2014;472(11):3536. doi:10.1007/s11999-014-3820-6.
26. Forsh DA, Ferguson TA. Contemporary management of femoral neck fractures: the young and the old. Curr Rev Musculoskelet Med. 2012;5(3):214. doi:10.1007/s12178-012-9127-x.
27. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287. doi:10.5435/00124635-200605000-00004.
28. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: Femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596. doi:10.5435/00124635-200810000-00005.
29. Probe R, Ward R. Internal fixation of femoral neck fractures. J Am Acad Orthop Surg. 2006;14(9):565. doi:10.5435/00124635-200609000-00006.
30. Jain NB, Losina E, Ward DM, Harris MB, Katz JN. Trends in surgical management of femoral neck fractures in the United States. Clin Orthop Relat Res. 2008;466(12):3116. doi:10.1007/s11999-008-0392-3.
31. Menendez ME, Neuhaus V, van Dijk CN, Ring D. The Elixhauser comorbidity method outperforms the Charlson index in predicting inpatient death after orthopaedic surgery. Clin Orthop Relat Res. 2014;472(9):2878. doi:10.1007/s11999-014-3686-7.
32. Van Walraven C, Austin PC, Jennings A, Quan H, Forster AJ. A modification of the Elixhauser Comorbidity measures into a point system for hospital death using administrative data. Med Care. 2009;47(6):626-633.
33. Best MJ, Buller LT, Falakassa J, Vecchione D. Risk factors for nonroutine discharge in patients undergoing spinal fusion for intervertebral disc disorders. Iowa Orthop J. 2015;35:147.
34. Schairer WW, Lane JM, Halsey DA, Iorio R, Padgett DE, McLawhorn AS. The Frank Stinchfield award: total hip arthroplasty for femoral neck fracture is not a typical DRG 470: A propensity-matched cohort study. Clin Orthop Relat Res. 2017;475(2):353-360. doi:10.1007/s11999-016-4868-2.
35. Nikkel LE, Fox EJ, Black KP, Davis C, Andersen L, Hollenbeak CS. Impact of comorbidities on hospitalization costs following hip fracture. J Bone Joint Surg Am. 2012;94(1):9. doi:10.2106/JBJS.J.01077.
36. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2 Suppl.):S14. doi:10.1016/j.amjmed.2008.12.003.
37. Siris ES, Pasquale MK, Wang Y, Watts NB. Estimating bisphosphonate use and fracture reduction among US women aged 45 years and older, 2001-2008. J Bone Miner Res Off J Am Soc Bone Miner Res. 2011;26(1):3. doi:10.1002/jbmr.189.
1. Bishop J, Yang A, Githens M, Sox AH. Evaluation of contemporary trends in femoral neck fracture management reveals discrepancies in treatment. Geriatr Orthop Surg Rehabil. 2016;7(3):135. doi:10.1177/2151458516658328.
2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res Off J Am Soc Bone Miner Res. 2007;22(3):465. doi:10.1359/jbmr.061113.
3. Kannus P, Parkkari J, Sievanen H, Heinonen A, Vuori I, Jarvinen M. Epidemiology of hip fractures. Bone. 1996;18(1 Suppl.):57s. doi:10.1016/8756-3282(95)00381-9.
4. Koval KJ, Zuckerman JD. Hip fractures: I. Overview and evaluation and treatment of femoral-neck fractures. J Am Acad Orthop Surg. 1994;2(3):141. doi:10.5435/00124635-199405000-00002.
5. Miller BJ, Callaghan JJ, Cram P, Karam M, Marsh JL, Noiseux NO. Changing trends in the treatment of femoral neck fractures: a review of the American Board of Orthopaedic Surgery database. J Bone Joint Surg. (American) 2014;96(17):e149. doi:10.2106/JBJS.M.01122.
6. Miller BJ, Lu X, Cram P. The trends in treatment of femoral neck fractures in the Medicare population from 1991 to 2008. J Bone Joint Surg. (American) 2013;95(18):e132. doi:10.2106/JBJS.L.01163.
7. Nwachukwu BU, McCormick F, Provencher MT, Roche M, Rubash HE. A comprehensive analysis of Medicare trends in utilization and hospital economics for total knee and hip arthroplasty from 2005 to 2011. J Arthroplast. 2015;30(1):15. doi:10.1016/j.arth.2014.08.025.
8. Su EP, Su SL. Femoral neck fractures: a changing paradigm. Bone Joint J. 2014;96-b(11) Supple A):43. doi:10.1302/0301-620X.96B11.34334.
9. Ahn J, Man LX, Park S, Sodl JF, Esterhai JL. Systematic review of cemented and uncemented hemiarthroplasty outcomes for femoral neck fractures. Clin Orthop Relat Res. 2008;466(10):2513. doi:10.1007/s11999-008-0368-3.
10. Alolabi B, Bajammal S, Shirali J, Karanicolas PJ, Gafni A, Bhandari M. Treatment of displaced femoral neck fractures in the elderly: a cost-benefit analysis. J Orthop Trauma. 2009;23(6):442. doi:10.1097/BOT.0b013e31817614dd.
11. Bentler SE, Liu L, Obrizan M, et al. The aftermath of hip fracture: discharge placement, functional status change, and mortality. Am J Epidemiol. 2009;170(10):1290. doi:10.1093/aje/kwp266.
12. Brox WT, Chan PH, Cafri G, Inacio MC. Similar mortality with general or regional anesthesia in elderly hip fracture patients. Acta Orthop. 2016;87(2):152. doi:10.3109/17453674.2015.1128781.
13. Catal B, Sener M. Treatment and displacement affect the reoperation rate for femoral neck fracture. Clin Orthop Relat Res. 2013;471(12):4096. doi:10.1007/s11999-013-3295-x.
14. Dailiana Z, Papakostidou I, Varitimidis S, Michalitsis S, Veloni A, Malizos K. Surgical treatment of hip fractures: factors influencing mortality. Hippokratia. 2013;17(3):252.
15. Deangelis JP, Ademi A, Staff I, Lewis CG. Cemented versus uncemented hemiarthroplasty for displaced femoral neck fractures: a prospective randomized trial with early follow-up. J Orthop Trauma. 2012;26(3):135. doi:10.1097/BOT.0b013e318238b7a5.
16. Hedbeck CJ, Inngul C, Blomfeldt R, Ponzer S, Tornkvist H, Enocson A. Internal fixation versus cemented hemiarthroplasty for displaced femoral neck fractures in patients with severe cognitive dysfunction: a randomized controlled trial. J Orthop Trauma. 2013;27(12):690. doi:10.1097/BOT.0b013e318291f544.
17. Jia Z, Ding F, Wu Y, et al. Unipolar versus bipolar hemiarthroplasty for displaced femoral neck fractures: a systematic review and meta-analysis of randomized controlled trials. J Orthop Surg Res. 2015;10:8. doi:10.1186/s13018-015-0165-0.
18. Lapidus LJ, Charalampidis A, Rundgren J, Enocson A. Internal fixation of garden I and II femoral neck fractures: posterior tilt did not influence the reoperation rate in 382 consecutive hips followed for a minimum of 5 years. J Orthop Trauma. 2013;27(7):386. doi:10.1097/BOT.0b013e318281da6e.
19. Mariconda M, Costa GG, Cerbasi S, et al. Factors predicting mobility and the change in Activities of Daily Living After hip fracture: A 1-year prospective cohort study. J Orthop Trauma. 2016;30(2):71. doi:10.1097/BOT.0000000000000448.
20. Nyholm AM, Gromov K, Palm H, et al. Time to surgery is associated with thirty-day and ninety-day mortality After proximal femoral fracture: A retrospective observational study on prospectively collected data from the Danish Fracture Database Collaborators. J Bone Joint Surg. (American) 2015;97(16):1333. doi:10.2106/JBJS.O.00029.
21. Samuel AM, Russo GS, Lukasiewicz AM, et al. Surgical treatment of femoral neck fractures after 24 hours in patients between the ages of 18 and 49 is associated with poor inpatient outcomes: an analysis of 1361 patients in the National Trauma Data Bank. J Orthop Trauma. 2016;30(2):89. doi:10.1097/BOT.0000000000000456.
22. Yu L, Wang Y, Chen J. Total hip arthroplasty versus hemiarthroplasty for displaced femoral neck fractures: meta-analysis of randomized trials. Clin Orthop Relat Res. 2012;470(8):2235. doi:10.1007/s11999-012-2293-8.
23. Zi-Sheng A, You-Shui G, Zhi-Zhen J, Ting Y, Chang-Qing Z. Hemiarthroplasty vs primary total hip arthroplasty for displaced fractures of the femoral neck in the elderly: a meta-analysis. J Arthroplast. 2012;27(4):583. doi:10.1016/j.arth.2011.07.009.
24. Zielinski SM, Keijsers NL, Praet SF, et al. Functional outcome after successful internal fixation versus salvage arthroplasty of patients with a femoral neck fracture. J Orthop Trauma. 2014;28(12):e273. doi:10.1097/BOT.0000000000000123.
25. Gu Q, Koenig L, Mather RC, 3rd, Tongue J. Surgery for hip fracture yields societal benefits that exceed the direct medical costs. Clin Orthop Relat Res. 2014;472(11):3536. doi:10.1007/s11999-014-3820-6.
26. Forsh DA, Ferguson TA. Contemporary management of femoral neck fractures: the young and the old. Curr Rev Musculoskelet Med. 2012;5(3):214. doi:10.1007/s12178-012-9127-x.
27. Macaulay W, Pagnotto MR, Iorio R, Mont MA, Saleh KJ. Displaced femoral neck fractures in the elderly: hemiarthroplasty versus total hip arthroplasty. J Am Acad Orthop Surg. 2006;14(5):287. doi:10.5435/00124635-200605000-00004.
28. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: Femoral neck fractures. J Am Acad Orthop Surg. 2008;16(10):596. doi:10.5435/00124635-200810000-00005.
29. Probe R, Ward R. Internal fixation of femoral neck fractures. J Am Acad Orthop Surg. 2006;14(9):565. doi:10.5435/00124635-200609000-00006.
30. Jain NB, Losina E, Ward DM, Harris MB, Katz JN. Trends in surgical management of femoral neck fractures in the United States. Clin Orthop Relat Res. 2008;466(12):3116. doi:10.1007/s11999-008-0392-3.
31. Menendez ME, Neuhaus V, van Dijk CN, Ring D. The Elixhauser comorbidity method outperforms the Charlson index in predicting inpatient death after orthopaedic surgery. Clin Orthop Relat Res. 2014;472(9):2878. doi:10.1007/s11999-014-3686-7.
32. Van Walraven C, Austin PC, Jennings A, Quan H, Forster AJ. A modification of the Elixhauser Comorbidity measures into a point system for hospital death using administrative data. Med Care. 2009;47(6):626-633.
33. Best MJ, Buller LT, Falakassa J, Vecchione D. Risk factors for nonroutine discharge in patients undergoing spinal fusion for intervertebral disc disorders. Iowa Orthop J. 2015;35:147.
34. Schairer WW, Lane JM, Halsey DA, Iorio R, Padgett DE, McLawhorn AS. The Frank Stinchfield award: total hip arthroplasty for femoral neck fracture is not a typical DRG 470: A propensity-matched cohort study. Clin Orthop Relat Res. 2017;475(2):353-360. doi:10.1007/s11999-016-4868-2.
35. Nikkel LE, Fox EJ, Black KP, Davis C, Andersen L, Hollenbeak CS. Impact of comorbidities on hospitalization costs following hip fracture. J Bone Joint Surg Am. 2012;94(1):9. doi:10.2106/JBJS.J.01077.
36. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2 Suppl.):S14. doi:10.1016/j.amjmed.2008.12.003.
37. Siris ES, Pasquale MK, Wang Y, Watts NB. Estimating bisphosphonate use and fracture reduction among US women aged 45 years and older, 2001-2008. J Bone Miner Res Off J Am Soc Bone Miner Res. 2011;26(1):3. doi:10.1002/jbmr.189.
TAKE-HOME POINTS
- The femoral neck patient population is older and has more medical comorbidities.
- Hemiarthroplasty (HA) is being performed more commonly in patients > 50 years old for femoral neck fractures.
- Open reduction and internal fixation is being performed more commonly in patients > 80 years old for femoral neck fractures.
- The rate of adverse events following femoral neck fracture is higher in the total hip arthroplasty (THA) group than in the HA group.
- THA is an independent risk factor for adverse events following femoral neck fracture.
Incidental Asymptomatic Fibular Stress Fractures Presenting as Varus Knee Osteoarthritis: A Case Report
ABSTRACT
Stress fractures are often missed, especially in unusual clinical settings. We report on 2 patients who presented to our orthopedic surgery clinic with incidental findings of asymptomatic proximal fibular tension side stress fractures in severe longstanding varus osteoarthritic knees. Initial plain films demonstrated an expansile deformity of the proximal fibular shaft, and differential diagnosis included a healed or healing fracture versus possible neoplasm. Magnetic resonance imaging with and without gadolinium was utilized to rule out the latter prior to planned total knee arthroplasty.
Continue to: The proximal fibula...
The proximal fibula is a rare site for stress fractures, with most of these fractures occurring in military recruits.1 To the authors’ knowledge, there has been only 1 documented case of a proximal fibular stress fracture in patients with severe osteoarthritis (OA) and fixed varus deformity, which mimicked L5 radiculopathy.2 We are not aware of any reports of asymptomatic tension-side fibular stress fractures in varus knees. In our 2 cases, the patients were indicated for total knee arthroplasty (TKA) for varus degenerative joint disease after failing nonoperative treatment; however, further work-up was justified to rule out neoplasm after plain films revealed expansile deformities of the proximal fibular shaft. Each patient subsequently underwent magnetic resonance imaging (MRI) with and without gadolinium contrast, which demonstrated a healed and healing proximal fibular stress fracture. Magnetic resonance imaging is rarely indicated in the evaluation of degenerative joint disease, and stress fractures about a varus knee generally occur on the compression side of the tibia and are symptomatic.3-7 The patients provided informed written consent for print and electronic publication of this case report.
CASE REPORT
The first patient was a 77-year-old male who presented with longstanding knee pain, left greater than right, exacerbated by weight-bearing activities. The patient had no improvement with physical therapy or anti-inflammatory medication. He denied any history of trauma, weakness, paresthesias, or a recent increase in activity. The patient also denied any fevers, chills, night sweats, or other constitutional symptoms. On physical examination, the patient had an antalgic gait and limited range of motion bilaterally. Examination of his right lower extremity demonstrated a fixed 5° varus deformity. No distinct point tenderness was noted.
Radiographs of the right knee demonstrated varus deformity and tricompartmental degenerative changes with severe medial joint space narrowing. An expansile deformity of the proximal right fibular shaft was also noted (Figure 1), which was not present on the films 2 years earlier (Figure 2). The absence of this deformity on previous imaging raised the suspicion of a tumor. An MRI with and without gadolinium, which was obtained to rule out a neoplastic process, showed an old, healed proximal fibular shaft fracture with chronic periosteal reaction (Figure 3). There was no marrow edema to suggest acute injury and no neoplastic lesion. He was reassured regarding the benign findings and was scheduled for a left TKA, as his pain was more severe on the left knee. The patient’s stress fracture healed without complications, and he underwent a successful left TKA. He returned approximately 6 months after his procedure with worsening right knee pain and underwent a successful TKA on the right knee as well.
The second patient was a 67-year-old male with longstanding bilateral knee pain, right greater than left, with no antecedent trauma. He denied a history of increased activity, or weakness or paresthesias. He denied any fevers, chills, night sweats, or other constitutional symptoms. One year prior to presentation at our clinic, he had received corticosteroid injections and hyaluronic acid, without relief. The patient also had a history with another surgeon of arthroscopy 1 year earlier and subchondroplasty 3 years before presentation to our clinic. On physical examination, the patient’s right knee displayed a fixed 7° varus deformity with decreased range of motion, effusion, and diffuse crepitus. Further examination revealed tenderness to palpation of the proximal fibula.
Radiographs of the right knee showed degenerative joint disease with varus deformity and medial compartment joint space narrowing. They also demonstrated an expansile deformity of mixed lucency and sclerosis involving the proximal right fibular shaft (Figure 4). Although these findings appeared to be consistent with a stress fracture, their appearance was also suspicious for a neoplasm. To rule out malignancy, an MRI with and without gadolinium was obtained that revealed a healing stress fracture of the proximal fibula (Figure 5). The patient was reassured, and plans were made to proceed with a TKA. The patient’s stress fracture healed without complications, and he underwent successful right TKA. Radiographs from the patient’s 8-week follow-up showed a healed fibular stress fracture (Figure 6).
Continue to: DISCUSSION
DISCUSSION
To our knowledge, this is the first report of incidental tension-side stress fractures in varus osteoarthritic knees. Stress fractures have been classified into 2 groups, fatigue fractures and insufficiency fractures. Fatigue fractures occur when abnormal stress is applied to normal bones, and insufficiency fractures result when normal stress is applied to abnormal bones.8 Stress fractures can also be classified into risk categories based on which bone is involved and the loading of the bone.9 Sites loaded in tension have increased risk of nonunion, progression to complete fracture, and reoccurrence compared with sites loaded in compression.9 Stress fractures of the fibula occur rarely, and when present, they are more commonly observed in the distal fibula in athletes and military recruits.1 Stress fractures occur rarely in patients with primary OA, and when present in this setting, obesity and malalignment are the contributing factors.3 Neither patient was obese in our case (body mass index of 27 and 28, respectively), but significant varus deformity was present in both patients. Stress fractures occurring near the knee in the setting of a varus deformity generally occur on the compression side of the tibia and are symptomatic.3-7
Regarding malalignment, Cheung and colleagues10 reported about a case of an elderly female with OA of the knee with valgus deformity that initially developed a proximal fibular stress fracture followed by a proximal tibial stress fracture. However, both of our patients had varus deformities. Mullaji and Shetty3 documented stress fractures in 34 patients with OA, a majority with varus deformities, but did not report any isolated proximal fibular stress fractures. Manish and colleagues2 reported the only documented case of an isolated proximal fibular stress fracture in a patient with osteoarthritic varus deformity. The patient presented initially with pain and paresthesias of the lower thigh and leg consistent with an L5 radiculopathy. They believed that the varus deformity and the repetitive contraction of the lateral knee muscles put increased shear forces on the fibula leading to the stress fracture. Our patients did not present with any radicular symptoms, a history of acute worsening pain, or an increased activity concerning for a stress fracture. Instead, our patients presented with progressively worsening knee pain typical of severe OA and incidental findings on imaging of tension-side fibular stress fractures. An MRI with and without gadolinium confirmed the diagnosis of a healed fracture in our first patient and a healing fracture in our second patient.
CONCLUSION
Although exceedingly rare in osteoarthritic varus knees, we presented 2 cases of MRI-confirmed proximal fibular stress fractures in this report. As demonstrated, patients may present with symptoms of OA or radicular symptoms as described by Manish and colleagues.2 Presentation may also include an expansile lesion on imaging, prompting a differential diagnosis that includes a neoplasm. If present in the setting of an osteoarthritic varus knee, stress fractures of the proximal fibula should heal with conservative treatment and not affect the plan or outcome of TKA.
- Devas MB, Sweetnam R. Stress fractures of the fibula; a review of fifty cases in athletes. J Bone Joint Surg Br. 1956;38-B(4):818-829.
- Manish KK, Agnivesh T, Pramod PS, Samir SD. Isolated proximal fibular stress fracture in osteoarthritis knee presenting as L5 radiculopathy. J Orthop Case Reports. 2015;5(3):75-77. doi:10.13107/jocr.2250-0685.315.
- Mullaji A, Shetty G. Total knee arthroplasty for arthritic knees with tibiofibular stress fractures: classification and treatment guidelines. J Arthroplasty. 2010;25(2):295-301. doi:10.1016/j.arth.2008.11.012.
- Sourlas I, Papachristou G, Pilichou A, Giannoudis PV, Efstathopoulos N, Nikolaou VS. Proximal tibial stress fractures associated with primary degenerative knee osteoarthritis. Am J Orthop (Belle Mead NJ). 2009;38(3):120-124
- Demir B, Gursu S, Oke R, Ozturk K, Sahin V. Proximal tibia stress fracture caused by severe arthrosis of the knee with varus deformity. Am J Orthop (Belle Mead NJ). 2009;38(9):457-459.
- Satku K, Kumar VP, Pho RW. Stress fractures of the tibia in osteoarthritis of the knee. J Bone Joint Surg Br. 1987;69(2):309-311. doi:10.1302/0301-620X.69B2.3818767.
- Martin LM, Bourne RB, Rorabeck CH. Stress fractures associated with osteoarthritis of the knee. A report of three cases. J Bone Joint Surg Am. 1988;70(5):771-774.
- Hong SH, Chu IT. Stress fracture of the proximal fibula in military recruits. Clin Orthop Surg. 2009;1(3):161-164. doi:10.4055/cios.2009.1.3.161
- Knapik JJ, Reynolds K, Hoedebecke KL. Stress fractures: Etiology, epidemiology, diagnosis, treatment, and prevention. J Spec Oper Med. 17(2):120-130.
- Cheung MHS, Lee M-F, Lui TH. Insufficiency fracture of the proximal fibula and then tibia: A case report. J Orthop Surg. 2013;21(1):103-105. doi:10.1177/230949901302100126
ABSTRACT
Stress fractures are often missed, especially in unusual clinical settings. We report on 2 patients who presented to our orthopedic surgery clinic with incidental findings of asymptomatic proximal fibular tension side stress fractures in severe longstanding varus osteoarthritic knees. Initial plain films demonstrated an expansile deformity of the proximal fibular shaft, and differential diagnosis included a healed or healing fracture versus possible neoplasm. Magnetic resonance imaging with and without gadolinium was utilized to rule out the latter prior to planned total knee arthroplasty.
Continue to: The proximal fibula...
The proximal fibula is a rare site for stress fractures, with most of these fractures occurring in military recruits.1 To the authors’ knowledge, there has been only 1 documented case of a proximal fibular stress fracture in patients with severe osteoarthritis (OA) and fixed varus deformity, which mimicked L5 radiculopathy.2 We are not aware of any reports of asymptomatic tension-side fibular stress fractures in varus knees. In our 2 cases, the patients were indicated for total knee arthroplasty (TKA) for varus degenerative joint disease after failing nonoperative treatment; however, further work-up was justified to rule out neoplasm after plain films revealed expansile deformities of the proximal fibular shaft. Each patient subsequently underwent magnetic resonance imaging (MRI) with and without gadolinium contrast, which demonstrated a healed and healing proximal fibular stress fracture. Magnetic resonance imaging is rarely indicated in the evaluation of degenerative joint disease, and stress fractures about a varus knee generally occur on the compression side of the tibia and are symptomatic.3-7 The patients provided informed written consent for print and electronic publication of this case report.
CASE REPORT
The first patient was a 77-year-old male who presented with longstanding knee pain, left greater than right, exacerbated by weight-bearing activities. The patient had no improvement with physical therapy or anti-inflammatory medication. He denied any history of trauma, weakness, paresthesias, or a recent increase in activity. The patient also denied any fevers, chills, night sweats, or other constitutional symptoms. On physical examination, the patient had an antalgic gait and limited range of motion bilaterally. Examination of his right lower extremity demonstrated a fixed 5° varus deformity. No distinct point tenderness was noted.
Radiographs of the right knee demonstrated varus deformity and tricompartmental degenerative changes with severe medial joint space narrowing. An expansile deformity of the proximal right fibular shaft was also noted (Figure 1), which was not present on the films 2 years earlier (Figure 2). The absence of this deformity on previous imaging raised the suspicion of a tumor. An MRI with and without gadolinium, which was obtained to rule out a neoplastic process, showed an old, healed proximal fibular shaft fracture with chronic periosteal reaction (Figure 3). There was no marrow edema to suggest acute injury and no neoplastic lesion. He was reassured regarding the benign findings and was scheduled for a left TKA, as his pain was more severe on the left knee. The patient’s stress fracture healed without complications, and he underwent a successful left TKA. He returned approximately 6 months after his procedure with worsening right knee pain and underwent a successful TKA on the right knee as well.
The second patient was a 67-year-old male with longstanding bilateral knee pain, right greater than left, with no antecedent trauma. He denied a history of increased activity, or weakness or paresthesias. He denied any fevers, chills, night sweats, or other constitutional symptoms. One year prior to presentation at our clinic, he had received corticosteroid injections and hyaluronic acid, without relief. The patient also had a history with another surgeon of arthroscopy 1 year earlier and subchondroplasty 3 years before presentation to our clinic. On physical examination, the patient’s right knee displayed a fixed 7° varus deformity with decreased range of motion, effusion, and diffuse crepitus. Further examination revealed tenderness to palpation of the proximal fibula.
Radiographs of the right knee showed degenerative joint disease with varus deformity and medial compartment joint space narrowing. They also demonstrated an expansile deformity of mixed lucency and sclerosis involving the proximal right fibular shaft (Figure 4). Although these findings appeared to be consistent with a stress fracture, their appearance was also suspicious for a neoplasm. To rule out malignancy, an MRI with and without gadolinium was obtained that revealed a healing stress fracture of the proximal fibula (Figure 5). The patient was reassured, and plans were made to proceed with a TKA. The patient’s stress fracture healed without complications, and he underwent successful right TKA. Radiographs from the patient’s 8-week follow-up showed a healed fibular stress fracture (Figure 6).
Continue to: DISCUSSION
DISCUSSION
To our knowledge, this is the first report of incidental tension-side stress fractures in varus osteoarthritic knees. Stress fractures have been classified into 2 groups, fatigue fractures and insufficiency fractures. Fatigue fractures occur when abnormal stress is applied to normal bones, and insufficiency fractures result when normal stress is applied to abnormal bones.8 Stress fractures can also be classified into risk categories based on which bone is involved and the loading of the bone.9 Sites loaded in tension have increased risk of nonunion, progression to complete fracture, and reoccurrence compared with sites loaded in compression.9 Stress fractures of the fibula occur rarely, and when present, they are more commonly observed in the distal fibula in athletes and military recruits.1 Stress fractures occur rarely in patients with primary OA, and when present in this setting, obesity and malalignment are the contributing factors.3 Neither patient was obese in our case (body mass index of 27 and 28, respectively), but significant varus deformity was present in both patients. Stress fractures occurring near the knee in the setting of a varus deformity generally occur on the compression side of the tibia and are symptomatic.3-7
Regarding malalignment, Cheung and colleagues10 reported about a case of an elderly female with OA of the knee with valgus deformity that initially developed a proximal fibular stress fracture followed by a proximal tibial stress fracture. However, both of our patients had varus deformities. Mullaji and Shetty3 documented stress fractures in 34 patients with OA, a majority with varus deformities, but did not report any isolated proximal fibular stress fractures. Manish and colleagues2 reported the only documented case of an isolated proximal fibular stress fracture in a patient with osteoarthritic varus deformity. The patient presented initially with pain and paresthesias of the lower thigh and leg consistent with an L5 radiculopathy. They believed that the varus deformity and the repetitive contraction of the lateral knee muscles put increased shear forces on the fibula leading to the stress fracture. Our patients did not present with any radicular symptoms, a history of acute worsening pain, or an increased activity concerning for a stress fracture. Instead, our patients presented with progressively worsening knee pain typical of severe OA and incidental findings on imaging of tension-side fibular stress fractures. An MRI with and without gadolinium confirmed the diagnosis of a healed fracture in our first patient and a healing fracture in our second patient.
CONCLUSION
Although exceedingly rare in osteoarthritic varus knees, we presented 2 cases of MRI-confirmed proximal fibular stress fractures in this report. As demonstrated, patients may present with symptoms of OA or radicular symptoms as described by Manish and colleagues.2 Presentation may also include an expansile lesion on imaging, prompting a differential diagnosis that includes a neoplasm. If present in the setting of an osteoarthritic varus knee, stress fractures of the proximal fibula should heal with conservative treatment and not affect the plan or outcome of TKA.
ABSTRACT
Stress fractures are often missed, especially in unusual clinical settings. We report on 2 patients who presented to our orthopedic surgery clinic with incidental findings of asymptomatic proximal fibular tension side stress fractures in severe longstanding varus osteoarthritic knees. Initial plain films demonstrated an expansile deformity of the proximal fibular shaft, and differential diagnosis included a healed or healing fracture versus possible neoplasm. Magnetic resonance imaging with and without gadolinium was utilized to rule out the latter prior to planned total knee arthroplasty.
Continue to: The proximal fibula...
The proximal fibula is a rare site for stress fractures, with most of these fractures occurring in military recruits.1 To the authors’ knowledge, there has been only 1 documented case of a proximal fibular stress fracture in patients with severe osteoarthritis (OA) and fixed varus deformity, which mimicked L5 radiculopathy.2 We are not aware of any reports of asymptomatic tension-side fibular stress fractures in varus knees. In our 2 cases, the patients were indicated for total knee arthroplasty (TKA) for varus degenerative joint disease after failing nonoperative treatment; however, further work-up was justified to rule out neoplasm after plain films revealed expansile deformities of the proximal fibular shaft. Each patient subsequently underwent magnetic resonance imaging (MRI) with and without gadolinium contrast, which demonstrated a healed and healing proximal fibular stress fracture. Magnetic resonance imaging is rarely indicated in the evaluation of degenerative joint disease, and stress fractures about a varus knee generally occur on the compression side of the tibia and are symptomatic.3-7 The patients provided informed written consent for print and electronic publication of this case report.
CASE REPORT
The first patient was a 77-year-old male who presented with longstanding knee pain, left greater than right, exacerbated by weight-bearing activities. The patient had no improvement with physical therapy or anti-inflammatory medication. He denied any history of trauma, weakness, paresthesias, or a recent increase in activity. The patient also denied any fevers, chills, night sweats, or other constitutional symptoms. On physical examination, the patient had an antalgic gait and limited range of motion bilaterally. Examination of his right lower extremity demonstrated a fixed 5° varus deformity. No distinct point tenderness was noted.
Radiographs of the right knee demonstrated varus deformity and tricompartmental degenerative changes with severe medial joint space narrowing. An expansile deformity of the proximal right fibular shaft was also noted (Figure 1), which was not present on the films 2 years earlier (Figure 2). The absence of this deformity on previous imaging raised the suspicion of a tumor. An MRI with and without gadolinium, which was obtained to rule out a neoplastic process, showed an old, healed proximal fibular shaft fracture with chronic periosteal reaction (Figure 3). There was no marrow edema to suggest acute injury and no neoplastic lesion. He was reassured regarding the benign findings and was scheduled for a left TKA, as his pain was more severe on the left knee. The patient’s stress fracture healed without complications, and he underwent a successful left TKA. He returned approximately 6 months after his procedure with worsening right knee pain and underwent a successful TKA on the right knee as well.
The second patient was a 67-year-old male with longstanding bilateral knee pain, right greater than left, with no antecedent trauma. He denied a history of increased activity, or weakness or paresthesias. He denied any fevers, chills, night sweats, or other constitutional symptoms. One year prior to presentation at our clinic, he had received corticosteroid injections and hyaluronic acid, without relief. The patient also had a history with another surgeon of arthroscopy 1 year earlier and subchondroplasty 3 years before presentation to our clinic. On physical examination, the patient’s right knee displayed a fixed 7° varus deformity with decreased range of motion, effusion, and diffuse crepitus. Further examination revealed tenderness to palpation of the proximal fibula.
Radiographs of the right knee showed degenerative joint disease with varus deformity and medial compartment joint space narrowing. They also demonstrated an expansile deformity of mixed lucency and sclerosis involving the proximal right fibular shaft (Figure 4). Although these findings appeared to be consistent with a stress fracture, their appearance was also suspicious for a neoplasm. To rule out malignancy, an MRI with and without gadolinium was obtained that revealed a healing stress fracture of the proximal fibula (Figure 5). The patient was reassured, and plans were made to proceed with a TKA. The patient’s stress fracture healed without complications, and he underwent successful right TKA. Radiographs from the patient’s 8-week follow-up showed a healed fibular stress fracture (Figure 6).
Continue to: DISCUSSION
DISCUSSION
To our knowledge, this is the first report of incidental tension-side stress fractures in varus osteoarthritic knees. Stress fractures have been classified into 2 groups, fatigue fractures and insufficiency fractures. Fatigue fractures occur when abnormal stress is applied to normal bones, and insufficiency fractures result when normal stress is applied to abnormal bones.8 Stress fractures can also be classified into risk categories based on which bone is involved and the loading of the bone.9 Sites loaded in tension have increased risk of nonunion, progression to complete fracture, and reoccurrence compared with sites loaded in compression.9 Stress fractures of the fibula occur rarely, and when present, they are more commonly observed in the distal fibula in athletes and military recruits.1 Stress fractures occur rarely in patients with primary OA, and when present in this setting, obesity and malalignment are the contributing factors.3 Neither patient was obese in our case (body mass index of 27 and 28, respectively), but significant varus deformity was present in both patients. Stress fractures occurring near the knee in the setting of a varus deformity generally occur on the compression side of the tibia and are symptomatic.3-7
Regarding malalignment, Cheung and colleagues10 reported about a case of an elderly female with OA of the knee with valgus deformity that initially developed a proximal fibular stress fracture followed by a proximal tibial stress fracture. However, both of our patients had varus deformities. Mullaji and Shetty3 documented stress fractures in 34 patients with OA, a majority with varus deformities, but did not report any isolated proximal fibular stress fractures. Manish and colleagues2 reported the only documented case of an isolated proximal fibular stress fracture in a patient with osteoarthritic varus deformity. The patient presented initially with pain and paresthesias of the lower thigh and leg consistent with an L5 radiculopathy. They believed that the varus deformity and the repetitive contraction of the lateral knee muscles put increased shear forces on the fibula leading to the stress fracture. Our patients did not present with any radicular symptoms, a history of acute worsening pain, or an increased activity concerning for a stress fracture. Instead, our patients presented with progressively worsening knee pain typical of severe OA and incidental findings on imaging of tension-side fibular stress fractures. An MRI with and without gadolinium confirmed the diagnosis of a healed fracture in our first patient and a healing fracture in our second patient.
CONCLUSION
Although exceedingly rare in osteoarthritic varus knees, we presented 2 cases of MRI-confirmed proximal fibular stress fractures in this report. As demonstrated, patients may present with symptoms of OA or radicular symptoms as described by Manish and colleagues.2 Presentation may also include an expansile lesion on imaging, prompting a differential diagnosis that includes a neoplasm. If present in the setting of an osteoarthritic varus knee, stress fractures of the proximal fibula should heal with conservative treatment and not affect the plan or outcome of TKA.
- Devas MB, Sweetnam R. Stress fractures of the fibula; a review of fifty cases in athletes. J Bone Joint Surg Br. 1956;38-B(4):818-829.
- Manish KK, Agnivesh T, Pramod PS, Samir SD. Isolated proximal fibular stress fracture in osteoarthritis knee presenting as L5 radiculopathy. J Orthop Case Reports. 2015;5(3):75-77. doi:10.13107/jocr.2250-0685.315.
- Mullaji A, Shetty G. Total knee arthroplasty for arthritic knees with tibiofibular stress fractures: classification and treatment guidelines. J Arthroplasty. 2010;25(2):295-301. doi:10.1016/j.arth.2008.11.012.
- Sourlas I, Papachristou G, Pilichou A, Giannoudis PV, Efstathopoulos N, Nikolaou VS. Proximal tibial stress fractures associated with primary degenerative knee osteoarthritis. Am J Orthop (Belle Mead NJ). 2009;38(3):120-124
- Demir B, Gursu S, Oke R, Ozturk K, Sahin V. Proximal tibia stress fracture caused by severe arthrosis of the knee with varus deformity. Am J Orthop (Belle Mead NJ). 2009;38(9):457-459.
- Satku K, Kumar VP, Pho RW. Stress fractures of the tibia in osteoarthritis of the knee. J Bone Joint Surg Br. 1987;69(2):309-311. doi:10.1302/0301-620X.69B2.3818767.
- Martin LM, Bourne RB, Rorabeck CH. Stress fractures associated with osteoarthritis of the knee. A report of three cases. J Bone Joint Surg Am. 1988;70(5):771-774.
- Hong SH, Chu IT. Stress fracture of the proximal fibula in military recruits. Clin Orthop Surg. 2009;1(3):161-164. doi:10.4055/cios.2009.1.3.161
- Knapik JJ, Reynolds K, Hoedebecke KL. Stress fractures: Etiology, epidemiology, diagnosis, treatment, and prevention. J Spec Oper Med. 17(2):120-130.
- Cheung MHS, Lee M-F, Lui TH. Insufficiency fracture of the proximal fibula and then tibia: A case report. J Orthop Surg. 2013;21(1):103-105. doi:10.1177/230949901302100126
- Devas MB, Sweetnam R. Stress fractures of the fibula; a review of fifty cases in athletes. J Bone Joint Surg Br. 1956;38-B(4):818-829.
- Manish KK, Agnivesh T, Pramod PS, Samir SD. Isolated proximal fibular stress fracture in osteoarthritis knee presenting as L5 radiculopathy. J Orthop Case Reports. 2015;5(3):75-77. doi:10.13107/jocr.2250-0685.315.
- Mullaji A, Shetty G. Total knee arthroplasty for arthritic knees with tibiofibular stress fractures: classification and treatment guidelines. J Arthroplasty. 2010;25(2):295-301. doi:10.1016/j.arth.2008.11.012.
- Sourlas I, Papachristou G, Pilichou A, Giannoudis PV, Efstathopoulos N, Nikolaou VS. Proximal tibial stress fractures associated with primary degenerative knee osteoarthritis. Am J Orthop (Belle Mead NJ). 2009;38(3):120-124
- Demir B, Gursu S, Oke R, Ozturk K, Sahin V. Proximal tibia stress fracture caused by severe arthrosis of the knee with varus deformity. Am J Orthop (Belle Mead NJ). 2009;38(9):457-459.
- Satku K, Kumar VP, Pho RW. Stress fractures of the tibia in osteoarthritis of the knee. J Bone Joint Surg Br. 1987;69(2):309-311. doi:10.1302/0301-620X.69B2.3818767.
- Martin LM, Bourne RB, Rorabeck CH. Stress fractures associated with osteoarthritis of the knee. A report of three cases. J Bone Joint Surg Am. 1988;70(5):771-774.
- Hong SH, Chu IT. Stress fracture of the proximal fibula in military recruits. Clin Orthop Surg. 2009;1(3):161-164. doi:10.4055/cios.2009.1.3.161
- Knapik JJ, Reynolds K, Hoedebecke KL. Stress fractures: Etiology, epidemiology, diagnosis, treatment, and prevention. J Spec Oper Med. 17(2):120-130.
- Cheung MHS, Lee M-F, Lui TH. Insufficiency fracture of the proximal fibula and then tibia: A case report. J Orthop Surg. 2013;21(1):103-105. doi:10.1177/230949901302100126
TAKE-HOME POINTS
- Proximal fibular stress fractures in patients with primary osteoarthritis and fixed varus deformity have rarely been reported.
- Stress fractures occurring near the knee in the setting of a varus deformity generally occur on the compression side of the tibia and are symptomatic.
- Proximal fibular stress fractures may present as an incidental finding of an expansile deformity on plain films in patients with varus osteoarthritic knees.
- Magnetic resonance imaging is rarely indicated in the evaluation of degenerative joint disease; however, it was justified in our case to rule out neoplasm.
- When present in the setting of an osteoarthritic varus knee, stress fractures of the proximal fibula should heal with conservative treatment and should not affect the plan or outcome of TKA.
Arthroscopic SLAP IIb Repair Using Knot-Tying Versus Knotless Suture Anchors: Is There a Difference?
ABSTRACT
The use of knotless suture anchors has increased in popularity; however, there is a paucity of literature examining the difference in clinical outcomes with traditional knotted fixation. It was hypothesized that knotless fixation would provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears. Seventy-four athletes who underwent arthroscopic SLAP IIb repair with traditional (n = 42) and knotless anchors (n = 32) by a single surgeon were evaluated after a minimum 2-year follow. Demographic and surgical data, RTP, Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, strength, and pain scores were compared. Knotless anchors had slightly higher RTP (93.5% vs 90.2%, P = .94) and RTP at the same level (58.1% vs 53.7% P = .81) compared with knotted fixation, but the difference did not reach statistical significance. Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but the difference was not statistically significant. When comparing knotless and traditional knotted suture anchor repair of type llb SLAP tears, knotless fixation required less revision surgery and had higher RTP, ASES, and KJOC scores; however, statistical significance was not achieved in this relatively small cohort.
Continue to: Injury of the anterosuperior...
Injury of the anterosuperior labrum near the biceps origin was first described by Andrews and colleagues in 1985 in overhead athletes.1 The term SLAP, or a tear in the superior labrum anterior to posterior, was coined a few years later by Snyder and colleagues.2 They described an injury to the superior labrum beginning posteriorly and extending anteriorly, including the “anchor” of the biceps tendon to the labrum. Snyder further delineated SLAP lesions into 4 subtypes, the most common being type II, which he described as “degenerative fraying of the labrum with additional detachment of the superior labrum and biceps from the glenoid resulting in an unstable labral anchor.”2,3 Type II tears are of particular importance as they are the most common SLAP lesions, with an incidence of 55%, and comprise nearly 75% of SLAP repairs performed.2,4
Morgan and colleagues further delineated type II SLAP tears into IIa (anterior), IIb (posterior), and IIc (combined). Their group found that SLAP IIb tears were the most common type in overhead throwers, accounting for 47% of overhead athletes with type II tears.5 Further, type IIb tears can have a significant impact in throwers, in part due to greater shoulder instability as well as anterior pseudolaxity.5 SLAP injuries typically have been difficult to successfully treat nonoperatively in overhead athletes.6 A study by Edwards and colleagues6 examined 39 patients with all types of SLAP tears. Although, in their study, nonoperative management failed in 20 patients and they required surgery, 10 of the 15 overhead athletes in whom nonoperative treatment did not fail initially returned to sport at a level equal to or better than their pre-injury level, indicating that nonoperative treatment may play a role in some patients’ recovery.6
Surgical outcomes of SLAP IIb repairs have traditionally been less predictable than those of other shoulder injuries. Some believe that traditional knotted anchors may be partially to blame by abrading the rotator cuff, possibly leading to rotator cuff tears and pain. Further, knotted anchors are typically bulkier and require more experience with tying and tensioning and, therefore, may lead to less consistent results.7 The purpose of this study was to investigate if knotless anchors result in more favorable outcomes in repair of type IIb SLAP lesions when compared with traditional knotted anchors. It was hypothesized that knotless fixation will provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears.
METHODS
PATIENT SELECTION
The authors retrospectively reviewed SLAP tears repaired by the senior author from June 2000 to September 2015. The inclusion criteria consisted of all athletes at any level who were diagnosed intraoperatively with a type IIb SLAP tear as defined by Morgan and colleagues5 with a minimum 2-year follow-up. The exclusion criteria were any patients with a previous shoulder surgery and the presence of any labral pathology aside from a SLAP IIb tear. Patients with rotator cuff or biceps pathologies were included. In all included patients, an initial course of preoperative physical therapy, including strengthening and stabilization of the scapulothoracic joint, had failed. Patient-directed surveys evaluated RTP, as well as the Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, range of motion (ROM), strength, and pain scores, as previously described.8-10 Institutional Review Board and informed consent approval were acquired prior to initiation of the study.
PATIENT EVALUATION
An appropriate preoperative history was taken, and physical examinations were performed, including evaluation of the scapulothoracic joint, as well as tests to evaluate the presence of a SLAP tear, anterior instability, posterior instability, multi-directional instability, and rotator cuff tears, as previously described.11 Patients with a history and physical examination concerning SLAP pathology underwent an magnetic resonance imaging (MRI) arthrogram, which was used in conjunction with intraoperative findings to diagnose type IIb SLAP tears.
Continue to: SURGICAL TECHNIQUE
SURGICAL TECHNIQUE
All surgeries were performed arthroscopically with the patient in the lateral decubitus position. The SLAP lesions were subsequently repaired using a technique similar to that described by Burkhart and colleagues.12 The traditional knotted fixation incorporated the use of 3.0 Bio-FASTak (Arthrex) with #2 FiberWire (Arthrex). Knotless anchor fixation was performed using 2.9 mm × 12.5 mm or 2.4 mm × 11.3 mm BioComposite PushLock (Arthrex) suture anchors, based on the size of the glenoid, with LabralTape or SutureTape (Arthrex). Patients who had surgery before January 1, 2013 underwent fixation with traditional knotted fixation; after that date, patients underwent fixation with knotless anchors.
POSTOPERATIVE REHABILITATION
Patients underwent a strict postoperative protocol in which they were kept in a sling with an abduction pillow for the first 6 weeks and performed pendulum exercises and passive motion only. A formal physical therapy regimen started at 4 weeks with passive ROM, passive posterior capsular and internal rotation stretching, scapulothoracic mobility, and biceps, rotator cuff, and capsular stabilizer strengthening. At 10 weeks, patients began biceps, rotator cuff, and scapular stabilizer resistance exercises, and at 16 weeks, throwing athletes began an interval throwing program. Patients were first eligible to return to sport without limitation at 9 months.
STATISTICAL ANALYSIS
Return to play, KJOC, ASES, stability, ROM, strength, and pain scores were analyzed and compared using Fisher exact test, the Kruskal-Wallis test, and the Wilcoxon rank sum test, where appropriate. The level of statistical significance was α = 0.05.
RESULTS
Table 1. Patient Demographics | |
Athletes (N) | 74 |
Age (yr) | 30.1 (14-64) |
Knotless anchors | 32 (43.2%) |
Knotted anchors | 42 (56.8%) |
Overhead athletes | 53 (72%) |
Throwing athletes | 29 (39%) |
Follow-up (yr) | 6.5 (2-12) |
Of the 74 athletes who met inclusion criteria, 28 were female (37.8%) and 46 (62.2%) were male. The average follow-up was 6.5 years with a minimum of 2 years and a maximum of 12 years. Forty-two (56.8%) patients underwent traditional knotted suture anchor fixation and 32 (43.2%) underwent knotless anchor fixation. The average age was 30.1 +/– 13.6 years, with a range of 14 to 64 years. The majority of athletes were right hand dominant (79.9%). Fifty-three (72%) were overhead athletes and 29 (39%) were throwing athletes (Table 1). The average age in the knotted group was 33.3 years: 29 of 42 (69%) were overhead athletes and 20 (47.6%) were throwing athletes. In the knotless group, the average age was 25.8 years: 24 of 32 (75.0%) were overhead athletes and 9 (28.1%) were throwing athletes. Primary sports at the time of injury are listed in Table 2. The average number of anchors used was 3.1, with 17 patients (23.0%) requiring ≤2 anchors, 39 (52.7%) requiring 3 anchors, and 18 (24.3%) requiring ≥4 anchors for repair. The number of anchors used was determined intraoperatively by the surgeon on the basis of the size and extent of the tear. Of the entire group of 74 patients, 91.9% returned to sport, 56.8% returned to the same level, 35.1% returned at a lower capacity, and 8.1% were unable to return to sport. Knotless anchors had a slightly higher overall RTP compared with traditional anchors (93.5% vs 90.2%, P = .94), as well as a higher RTP at the same level (58.1% vs 53.7%, P = .81). These differences were, however, not statistically significant (Table 3).
Table 2. Primary Sport at Time of SLAP IIb Injury | |
Primary Sport | n (%) |
Baseball | 14 (19.7%) |
Softball | 8 (11.3%) |
Volleyball | 6 (8.5%) |
Basketball | 5 (7.0%) |
Golf | 5 (7.0%) |
Other Sport | 33 (46.5%) |
No Primary Sport | 3 (4.1%) |
Abbreviation: SLAP, superior labrum anterior to posterior.
Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but this difference was not statistically significant (Table 3). In the knotted group, 5 patients had revision surgery for rotator cuff tears, and 2 patients had recurrent SLAP tears. In the knotless group, 2 patients had revision surgeries for a torn rotator cuff, and 1 patient had a snapping scapula. A power analysis found that it would take over 300 athletes in each group to detect a significant difference in the revision rate between knotless and traditional anchors.
Table 3. Comparison of Anchor Type in Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | KJOC | Revision Rate |
Knotless anchors (n = 32) | 93.5% | 58.1% | 86.3 + 10.5 | 66.1 + 29.6 | 9% |
Traditional anchors (n = 42) | 90.2% | 53.7% | 85.3 + 15.6 | 65.6 + 27.2 | 17% |
P-value | .94 | .81 | .79 | .61 | .50 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
Continue to: Although KJOC...
Although KJOC (66.1 vs 65.6 P = .61) and ASES (86.3 vs 85.3 P = .79) scores were also superior with knotless anchors, these differences in scores were not statistically significant (Table 3). Pain was the only variable that was linked to decreased RTP, as patients who rated higher on a pain scale of 0 to 10 were less likely to return to their sport (P < .0001). There was no correlation in outcome measures or RTP with gender, age, number of anchors, or sport type (P > .05). There was no statistically significant difference in RTP, KJOC, or ASES scores between non-overhead and overhead athletes (Table 4). Overall return to sport in throwers was 85.7% (24/28), while 39.3% (11/28) returned at the same level, 46.4% (13/28) at a lower level, and 14.3% (4/28) did not return to sport.
Table 4. Overhead vs Non-Overhead Athletes After Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | ASES Good-Excellent | KJOC |
Overhead | 90.6% | 52.3% | 91.7 + 14.1 | 98.1% | 64.6 + 25.7 |
Non-Overhead | 95.5% | 72.7% | 86.7 + 12.7 | 100% | 88.5 + 29.6 |
P value | 0.1 | 0.29 | 0.76 | 0.50 | 0.49 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
DISCUSSION
There was no significant difference between knotted and knotless fixation in clinical outcomes or return to sport in the repair of SLAP IIb tears; however, there was a trend toward knotless anchors requiring less revision surgery and having higher RTP, ASES, and KJOC scores than knotted fixation. Despite the inclusion of 74 patients, this study was significantly underpowered, as a power analysis calculated that over 300 athletes would be required in each group to detect a difference in the revision rate.
SLAP tears, traditionally treated with knotted suture anchors, have yielded varying results in the literature, with good to excellent results being reported in 65% to 94% of patients.13-17 The success of SLAP repairs in athletes, especially overhead athletes, remains a difficult problem, as they are common injuries, and RTP is less predictable. Studies differ with regard to the percentage of overhead athletes who are able to return to their previous level of sport, with ranges being reported from 22% to 92%.16,18,19 In a systematic review of 198 patients, Sayde and colleagues16 found that 63% of overhead athletes treated with anchor fixation, tacks, or staples were able to return to their previous level of play. Morgan and colleagues5 found a higher return to sport when compared with other studies, reporting that 83% of patients undergoing SLAP repairs using traditional suture anchors had excellent results, and 87% of the 53 overhead athletes had excellent results based on UCLA shoulder scores. Further, 37 of the 44 pitchers examined (84%) were able to return to their pre-injury levels.5 This is in contrast to Friel and colleagues20 who found that in 48 patients with type II SLAP tears treated with traditional anchors, 23% reported excellent and 56% reported good results in regards to UCLA shoulder scores. Friel and colleagues also found that 62% of all athletes and 59% of overhead athletes were able to return to their previous levels of sport, which is similar to the current study.20 The large discrepancy in RTP at the pre-injury level between this study and that of Morgan and colleagues5 may be due to the shorter minimum follow-up of 1 year as well as the inclusion of all subtypes of SLAP II tears in the latter. The current study had a minimum 2-year follow-up period, with an average of 6.5 years, and was limited to SLAP IIb tears. With a longer follow-up period, patient outcomes and RTP, particularly in overhead sports, may deteriorate; therefore, the current study likely shows a more complete and accurate result.
Knotless anchors were originally introduced as a less time consuming, lower profile, and simpler device to learn and use for arthroscopic procedures.21 Kocaoglu and colleagues22 found that in Bankart repairs, the mean time per anchor placement for knotted anchors was 380 seconds, whereas placement of knotless anchors took on average 225 seconds. A learning curve also exists for proper and efficient knot tying.7 There is also variation in knot tying between surgeons, as evidenced by a wide range in both load to failure and knot height.7 A study performed by Hanypsiak and colleagues7 found that the surgical knot was the weakest portion of the suture-anchor construct, as the knot’s load to failure was less than the pullout strength of the anchor.
There is also concern for the added height associated with traditional knotted fixation, which has been supported by case reports of knot-induced glenoid erosion after arthroscopic fixation of a SLAP tear.23 Hanypsiak and colleagues7 also found that the average knot height occupied 50% to 95% of the space between the humeral head and the acromion when the shoulder is in a neutral position, indicating that the higher profile knotted anchors may contact the undersurface of the acromion, which could affect the labral repair as well as cause rotator cuff injury. Abrasion of the rotator cuff by a prominent knot may cause pain, tearing, and disability. A recent study by Park and colleagues24 reported on 11 patients with knot-induced pain after type II SLAP repair. All complained of sharp pain, with 64% also complaining of clicking. Knot location did not seem to matter, as there was no difference in preoperative symptoms, with 5 of the 11 patients having knots on the glenoid side of the repair on repeat arthroscopy. Patients with knots on the labral side did, however, have humeral head cartilage damage. The knots appeared to be the cause of pain and clicking, as after arthroscopic knot removal, dramatic pain relief was seen, with Constant and UCLA scores significantly improving in all 11 patients. All patients also had positive preoperative compression-rotation testing, and at 6 weeks after surgical knot removal, all were negative.24
Continue to: Further, as shown by Dines and colleagues...
Further, as shown by Dines and colleagues25, knotless anchors may help to better restore the meniscoid anatomy of the superior labrum better than knotted suture anchors. With regards to fixation strength, Uggen and colleagues26, using a cadaveric model, found no difference in initial fixation strength of knotless and traditional suture anchor repair of SLAP II tears, and both restored glenohumeral rotation without over-constraining the shoulder.
Despite the shorter operative time, lower profile, and more consistent tensioning with knotless anchors, the literature is limited with regard to evaluating patient outcomes. In a study by Yung and colleagues13 14 of the 16 patients with type II SLAP tears were treated with knotless anchors, and the authors found that 31.3% of patients had an excellent UCLA score while 43.8% had a good score. This is similar to the outcomes illustrated in studies by both Friel and colleagues20 and Sayde and colleagues.16 In a more recent study, Yang and colleagues27 did find some benefit in regard to ROM with knotless fixation. Their study consisted of 21 patients who underwent surgery with traditional knotted anchor fixation and 20 who underwent knotless horizontal mattress fixation. They found an average UCLA score of 37.6 and ASES score of 91.5 in patients undergoing knotless fixation, and the knotless fixation group had 5% greater total ROM, 15.6% more internal rotation at abduction, and 11.4% more external rotation at the side as compared with patients undergoing the traditional knotted technique. When compared with the current study, this study also had a significantly shorter follow-up period of 3 years.27 In a 2017 study, Bents and colleagues28 compared 44 patients who underwent knotless and 119 who underwent knotted fixation of SLAP tears. They found no statistically significant difference between knotless and knotted fixation in the ASES score, Visual Analog Scale (VAS), ASES, or Veterans RAND 12-Item Health Survey (VR-12) at 1 year postoperatively. Their outcomes were similar to those of the current study, but as in other mentioned literature, the study by Bents and colleagues28 included multiple surgeons with different postoperative protocols, was not limited to SLAP IIb tears, and also had a shorter follow-up of 1 year. Like Kocaoglu and colleagues22, Bents and colleagues did find knotless anchors to be more efficient, as operative time was reduced by 5.3 minutes per anchor. This likely would have a significant impact on surgical cost and surgeon productivity.28
One limitation of the current study was that despite the inclusion of >70 patients, the study was still significantly underpowered. It was determined that >300 patients in each group would be required to detect a significant difference in the revision rate between the 2 anchor types. Also, due to the retrospective nature of this study, no preoperative scores were collected. The inclusion of objective clinical measurements and follow-up imaging evaluating the rotator cuff and other anatomy would also be of interest.
Although statistical significance was not achieved, there was a trend toward knotless fixation requiring less revision surgery and having higher RTP, ASES, and KJOC scores when compared with traditional knotted fixation at 6.5-year follow-up. Larger studies with longer follow-up periods are necessary to determine the effects of knotted and knotless anchors on rotator cuff tears, patient reported outcomes, and RTP. These complications have been shown in the literature, mostly in case reports, and typically develop over a longer period.23 Despite this, other advantages of knotless fixation, such as its lower profile, the ability to better provide consistent tensioning, and decreased surgical time are important to consider.
1. Andrews JR, Carson WG, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341. doi:10.1177/036354658501300508.
2. Snyder SJ, Karzel RP, Pizzo WD, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthrosc J Arthrosc Relat Surg. 1990;6(4):274-279. doi:10.1016/0749-8063(90)90056-J.
3. Ahsan ZS, Hsu JE, Gee AO. The Snyder classification of superior labrum anterior and posterior (SLAP) lesions. Clin Orthop. 2016;474(9):2075-2078. doi:10.1007/s11999-016-4826-z.
4. Erickson BJ, Jain A, Abrams GD, et al. SLAP Lesions: Trends in treatment. Arthrosc J Arthrosc Relat Surg. 2016;32(6):976-981. doi:10.1016/j.arthro.2015.11.044.
5. Morgan C, Burkhart S, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthrosc J Arthrosc Relat Surg. 1998;14(6):553-565. doi:10.1016/S0749-8063(98)70049-0.
6. Edwards SL, Lee JA, Bell J-E, et al. nonoperative treatment of superior labrum anterior posterior tears: Improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456-1461. doi:10.1177/0363546510370937.
7. Hanypsiak BT, DeLong JM, Simmons L, Lowe W, Burkhart S. Knot strength varies widely among expert arthroscopists. Am J Sports Med. 2014;42(8):1978-1984. doi:10.1177/0363546514535554.
8. Alberta FG, ElAttrache NS, Bissell S, et al. The development and validation of a functional assessment tool for the upper extremity in the overhead athlete. Am J Sports Med. 2010;38(5):903-911. doi:10.1177/0363546509355642.
9. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014. doi:10.1177/0363546513493599.
10. Michener LA, McClure PW, Sennett BJ. American shoulder and elbow surgeons standardized shoulder assessment form, patient self-report section: Reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594. doi:10.1067/mse.2002.127096.
11. Cook C, Hegedus EJ. Orthopedic Physical Examination Tests: An Evidence-Based Approach. Upper Saddle River, NJ: PearsonPrentice Hall; 2008.
12. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology part I: Pathoanatomy and biomechanics. Arthrosc J Arthrosc Relat Surg. 2003;19(4):404-420. doi:10.1053/jars.2003.50128.
13. Yung PS-H, Fong DT-P, Kong M-F, et al. Arthroscopic repair of isolated type II superior labrum anterior–posterior lesion. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1151-1157. doi:10.1007/s00167-008-0629-4.
14. Brockmeier SF, Voos JE, Williams RJ, Altchek DW, Cordasco FA, Allen AA. Outcomes After Arthroscopic Repair of Type-II SLAP Lesions: J Bone Jt Surg-Am Vol. 2009;91(7):1595-1603. doi:10.2106/JBJS.H.00205.
15. Galano GJ, Ahmad CS, Bigliani L, Levine W. Percutaneous SLAP lesion repair technique is an effective alternative to portal of Wilmington. Orthopedics. 2010;33(11). doi:10.3928/01477447-20100924-15.
16. Sayde WM, Cohen SB, Ciccotti MG, Dodson CC. Return to play after type II superior labral anterior-posterior lesion repairs in athletes: A systematic review. Clin Orthop Relat Res. 2012;470(6):1595-1600. doi:10.1007/s11999-012-2295-6.
17. Kim K-H, Bin S-I, Kim J-M. The correlation between posterior tibial slope and maximal angle of flexion after total knee arthroplasty. Knee Surg Relat Res. 2012;24(3):158-163. doi:10.5792/ksrr.2012.24.3.158.
18. Kim S-H, Ha K-I, Kim S-H, Choi H-J. Results of arthroscopic treatment of superior labral lesions. J Bone Joint Surg Am. 2002;84-A(6):981-985.
19. Pagnani MJ, Speer KP, Altchek DW, Warren RF, Dines DM. Arthroscopic fixation of superior labral lesions using a biodegradable implant: a preliminary report. Arthrosc J Arthrosc Relat Surg Off Publ Arthrosc Assoc N Am Int Arthrosc Assoc. 1995;11(2):194-198.
20. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: Prospective evaluation at a minimum two-year follow-up. J Shoulder Elbow Surg. 2010;19(6):859-867. doi:10.1016/j.jse.2010.03.004.
21. Thal R. A knotless suture anchor. Arthrosc J Arthrosc Relat Surg. 2001;17(2):213-218. doi:10.1053/jars.2001.20666.
22. Kocaoglu B, Guven O, Nalbantoglu U, Aydin N, Haklar U. No difference between knotless sutures and suture anchors in arthroscopic repair of Bankart lesions in collision athletes. Knee Surg Sports Traumatol Arthrosc. 2009;17(7):844-849. doi:10.1007/s00167-009-0811-3.
23. Rhee YG, Ha JH. Knot-induced glenoid erosion after arthroscopic fixation for unstable superior labrum anterior-posterior lesion: Case report. J Shoulder Elbow Surg. 2006;15(3):391-393. doi:10.1016/j.jse.2005.03.010.
24. Park JG, Cho NS, Kim JY, Song JH, Hong SJ, Rhee YG. Arthroscopic Knot Removal for Failed Superior Labrum Anterior-Posterior Repair Secondary to Knot-Induced Pain. Am J Sports Med. 2017;45(11):2563-2568. doi:10.1177/0363546517713662.
25. Dines JS, ElAttrache NS. Horizontal Mattress With a Knotless Anchor to Better Recreate the Normal Superior Labrum Anatomy. Arthrosc J Arthrosc Relat Surg. 2008;24(12):1422-1425. doi:10.1016/j.arthro.2008.06.012.
26. Uggen C, Wei A, Glousman RE, et al. Biomechanical Comparison of Knotless Anchor Repair Versus Simple Suture Repair for Type II SLAP Lesions. Arthrosc J Arthrosc Relat Surg. 2009;25(10):1085-1092. doi:10.1016/j.arthro.2009.03.022.
27. Yang HJ, Yoon K, Jin H, Song HS. Clinical outcome of arthroscopic SLAP repair: conventional vertical knot versus knotless horizontal mattress sutures. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):464-469. doi:10.1007/s00167-014-3449-8.
28. Bents EJ, Brady PC, Adams CR, Tokish JM, Higgins LD, Denard PJ. Patient-reported outcomes of knotted and knotless glenohumeral labral repairs are equivalent. Am J Orthop. 2017;46(6):279-283.
ABSTRACT
The use of knotless suture anchors has increased in popularity; however, there is a paucity of literature examining the difference in clinical outcomes with traditional knotted fixation. It was hypothesized that knotless fixation would provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears. Seventy-four athletes who underwent arthroscopic SLAP IIb repair with traditional (n = 42) and knotless anchors (n = 32) by a single surgeon were evaluated after a minimum 2-year follow. Demographic and surgical data, RTP, Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, strength, and pain scores were compared. Knotless anchors had slightly higher RTP (93.5% vs 90.2%, P = .94) and RTP at the same level (58.1% vs 53.7% P = .81) compared with knotted fixation, but the difference did not reach statistical significance. Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but the difference was not statistically significant. When comparing knotless and traditional knotted suture anchor repair of type llb SLAP tears, knotless fixation required less revision surgery and had higher RTP, ASES, and KJOC scores; however, statistical significance was not achieved in this relatively small cohort.
Continue to: Injury of the anterosuperior...
Injury of the anterosuperior labrum near the biceps origin was first described by Andrews and colleagues in 1985 in overhead athletes.1 The term SLAP, or a tear in the superior labrum anterior to posterior, was coined a few years later by Snyder and colleagues.2 They described an injury to the superior labrum beginning posteriorly and extending anteriorly, including the “anchor” of the biceps tendon to the labrum. Snyder further delineated SLAP lesions into 4 subtypes, the most common being type II, which he described as “degenerative fraying of the labrum with additional detachment of the superior labrum and biceps from the glenoid resulting in an unstable labral anchor.”2,3 Type II tears are of particular importance as they are the most common SLAP lesions, with an incidence of 55%, and comprise nearly 75% of SLAP repairs performed.2,4
Morgan and colleagues further delineated type II SLAP tears into IIa (anterior), IIb (posterior), and IIc (combined). Their group found that SLAP IIb tears were the most common type in overhead throwers, accounting for 47% of overhead athletes with type II tears.5 Further, type IIb tears can have a significant impact in throwers, in part due to greater shoulder instability as well as anterior pseudolaxity.5 SLAP injuries typically have been difficult to successfully treat nonoperatively in overhead athletes.6 A study by Edwards and colleagues6 examined 39 patients with all types of SLAP tears. Although, in their study, nonoperative management failed in 20 patients and they required surgery, 10 of the 15 overhead athletes in whom nonoperative treatment did not fail initially returned to sport at a level equal to or better than their pre-injury level, indicating that nonoperative treatment may play a role in some patients’ recovery.6
Surgical outcomes of SLAP IIb repairs have traditionally been less predictable than those of other shoulder injuries. Some believe that traditional knotted anchors may be partially to blame by abrading the rotator cuff, possibly leading to rotator cuff tears and pain. Further, knotted anchors are typically bulkier and require more experience with tying and tensioning and, therefore, may lead to less consistent results.7 The purpose of this study was to investigate if knotless anchors result in more favorable outcomes in repair of type IIb SLAP lesions when compared with traditional knotted anchors. It was hypothesized that knotless fixation will provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears.
METHODS
PATIENT SELECTION
The authors retrospectively reviewed SLAP tears repaired by the senior author from June 2000 to September 2015. The inclusion criteria consisted of all athletes at any level who were diagnosed intraoperatively with a type IIb SLAP tear as defined by Morgan and colleagues5 with a minimum 2-year follow-up. The exclusion criteria were any patients with a previous shoulder surgery and the presence of any labral pathology aside from a SLAP IIb tear. Patients with rotator cuff or biceps pathologies were included. In all included patients, an initial course of preoperative physical therapy, including strengthening and stabilization of the scapulothoracic joint, had failed. Patient-directed surveys evaluated RTP, as well as the Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, range of motion (ROM), strength, and pain scores, as previously described.8-10 Institutional Review Board and informed consent approval were acquired prior to initiation of the study.
PATIENT EVALUATION
An appropriate preoperative history was taken, and physical examinations were performed, including evaluation of the scapulothoracic joint, as well as tests to evaluate the presence of a SLAP tear, anterior instability, posterior instability, multi-directional instability, and rotator cuff tears, as previously described.11 Patients with a history and physical examination concerning SLAP pathology underwent an magnetic resonance imaging (MRI) arthrogram, which was used in conjunction with intraoperative findings to diagnose type IIb SLAP tears.
Continue to: SURGICAL TECHNIQUE
SURGICAL TECHNIQUE
All surgeries were performed arthroscopically with the patient in the lateral decubitus position. The SLAP lesions were subsequently repaired using a technique similar to that described by Burkhart and colleagues.12 The traditional knotted fixation incorporated the use of 3.0 Bio-FASTak (Arthrex) with #2 FiberWire (Arthrex). Knotless anchor fixation was performed using 2.9 mm × 12.5 mm or 2.4 mm × 11.3 mm BioComposite PushLock (Arthrex) suture anchors, based on the size of the glenoid, with LabralTape or SutureTape (Arthrex). Patients who had surgery before January 1, 2013 underwent fixation with traditional knotted fixation; after that date, patients underwent fixation with knotless anchors.
POSTOPERATIVE REHABILITATION
Patients underwent a strict postoperative protocol in which they were kept in a sling with an abduction pillow for the first 6 weeks and performed pendulum exercises and passive motion only. A formal physical therapy regimen started at 4 weeks with passive ROM, passive posterior capsular and internal rotation stretching, scapulothoracic mobility, and biceps, rotator cuff, and capsular stabilizer strengthening. At 10 weeks, patients began biceps, rotator cuff, and scapular stabilizer resistance exercises, and at 16 weeks, throwing athletes began an interval throwing program. Patients were first eligible to return to sport without limitation at 9 months.
STATISTICAL ANALYSIS
Return to play, KJOC, ASES, stability, ROM, strength, and pain scores were analyzed and compared using Fisher exact test, the Kruskal-Wallis test, and the Wilcoxon rank sum test, where appropriate. The level of statistical significance was α = 0.05.
RESULTS
Table 1. Patient Demographics | |
Athletes (N) | 74 |
Age (yr) | 30.1 (14-64) |
Knotless anchors | 32 (43.2%) |
Knotted anchors | 42 (56.8%) |
Overhead athletes | 53 (72%) |
Throwing athletes | 29 (39%) |
Follow-up (yr) | 6.5 (2-12) |
Of the 74 athletes who met inclusion criteria, 28 were female (37.8%) and 46 (62.2%) were male. The average follow-up was 6.5 years with a minimum of 2 years and a maximum of 12 years. Forty-two (56.8%) patients underwent traditional knotted suture anchor fixation and 32 (43.2%) underwent knotless anchor fixation. The average age was 30.1 +/– 13.6 years, with a range of 14 to 64 years. The majority of athletes were right hand dominant (79.9%). Fifty-three (72%) were overhead athletes and 29 (39%) were throwing athletes (Table 1). The average age in the knotted group was 33.3 years: 29 of 42 (69%) were overhead athletes and 20 (47.6%) were throwing athletes. In the knotless group, the average age was 25.8 years: 24 of 32 (75.0%) were overhead athletes and 9 (28.1%) were throwing athletes. Primary sports at the time of injury are listed in Table 2. The average number of anchors used was 3.1, with 17 patients (23.0%) requiring ≤2 anchors, 39 (52.7%) requiring 3 anchors, and 18 (24.3%) requiring ≥4 anchors for repair. The number of anchors used was determined intraoperatively by the surgeon on the basis of the size and extent of the tear. Of the entire group of 74 patients, 91.9% returned to sport, 56.8% returned to the same level, 35.1% returned at a lower capacity, and 8.1% were unable to return to sport. Knotless anchors had a slightly higher overall RTP compared with traditional anchors (93.5% vs 90.2%, P = .94), as well as a higher RTP at the same level (58.1% vs 53.7%, P = .81). These differences were, however, not statistically significant (Table 3).
Table 2. Primary Sport at Time of SLAP IIb Injury | |
Primary Sport | n (%) |
Baseball | 14 (19.7%) |
Softball | 8 (11.3%) |
Volleyball | 6 (8.5%) |
Basketball | 5 (7.0%) |
Golf | 5 (7.0%) |
Other Sport | 33 (46.5%) |
No Primary Sport | 3 (4.1%) |
Abbreviation: SLAP, superior labrum anterior to posterior.
Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but this difference was not statistically significant (Table 3). In the knotted group, 5 patients had revision surgery for rotator cuff tears, and 2 patients had recurrent SLAP tears. In the knotless group, 2 patients had revision surgeries for a torn rotator cuff, and 1 patient had a snapping scapula. A power analysis found that it would take over 300 athletes in each group to detect a significant difference in the revision rate between knotless and traditional anchors.
Table 3. Comparison of Anchor Type in Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | KJOC | Revision Rate |
Knotless anchors (n = 32) | 93.5% | 58.1% | 86.3 + 10.5 | 66.1 + 29.6 | 9% |
Traditional anchors (n = 42) | 90.2% | 53.7% | 85.3 + 15.6 | 65.6 + 27.2 | 17% |
P-value | .94 | .81 | .79 | .61 | .50 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
Continue to: Although KJOC...
Although KJOC (66.1 vs 65.6 P = .61) and ASES (86.3 vs 85.3 P = .79) scores were also superior with knotless anchors, these differences in scores were not statistically significant (Table 3). Pain was the only variable that was linked to decreased RTP, as patients who rated higher on a pain scale of 0 to 10 were less likely to return to their sport (P < .0001). There was no correlation in outcome measures or RTP with gender, age, number of anchors, or sport type (P > .05). There was no statistically significant difference in RTP, KJOC, or ASES scores between non-overhead and overhead athletes (Table 4). Overall return to sport in throwers was 85.7% (24/28), while 39.3% (11/28) returned at the same level, 46.4% (13/28) at a lower level, and 14.3% (4/28) did not return to sport.
Table 4. Overhead vs Non-Overhead Athletes After Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | ASES Good-Excellent | KJOC |
Overhead | 90.6% | 52.3% | 91.7 + 14.1 | 98.1% | 64.6 + 25.7 |
Non-Overhead | 95.5% | 72.7% | 86.7 + 12.7 | 100% | 88.5 + 29.6 |
P value | 0.1 | 0.29 | 0.76 | 0.50 | 0.49 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
DISCUSSION
There was no significant difference between knotted and knotless fixation in clinical outcomes or return to sport in the repair of SLAP IIb tears; however, there was a trend toward knotless anchors requiring less revision surgery and having higher RTP, ASES, and KJOC scores than knotted fixation. Despite the inclusion of 74 patients, this study was significantly underpowered, as a power analysis calculated that over 300 athletes would be required in each group to detect a difference in the revision rate.
SLAP tears, traditionally treated with knotted suture anchors, have yielded varying results in the literature, with good to excellent results being reported in 65% to 94% of patients.13-17 The success of SLAP repairs in athletes, especially overhead athletes, remains a difficult problem, as they are common injuries, and RTP is less predictable. Studies differ with regard to the percentage of overhead athletes who are able to return to their previous level of sport, with ranges being reported from 22% to 92%.16,18,19 In a systematic review of 198 patients, Sayde and colleagues16 found that 63% of overhead athletes treated with anchor fixation, tacks, or staples were able to return to their previous level of play. Morgan and colleagues5 found a higher return to sport when compared with other studies, reporting that 83% of patients undergoing SLAP repairs using traditional suture anchors had excellent results, and 87% of the 53 overhead athletes had excellent results based on UCLA shoulder scores. Further, 37 of the 44 pitchers examined (84%) were able to return to their pre-injury levels.5 This is in contrast to Friel and colleagues20 who found that in 48 patients with type II SLAP tears treated with traditional anchors, 23% reported excellent and 56% reported good results in regards to UCLA shoulder scores. Friel and colleagues also found that 62% of all athletes and 59% of overhead athletes were able to return to their previous levels of sport, which is similar to the current study.20 The large discrepancy in RTP at the pre-injury level between this study and that of Morgan and colleagues5 may be due to the shorter minimum follow-up of 1 year as well as the inclusion of all subtypes of SLAP II tears in the latter. The current study had a minimum 2-year follow-up period, with an average of 6.5 years, and was limited to SLAP IIb tears. With a longer follow-up period, patient outcomes and RTP, particularly in overhead sports, may deteriorate; therefore, the current study likely shows a more complete and accurate result.
Knotless anchors were originally introduced as a less time consuming, lower profile, and simpler device to learn and use for arthroscopic procedures.21 Kocaoglu and colleagues22 found that in Bankart repairs, the mean time per anchor placement for knotted anchors was 380 seconds, whereas placement of knotless anchors took on average 225 seconds. A learning curve also exists for proper and efficient knot tying.7 There is also variation in knot tying between surgeons, as evidenced by a wide range in both load to failure and knot height.7 A study performed by Hanypsiak and colleagues7 found that the surgical knot was the weakest portion of the suture-anchor construct, as the knot’s load to failure was less than the pullout strength of the anchor.
There is also concern for the added height associated with traditional knotted fixation, which has been supported by case reports of knot-induced glenoid erosion after arthroscopic fixation of a SLAP tear.23 Hanypsiak and colleagues7 also found that the average knot height occupied 50% to 95% of the space between the humeral head and the acromion when the shoulder is in a neutral position, indicating that the higher profile knotted anchors may contact the undersurface of the acromion, which could affect the labral repair as well as cause rotator cuff injury. Abrasion of the rotator cuff by a prominent knot may cause pain, tearing, and disability. A recent study by Park and colleagues24 reported on 11 patients with knot-induced pain after type II SLAP repair. All complained of sharp pain, with 64% also complaining of clicking. Knot location did not seem to matter, as there was no difference in preoperative symptoms, with 5 of the 11 patients having knots on the glenoid side of the repair on repeat arthroscopy. Patients with knots on the labral side did, however, have humeral head cartilage damage. The knots appeared to be the cause of pain and clicking, as after arthroscopic knot removal, dramatic pain relief was seen, with Constant and UCLA scores significantly improving in all 11 patients. All patients also had positive preoperative compression-rotation testing, and at 6 weeks after surgical knot removal, all were negative.24
Continue to: Further, as shown by Dines and colleagues...
Further, as shown by Dines and colleagues25, knotless anchors may help to better restore the meniscoid anatomy of the superior labrum better than knotted suture anchors. With regards to fixation strength, Uggen and colleagues26, using a cadaveric model, found no difference in initial fixation strength of knotless and traditional suture anchor repair of SLAP II tears, and both restored glenohumeral rotation without over-constraining the shoulder.
Despite the shorter operative time, lower profile, and more consistent tensioning with knotless anchors, the literature is limited with regard to evaluating patient outcomes. In a study by Yung and colleagues13 14 of the 16 patients with type II SLAP tears were treated with knotless anchors, and the authors found that 31.3% of patients had an excellent UCLA score while 43.8% had a good score. This is similar to the outcomes illustrated in studies by both Friel and colleagues20 and Sayde and colleagues.16 In a more recent study, Yang and colleagues27 did find some benefit in regard to ROM with knotless fixation. Their study consisted of 21 patients who underwent surgery with traditional knotted anchor fixation and 20 who underwent knotless horizontal mattress fixation. They found an average UCLA score of 37.6 and ASES score of 91.5 in patients undergoing knotless fixation, and the knotless fixation group had 5% greater total ROM, 15.6% more internal rotation at abduction, and 11.4% more external rotation at the side as compared with patients undergoing the traditional knotted technique. When compared with the current study, this study also had a significantly shorter follow-up period of 3 years.27 In a 2017 study, Bents and colleagues28 compared 44 patients who underwent knotless and 119 who underwent knotted fixation of SLAP tears. They found no statistically significant difference between knotless and knotted fixation in the ASES score, Visual Analog Scale (VAS), ASES, or Veterans RAND 12-Item Health Survey (VR-12) at 1 year postoperatively. Their outcomes were similar to those of the current study, but as in other mentioned literature, the study by Bents and colleagues28 included multiple surgeons with different postoperative protocols, was not limited to SLAP IIb tears, and also had a shorter follow-up of 1 year. Like Kocaoglu and colleagues22, Bents and colleagues did find knotless anchors to be more efficient, as operative time was reduced by 5.3 minutes per anchor. This likely would have a significant impact on surgical cost and surgeon productivity.28
One limitation of the current study was that despite the inclusion of >70 patients, the study was still significantly underpowered. It was determined that >300 patients in each group would be required to detect a significant difference in the revision rate between the 2 anchor types. Also, due to the retrospective nature of this study, no preoperative scores were collected. The inclusion of objective clinical measurements and follow-up imaging evaluating the rotator cuff and other anatomy would also be of interest.
Although statistical significance was not achieved, there was a trend toward knotless fixation requiring less revision surgery and having higher RTP, ASES, and KJOC scores when compared with traditional knotted fixation at 6.5-year follow-up. Larger studies with longer follow-up periods are necessary to determine the effects of knotted and knotless anchors on rotator cuff tears, patient reported outcomes, and RTP. These complications have been shown in the literature, mostly in case reports, and typically develop over a longer period.23 Despite this, other advantages of knotless fixation, such as its lower profile, the ability to better provide consistent tensioning, and decreased surgical time are important to consider.
ABSTRACT
The use of knotless suture anchors has increased in popularity; however, there is a paucity of literature examining the difference in clinical outcomes with traditional knotted fixation. It was hypothesized that knotless fixation would provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears. Seventy-four athletes who underwent arthroscopic SLAP IIb repair with traditional (n = 42) and knotless anchors (n = 32) by a single surgeon were evaluated after a minimum 2-year follow. Demographic and surgical data, RTP, Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, strength, and pain scores were compared. Knotless anchors had slightly higher RTP (93.5% vs 90.2%, P = .94) and RTP at the same level (58.1% vs 53.7% P = .81) compared with knotted fixation, but the difference did not reach statistical significance. Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but the difference was not statistically significant. When comparing knotless and traditional knotted suture anchor repair of type llb SLAP tears, knotless fixation required less revision surgery and had higher RTP, ASES, and KJOC scores; however, statistical significance was not achieved in this relatively small cohort.
Continue to: Injury of the anterosuperior...
Injury of the anterosuperior labrum near the biceps origin was first described by Andrews and colleagues in 1985 in overhead athletes.1 The term SLAP, or a tear in the superior labrum anterior to posterior, was coined a few years later by Snyder and colleagues.2 They described an injury to the superior labrum beginning posteriorly and extending anteriorly, including the “anchor” of the biceps tendon to the labrum. Snyder further delineated SLAP lesions into 4 subtypes, the most common being type II, which he described as “degenerative fraying of the labrum with additional detachment of the superior labrum and biceps from the glenoid resulting in an unstable labral anchor.”2,3 Type II tears are of particular importance as they are the most common SLAP lesions, with an incidence of 55%, and comprise nearly 75% of SLAP repairs performed.2,4
Morgan and colleagues further delineated type II SLAP tears into IIa (anterior), IIb (posterior), and IIc (combined). Their group found that SLAP IIb tears were the most common type in overhead throwers, accounting for 47% of overhead athletes with type II tears.5 Further, type IIb tears can have a significant impact in throwers, in part due to greater shoulder instability as well as anterior pseudolaxity.5 SLAP injuries typically have been difficult to successfully treat nonoperatively in overhead athletes.6 A study by Edwards and colleagues6 examined 39 patients with all types of SLAP tears. Although, in their study, nonoperative management failed in 20 patients and they required surgery, 10 of the 15 overhead athletes in whom nonoperative treatment did not fail initially returned to sport at a level equal to or better than their pre-injury level, indicating that nonoperative treatment may play a role in some patients’ recovery.6
Surgical outcomes of SLAP IIb repairs have traditionally been less predictable than those of other shoulder injuries. Some believe that traditional knotted anchors may be partially to blame by abrading the rotator cuff, possibly leading to rotator cuff tears and pain. Further, knotted anchors are typically bulkier and require more experience with tying and tensioning and, therefore, may lead to less consistent results.7 The purpose of this study was to investigate if knotless anchors result in more favorable outcomes in repair of type IIb SLAP lesions when compared with traditional knotted anchors. It was hypothesized that knotless fixation will provide superior clinical outcomes, improved return to play (RTP), and lower revision rates as compared with traditional knotted fixation in the repair of SLAP IIb tears.
METHODS
PATIENT SELECTION
The authors retrospectively reviewed SLAP tears repaired by the senior author from June 2000 to September 2015. The inclusion criteria consisted of all athletes at any level who were diagnosed intraoperatively with a type IIb SLAP tear as defined by Morgan and colleagues5 with a minimum 2-year follow-up. The exclusion criteria were any patients with a previous shoulder surgery and the presence of any labral pathology aside from a SLAP IIb tear. Patients with rotator cuff or biceps pathologies were included. In all included patients, an initial course of preoperative physical therapy, including strengthening and stabilization of the scapulothoracic joint, had failed. Patient-directed surveys evaluated RTP, as well as the Kerlan-Jobe Orthopaedic Clinic (KJOC) score, American Shoulder and Elbow Surgeons (ASES) score, stability, range of motion (ROM), strength, and pain scores, as previously described.8-10 Institutional Review Board and informed consent approval were acquired prior to initiation of the study.
PATIENT EVALUATION
An appropriate preoperative history was taken, and physical examinations were performed, including evaluation of the scapulothoracic joint, as well as tests to evaluate the presence of a SLAP tear, anterior instability, posterior instability, multi-directional instability, and rotator cuff tears, as previously described.11 Patients with a history and physical examination concerning SLAP pathology underwent an magnetic resonance imaging (MRI) arthrogram, which was used in conjunction with intraoperative findings to diagnose type IIb SLAP tears.
Continue to: SURGICAL TECHNIQUE
SURGICAL TECHNIQUE
All surgeries were performed arthroscopically with the patient in the lateral decubitus position. The SLAP lesions were subsequently repaired using a technique similar to that described by Burkhart and colleagues.12 The traditional knotted fixation incorporated the use of 3.0 Bio-FASTak (Arthrex) with #2 FiberWire (Arthrex). Knotless anchor fixation was performed using 2.9 mm × 12.5 mm or 2.4 mm × 11.3 mm BioComposite PushLock (Arthrex) suture anchors, based on the size of the glenoid, with LabralTape or SutureTape (Arthrex). Patients who had surgery before January 1, 2013 underwent fixation with traditional knotted fixation; after that date, patients underwent fixation with knotless anchors.
POSTOPERATIVE REHABILITATION
Patients underwent a strict postoperative protocol in which they were kept in a sling with an abduction pillow for the first 6 weeks and performed pendulum exercises and passive motion only. A formal physical therapy regimen started at 4 weeks with passive ROM, passive posterior capsular and internal rotation stretching, scapulothoracic mobility, and biceps, rotator cuff, and capsular stabilizer strengthening. At 10 weeks, patients began biceps, rotator cuff, and scapular stabilizer resistance exercises, and at 16 weeks, throwing athletes began an interval throwing program. Patients were first eligible to return to sport without limitation at 9 months.
STATISTICAL ANALYSIS
Return to play, KJOC, ASES, stability, ROM, strength, and pain scores were analyzed and compared using Fisher exact test, the Kruskal-Wallis test, and the Wilcoxon rank sum test, where appropriate. The level of statistical significance was α = 0.05.
RESULTS
Table 1. Patient Demographics | |
Athletes (N) | 74 |
Age (yr) | 30.1 (14-64) |
Knotless anchors | 32 (43.2%) |
Knotted anchors | 42 (56.8%) |
Overhead athletes | 53 (72%) |
Throwing athletes | 29 (39%) |
Follow-up (yr) | 6.5 (2-12) |
Of the 74 athletes who met inclusion criteria, 28 were female (37.8%) and 46 (62.2%) were male. The average follow-up was 6.5 years with a minimum of 2 years and a maximum of 12 years. Forty-two (56.8%) patients underwent traditional knotted suture anchor fixation and 32 (43.2%) underwent knotless anchor fixation. The average age was 30.1 +/– 13.6 years, with a range of 14 to 64 years. The majority of athletes were right hand dominant (79.9%). Fifty-three (72%) were overhead athletes and 29 (39%) were throwing athletes (Table 1). The average age in the knotted group was 33.3 years: 29 of 42 (69%) were overhead athletes and 20 (47.6%) were throwing athletes. In the knotless group, the average age was 25.8 years: 24 of 32 (75.0%) were overhead athletes and 9 (28.1%) were throwing athletes. Primary sports at the time of injury are listed in Table 2. The average number of anchors used was 3.1, with 17 patients (23.0%) requiring ≤2 anchors, 39 (52.7%) requiring 3 anchors, and 18 (24.3%) requiring ≥4 anchors for repair. The number of anchors used was determined intraoperatively by the surgeon on the basis of the size and extent of the tear. Of the entire group of 74 patients, 91.9% returned to sport, 56.8% returned to the same level, 35.1% returned at a lower capacity, and 8.1% were unable to return to sport. Knotless anchors had a slightly higher overall RTP compared with traditional anchors (93.5% vs 90.2%, P = .94), as well as a higher RTP at the same level (58.1% vs 53.7%, P = .81). These differences were, however, not statistically significant (Table 3).
Table 2. Primary Sport at Time of SLAP IIb Injury | |
Primary Sport | n (%) |
Baseball | 14 (19.7%) |
Softball | 8 (11.3%) |
Volleyball | 6 (8.5%) |
Basketball | 5 (7.0%) |
Golf | 5 (7.0%) |
Other Sport | 33 (46.5%) |
No Primary Sport | 3 (4.1%) |
Abbreviation: SLAP, superior labrum anterior to posterior.
Knotless anchors were less likely to require revision surgery than traditional anchors (9% vs 17%, P = .50), but this difference was not statistically significant (Table 3). In the knotted group, 5 patients had revision surgery for rotator cuff tears, and 2 patients had recurrent SLAP tears. In the knotless group, 2 patients had revision surgeries for a torn rotator cuff, and 1 patient had a snapping scapula. A power analysis found that it would take over 300 athletes in each group to detect a significant difference in the revision rate between knotless and traditional anchors.
Table 3. Comparison of Anchor Type in Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | KJOC | Revision Rate |
Knotless anchors (n = 32) | 93.5% | 58.1% | 86.3 + 10.5 | 66.1 + 29.6 | 9% |
Traditional anchors (n = 42) | 90.2% | 53.7% | 85.3 + 15.6 | 65.6 + 27.2 | 17% |
P-value | .94 | .81 | .79 | .61 | .50 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
Continue to: Although KJOC...
Although KJOC (66.1 vs 65.6 P = .61) and ASES (86.3 vs 85.3 P = .79) scores were also superior with knotless anchors, these differences in scores were not statistically significant (Table 3). Pain was the only variable that was linked to decreased RTP, as patients who rated higher on a pain scale of 0 to 10 were less likely to return to their sport (P < .0001). There was no correlation in outcome measures or RTP with gender, age, number of anchors, or sport type (P > .05). There was no statistically significant difference in RTP, KJOC, or ASES scores between non-overhead and overhead athletes (Table 4). Overall return to sport in throwers was 85.7% (24/28), while 39.3% (11/28) returned at the same level, 46.4% (13/28) at a lower level, and 14.3% (4/28) did not return to sport.
Table 4. Overhead vs Non-Overhead Athletes After Surgical Fixation of SLAP IIb Tears | |||||
| RTP | RTP Same Level | ASES | ASES Good-Excellent | KJOC |
Overhead | 90.6% | 52.3% | 91.7 + 14.1 | 98.1% | 64.6 + 25.7 |
Non-Overhead | 95.5% | 72.7% | 86.7 + 12.7 | 100% | 88.5 + 29.6 |
P value | 0.1 | 0.29 | 0.76 | 0.50 | 0.49 |
Abbreviations: ASES, American Shoulder and Elbow Surgeons; KJOC, Kerlan-Jobe Orthopaedic Clinic; RTP: return to play. | |||||
DISCUSSION
There was no significant difference between knotted and knotless fixation in clinical outcomes or return to sport in the repair of SLAP IIb tears; however, there was a trend toward knotless anchors requiring less revision surgery and having higher RTP, ASES, and KJOC scores than knotted fixation. Despite the inclusion of 74 patients, this study was significantly underpowered, as a power analysis calculated that over 300 athletes would be required in each group to detect a difference in the revision rate.
SLAP tears, traditionally treated with knotted suture anchors, have yielded varying results in the literature, with good to excellent results being reported in 65% to 94% of patients.13-17 The success of SLAP repairs in athletes, especially overhead athletes, remains a difficult problem, as they are common injuries, and RTP is less predictable. Studies differ with regard to the percentage of overhead athletes who are able to return to their previous level of sport, with ranges being reported from 22% to 92%.16,18,19 In a systematic review of 198 patients, Sayde and colleagues16 found that 63% of overhead athletes treated with anchor fixation, tacks, or staples were able to return to their previous level of play. Morgan and colleagues5 found a higher return to sport when compared with other studies, reporting that 83% of patients undergoing SLAP repairs using traditional suture anchors had excellent results, and 87% of the 53 overhead athletes had excellent results based on UCLA shoulder scores. Further, 37 of the 44 pitchers examined (84%) were able to return to their pre-injury levels.5 This is in contrast to Friel and colleagues20 who found that in 48 patients with type II SLAP tears treated with traditional anchors, 23% reported excellent and 56% reported good results in regards to UCLA shoulder scores. Friel and colleagues also found that 62% of all athletes and 59% of overhead athletes were able to return to their previous levels of sport, which is similar to the current study.20 The large discrepancy in RTP at the pre-injury level between this study and that of Morgan and colleagues5 may be due to the shorter minimum follow-up of 1 year as well as the inclusion of all subtypes of SLAP II tears in the latter. The current study had a minimum 2-year follow-up period, with an average of 6.5 years, and was limited to SLAP IIb tears. With a longer follow-up period, patient outcomes and RTP, particularly in overhead sports, may deteriorate; therefore, the current study likely shows a more complete and accurate result.
Knotless anchors were originally introduced as a less time consuming, lower profile, and simpler device to learn and use for arthroscopic procedures.21 Kocaoglu and colleagues22 found that in Bankart repairs, the mean time per anchor placement for knotted anchors was 380 seconds, whereas placement of knotless anchors took on average 225 seconds. A learning curve also exists for proper and efficient knot tying.7 There is also variation in knot tying between surgeons, as evidenced by a wide range in both load to failure and knot height.7 A study performed by Hanypsiak and colleagues7 found that the surgical knot was the weakest portion of the suture-anchor construct, as the knot’s load to failure was less than the pullout strength of the anchor.
There is also concern for the added height associated with traditional knotted fixation, which has been supported by case reports of knot-induced glenoid erosion after arthroscopic fixation of a SLAP tear.23 Hanypsiak and colleagues7 also found that the average knot height occupied 50% to 95% of the space between the humeral head and the acromion when the shoulder is in a neutral position, indicating that the higher profile knotted anchors may contact the undersurface of the acromion, which could affect the labral repair as well as cause rotator cuff injury. Abrasion of the rotator cuff by a prominent knot may cause pain, tearing, and disability. A recent study by Park and colleagues24 reported on 11 patients with knot-induced pain after type II SLAP repair. All complained of sharp pain, with 64% also complaining of clicking. Knot location did not seem to matter, as there was no difference in preoperative symptoms, with 5 of the 11 patients having knots on the glenoid side of the repair on repeat arthroscopy. Patients with knots on the labral side did, however, have humeral head cartilage damage. The knots appeared to be the cause of pain and clicking, as after arthroscopic knot removal, dramatic pain relief was seen, with Constant and UCLA scores significantly improving in all 11 patients. All patients also had positive preoperative compression-rotation testing, and at 6 weeks after surgical knot removal, all were negative.24
Continue to: Further, as shown by Dines and colleagues...
Further, as shown by Dines and colleagues25, knotless anchors may help to better restore the meniscoid anatomy of the superior labrum better than knotted suture anchors. With regards to fixation strength, Uggen and colleagues26, using a cadaveric model, found no difference in initial fixation strength of knotless and traditional suture anchor repair of SLAP II tears, and both restored glenohumeral rotation without over-constraining the shoulder.
Despite the shorter operative time, lower profile, and more consistent tensioning with knotless anchors, the literature is limited with regard to evaluating patient outcomes. In a study by Yung and colleagues13 14 of the 16 patients with type II SLAP tears were treated with knotless anchors, and the authors found that 31.3% of patients had an excellent UCLA score while 43.8% had a good score. This is similar to the outcomes illustrated in studies by both Friel and colleagues20 and Sayde and colleagues.16 In a more recent study, Yang and colleagues27 did find some benefit in regard to ROM with knotless fixation. Their study consisted of 21 patients who underwent surgery with traditional knotted anchor fixation and 20 who underwent knotless horizontal mattress fixation. They found an average UCLA score of 37.6 and ASES score of 91.5 in patients undergoing knotless fixation, and the knotless fixation group had 5% greater total ROM, 15.6% more internal rotation at abduction, and 11.4% more external rotation at the side as compared with patients undergoing the traditional knotted technique. When compared with the current study, this study also had a significantly shorter follow-up period of 3 years.27 In a 2017 study, Bents and colleagues28 compared 44 patients who underwent knotless and 119 who underwent knotted fixation of SLAP tears. They found no statistically significant difference between knotless and knotted fixation in the ASES score, Visual Analog Scale (VAS), ASES, or Veterans RAND 12-Item Health Survey (VR-12) at 1 year postoperatively. Their outcomes were similar to those of the current study, but as in other mentioned literature, the study by Bents and colleagues28 included multiple surgeons with different postoperative protocols, was not limited to SLAP IIb tears, and also had a shorter follow-up of 1 year. Like Kocaoglu and colleagues22, Bents and colleagues did find knotless anchors to be more efficient, as operative time was reduced by 5.3 minutes per anchor. This likely would have a significant impact on surgical cost and surgeon productivity.28
One limitation of the current study was that despite the inclusion of >70 patients, the study was still significantly underpowered. It was determined that >300 patients in each group would be required to detect a significant difference in the revision rate between the 2 anchor types. Also, due to the retrospective nature of this study, no preoperative scores were collected. The inclusion of objective clinical measurements and follow-up imaging evaluating the rotator cuff and other anatomy would also be of interest.
Although statistical significance was not achieved, there was a trend toward knotless fixation requiring less revision surgery and having higher RTP, ASES, and KJOC scores when compared with traditional knotted fixation at 6.5-year follow-up. Larger studies with longer follow-up periods are necessary to determine the effects of knotted and knotless anchors on rotator cuff tears, patient reported outcomes, and RTP. These complications have been shown in the literature, mostly in case reports, and typically develop over a longer period.23 Despite this, other advantages of knotless fixation, such as its lower profile, the ability to better provide consistent tensioning, and decreased surgical time are important to consider.
1. Andrews JR, Carson WG, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341. doi:10.1177/036354658501300508.
2. Snyder SJ, Karzel RP, Pizzo WD, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthrosc J Arthrosc Relat Surg. 1990;6(4):274-279. doi:10.1016/0749-8063(90)90056-J.
3. Ahsan ZS, Hsu JE, Gee AO. The Snyder classification of superior labrum anterior and posterior (SLAP) lesions. Clin Orthop. 2016;474(9):2075-2078. doi:10.1007/s11999-016-4826-z.
4. Erickson BJ, Jain A, Abrams GD, et al. SLAP Lesions: Trends in treatment. Arthrosc J Arthrosc Relat Surg. 2016;32(6):976-981. doi:10.1016/j.arthro.2015.11.044.
5. Morgan C, Burkhart S, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthrosc J Arthrosc Relat Surg. 1998;14(6):553-565. doi:10.1016/S0749-8063(98)70049-0.
6. Edwards SL, Lee JA, Bell J-E, et al. nonoperative treatment of superior labrum anterior posterior tears: Improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456-1461. doi:10.1177/0363546510370937.
7. Hanypsiak BT, DeLong JM, Simmons L, Lowe W, Burkhart S. Knot strength varies widely among expert arthroscopists. Am J Sports Med. 2014;42(8):1978-1984. doi:10.1177/0363546514535554.
8. Alberta FG, ElAttrache NS, Bissell S, et al. The development and validation of a functional assessment tool for the upper extremity in the overhead athlete. Am J Sports Med. 2010;38(5):903-911. doi:10.1177/0363546509355642.
9. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014. doi:10.1177/0363546513493599.
10. Michener LA, McClure PW, Sennett BJ. American shoulder and elbow surgeons standardized shoulder assessment form, patient self-report section: Reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594. doi:10.1067/mse.2002.127096.
11. Cook C, Hegedus EJ. Orthopedic Physical Examination Tests: An Evidence-Based Approach. Upper Saddle River, NJ: PearsonPrentice Hall; 2008.
12. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology part I: Pathoanatomy and biomechanics. Arthrosc J Arthrosc Relat Surg. 2003;19(4):404-420. doi:10.1053/jars.2003.50128.
13. Yung PS-H, Fong DT-P, Kong M-F, et al. Arthroscopic repair of isolated type II superior labrum anterior–posterior lesion. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1151-1157. doi:10.1007/s00167-008-0629-4.
14. Brockmeier SF, Voos JE, Williams RJ, Altchek DW, Cordasco FA, Allen AA. Outcomes After Arthroscopic Repair of Type-II SLAP Lesions: J Bone Jt Surg-Am Vol. 2009;91(7):1595-1603. doi:10.2106/JBJS.H.00205.
15. Galano GJ, Ahmad CS, Bigliani L, Levine W. Percutaneous SLAP lesion repair technique is an effective alternative to portal of Wilmington. Orthopedics. 2010;33(11). doi:10.3928/01477447-20100924-15.
16. Sayde WM, Cohen SB, Ciccotti MG, Dodson CC. Return to play after type II superior labral anterior-posterior lesion repairs in athletes: A systematic review. Clin Orthop Relat Res. 2012;470(6):1595-1600. doi:10.1007/s11999-012-2295-6.
17. Kim K-H, Bin S-I, Kim J-M. The correlation between posterior tibial slope and maximal angle of flexion after total knee arthroplasty. Knee Surg Relat Res. 2012;24(3):158-163. doi:10.5792/ksrr.2012.24.3.158.
18. Kim S-H, Ha K-I, Kim S-H, Choi H-J. Results of arthroscopic treatment of superior labral lesions. J Bone Joint Surg Am. 2002;84-A(6):981-985.
19. Pagnani MJ, Speer KP, Altchek DW, Warren RF, Dines DM. Arthroscopic fixation of superior labral lesions using a biodegradable implant: a preliminary report. Arthrosc J Arthrosc Relat Surg Off Publ Arthrosc Assoc N Am Int Arthrosc Assoc. 1995;11(2):194-198.
20. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: Prospective evaluation at a minimum two-year follow-up. J Shoulder Elbow Surg. 2010;19(6):859-867. doi:10.1016/j.jse.2010.03.004.
21. Thal R. A knotless suture anchor. Arthrosc J Arthrosc Relat Surg. 2001;17(2):213-218. doi:10.1053/jars.2001.20666.
22. Kocaoglu B, Guven O, Nalbantoglu U, Aydin N, Haklar U. No difference between knotless sutures and suture anchors in arthroscopic repair of Bankart lesions in collision athletes. Knee Surg Sports Traumatol Arthrosc. 2009;17(7):844-849. doi:10.1007/s00167-009-0811-3.
23. Rhee YG, Ha JH. Knot-induced glenoid erosion after arthroscopic fixation for unstable superior labrum anterior-posterior lesion: Case report. J Shoulder Elbow Surg. 2006;15(3):391-393. doi:10.1016/j.jse.2005.03.010.
24. Park JG, Cho NS, Kim JY, Song JH, Hong SJ, Rhee YG. Arthroscopic Knot Removal for Failed Superior Labrum Anterior-Posterior Repair Secondary to Knot-Induced Pain. Am J Sports Med. 2017;45(11):2563-2568. doi:10.1177/0363546517713662.
25. Dines JS, ElAttrache NS. Horizontal Mattress With a Knotless Anchor to Better Recreate the Normal Superior Labrum Anatomy. Arthrosc J Arthrosc Relat Surg. 2008;24(12):1422-1425. doi:10.1016/j.arthro.2008.06.012.
26. Uggen C, Wei A, Glousman RE, et al. Biomechanical Comparison of Knotless Anchor Repair Versus Simple Suture Repair for Type II SLAP Lesions. Arthrosc J Arthrosc Relat Surg. 2009;25(10):1085-1092. doi:10.1016/j.arthro.2009.03.022.
27. Yang HJ, Yoon K, Jin H, Song HS. Clinical outcome of arthroscopic SLAP repair: conventional vertical knot versus knotless horizontal mattress sutures. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):464-469. doi:10.1007/s00167-014-3449-8.
28. Bents EJ, Brady PC, Adams CR, Tokish JM, Higgins LD, Denard PJ. Patient-reported outcomes of knotted and knotless glenohumeral labral repairs are equivalent. Am J Orthop. 2017;46(6):279-283.
1. Andrews JR, Carson WG, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341. doi:10.1177/036354658501300508.
2. Snyder SJ, Karzel RP, Pizzo WD, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthrosc J Arthrosc Relat Surg. 1990;6(4):274-279. doi:10.1016/0749-8063(90)90056-J.
3. Ahsan ZS, Hsu JE, Gee AO. The Snyder classification of superior labrum anterior and posterior (SLAP) lesions. Clin Orthop. 2016;474(9):2075-2078. doi:10.1007/s11999-016-4826-z.
4. Erickson BJ, Jain A, Abrams GD, et al. SLAP Lesions: Trends in treatment. Arthrosc J Arthrosc Relat Surg. 2016;32(6):976-981. doi:10.1016/j.arthro.2015.11.044.
5. Morgan C, Burkhart S, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthrosc J Arthrosc Relat Surg. 1998;14(6):553-565. doi:10.1016/S0749-8063(98)70049-0.
6. Edwards SL, Lee JA, Bell J-E, et al. nonoperative treatment of superior labrum anterior posterior tears: Improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456-1461. doi:10.1177/0363546510370937.
7. Hanypsiak BT, DeLong JM, Simmons L, Lowe W, Burkhart S. Knot strength varies widely among expert arthroscopists. Am J Sports Med. 2014;42(8):1978-1984. doi:10.1177/0363546514535554.
8. Alberta FG, ElAttrache NS, Bissell S, et al. The development and validation of a functional assessment tool for the upper extremity in the overhead athlete. Am J Sports Med. 2010;38(5):903-911. doi:10.1177/0363546509355642.
9. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014. doi:10.1177/0363546513493599.
10. Michener LA, McClure PW, Sennett BJ. American shoulder and elbow surgeons standardized shoulder assessment form, patient self-report section: Reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11(6):587-594. doi:10.1067/mse.2002.127096.
11. Cook C, Hegedus EJ. Orthopedic Physical Examination Tests: An Evidence-Based Approach. Upper Saddle River, NJ: PearsonPrentice Hall; 2008.
12. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology part I: Pathoanatomy and biomechanics. Arthrosc J Arthrosc Relat Surg. 2003;19(4):404-420. doi:10.1053/jars.2003.50128.
13. Yung PS-H, Fong DT-P, Kong M-F, et al. Arthroscopic repair of isolated type II superior labrum anterior–posterior lesion. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1151-1157. doi:10.1007/s00167-008-0629-4.
14. Brockmeier SF, Voos JE, Williams RJ, Altchek DW, Cordasco FA, Allen AA. Outcomes After Arthroscopic Repair of Type-II SLAP Lesions: J Bone Jt Surg-Am Vol. 2009;91(7):1595-1603. doi:10.2106/JBJS.H.00205.
15. Galano GJ, Ahmad CS, Bigliani L, Levine W. Percutaneous SLAP lesion repair technique is an effective alternative to portal of Wilmington. Orthopedics. 2010;33(11). doi:10.3928/01477447-20100924-15.
16. Sayde WM, Cohen SB, Ciccotti MG, Dodson CC. Return to play after type II superior labral anterior-posterior lesion repairs in athletes: A systematic review. Clin Orthop Relat Res. 2012;470(6):1595-1600. doi:10.1007/s11999-012-2295-6.
17. Kim K-H, Bin S-I, Kim J-M. The correlation between posterior tibial slope and maximal angle of flexion after total knee arthroplasty. Knee Surg Relat Res. 2012;24(3):158-163. doi:10.5792/ksrr.2012.24.3.158.
18. Kim S-H, Ha K-I, Kim S-H, Choi H-J. Results of arthroscopic treatment of superior labral lesions. J Bone Joint Surg Am. 2002;84-A(6):981-985.
19. Pagnani MJ, Speer KP, Altchek DW, Warren RF, Dines DM. Arthroscopic fixation of superior labral lesions using a biodegradable implant: a preliminary report. Arthrosc J Arthrosc Relat Surg Off Publ Arthrosc Assoc N Am Int Arthrosc Assoc. 1995;11(2):194-198.
20. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: Prospective evaluation at a minimum two-year follow-up. J Shoulder Elbow Surg. 2010;19(6):859-867. doi:10.1016/j.jse.2010.03.004.
21. Thal R. A knotless suture anchor. Arthrosc J Arthrosc Relat Surg. 2001;17(2):213-218. doi:10.1053/jars.2001.20666.
22. Kocaoglu B, Guven O, Nalbantoglu U, Aydin N, Haklar U. No difference between knotless sutures and suture anchors in arthroscopic repair of Bankart lesions in collision athletes. Knee Surg Sports Traumatol Arthrosc. 2009;17(7):844-849. doi:10.1007/s00167-009-0811-3.
23. Rhee YG, Ha JH. Knot-induced glenoid erosion after arthroscopic fixation for unstable superior labrum anterior-posterior lesion: Case report. J Shoulder Elbow Surg. 2006;15(3):391-393. doi:10.1016/j.jse.2005.03.010.
24. Park JG, Cho NS, Kim JY, Song JH, Hong SJ, Rhee YG. Arthroscopic Knot Removal for Failed Superior Labrum Anterior-Posterior Repair Secondary to Knot-Induced Pain. Am J Sports Med. 2017;45(11):2563-2568. doi:10.1177/0363546517713662.
25. Dines JS, ElAttrache NS. Horizontal Mattress With a Knotless Anchor to Better Recreate the Normal Superior Labrum Anatomy. Arthrosc J Arthrosc Relat Surg. 2008;24(12):1422-1425. doi:10.1016/j.arthro.2008.06.012.
26. Uggen C, Wei A, Glousman RE, et al. Biomechanical Comparison of Knotless Anchor Repair Versus Simple Suture Repair for Type II SLAP Lesions. Arthrosc J Arthrosc Relat Surg. 2009;25(10):1085-1092. doi:10.1016/j.arthro.2009.03.022.
27. Yang HJ, Yoon K, Jin H, Song HS. Clinical outcome of arthroscopic SLAP repair: conventional vertical knot versus knotless horizontal mattress sutures. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):464-469. doi:10.1007/s00167-014-3449-8.
28. Bents EJ, Brady PC, Adams CR, Tokish JM, Higgins LD, Denard PJ. Patient-reported outcomes of knotted and knotless glenohumeral labral repairs are equivalent. Am J Orthop. 2017;46(6):279-283.
TAKE-HOME POINTS
- SLAP IIb tears are common injuries in overhead athletes, yet surgical outcomes are variable, with throwers commonly having difficulty with return to play at the same level.
- In this study, 92% of athletes returned to play post-operatively, yet only around 55% returned at the same level.
- In overhead athletes, overall return to play was 85.7%, yet only 39.3% returned at the same level.
- Knotless fixation required less revision surgery and had higher outcome scores and return to play when compared to knotted fixation; however, this did not reach statistical significance.
- Knotless fixation should be considered in SLAP IIb repairs given their lower profile leading to less rotator cuff irritation, the ability to better provide more consistent tensioning, and decreased surgical time.
Nutrition-Related Considerations in Soccer: A Review
Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.
Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.
Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.
ENERGY METABOLISM IN SOCCER
Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.1 Krustrup and colleagues2 found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.
ENERGY EXPENDITURE
Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.6 Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.7 In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.8
Continue to: FUELING THE SOCCER PLAYER
FUELING THE SOCCER PLAYER
Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.
- Carbohydrates: 5–10 g/kg/day
- Protein: 1.2–2.0 g/kg/day
- Fat: 0.8–1.5 g/kg/day
CARBOHYDRATE AND SOCCER PERFORMANCE
Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.9 This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.10 On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high11 or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.
Table 1. Carbohydrates | ||
Timing | Amount | Application |
| Daily | 5–7 g/kg/day | Low–moderate training load. Match amount to training session intensity. |
Pre-Training/Match | 1–4 gm/kg | Adjust to players’ tolerance, preferences and training load. |
| During Training | 0–30 g/h | Light training session |
| Recovery/After Training | Balance meal 1.0–1.2 g/kg/h, ASAP. | Light training: < 2 h Heavy training/2 sessions/day |
| Match day -1, match day, match day +1 | 7–10 g/kg/d | Adjust to players’ tolerance, preferences. |
| During/half time | 30–60 g/h | High glycemic carbohydrates |
| Recovery/after match | 1.0–1.2 g/kg/h | High glycemic carbohydrates |
However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.10 In the early 1970s, Saltin and colleagues12 showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.19 This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.
An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues10 looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.
PROTEIN AND SOCCER PERFORMANCE
Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.20 Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage21 especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.22,23
Table 2. Protein | ||
Timing | Amount | Application |
| Daily | 1.2–2.0 g/kg | High quality sources; chicken, lean meats, fish, seafood, eggs, dairy, beans, soy |
Pre-training/match; | 20–40 g or 0.25–0.40 g/kg | Meal/snack |
| During training/match | None needed | If training session <3 h |
| Recovery/after training Night-time feeding | 20–40 g | <30–60 min, whey, casein/whey, pea, soy protein Casein (slow-absorbing protein), strength training days |
Continue to: FAT AND SOCCER PERFORMANCE
FAT AND SOCCER PERFORMANCE
Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.
Table 3. Fat | ||
Timing | Amount | Application |
Daily | 0.8–1.5 g/kg | Include well balanced meals, primarily polyunsaturated and monounsaturated fats. |
Pre-Training/Match; | ~10–30 g/meal | Limit amount. Avoid digestion and gastrointestinal issues. |
During Training/Match | None needed | Risk of gastrointestinal intolerances. |
Recovery/After Training | ~10–30 g | Include well-balanced meals, primarily polyunsaturated and monounsaturated fats. |
The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.23 Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.
In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.25 More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.
MICRONUTRIENTS, VITAMINS, AND MINERALS
Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.
IRON
Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.28 Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.29,30
Continue to: Landahl and colleagues...
Landahl and colleagues31 found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.
VITAMIN D
Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.34 In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.34,36-38
Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.32 Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.33
CALCIUM
Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.39 Calcium and vitamin D are also important for muscle contraction.
Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.
Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS
FLUID REQUIREMENTS FOR SOCCER PLAYERS
Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.
Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.40, 41 Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.41 Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.
Table 4. Sweat Rate Calculation Steps | ||
|
Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.42 Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.39 Soccer players will lose ~1.5 to 4.5 liters during match play.43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.
Table 5. Performance Outcomes at Various Dehydration Levels | ||
|
ELECTROLYTES
Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.42, 51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.
REHYDRATION AFTER TRAINING OR COMPETITION
Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.52
Table 6. Hydration | ||
Timing | Amount | Application |
Daily | 3.7 L adult males | Monitor urine color. |
Pre-training/match; | 16 oz or 5–7 mL/kg | Monitor urine production and color |
During training/match | 13–28 oz/h (400- | Every 15–20 min. *Dependent on sweat rate. |
Recovery/after training | 22–24 oz/1 lb body weight lost | Water + food (carbohydrates/electrolytes) |
- Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports Sci. 2003;21:519-528.
- Krustrup P, Mohr M, Steensberg A, Bencke J, Kjaer M, Bangsbo J. Muscle and blood metabolites during a soccer game: implications for sprint performance. Med Sci Sports Exerc. 2006;38:1165-1174.
- Di Salvo V, Gregson W, Atkinson G, Tordoff P, Drust B. Analysis of high intensity activity in Premier League soccer. Int J Sports Med. 2009;30:205-212.
- Di Salvo V, Baron R, Tschan H, Calderon Montero FJ, Bachl N, Pigozzi F. Performance characteristics according to playing position in elite soccer. Int J Sports Med. 2007;28:222-227.
- Reilly T, Thomas V. Estimated daily energy expenditures of professional association footballers. Ergonomics. 1979;22:541-548.
- Osgnach C, Poser S, Bernardini R, Rinaldo R, di Prampero P.E. Energy cost and metabolic power in elite soccer: A new match analysis approach. Med Sci Sports Exerc. 2010;42:170-178.
- Anderson L, Orme P, Naughton RJ, Close, GL, Milsom J, Rydings D, et al. Energy intake and expenditure of professional soccer players of the English Premier League: evidence of carbohydrate periodization. Int J Sport Nutr Exerc Metab. 2017;1-25.
- Mara JK, Thompson KG, Pumpa KL. Assessing the energy expenditure of elite female soccer layers: a preliminary study. J Strength Cond Res. 2015;2780-2786.
- Bartlett JD, Hawley JA, Morton JP. Eur J Sport Sci. 2015;15(1):1, 3-12.
- Anderson L, Orme P, Di Michele R, Close GL, Morgans R, Drust B, Morton JP. Quantification of training load during one-, two- and three-game week schedules in professional soccer players from the English Premier League: implications for carbohydrate periodisation. J Sports Sci. 2016;34;1250-1259.
- Hawley JA, Morton JP. Ramping up the signal: promoting endurance training adaptation in skeletal muscle by nutritional manipulation. Clin Exp Pharmacol Physiol. 2014;41:608-613.
- Saltin B. Metabolic fundamentals in exercise. 1973;:137-146.
- Balsom PD, Wood K, Olsson P, Ekblom B. Carbohydrate intake and multiple sprint sports: With special reference to football (soccer). Int J Sports Med. 1999;20:48-52.
- Neufer PD, Costill DL, Flynn MG, Kirwan JP, Mitchell JB, Houmard J. Improvements in exercise performance: Effects of carbohydrate feedings and diet. J Appl Physiol. 1987;62:983-988.
- Sherman WM, Brodowicz G, Wright DA, Allen WK, Simonsen J, Dernbach A. Effects of 4 h preexercise carbohydrate feedings on cycling performance. Med Sci Sports Exerc. 1989;21:598-604.
- Baker LB, Rollo I, Stein KW, Jeukendrup AE. Acute effects of carbohydrate supplementation on intermittent sports performance. Nutrients. 2015;7:5733-5763.
- Goedecke JH, White NJ, Chicktay W, Mahomed H, Durandt J, Lambert MI. The effect of carbohydrate ingestion on performance during a simulated soccer match. Nutrients. 2013;5:5193-5204.
- Nicholas CW, Williams C, Lakomy HK, Phillips G, Nowitz A. Influence of ingesting a carbohydrate-electrolyte solution on endurance capacity during intermittent, high-intensity shuttle running. J Sports Sci. 1995;13:283-290.
- Burke LM, van Loon LJC, Hawley JA. Post-exercise muscle glycogen resynthesis in humans. J Appl Physiol. 2016;122:1055-1067.
- Rodriquez NR, DiMarco NM, Langley S. Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and athletic performance. J Am Diet Assoc. 2009;109(3):509-527.
- Romagnoli M, Sanchis-Gomar F, Alis R, Risso-Ballester J, Bosio A, Graziani RL, Rampinini E. Changes in muscle damage, inflammation, and fatigue-related parameters in young elite soccer players after a match. J. Sports Med Phys Fit. 2016;56:1198-1205.
- Res PT, Groen B, Pennings B, Beelen M, Wallis GA, Gijsen AP, et al.Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc. 2012;44:1560-1569.
- Snijders T, Res PT, Smeets JSJ, Van Vliet S, Van Kranenburg J, Maase K, et al.Protein ingestion before sleep increases muscle mass and strength gains during prolonged resistance-type exercise training in healthy young men. J Nutr. 2015;145:1178-1184.
- Simopoulos AP. Omega-3 fatty acids and athletics. Curr Sports Med Rep. 2007;6230-236.
- Peoples GE, McLennan PL, Howe P, Groeller H. Fish oil reduces apparent myocardial oxygen consumption in trained cyclists but does not change time to fatigue. Presented at the Fourth International Conference on Nutrition and Fitness; May 25-29, 2000; Ancient Olympia, Greece.
- Burke LM, Collier GR, Beasley S.K, Davis PG, Fricker PA, Heeley P, et al. Effect of coingestion of fat and protein with carbohydrate feedings on muscle glycogen storage. J Appl Physiol. 1995;78:2187-2192.
- Roy BD, Tarnopolsky MA. Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol. 1998;84:890-896.
- Reinke S, Taylor W.R, Duda GN, von Haehling S, Reinke P, Volk H-D et al. Absolute and functional iron deficiency in professional athletes during training and recovery. Int J Cardiol. 2012;156:186-191.
- Escanero JF, Villanueva J, Rojo A, Herrera A, del Diego C, Guerra M. Iron stores in professional athletes throughout the sports season. Physiol Behav. 1997;62:811-814.
- Heisterberg MF, Fahrenkrug J, Krustrup P, Storskov A, Kjær, M, Andersen JL. Extensive monitoring
- Landahl G, Adolfsson P, Borjesson M, Mannheimer C, Rodjer S. Iron deficiency and anemia: a common problem in female elite soccer players. Int J Sport Nutr Exerc Metab. 2005;15(6):689-694.
- Sinha A, Hollingsworth K, Ball S, Cheetham T. Improving the vitamin D status of vitamin D deficient adults is associated with improved mitochondrial oxidative function in skeletal muscle. Endocrine Abstracts, 2013;31.OC1.6
- Shuler FD, Wingate MK, Moore GH, Giangarra C. Sports health benefits of vitamin D. Sports Health. 2012;4:496-501.
- Hamilton B, Whiteley R, Farooq A, Chalabi H. Vitamin D concentration in 342 professional football players and association with lower limb isokinetic function. J Sci. Med Sport. 2014;17:139-143.
- Ksiażek A, Zagrodna A, Dziubek W, Pietraszewski B, Ochmann B, Słowińska-Lisowska M,25(OH)D3 levels relative to muscle strength and maximum oxygen uptake in athletes. J Hum Kinet. 2016;50:71-77.
- Kopeć A, Solarz K, Majda F, Słowińska-Lisowska M, Medraś M. An evaluation of the levels of vitamin D and bone turnover markers after the summer and winter periods in Polish professional soccer players. J Hum Kinet. 2013;38:135-140.
- Vander Slagmolen G, van Hellemondt FJ, Wielders JPM. Do professional soccer players have a vitamin D status supporting optimal performance in winter time? J Sports Med Doping Stud. 2014,4:2.
- Morton JP, Iqbal Z, Drust B, Burgess D, Close GL, Brukner PD. Seasonal variation in vitamin D status in professional soccer players of the English Premier League. Appl Physiol Nutr Metab. 2012;37:798-802.
- Lozano-Berges G, Matute-Llorente A, Gonzalez-Aguero A, Gomez-Bruton A, Gomez-Cabelloa A, Vincente-Rodriguez G, Casajus JA. Soccer helps build strong bones during growth: a systematic review and meta-analysis. Eur J Pediatr. 2018;177(3):295-310.
- Burke LM. Fluid balance during team sports. J Sports Sci. 1997;15:287-295.
- Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004;14:333-346.
- Brendon P, McDermott, P, Anderson SA, Armstrong LE, Casa DJ, Cheuvront SN, et al. National Athletic Trainers’ Association Position Statement: Fluid Replacement for the Physically Active. J Athl Train. 2017;52(9):877-895.
- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26: 90-95.
- Maughan RJ, Watson P, Evans GH, Broad N, Shirreffs SM. Water balance and salt losses in competitive football. Int J Sport Nutr Exerc Metab. 2007;17:583-594.
- Aragón-Vargas LF, Moncada-Jiménez J, Hernández-Elizondo J, Barrenechea A,Monge-Alvarado M. Evaluation of pre-game hydration status, heat stress, and fluid balance during professional soccer competition in the heat. Eur J Sport Sci. 2009;9:269-276.
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- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26:90-95.
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Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.
Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.
Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.
ENERGY METABOLISM IN SOCCER
Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.1 Krustrup and colleagues2 found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.
ENERGY EXPENDITURE
Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.6 Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.7 In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.8
Continue to: FUELING THE SOCCER PLAYER
FUELING THE SOCCER PLAYER
Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.
- Carbohydrates: 5–10 g/kg/day
- Protein: 1.2–2.0 g/kg/day
- Fat: 0.8–1.5 g/kg/day
CARBOHYDRATE AND SOCCER PERFORMANCE
Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.9 This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.10 On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high11 or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.
Table 1. Carbohydrates | ||
Timing | Amount | Application |
| Daily | 5–7 g/kg/day | Low–moderate training load. Match amount to training session intensity. |
Pre-Training/Match | 1–4 gm/kg | Adjust to players’ tolerance, preferences and training load. |
| During Training | 0–30 g/h | Light training session |
| Recovery/After Training | Balance meal 1.0–1.2 g/kg/h, ASAP. | Light training: < 2 h Heavy training/2 sessions/day |
| Match day -1, match day, match day +1 | 7–10 g/kg/d | Adjust to players’ tolerance, preferences. |
| During/half time | 30–60 g/h | High glycemic carbohydrates |
| Recovery/after match | 1.0–1.2 g/kg/h | High glycemic carbohydrates |
However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.10 In the early 1970s, Saltin and colleagues12 showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.19 This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.
An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues10 looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.
PROTEIN AND SOCCER PERFORMANCE
Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.20 Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage21 especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.22,23
Table 2. Protein | ||
Timing | Amount | Application |
| Daily | 1.2–2.0 g/kg | High quality sources; chicken, lean meats, fish, seafood, eggs, dairy, beans, soy |
Pre-training/match; | 20–40 g or 0.25–0.40 g/kg | Meal/snack |
| During training/match | None needed | If training session <3 h |
| Recovery/after training Night-time feeding | 20–40 g | <30–60 min, whey, casein/whey, pea, soy protein Casein (slow-absorbing protein), strength training days |
Continue to: FAT AND SOCCER PERFORMANCE
FAT AND SOCCER PERFORMANCE
Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.
Table 3. Fat | ||
Timing | Amount | Application |
Daily | 0.8–1.5 g/kg | Include well balanced meals, primarily polyunsaturated and monounsaturated fats. |
Pre-Training/Match; | ~10–30 g/meal | Limit amount. Avoid digestion and gastrointestinal issues. |
During Training/Match | None needed | Risk of gastrointestinal intolerances. |
Recovery/After Training | ~10–30 g | Include well-balanced meals, primarily polyunsaturated and monounsaturated fats. |
The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.23 Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.
In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.25 More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.
MICRONUTRIENTS, VITAMINS, AND MINERALS
Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.
IRON
Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.28 Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.29,30
Continue to: Landahl and colleagues...
Landahl and colleagues31 found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.
VITAMIN D
Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.34 In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.34,36-38
Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.32 Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.33
CALCIUM
Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.39 Calcium and vitamin D are also important for muscle contraction.
Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.
Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS
FLUID REQUIREMENTS FOR SOCCER PLAYERS
Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.
Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.40, 41 Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.41 Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.
Table 4. Sweat Rate Calculation Steps | ||
|
Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.42 Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.39 Soccer players will lose ~1.5 to 4.5 liters during match play.43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.
Table 5. Performance Outcomes at Various Dehydration Levels | ||
|
ELECTROLYTES
Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.42, 51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.
REHYDRATION AFTER TRAINING OR COMPETITION
Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.52
Table 6. Hydration | ||
Timing | Amount | Application |
Daily | 3.7 L adult males | Monitor urine color. |
Pre-training/match; | 16 oz or 5–7 mL/kg | Monitor urine production and color |
During training/match | 13–28 oz/h (400- | Every 15–20 min. *Dependent on sweat rate. |
Recovery/after training | 22–24 oz/1 lb body weight lost | Water + food (carbohydrates/electrolytes) |
Soccer is the world’s most popular sport. As the sport has grown, so have the physical demands and the search for ways to edge out the competition with the use of sports science and nutrition. The demands, which include intense training, ≥90 minutes matches, congested fixtures, and travel, lead to increased energy and nutrient requirements, stress on the body, and risk of impaired sleep cycles. Identifying key areas to enhance a player’s performance is an ongoing effort because of individual differences. Moreover, new information is being discovered via research, and advancing technology to measure performance is always evolving. This article focuses on the core nutrition principles known to lay the foundation for a better soccer player. These principles are obvious for some; however, nutrition and hydration are often undervalued, leaving the individual player with the responsibility to eat right. This review addresses the most applicable nutrition-related recommendations for soccer players.
Technical, tactical, and physical skills are key factors in a soccer player’s performance. However, energy demands of matches and training sessions require adequate fuel and hydration to maximize those key factors. Athletes may need to manage carbohydrates, protein, and fat separately to achieve optimal body size and body composition, and to maximize performance.
Nutrition plays a vital role in keeping the player healthy, reducing risk of injuries, speeding up recovery, and enhancing training adaptations. Research has shown what we eat and when we eat can significantly impact skeletal muscle adaptation, inflammation, immune response, and energy metabolism. These are all essential nutrition considerations for soccer players.
ENERGY METABOLISM IN SOCCER
Understanding energy demands will help determine energy requirements: type, amount, and timing of macronutrients and micronutrients. Soccer utilizes both aerobic and anaerobic energy systems. Soccer is an intermittent team-based sport; thus, it contains various high-intensity movements, such as sprinting, jumping, dribbling, and frequent changing of direction performed in between numerous low-intensity slow movements. The high intense movements collectively account for about 30% of match play, whereas 70% is walking, jogging, and standing. Although sprinting and jumping are not a large part of the 90 minutes of match play, they have a huge impact on the outcome of the match. Distance covered in the last 15 minutes of match play decreases by 14% to 45% compared with the first 15 minutes of play.1 Krustrup and colleagues2 found muscles in the quadriceps to be empty or nearly empty of glycogen (stored carbohydrates) after match play. This phenomenon can help explain a significant decrease in sprinting, jumping, and intermittent movements toward the end of a match—energy demands that rely on glycogen as the primary fuel source. Being well-fueled and hydrated and having the ability to delay fatigue can place a team at a performance advantage.
ENERGY EXPENDITURE
Beyond training load or match intensity, a soccer player’s body composition, gender, age, and position can affect energy needs. Position differences in elite soccer players show that the greatest total distance covered is by central midfielders and wide midfielders (~12 km –13 km), whereas central defenders cover the least area of the field players (≤~10 km).3,4 The environment can also play a role in energy expenditure. To further understand calorie needs, total daily energy expenditure in soccer players has been measured using doubly labeled water and estimated using heart rate, global positioning system, video match analysis, and activity records.5,6 One study estimated that energy expended during a training day for elite male soccer players is between 3442 kcal and 3824 kcal.6 Another study using doubly labeled water concluded that mean energy expenditure of elite male soccer players is 3566 kcal over a 7-day period, which included 5 training days and 2 matches.7 In terms of energy expenditure for elite female soccer players, the mean values for match day, training days, and rest days were 2914, 2783, and 2213 calories, respectively.8
Continue to: FUELING THE SOCCER PLAYER
FUELING THE SOCCER PLAYER
Depending on the match fixture, proper fueling can be a challenge due to the number of matches, travel time, and limited recovery time. Macronutrients will provide the mainstay of fuel for a player, specifically carbohydrates and fats. Carbohydrates are the preferred source of fuel for the majority of the calories consumed. Using body weight (kg) is a more current and accurate method of recommending the amount of each macronutrient an individual player should eat as compared to using a percentage of total daily calories.
- Carbohydrates: 5–10 g/kg/day
- Protein: 1.2–2.0 g/kg/day
- Fat: 0.8–1.5 g/kg/day
CARBOHYDRATE AND SOCCER PERFORMANCE
Carbohydrates are a limited supply of fuel compared with fat stores. They are an important fuel source for soccer players, as muscle glycogen is vital to performance during high intense training and match play (Table 1). Yet current research shows that a high carbohydrate intake is not required to be followed every day due to varied energy demands.9 This newer strategy is referred to as “training low,” allowing the athlete to train at a low-moderate intensity in a low glycogen state. The glycogen status of the muscle can alter the training adaptations through cellular changes in the mitochondria. Therefore, carbohydrate needs should reflect the work required or demand for optimal performance. However, on high-training load days or 24 hours pre-match, carbohydrate intake should be increased to maximize muscle glycogen stores. Soccer players need to consume up to 8-10 g/kg body weight during the 24 hours before a match.10 On low or rest days, carbohydrate intake should be reduced to reflect the decreased training load. For example, recent research has demonstrated potential training adaptations when muscle glycogen stores are not consistently high11 or intentionally kept low depending on the training load. Adjusting carbohydrate intake to the physical demands of an athlete is a strategy called nutrition periodization.
Table 1. Carbohydrates | ||
Timing | Amount | Application |
| Daily | 5–7 g/kg/day | Low–moderate training load. Match amount to training session intensity. |
Pre-Training/Match | 1–4 gm/kg | Adjust to players’ tolerance, preferences and training load. |
| During Training | 0–30 g/h | Light training session |
| Recovery/After Training | Balance meal 1.0–1.2 g/kg/h, ASAP. | Light training: < 2 h Heavy training/2 sessions/day |
| Match day -1, match day, match day +1 | 7–10 g/kg/d | Adjust to players’ tolerance, preferences. |
| During/half time | 30–60 g/h | High glycemic carbohydrates |
| Recovery/after match | 1.0–1.2 g/kg/h | High glycemic carbohydrates |
However, if glycogen stores are not well supplied before a match >90 minutes, then the muscles and the brain will become fatigued and lead to poor performance. Glycogen depletion contributes to fatigue toward the end of a match.10 In the early 1970s, Saltin and colleagues12 showed that players with high muscle glycogen stores (~400 mmol/kg dry wt) achieve higher movement intensities and cover more total distance than those players who start the match with low glycogen stores (~200 mmol/kg dry wt). Another study examined pre-match diets of male soccer players (65% vs 30% daily carbohydrate intake) to determine the effect on performance outcomes and glycogen concentrations. Results showed high-muscle glycogen concentrations in the 65% carbohydrate diet and a significantly higher amount of intense exercise bouts. More acutely, studies have shown a meal containing 200 to 300 grams of carbohydrates 2 to 4 hours before exercise prolongs endurance.13-15 Ideally, consuming fast-digesting carbohydrate sources during or at half time will help maintain blood glucose concentrations and spare muscle glycogen reserves. The majority of literature shows a 6% to 8% solution of combined fast-digesting carbohydrates (ie, glucose, fructose, sucrose, or maltodextrin) at a rate of 30 to 60 g/h enhances at least 1 aspect of performance in soccer.16-18 These performance benefits include increased running time, improved time to fatigue, and enhanced technical skills. Regarding recovery, soccer players should begin consuming carbohydrate-rich foods and beverages immediately after exhaustive training or a match to optimize glycogen reloading. Ingesting post-exercise carbohydrates stimulates muscle and liver glycogen synthesis up to tenfold compared with post-intake of no carbohydrates.19 This recovery period becomes vital when there are <8 hours between training sessions or another match, such as in youth tournaments. The form of carbohydrate, solid or liquid, can be based on preference and tolerance, as long as the source provides a large glycemic and insulin response.
An easy way to adjust daily carbohydrate intake is to schedule carbohydrate-rich foods at meals or snacks around important training sessions or before/during/after on match day. Anderson and colleagues10 looked at training loads for 1, 2, and 3 matches per week, recommending high carbohydrate intake match day minus 1, on match day, and match day plus 1 for 1 and 2 matches per week and lower carbohydrate intake on the other days. During a 3-match week, lowering carbohydrates any day of that week is not recommended. More research is needed to determine the best strategy for performance regarding carbohydrate periodization in soccer.
PROTEIN AND SOCCER PERFORMANCE
Protein is important to soccer players for muscle tissue repair, strength, bone health, and the immune system (Table 2). The American College of Sports Medicine, the Academy of Nutrition and Dietetics, and the Dietitians of Canada recommend 1.2 to 2.0 g/kg/day.20 Most soccer players meet the daily protein requirements; however, the key to optimizing the total daily amount is focusing on the source/amino acid profile, timing, and amount per feeding. Consuming divided doses of protein (20 g to 40 g) every 3 to 4 hours gives the body a continuous flow of amino acids to support muscle synthesis and recovery. In terms of body size, the recommendation is 0.25 to 0.4 g/kg every 3 to 4 hours, which includes pre-training/match and post-training/match. Protein/amino acids consumed around strength training and high-intensity sessions can promote muscle adaptations, minimize tissue breakdown, and speed recovery. Soccer matches lead to significant muscle damage21 especially at 2 sessions/day or multiple matches in a week. Protein is not a priority during training or matches, as its role is not to provide energy, and the primary goal during soccer activities is energy production. Research supports an intake of 30 to 40 g of casein, which is a slow digesting protein, at night before bed when a strength-training session has been performed that day.22,23
Table 2. Protein | ||
Timing | Amount | Application |
| Daily | 1.2–2.0 g/kg | High quality sources; chicken, lean meats, fish, seafood, eggs, dairy, beans, soy |
Pre-training/match; | 20–40 g or 0.25–0.40 g/kg | Meal/snack |
| During training/match | None needed | If training session <3 h |
| Recovery/after training Night-time feeding | 20–40 g | <30–60 min, whey, casein/whey, pea, soy protein Casein (slow-absorbing protein), strength training days |
Continue to: FAT AND SOCCER PERFORMANCE
FAT AND SOCCER PERFORMANCE
Fat is the primary source of energy at rest and at low-training intensities, such as walking or jogging for soccer players (Table 3). Besides providing slow, long-lasting energy, fat helps absorb vitamins A, D, E, and K; produce hormones; protect organs; and support the cell membrane structure. The dietary recommendations of total fat intake for athletes are similar to or slightly greater than those recommended for non-athletes. The total amount required depends on the training demands and the players’ goals. The recommended amount of dietary fat is between 20% and 35% of total daily energy intake.
Table 3. Fat | ||
Timing | Amount | Application |
Daily | 0.8–1.5 g/kg | Include well balanced meals, primarily polyunsaturated and monounsaturated fats. |
Pre-Training/Match; | ~10–30 g/meal | Limit amount. Avoid digestion and gastrointestinal issues. |
During Training/Match | None needed | Risk of gastrointestinal intolerances. |
Recovery/After Training | ~10–30 g | Include well-balanced meals, primarily polyunsaturated and monounsaturated fats. |
The key to gaining performance benefits from dietary fat depends on the type of fat selected. Some fats in excess, such as omega-6 fatty acids and saturated fats, may promote inflammation, hinder recovery, and affect brain health. Other types can help reduce inflammation, enhance muscle recovery, and improve brain health. These types include polyunsaturated omega-3 fatty acids, which are essential for the health of the athlete, allowing for a balanced fatty acid profile.23 Specific omega-3 fatty acids (EPA and DHA) have shown an improvement in the function of the mitochondria, enhancing energy cell metabolism. They also have potential to be highly anti-inflammatory, benefit rehabilitation during soft-tissue injury, and help decrease secondary damage from a concussion.
In addition, research shows that omega-3 may enhance the energy production of the mitochondria, resulting in less oxidative damage to the muscle cell.25 More research is needed on the effects of performance on soccer players. Given the slow digestion and absorption of fats, fat intake must be limited leading up to or during training sessions or matches, which may risk gastrointestinal issues and displacement of carbohydrates. Low to moderate monounsaturated and polyunsaturated fats in a recovery meal have not been shown to inhibit muscle glycogen reloading or muscle protein synthesis.26,27 In regard to fat intake post-match, fat is not a key nutrient of concern for muscle recovery, as it can be included in the next balanced meal.
MICRONUTRIENTS, VITAMINS, AND MINERALS
Exercise stresses many of the metabolic pathways where vitamins and minerals are required. High-level training demands may also increase the turnover rate of vitamins and minerals. As a result, greater dietary intakes of vitamins and minerals may be warranted. Soccer players at the greatest risk for poor vitamin and mineral levels are those who skip meals, who eliminate ≥1 of the food groups from their diet (such as vegans), or who consume unbalanced and highly processed foods. In soccer players, the micronutrients of concern include iron and vitamin D. In young female soccer players, calcium intake must be assessed along with adequate energy intake for optimal bone density. Vegetarians, vegans, and/or athletes who do not consume meat, eggs, and/or dairy in their diet are at risk for vitamin B12 deficiency. The key to obtaining all the vitamins and minerals an athlete will need is to eat a wide variety of nutrient-dense foods.
IRON
Iron deficiency, with or without anemia, may impair muscle function and limit exercise capacity. Adequate iron intake in athletes with iron deficiencies and/or anemia can improve exercise capacity. Iron depletion is 1 of the most common nutrient deficiencies observed among endurance athletes. Foot strike hemolysis can destroy red blood cells during activities such as running. Research has shown that 30% of professional male soccer players have ferritin levels <30 mcg/L at the end of a soccer season.28 Thus, fatigue and poor recovery time place soccer players at risk of an iron imbalance.29,30
Continue to: Landahl and colleagues...
Landahl and colleagues31 found that iron deficiency and iron deficiency anemia are common in female soccer players at the elite level. In their study of 28 female national soccer players, 57% had iron deficiency and 29% presented with iron deficiency anemia 6 months before the FIFA Women's World Cup. Testing hemoglobin alone is insufficient to detect relative anemia. Regular monitoring of hemoglobin and ferritin concentrations may be necessary to determine appropriate iron needs.
VITAMIN D
Vitamin D is required for optimal bone health, as it helps regulate calcium and phosphorus. Further research shows a link between vitamin D and non–bone-related functions, such as muscle health, immune support, and anti-inflammatory roles, which may be linked to performance. Soccer players with low levels of vitamin D (<30 ng/mL) may be more at risk for musculoskeletal injuries and stress fractures.34 In other sports, vitamin D may enhance muscle strength; however, no association between vitamin D and muscle strength has been found in soccer players.34,35 The geographic location of an athlete seems to be irrelevant to serum levels, as insufficient levels can be found at various latitudes.34,36-38
Evidence has shown that vitamin D may improve athletic performance in vitamin D-depleted athletes, thereby improving vertical jumps, lowering risks of muscle injury/strains and stress fractures, and reducing risk of colds/flu. In 2013, researchers showed for the first time a link between vitamin D and muscle aerobic metabolism by studying the energy efficiency of the mitochondria.32 Athletes with low vitamin D levels increased their ATP production within the muscle with vitamin D supplementation over 10 weeks to 12 weeks.33
CALCIUM
Soccer players present with stronger and denser bones than non-athletes due to running and jumping in their sport. Weight-bearing sites such as lumbar spine, hip, femoral neck, trochanter, intertrochanteric region, and both legs are sensitive to the impact of soccer movements.39 Calcium and vitamin D are also important for muscle contraction.
Given the variation in genetics, sports, and gender, optimal performance requires a healthy eating plan tailored to the individual athlete. A healthy eating plan allows an athlete to train longer and harder, delay the onset of fatigue, and speed recovery. Nutrition supports optimal performance through real food, proper hydration, nutrient timing, and supplementation.
Continue to: FLUID REQUIREMENTS FOR SOCCER PLAYERS
FLUID REQUIREMENTS FOR SOCCER PLAYERS
Many athletes overlook the importance of hydration on performance, either assuming they are hydrated or they miscalculate fluid and electrolyte needs to actual sweat losses. Numerous factors play a part in optimal hydration such as sweat rate, environment, training intensity, duration, body size, and body composition. Soccer players have fewer breaks to consume fluids during a match compared with basketball, baseball, or American football players. These breaks include a 15-minute half between coming off the pitch to the locker room and back, as well as time spent with coaches reviewing strategies; this short window of time must be maximized to rehydrate. Fluids with a carbohydrate concentration of 4% to 8% at 5 to 10 ounces and breaks every 15 to 20 minutes are optimal to maximize uptake while avoiding gastric intolerance.
Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses.40, 41 Maughan and colleagues measured high levels of urine osmolality in some soccer players, thereby indicating that the players started their training session dehydrated.41 Soccer players must begin training or a match well hydrated due to the limited opportunities after kick-off. The athlete should drink at least 4 hours prior to exercise; if no urine is produced or urine is dark in color, then the athlete should drink again 2 hours prior.
Table 4. Sweat Rate Calculation Steps | ||
|
Changes in body mass, urine color, and thirst offer clues to the need for rehydration. Advanced hydration measurement includes testing urine specific gravity (USG) values. For example, testing pre-training or pre-match can be conducted to determine hydration status and trending changes from day to day. A USG value >1.020 is considered dehydrated in accordance with the NATA position statement.42 Calculating a sweat rate is a practical approach to determining individual hydration needs (see Table 4). Sweat rates will vary between soccer players based on their position and intensity of play, along with total match time.39 Soccer players will lose ~1.5 to 4.5 liters during match play.43-46 In general, athletes, including soccer players, should limit body weight loss to ≤2% to 3% to maintain performance. Studies have shown that >2% body mass loss can hinder soccer-specific performance, such as dribbling skills and intermittent high intensity sprinting.49-51) Table 5 outlines the detrimental effects dehydration has on performance. Urine-specific gravity values between 1.021 and 1.030 may reflect 3% to 5% change in body weight.
Table 5. Performance Outcomes at Various Dehydration Levels | ||
|
ELECTROLYTES
Sodium is the primary electrolyte lost in sweat. Other electrolytes (potassium, magnesium, and calcium) are lost at much lower levels and typically replaced through diet. Soccer players can lose large amounts of sodium; between 700 and 1500 mg of sodium/L of sweat has been reported in several studies.42-44 Studies of professional male soccer players have shown potassium losses in the range of 165 mg/L to 234 mg/L.42, 51,52 Sodium in a sports drink or in food aids with water uptake from the intestines and enhances the thirst mechanism in the brain, resulting in additional fluid being retained in the body.
REHYDRATION AFTER TRAINING OR COMPETITION
Within 2 hours after training or competition, the rehydration strategy should provide water to restore body fluid status, carbohydrates to replenish glycogen (fuel) stores, and electrolytes to speed rehydration (Table 6). The volume of fluids and type of fluids over the next 24 hours dictate the hydration status prior to the next day’s training session. It is a continuous cycle. Over time, an athlete increases the risk of being in a chronic dehydrated state, resulting in lack of motivation, risk of injury, and illness, fatigue, and poor performance. The current recommendation is to drink ~50% more in volume than the amount of weight lost, such as 22 to 24 ounces/pound lost.52
Table 6. Hydration | ||
Timing | Amount | Application |
Daily | 3.7 L adult males | Monitor urine color. |
Pre-training/match; | 16 oz or 5–7 mL/kg | Monitor urine production and color |
During training/match | 13–28 oz/h (400- | Every 15–20 min. *Dependent on sweat rate. |
Recovery/after training | 22–24 oz/1 lb body weight lost | Water + food (carbohydrates/electrolytes) |
- Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports Sci. 2003;21:519-528.
- Krustrup P, Mohr M, Steensberg A, Bencke J, Kjaer M, Bangsbo J. Muscle and blood metabolites during a soccer game: implications for sprint performance. Med Sci Sports Exerc. 2006;38:1165-1174.
- Di Salvo V, Gregson W, Atkinson G, Tordoff P, Drust B. Analysis of high intensity activity in Premier League soccer. Int J Sports Med. 2009;30:205-212.
- Di Salvo V, Baron R, Tschan H, Calderon Montero FJ, Bachl N, Pigozzi F. Performance characteristics according to playing position in elite soccer. Int J Sports Med. 2007;28:222-227.
- Reilly T, Thomas V. Estimated daily energy expenditures of professional association footballers. Ergonomics. 1979;22:541-548.
- Osgnach C, Poser S, Bernardini R, Rinaldo R, di Prampero P.E. Energy cost and metabolic power in elite soccer: A new match analysis approach. Med Sci Sports Exerc. 2010;42:170-178.
- Anderson L, Orme P, Naughton RJ, Close, GL, Milsom J, Rydings D, et al. Energy intake and expenditure of professional soccer players of the English Premier League: evidence of carbohydrate periodization. Int J Sport Nutr Exerc Metab. 2017;1-25.
- Mara JK, Thompson KG, Pumpa KL. Assessing the energy expenditure of elite female soccer layers: a preliminary study. J Strength Cond Res. 2015;2780-2786.
- Bartlett JD, Hawley JA, Morton JP. Eur J Sport Sci. 2015;15(1):1, 3-12.
- Anderson L, Orme P, Di Michele R, Close GL, Morgans R, Drust B, Morton JP. Quantification of training load during one-, two- and three-game week schedules in professional soccer players from the English Premier League: implications for carbohydrate periodisation. J Sports Sci. 2016;34;1250-1259.
- Hawley JA, Morton JP. Ramping up the signal: promoting endurance training adaptation in skeletal muscle by nutritional manipulation. Clin Exp Pharmacol Physiol. 2014;41:608-613.
- Saltin B. Metabolic fundamentals in exercise. 1973;:137-146.
- Balsom PD, Wood K, Olsson P, Ekblom B. Carbohydrate intake and multiple sprint sports: With special reference to football (soccer). Int J Sports Med. 1999;20:48-52.
- Neufer PD, Costill DL, Flynn MG, Kirwan JP, Mitchell JB, Houmard J. Improvements in exercise performance: Effects of carbohydrate feedings and diet. J Appl Physiol. 1987;62:983-988.
- Sherman WM, Brodowicz G, Wright DA, Allen WK, Simonsen J, Dernbach A. Effects of 4 h preexercise carbohydrate feedings on cycling performance. Med Sci Sports Exerc. 1989;21:598-604.
- Baker LB, Rollo I, Stein KW, Jeukendrup AE. Acute effects of carbohydrate supplementation on intermittent sports performance. Nutrients. 2015;7:5733-5763.
- Goedecke JH, White NJ, Chicktay W, Mahomed H, Durandt J, Lambert MI. The effect of carbohydrate ingestion on performance during a simulated soccer match. Nutrients. 2013;5:5193-5204.
- Nicholas CW, Williams C, Lakomy HK, Phillips G, Nowitz A. Influence of ingesting a carbohydrate-electrolyte solution on endurance capacity during intermittent, high-intensity shuttle running. J Sports Sci. 1995;13:283-290.
- Burke LM, van Loon LJC, Hawley JA. Post-exercise muscle glycogen resynthesis in humans. J Appl Physiol. 2016;122:1055-1067.
- Rodriquez NR, DiMarco NM, Langley S. Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and athletic performance. J Am Diet Assoc. 2009;109(3):509-527.
- Romagnoli M, Sanchis-Gomar F, Alis R, Risso-Ballester J, Bosio A, Graziani RL, Rampinini E. Changes in muscle damage, inflammation, and fatigue-related parameters in young elite soccer players after a match. J. Sports Med Phys Fit. 2016;56:1198-1205.
- Res PT, Groen B, Pennings B, Beelen M, Wallis GA, Gijsen AP, et al.Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc. 2012;44:1560-1569.
- Snijders T, Res PT, Smeets JSJ, Van Vliet S, Van Kranenburg J, Maase K, et al.Protein ingestion before sleep increases muscle mass and strength gains during prolonged resistance-type exercise training in healthy young men. J Nutr. 2015;145:1178-1184.
- Simopoulos AP. Omega-3 fatty acids and athletics. Curr Sports Med Rep. 2007;6230-236.
- Peoples GE, McLennan PL, Howe P, Groeller H. Fish oil reduces apparent myocardial oxygen consumption in trained cyclists but does not change time to fatigue. Presented at the Fourth International Conference on Nutrition and Fitness; May 25-29, 2000; Ancient Olympia, Greece.
- Burke LM, Collier GR, Beasley S.K, Davis PG, Fricker PA, Heeley P, et al. Effect of coingestion of fat and protein with carbohydrate feedings on muscle glycogen storage. J Appl Physiol. 1995;78:2187-2192.
- Roy BD, Tarnopolsky MA. Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol. 1998;84:890-896.
- Reinke S, Taylor W.R, Duda GN, von Haehling S, Reinke P, Volk H-D et al. Absolute and functional iron deficiency in professional athletes during training and recovery. Int J Cardiol. 2012;156:186-191.
- Escanero JF, Villanueva J, Rojo A, Herrera A, del Diego C, Guerra M. Iron stores in professional athletes throughout the sports season. Physiol Behav. 1997;62:811-814.
- Heisterberg MF, Fahrenkrug J, Krustrup P, Storskov A, Kjær, M, Andersen JL. Extensive monitoring
- Landahl G, Adolfsson P, Borjesson M, Mannheimer C, Rodjer S. Iron deficiency and anemia: a common problem in female elite soccer players. Int J Sport Nutr Exerc Metab. 2005;15(6):689-694.
- Sinha A, Hollingsworth K, Ball S, Cheetham T. Improving the vitamin D status of vitamin D deficient adults is associated with improved mitochondrial oxidative function in skeletal muscle. Endocrine Abstracts, 2013;31.OC1.6
- Shuler FD, Wingate MK, Moore GH, Giangarra C. Sports health benefits of vitamin D. Sports Health. 2012;4:496-501.
- Hamilton B, Whiteley R, Farooq A, Chalabi H. Vitamin D concentration in 342 professional football players and association with lower limb isokinetic function. J Sci. Med Sport. 2014;17:139-143.
- Ksiażek A, Zagrodna A, Dziubek W, Pietraszewski B, Ochmann B, Słowińska-Lisowska M,25(OH)D3 levels relative to muscle strength and maximum oxygen uptake in athletes. J Hum Kinet. 2016;50:71-77.
- Kopeć A, Solarz K, Majda F, Słowińska-Lisowska M, Medraś M. An evaluation of the levels of vitamin D and bone turnover markers after the summer and winter periods in Polish professional soccer players. J Hum Kinet. 2013;38:135-140.
- Vander Slagmolen G, van Hellemondt FJ, Wielders JPM. Do professional soccer players have a vitamin D status supporting optimal performance in winter time? J Sports Med Doping Stud. 2014,4:2.
- Morton JP, Iqbal Z, Drust B, Burgess D, Close GL, Brukner PD. Seasonal variation in vitamin D status in professional soccer players of the English Premier League. Appl Physiol Nutr Metab. 2012;37:798-802.
- Lozano-Berges G, Matute-Llorente A, Gonzalez-Aguero A, Gomez-Bruton A, Gomez-Cabelloa A, Vincente-Rodriguez G, Casajus JA. Soccer helps build strong bones during growth: a systematic review and meta-analysis. Eur J Pediatr. 2018;177(3):295-310.
- Burke LM. Fluid balance during team sports. J Sports Sci. 1997;15:287-295.
- Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004;14:333-346.
- Brendon P, McDermott, P, Anderson SA, Armstrong LE, Casa DJ, Cheuvront SN, et al. National Athletic Trainers’ Association Position Statement: Fluid Replacement for the Physically Active. J Athl Train. 2017;52(9):877-895.
- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26: 90-95.
- Maughan RJ, Watson P, Evans GH, Broad N, Shirreffs SM. Water balance and salt losses in competitive football. Int J Sport Nutr Exerc Metab. 2007;17:583-594.
- Aragón-Vargas LF, Moncada-Jiménez J, Hernández-Elizondo J, Barrenechea A,Monge-Alvarado M. Evaluation of pre-game hydration status, heat stress, and fluid balance during professional soccer competition in the heat. Eur J Sport Sci. 2009;9:269-276.
- Maughan RJ, Shirreffs SM, Merson SJ, Horswill CA. Fluid and electrolyte balance in elite male football (soccer) players training in a cool environment. J Sports Sci. 2005;23:73-79.
- Duffield R, McCall A, Coutts AJ, Peiffer JJ. Hydration, sweat and thermoregulatory responses to professional football training in the heat. J Sports Sci. 2012;30:957-965.
- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26:90-95.
- Edwards AM, Mann ME, Marfell-Jones MJ, Rankin DM, Noakes TD, Shillington DP. Influence of moderate dehydration on soccer performance: Physiological responses to 45 min of outdoor match-play and the immediate subsequent performance of sport-specific and mental concentration tests. Br J Sports Med. 2007;41:385-391.
- McGregor SJ, Nicholas CW, Lakomy HK, Williams C. The influence of intermittent high-intensity shuttle running and fluid ingestion on the performance of a soccer skill. J Sports Sci. 1999;17:895-903.
- Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004;14:333-346.
- Shirreffs SM, Sawka MN, Stone M. Water and electrolyte needs for football training and match-play. J Sports Sci. 2006;24:699-707.
- Mohr M, Krustrup P, Bangsbo J. Match performance of high-standard soccer players with special reference to development of fatigue. J Sports Sci. 2003;21:519-528.
- Krustrup P, Mohr M, Steensberg A, Bencke J, Kjaer M, Bangsbo J. Muscle and blood metabolites during a soccer game: implications for sprint performance. Med Sci Sports Exerc. 2006;38:1165-1174.
- Di Salvo V, Gregson W, Atkinson G, Tordoff P, Drust B. Analysis of high intensity activity in Premier League soccer. Int J Sports Med. 2009;30:205-212.
- Di Salvo V, Baron R, Tschan H, Calderon Montero FJ, Bachl N, Pigozzi F. Performance characteristics according to playing position in elite soccer. Int J Sports Med. 2007;28:222-227.
- Reilly T, Thomas V. Estimated daily energy expenditures of professional association footballers. Ergonomics. 1979;22:541-548.
- Osgnach C, Poser S, Bernardini R, Rinaldo R, di Prampero P.E. Energy cost and metabolic power in elite soccer: A new match analysis approach. Med Sci Sports Exerc. 2010;42:170-178.
- Anderson L, Orme P, Naughton RJ, Close, GL, Milsom J, Rydings D, et al. Energy intake and expenditure of professional soccer players of the English Premier League: evidence of carbohydrate periodization. Int J Sport Nutr Exerc Metab. 2017;1-25.
- Mara JK, Thompson KG, Pumpa KL. Assessing the energy expenditure of elite female soccer layers: a preliminary study. J Strength Cond Res. 2015;2780-2786.
- Bartlett JD, Hawley JA, Morton JP. Eur J Sport Sci. 2015;15(1):1, 3-12.
- Anderson L, Orme P, Di Michele R, Close GL, Morgans R, Drust B, Morton JP. Quantification of training load during one-, two- and three-game week schedules in professional soccer players from the English Premier League: implications for carbohydrate periodisation. J Sports Sci. 2016;34;1250-1259.
- Hawley JA, Morton JP. Ramping up the signal: promoting endurance training adaptation in skeletal muscle by nutritional manipulation. Clin Exp Pharmacol Physiol. 2014;41:608-613.
- Saltin B. Metabolic fundamentals in exercise. 1973;:137-146.
- Balsom PD, Wood K, Olsson P, Ekblom B. Carbohydrate intake and multiple sprint sports: With special reference to football (soccer). Int J Sports Med. 1999;20:48-52.
- Neufer PD, Costill DL, Flynn MG, Kirwan JP, Mitchell JB, Houmard J. Improvements in exercise performance: Effects of carbohydrate feedings and diet. J Appl Physiol. 1987;62:983-988.
- Sherman WM, Brodowicz G, Wright DA, Allen WK, Simonsen J, Dernbach A. Effects of 4 h preexercise carbohydrate feedings on cycling performance. Med Sci Sports Exerc. 1989;21:598-604.
- Baker LB, Rollo I, Stein KW, Jeukendrup AE. Acute effects of carbohydrate supplementation on intermittent sports performance. Nutrients. 2015;7:5733-5763.
- Goedecke JH, White NJ, Chicktay W, Mahomed H, Durandt J, Lambert MI. The effect of carbohydrate ingestion on performance during a simulated soccer match. Nutrients. 2013;5:5193-5204.
- Nicholas CW, Williams C, Lakomy HK, Phillips G, Nowitz A. Influence of ingesting a carbohydrate-electrolyte solution on endurance capacity during intermittent, high-intensity shuttle running. J Sports Sci. 1995;13:283-290.
- Burke LM, van Loon LJC, Hawley JA. Post-exercise muscle glycogen resynthesis in humans. J Appl Physiol. 2016;122:1055-1067.
- Rodriquez NR, DiMarco NM, Langley S. Position of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: Nutrition and athletic performance. J Am Diet Assoc. 2009;109(3):509-527.
- Romagnoli M, Sanchis-Gomar F, Alis R, Risso-Ballester J, Bosio A, Graziani RL, Rampinini E. Changes in muscle damage, inflammation, and fatigue-related parameters in young elite soccer players after a match. J. Sports Med Phys Fit. 2016;56:1198-1205.
- Res PT, Groen B, Pennings B, Beelen M, Wallis GA, Gijsen AP, et al.Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc. 2012;44:1560-1569.
- Snijders T, Res PT, Smeets JSJ, Van Vliet S, Van Kranenburg J, Maase K, et al.Protein ingestion before sleep increases muscle mass and strength gains during prolonged resistance-type exercise training in healthy young men. J Nutr. 2015;145:1178-1184.
- Simopoulos AP. Omega-3 fatty acids and athletics. Curr Sports Med Rep. 2007;6230-236.
- Peoples GE, McLennan PL, Howe P, Groeller H. Fish oil reduces apparent myocardial oxygen consumption in trained cyclists but does not change time to fatigue. Presented at the Fourth International Conference on Nutrition and Fitness; May 25-29, 2000; Ancient Olympia, Greece.
- Burke LM, Collier GR, Beasley S.K, Davis PG, Fricker PA, Heeley P, et al. Effect of coingestion of fat and protein with carbohydrate feedings on muscle glycogen storage. J Appl Physiol. 1995;78:2187-2192.
- Roy BD, Tarnopolsky MA. Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol. 1998;84:890-896.
- Reinke S, Taylor W.R, Duda GN, von Haehling S, Reinke P, Volk H-D et al. Absolute and functional iron deficiency in professional athletes during training and recovery. Int J Cardiol. 2012;156:186-191.
- Escanero JF, Villanueva J, Rojo A, Herrera A, del Diego C, Guerra M. Iron stores in professional athletes throughout the sports season. Physiol Behav. 1997;62:811-814.
- Heisterberg MF, Fahrenkrug J, Krustrup P, Storskov A, Kjær, M, Andersen JL. Extensive monitoring
- Landahl G, Adolfsson P, Borjesson M, Mannheimer C, Rodjer S. Iron deficiency and anemia: a common problem in female elite soccer players. Int J Sport Nutr Exerc Metab. 2005;15(6):689-694.
- Sinha A, Hollingsworth K, Ball S, Cheetham T. Improving the vitamin D status of vitamin D deficient adults is associated with improved mitochondrial oxidative function in skeletal muscle. Endocrine Abstracts, 2013;31.OC1.6
- Shuler FD, Wingate MK, Moore GH, Giangarra C. Sports health benefits of vitamin D. Sports Health. 2012;4:496-501.
- Hamilton B, Whiteley R, Farooq A, Chalabi H. Vitamin D concentration in 342 professional football players and association with lower limb isokinetic function. J Sci. Med Sport. 2014;17:139-143.
- Ksiażek A, Zagrodna A, Dziubek W, Pietraszewski B, Ochmann B, Słowińska-Lisowska M,25(OH)D3 levels relative to muscle strength and maximum oxygen uptake in athletes. J Hum Kinet. 2016;50:71-77.
- Kopeć A, Solarz K, Majda F, Słowińska-Lisowska M, Medraś M. An evaluation of the levels of vitamin D and bone turnover markers after the summer and winter periods in Polish professional soccer players. J Hum Kinet. 2013;38:135-140.
- Vander Slagmolen G, van Hellemondt FJ, Wielders JPM. Do professional soccer players have a vitamin D status supporting optimal performance in winter time? J Sports Med Doping Stud. 2014,4:2.
- Morton JP, Iqbal Z, Drust B, Burgess D, Close GL, Brukner PD. Seasonal variation in vitamin D status in professional soccer players of the English Premier League. Appl Physiol Nutr Metab. 2012;37:798-802.
- Lozano-Berges G, Matute-Llorente A, Gonzalez-Aguero A, Gomez-Bruton A, Gomez-Cabelloa A, Vincente-Rodriguez G, Casajus JA. Soccer helps build strong bones during growth: a systematic review and meta-analysis. Eur J Pediatr. 2018;177(3):295-310.
- Burke LM. Fluid balance during team sports. J Sports Sci. 1997;15:287-295.
- Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004;14:333-346.
- Brendon P, McDermott, P, Anderson SA, Armstrong LE, Casa DJ, Cheuvront SN, et al. National Athletic Trainers’ Association Position Statement: Fluid Replacement for the Physically Active. J Athl Train. 2017;52(9):877-895.
- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26: 90-95.
- Maughan RJ, Watson P, Evans GH, Broad N, Shirreffs SM. Water balance and salt losses in competitive football. Int J Sport Nutr Exerc Metab. 2007;17:583-594.
- Aragón-Vargas LF, Moncada-Jiménez J, Hernández-Elizondo J, Barrenechea A,Monge-Alvarado M. Evaluation of pre-game hydration status, heat stress, and fluid balance during professional soccer competition in the heat. Eur J Sport Sci. 2009;9:269-276.
- Maughan RJ, Shirreffs SM, Merson SJ, Horswill CA. Fluid and electrolyte balance in elite male football (soccer) players training in a cool environment. J Sports Sci. 2005;23:73-79.
- Duffield R, McCall A, Coutts AJ, Peiffer JJ. Hydration, sweat and thermoregulatory responses to professional football training in the heat. J Sports Sci. 2012;30:957-965.
- Shirreffs SM, Aragon-Vargas LF, Chamorro M, Maughan RJ, Serratosa L, Zachwieja JJ. The sweating response of elite professional soccer players to training in the heat. Int J Sports Med. 2005;26:90-95.
- Edwards AM, Mann ME, Marfell-Jones MJ, Rankin DM, Noakes TD, Shillington DP. Influence of moderate dehydration on soccer performance: Physiological responses to 45 min of outdoor match-play and the immediate subsequent performance of sport-specific and mental concentration tests. Br J Sports Med. 2007;41:385-391.
- McGregor SJ, Nicholas CW, Lakomy HK, Williams C. The influence of intermittent high-intensity shuttle running and fluid ingestion on the performance of a soccer skill. J Sports Sci. 1999;17:895-903.
- Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004;14:333-346.
- Shirreffs SM, Sawka MN, Stone M. Water and electrolyte needs for football training and match-play. J Sports Sci. 2006;24:699-707.
TAKE-HOME POINTS:
- Nutrition plays a vital role in keeping the player healthy, reducing risk for injury, speeding up recovery, and enhancing training adaptations.
- Average energy expenditure during a training day is ~3500-3600 kcal for elite male soccer players and ~2700-2800 kcal for elite female soccer players.
- Carbohydrate needs should reflect the work required/demand to produce optimal performance.
- Vitamin D and iron are two common nutrients of concern for soccer players.
- Studies have shown that most players do not drink sufficiently during a match to optimize hydration, replacing only ~40% to 45% of their sweat losses. Soccer players can also lose large amounts of sodium: between 700 and 1500 mg of sodium/L of sweat.
Lower Extremity Injuries in Ice Hockey: Current Concepts
ABSTRACT
Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.
“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)
Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.3 Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.5
During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.6 They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.2
One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.7 More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).2
Continue to: Hip and groin...
EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES
HIP INJURIES
Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.1 Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues12 performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.12
Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries | ||
Lower Extremity Injury | Treatment Options | Return-to-the-Rink Goal |
FAI | In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery | Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
|
Sports hernia/athletic pubalgia
| In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success
| Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
|
Adductor strains | Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice | Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
|
Quadriceps contusion
| Hinged knee brace to maintain 120° of flexion, ice, compression wrap.
| When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
|
MCL | Hinged knee brace, shin pad modification, ice, NSAIDs | Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
|
ACL | Surgery autograft BTB autograft soft tissue
| 9-10 mo41 |
Meniscus tear | Depends on type of tear and seasonal timing (in-season or off-season) | If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
|
High ankle sprain
| Cam boot, NSAIDS, ice and physical therapy
| 6 wk49 |
Boot top laceration | Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks | If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
|
Lace bite
| Bunga pad, ice, diclofenac gel
| Couple of days to up to 2 wk in recalcitrant cases3 |
Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.
Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.13 The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.
In the recent study by Ross and colleagues,15 the authors focused on symptomatic hip impingement in ice hockey goalies.15 Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates16 have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.
Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.15 Goalies had a significantly lower mean lateral center-edge angle (27.3° vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.13
Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.17 On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).20,21
In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.22 A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.23-25
For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.
Continue to: For athletes who...
For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues26 have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.27
One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.28 Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.29 On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.30 An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.31
Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,32 they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.29 At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.29 Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.33
Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.34 Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.35 Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.36 A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.37
These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.37 The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.37 Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.
Continue to: Contact injuries may...
Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.23 The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.38 Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.8
KNEE INJURIES
Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.39 Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).39 One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,39 with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.8,9
Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.41 The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.42 Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.41 Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.41 Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.41
Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.41 The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.42 Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.38 A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.43 In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).41
Continue to: The presence of...
The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.
Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.44Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.45 It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others8 have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.
FOOT AND ANKLE
Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.47 The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.47 Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.48
Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.49
Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.49,51,52
Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues4 demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.4 Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.4 The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.53 The study acknowledged a major limitation being a public source for identifying players with fractures.
Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).
SUMMARY
Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.
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13. Epstein DM, McHugh M, Yorio M, Neri B. Intra-articular hip injuries in national hockey league players: a descriptive epidemiological study. Am J Sports Med. 2013;41(2):343-348.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Ross JR, Bedi A, Stone RM, Sibilsky Enselman E, Kelly BT, Larson CM. Characterization of symptomatic hip impingement in butterfly ice hockey goalies. Arthroscopy. 2015;31(4):635-642.
16. Bedi A, Dolan M, Hetsroni I, et al. Surgical treatment of femoroacetabular impingement improves hip kinematics: a computer-assisted model. Am J Sports Med. 2011;39(Suppl):43S-49S.
17. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
18. Nepple JJ, Goljan P, Briggs KK, Garvey SE, Ryan M, Philippon MJ. Hip strength deficits in patients with symptomatic femoroacetabular impingement and labral ears. Arthroscopy. 2015;31(11):2106-2111.
19. Audenaert EA, Peeters I, Vigneron L, Baelde N, Pattyn C. Hip morphological characteristics and range of internal rotation in femoroacetabular impingement. Am J Sports Med. 2012;40(6):1329-1336.
20. Notzli HP, Wyss TF, Stoecklin CH, Schmid MR, Treiber K, Hodler J. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br. 2002;84(4):556-560.
21. Kuhn AW, Ross JR, Bedi A. Three-dimensional imaging and computer navigation in planning for hip preservation surgery. Sports Med Arthrosc Rev. 2015;23(4):e31-e38.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Kuhn AW, Noonan BC, Kelly BT, Larson CM, Bedi A. The hip in ice hockey: a current concepts review. Arthroscopy. 2016;32(9):1928-1938.
24. O'Connor M, Minkara AA, Westermann RW, Rosneck J, Lynch TS. Return to play after hip arthroscopy: a systematic review and meta-analysis. Am J Sports Med. 2018:46(11):2780-2788.
25. Minkara AA, Westermann RW, Rosneck J, Lynch TS. Systematic review and meta-analysis of outcomes after hip arthroscopy in femoroacetabular impingement. Am J Sports Med. 2018:363546517749475.
26. Philippon MJ, Weiss DR, Kuppersmith DA, Briggs KK, Hay CJ. Arthroscopic labral repair and treatment of femoroacetabular impingement in professional hockey players. Am J Sports Med. 2010;38(1):99-104.
27. Pierce CM, Laprade RF, Wahoff M, O'Brien L, Philippon MJ. Ice hockey goaltender rehabilitation, including on-ice progression, after arthroscopic hip surgery for femoroacetabular impingement. J Orthop Sports Phys Ther. 2013;43(3):129-141.
28. MacLeod DA, Gibbon WW. The sportsman's groin. Br J Surg. 1999;86(7):849-850.
29. Irshad K, Feldman LS, Lavoie C, Lacroix VJ, Mulder DS, Brown RA. Operative management of "hockey groin syndrome": 12 years of experience in National Hockey League players. Surgery. 2001;130(4):759-764; discussion 764-756.
30. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
31. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the "sports hernia": MR imaging findings. Radiology. 2008;247(3):797-807.
32. Jakoi A, O'Neill C, Damsgaard C, Fehring K, Tom J. Sports hernia in National Hockey League players: does surgery affect performance? Am J Sports Med. 2013;41(1):107-110.
33. Larson CM, Pierce BR, Giveans MR. Treatment of athletes with symptomatic intra-articular hip pathology and athletic pubalgia/sports hernia: a case series. Arthroscopy.2011;27(6):768-775.
34. Lorentzon R, Wedren H, Pietila 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.
35. Holmich P, Uhrskou P, Ulnits L, et al. Effectiveness of active physical training as treatment for long-standing adductor-related groin pain in athletes: randomised trial. Lancet. 1999;353(9151):439-443.
36. Sim FH, Chao EY. Injury potential in modern ice hockey. Am J Sports Med. 1978;6(6):378-384.
37. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
38. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. BrJ Sports Med. 2009;43(13):1000-1005.
39. Grant JA, Bedi A, Kurz J, Bancroft R, Miller BS. Incidence and injury characteristics of medial collateral ligament injuries in male collegiate ice hockey players. Sports Health. 2013;5(3):270-272.
40. Erickson BJ, Harris JD, Cole BJ, et al. Performance and return to sport after anterior cruciate ligament reconstruction in National Hockey League players. Orthop J Sports Med. 2014;2(9):2325967114548831.
41. Sikka R, Kurtenbach C, Steubs JT, Boyd JL, Nelson BJ. Anterior Cruciate Ligament Injuries in Professional Hockey Players. Am J Sports Med. 2016;44(2):378-383.
42. Friden T, Erlandsson T, Zatterstrom R, Lindstrand A, Moritz U. Compression or distraction of the anterior cruciate injured knee: variations in injury pattern in contact sports and downhill skiing. Knee Surg Sports Traumatol Arthrosc. 1995;3(3):144-147.
43. Kluczynski MA, Kang JV, Marzo JM, Bisson LJ. Magnetic resonance imaging and intra-articular findings after anterior cruciate ligament injuries in ice hockey versus other sports. Orthop J Sports Med. 2016;4(5):2325967116646534. 44. Beiner JM, Jokl P. Muscle contusion injuries: current treatment options. J Am Acad Orthop Surg. 2001;9(4):227-237.
45. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.
46. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.
47. Johnson PN, Mark; Green, Eric. Boot-top lacerations in ice hockey players: a new injury. Clin J Sports Med. 1991:205-208.
48. Nauth A, Aziz M, Tsuji M, Whalen DB, Theodoropoulos JS, Zdero R. The protective effect of Kevlar socks against hockey skate blade injuries: a biomechanical study. Orthop J Sports Med. 2014;2(Suppl 2):7.
49. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
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ABSTRACT
Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.
“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)
Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.3 Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.5
During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.6 They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.2
One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.7 More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).2
Continue to: Hip and groin...
EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES
HIP INJURIES
Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.1 Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues12 performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.12
Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries | ||
Lower Extremity Injury | Treatment Options | Return-to-the-Rink Goal |
FAI | In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery | Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
|
Sports hernia/athletic pubalgia
| In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success
| Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
|
Adductor strains | Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice | Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
|
Quadriceps contusion
| Hinged knee brace to maintain 120° of flexion, ice, compression wrap.
| When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
|
MCL | Hinged knee brace, shin pad modification, ice, NSAIDs | Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
|
ACL | Surgery autograft BTB autograft soft tissue
| 9-10 mo41 |
Meniscus tear | Depends on type of tear and seasonal timing (in-season or off-season) | If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
|
High ankle sprain
| Cam boot, NSAIDS, ice and physical therapy
| 6 wk49 |
Boot top laceration | Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks | If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
|
Lace bite
| Bunga pad, ice, diclofenac gel
| Couple of days to up to 2 wk in recalcitrant cases3 |
Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.
Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.13 The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.
In the recent study by Ross and colleagues,15 the authors focused on symptomatic hip impingement in ice hockey goalies.15 Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates16 have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.
Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.15 Goalies had a significantly lower mean lateral center-edge angle (27.3° vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.13
Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.17 On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).20,21
In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.22 A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.23-25
For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.
Continue to: For athletes who...
For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues26 have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.27
One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.28 Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.29 On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.30 An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.31
Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,32 they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.29 At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.29 Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.33
Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.34 Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.35 Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.36 A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.37
These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.37 The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.37 Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.
Continue to: Contact injuries may...
Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.23 The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.38 Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.8
KNEE INJURIES
Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.39 Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).39 One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,39 with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.8,9
Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.41 The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.42 Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.41 Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.41 Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.41
Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.41 The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.42 Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.38 A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.43 In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).41
Continue to: The presence of...
The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.
Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.44Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.45 It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others8 have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.
FOOT AND ANKLE
Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.47 The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.47 Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.48
Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.49
Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.49,51,52
Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues4 demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.4 Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.4 The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.53 The study acknowledged a major limitation being a public source for identifying players with fractures.
Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).
SUMMARY
Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.
ABSTRACT
Ice hockey is a fast-paced, collision sport requiring tremendous skill and finesse, yet ice hockey can be a harsh and violent game. It has one of the highest musculoskeletal injury rates in all of competitive sports. Razor sharp skates, aluminum sticks and boards made from high density polyethylene (HDPE), all contribute to the intrinsic hazards of the game. The objective of this article is to review evaluation, management, and return-to-the-rink guidelines after common lower extremity ice hockey injuries.
“Hockey is a fast body-contact game played by men with clubs in their hands and knives laced to their feet, since the skates are razor sharp, and before the evening is over it is almost a certainty that someone will be hurt and will fleck the ice with a generous contribution of gore before he is led away to be hemstitched together again.” —Paul Gallico in Farewell to Sport (1938)
Ice hockey is a collision sport with player speeds in excess of 30 miles/hour, on a sheet of ice surrounded by unforgiving boards, with a vulcanized rubber puck moving at speeds approaching 100 miles/hour.1-3 Understanding injuries specific to this fast-paced sport is an essential part of being a team physician at any level of competitive ice hockey. We are continuing to improve our ability to correctly identify and treat injuries in ice hockey players.2,4 On the prevention side, rule changes in hockey have been implemented, such as raising the age to allow checking and penalties for deliberate hits to the head and checking from behind, to make the game safer to play.3 Additionally, advancements in biomechanical research and 3D modeling are providing new insights into the pathoanatomy of the hip joint, which can be utilized for surgical planning in hockey players and goalies suffering from symptomatic femoroacetabular impingement (FAI) of the hip.5
During the 2010 Winter Olympics, more than 30% of ice hockey players were injured, which was the highest percentage amongst all competing sports.6 They also tallied the highest percentage of player-to-player injuries during the Olympics of any sport. Consequently, the team physician covering ice hockey should be prepared to manage upper and lower extremity musculoskeletal injuries, but also concussions, cervical spine injuries, and ocular and dental trauma.2
One of the earliest epidemiological studies of ice hockey injuries looked at elite Danish hockey players over 2 seasons and found that head trauma accounted for 28% of all injuries, followed by lower extremity injuries at 27% with upper extremity injuries accounting for 19%.7 More recent epidemiological studies have shown similar rates based on body region while further defining individual diagnoses and their incidence. This should help clinicians and researchers develop prevention strategies, as well as improve treatments to optimize player outcomes and return to sport.8,9 Our group recently reviewed the evaluation and management of common head, neck, and shoulder injuries at all competitive levels of ice hockey, and this article serves to complement the former by focusing on lower extremity injuries (Table).2
Continue to: Hip and groin...
EVALUATION AND MANAGEMENT OF COMMON LOWER EXTREMITY HOCKEY INJURIES
HIP INJURIES
Hip and groin injuries are very common amongst this group of athletes and account for approximately 9% of all ice hockey injuries.1 Unfortunately, they are also known for their high recurrence rates, which may be in part due to delayed diagnosis, inadequate rest and rehabilitation, as well as the extreme loads that are placed on the hip during competition.10,11 In hockey, the most commonly reported hip injuries include goaltender’s hip, FAI, sports hernia/hockey groin syndrome, adductor strains, hip pointer, and quadriceps contusions. Dalton and colleagues12 performed the largest epidemiological study to date on hip and groin injuries amongst National Collegiate Athletic Association ice hockey players and reported that the most common injury mechanism was noncontact in nature. Contact injuries accounted for 13% (55 of 421) in men’s ice hockey players while less than 4% (4 of 114) injuries in female ice hockey players, which is likely attributed to a no checking rule in the women’s division. Some of these hip and groin injuries are difficult to diagnose so it is important for the team physician to perform a thorough history and physical examination. Advanced imaging (magnetic resonance imaging [MRI] or a computed tomography (CT) scan with 3D reconstructions) may be necessary to make the correct diagnosis. This is important for providing proper treatment as well as setting player expectations for return to sport.12
Table 1. Return-to-Play Guidelines for Common Lower Extremity Ice Hockey Injuries | ||
Lower Extremity Injury | Treatment Options | Return-to-the-Rink Goal |
FAI | In-season: injection, physical therapy program, NSAIDS. Off-season or unable to play: requires arthroscopic surgery | Nonoperative can take up to 6 weeks. Surgical depends on what is fixed but goal is 4 months to return to ice24,26
|
Sports hernia/athletic pubalgia
| In-season: physical therapy program, NSAIDS Off-season or unable to play requiring surgery. Essential to make sure no other pathology (eg, FAI, osteitis pubis, adductor strain) to maximize success
| Nonoperative 6-8 wk trial of physical therapy Operative: depends if concomitant FAI but in isolation goal is 3-4 mo33,54
|
Adductor strains | Ice, NSAIDS, physical therapy, use of Hypervolt Hyperice | Depends on position (goalie vs skater) and severity; can take up to 4-8 wk to return to ice. Want 70% strength and painless ROM to skate successfully;55 in chronic cases, may take up to 6 mo35
|
Quadriceps contusion
| Hinged knee brace to maintain 120° of flexion, ice, compression wrap.
| When player regains motion and strength, return to ice can be as fast a couple of days or as long as 3 wk8,46
|
MCL | Hinged knee brace, shin pad modification, ice, NSAIDs | Depends on Grade; if Grade I, 1-2 wk; Grade II, 2-4 wk; Grade III, 4-6 wk8
|
ACL | Surgery autograft BTB autograft soft tissue
| 9-10 mo41 |
Meniscus tear | Depends on type of tear and seasonal timing (in-season or off-season) | If surgical, 3-4 mo; if repair, 4-6 wk if partial menisectomy
|
High ankle sprain
| Cam boot, NSAIDS, ice and physical therapy
| 6 wk49 |
Boot top laceration | Repair of cut structures, depends on depth and what is injured; best treatment is prevention with Kevlar socks | If laceration is deep and severs any medial tendons/vascular structures, return to ice can be ≥6 mo
|
Lace bite
| Bunga pad, ice, diclofenac gel
| Couple of days to up to 2 wk in recalcitrant cases3 |
Abbreviations: ACL, anterior cruciate ligament; BTB, bone-patellar tendon-bone; Cam, controlled ankle motion boot; MCL, medial collateral ligament; FAI, femoroacetabular impingement; NSAIDS, nonsteroidal anti-inflammatory drugs; ROM, range of motion.
Throughout the hockey community, FAI is being examined as a possible source of symptomatic hip pain amongst players at all levels. A recent study, which utilized the National Hockey League (NHL) injury surveillance database, reported that FAI accounted for 5.3% of all hip and groin injuries.13 The etiology of FAI is thought to arise from a combination of genetic predisposition coupled with repetitive axial loading/hip flexion. This causes a bony overgrowth of the proximal femoral physes resulting in a cam deformity (Figure 1).5,14 The abnormal bony anatomy allows for impingement between the acetabulum and proximal femur, which can injure the labrum and articular cartilage of the hip joint.
In the recent study by Ross and colleagues,15 the authors focused on symptomatic hip impingement in ice hockey goalies.15 Goaltender’s hip may be the result of the “butterfly style,” which is a technique of goaltending that emphasizes guarding the lower part of the goal. The goalie drops to his/her knees and internally rotates the hips to allow the leg pads to be parallel to the ice. This style acquired the name butterfly because of the resemblance of the spread goalie pads to a butterfly’s wings. Bedi and associates16 have evaluated hip biomechanics using 3D-generated bone models and showed in their study that arthroscopic treatment can improve hip kinematics and range of motion.
Plain radiographs showed that 90% (61 of 68) of hockey goalies had an elevated alpha angle signifying a femoral cam-type deformity.15 Goalies had a significantly lower mean lateral center-edge angle (27.3° vs 29.6°; P = .03) and 13.2% of them were found to have acetabular dysplasia (lateral center-edge angle<20°) compared to only 3% of positional players. The CT scan measurements demonstrated that hockey goalies have a unique cam-type deformity that is located more lateral (1:00 o’clock vs 1:45 o’clock; P < .0001) along the proximal femur, an elevated maximum alpha angle (80.9° vs 68.6°; P < .0001) and loss of offset, when compared to positional players. These findings provide an anatomical basis in support of reports that goaltenders are more likely to experience intra-articular hip injuries compared to other positional players.13
Regardless of position, symptomatic FAI in a hockey player is generally a problem that slowly builds and is made worse with activity.17 On examination, the player may have limited hip flexion and internal rotation, as well as weakness compared to the contralateral side when testing hip flexion and abduction.18,19 Plain radiographs plus MRI or CT allow for proper characterization and diagnosis (to include underlying chondrolabral pathology).20,21
In the young athlete, initial management includes physical therapy, which focuses on core strengthening. Emphasis is placed on hip flexion and extension, as well as abduction and external rotation with the goal of reducing symptoms and avoiding injuries.22 A similar approach may be applied to the elite athlete, but failure of nonoperative management may necessitate surgical intervention. Hip arthroscopy continues to grow in popularity over open surgical dislocation with low complication rate and high return-to-play rate.23-25
For the in-season athlete, attempts to continue to play can be assisted with the role of an intra-articular corticosteroid injection, which can help calm inflammation within the hip joint and mitigate pain, while rehabilitation focuses on core stabilization, postural retraining and focusing on any muscle imbalances that might be present. For positional players, ice time and shift duration can be adjusted to give the player’s hip a period of rest; meanwhile, for goaltenders, shot volumes in practice can be decreased.
Continue to: For athletes who...
For athletes who fail nonoperative care, surgical treatment varies depending on underlying hip pathology and may include femoroplasty, acetabuloplasty, and microfracture as well as labral repair or debridement. Though data are limited, Philippon and colleagues26 have published promising results in a case series of 28 NHL players after surgical intervention for FAI. All players returned to sport at an average of 3.8 months and players who had surgery within 1 year of injury returned on average 1.1 months sooner than those who waited more than 1 year. Rehabilitation protocol varies between goaltenders compared to defensemen and offensive players due to the different demands required for blocking shots on goal.27
One of the most challenging injuries to correctly identify in the hip area is athletic pubalgia (also referred to as sports hernia or core muscle injury) because pain in the groin may be referred from the lumbar spine, hip joint, urologic, or perineal etiologies.28 Sports hernias involve dilatation of the external ring of the inguinal canal and thinning of the posterior wall. Players may report to the athletic trainer or team physician with a complaint of groin pain that is worse when pushing off with their skate or taking a slap shot.29 On exam, pain can be reproduced by hip extension, contralateral torso rotation, or with a resisted sit-up with palpation of the inferolateral edge of the distal rectus abdominus.30 An MRI with specific sequences centered over the pubic symphysis is usually warranted to aid in the workup of sports hernia. An MRI in these cases may also demonstrate avulsions of the rectus abdominus.31
Most of these injuries are managed conservatively but can warrant surgical intervention if the symptoms persist. In the study by Jakoi and colleagues,32 they identified 43 ice hockey players over an 8-year period (2001-2008) who had repairs of their sports hernias and assessed the statistics during the 2 years prior and 2 years after surgery. The authors found that 80% of these players were able to return to the ice for 2 or more full seasons. The return-to-sport rate was comparable to other sports after sports hernia repair, but players who had played in ≥7 seasons demonstrated a greater decrease in number of games played, goals, assists and time on ice compared to those who had played in ≤6 seasons prior to the time of injury. Between 1989 and 2000, 22 NHL players who failed to respond to nonoperative management of their groin injuries underwent surgical exploration.29 At the time of surgical exploration, their hockey groin syndrome, consisted of small tears in the external oblique aponeurosis through which branches of the ilioinguinal or iliohypogastric could be identified. These surgical procedures were all through a standard inguinal approach and the perforating neurovascular structures were excised, while the main trunk of the ilioinguinal nerve was ablated and the external oblique aponeurosis was repaired and reinforced with Goretex (W.L. Gore & Associates Inc, Flagstaff, AZ). At follow-up, 18 of the 22 players (82%) had no pain and 19 (86%) were able to resume their careers in the NHL.29 Ice hockey players with sports hernias or hockey groin syndrome often return to the sport, but it is important to identify these problems early so that surgical options can be discussed if the player fails conservative management. It is also critical to make sure that all pathology is identified, because in players with mixed sports hernia and FAI, return-to-play results improve when both issues are addressed. In a study of athletes (some of whom were ice hockey players), who had both FAI and sports hernia, and only hernia/pubalgia surgery was performed, 25% of these athletes returned to sport. If only FAI was addressed, 50% of the athletes returned to sport; however, when hernia and FAI were treated, 89% returned to play.33
Adductor strains includes injury to the adductor muscles, pectineus, obturator externus and gracilis, and are prevalent in ice hockey players. A study of elite Swedish ice hockey players published in 1988 reported that adductor strains accounted for 10% (10 of 95) of all injuries.34 Given the prevalence of these injuries, considerable research has been dedicated to understanding their mechanism and prevention.35 Adductor strains within the ice hockey population have been attributed to the eccentric forces on the adductors when players attempt to decelerate the leg during a stride.36 A study of NHL players revealed that a ratio <80% of adductor-to-abductor muscle is the best predictor of a groin strain.37
These injuries are also well known for their recurrence rates, as was the case in an NHL study where 4 of the 9 adductor strains (44%) were recurrent injuries.37 The authors attributed the recurrence to an incomplete rehabilitation program and an accelerated return to sport. This was followed by an NHL prevention program that spanned 2 seasons and analyzed 58 players whose adductor-to-abductor ratio was <80% and placed them into a 6-week intervention program during the preseason.37 Only 3 players sustained an adductor strain in the 2 subsequent seasons after the intervention, compared to 11 strains in the previous 2 seasons. Thus, early identification of muscle strength imbalance coupled with an appropriate intervention program has proven to be an effective means of reducing adductor strains in this at-risk population.
Continue to: Contact injuries may...
Contact injuries may vary with checking into the boards being unique to men’s ice hockey. Hip pointers occur as a result of a direct compression injury to the iliac crest, which causes trauma to the bone but also to the overlying hip abductor musculature, and represent roughly 2.4% of ice hockey injuries.23 The resulting contusion may cause a local hematoma formation. Early identification of the injury plus treatment with RICE (rest, ice, compression, elevation) coupled with crutches to limit weight-bearing status may minimize soft tissue trauma and swelling, and ultimately aid in pain control and return to sport.38 Hip abductor strengthening, added padding over the injured area, as well as a compressive hip spica wrapping, have all been suggested to expedite return to play and help prevent recurrence of the hip pointer.8
KNEE INJURIES
Injury to the medial collateral ligament (MCL) is the most commonly reported knee injury (Figure 2) and second only to concussion amongst all injuries in National Collegiate Athletic Association ice hockey players.8,39 The mechanism of injury typically involves a valgus force on the knee, which is often caused by collision into another player.39 Valgus stress testing with the knee in 30° of flexion is used to grade the severity of injury (Grade I: 0-5 mm of medial opening; Grade II: 5-10 mm of medial opening; Grade III: >10 mm of medial opening).39 One study that followed a single college hockey team for 8 seasons reported that 77% of injuries (10 of 13) occurred during player-to-player collision,39 with 5 being Grade 1 injuries, 6 Grade 2 injuries, 1 Grade 3; information was missing for 1 player. Nonoperative management of incomplete injuries, grade 1 and 2 sprains, with RICE and early physical therapy intervention to work on knee range of motion and quadriceps strengthening typically helps the player return to sport within days for grade 1 and 2 injuries to 3 weeks for grade 2 injuries. Complete tears have been managed both operatively and nonoperatively with evidence to suggest better outcomes after surgical intervention if there is a concomitant ACL injury requiring reconstruction.8,9
Anterior cruciate ligament (ACL) tears occur less frequently in hockey players compared to the players in other sports such as football and basketball.38,40 Between 2006 and 2010, 47 players were identified by the NHL Injury Surveillance System as having sustained an ACL injury, which equates to an incidence of 9.4 ACL injuries per NHL season over this time span.41 The mechanism of ACL tears in ice hockey players appears to be different from other sports players based on a recent MRI study that evaluated players for concomitant injuries following ACL tear and noted significantly fewer bone bruises on the lateral femoral condyle compared to players in other sports.42 Early evaluation after injury with Lachman and/or pivot shift tests aids the diagnosis. Data from the NHL study identified 32 players (68%) with concomitant meniscal injuries and 32 (68%) had MCL injuries in conjunction with their ACL tears.41 Average length in the league prior to injury was 5.65 seasons. Twenty-nine of the injured players (61.7%) underwent reconstruction with a patellar tendon autograft, 13 (27.7%) had a hamstring autograft, and 5 (10.6%) had either a patellar tendon or hamstring allograft.41 Meniscus and ACL injuries were associated with a decreased length of career compared to age-matched controls and, notably, players >30 years at the time of injury had only a 67% rate of return to sport whereas those <30 years had a return-to-sport rate of 80%. Players who were able to return did so at an average of 9.8 months (range, 6-21 months) and had a significant reduction in total number of goals, assists, and points scored compared to controls. Decline in performance was typically associated with forwards and wings, while defensemen did not demonstrate the same decrease in performance following return to ice hockey.41
Meniscal tears are a well-documented concomitant injury with ruptures of the ACL, and the combination is a known pattern associated with shorter careers compared to isolated ACL tears in ice hockey players.41 The lateral meniscus is known for increased mobility compared to the medial meniscus and is more commonly injured (39% vs 8.5%) in ACL tears that occur in contact sports and downhill skiing.42 Ice hockey presents a scenario that is different from other contact sports because of the near frictionless interaction between the player’s ice skates and playing surface. This likely equates to a different injury mechanism and dissipation of energy after contact as well as non-contact injuries.38 A recent study reviewed knee MRI findings associated with ACL tears in collegiate ice hockey players and compared to other sports known for their high rates of concomitant meniscal pathology. The authors reported a statistically significant decrease in lateral meniscus tears and bone-bruising patterns in ice hockey players with ACL injuries compared to athletes with ACL tears in other sports.43 In contrast, an NHL study of ACL tears in professional ice hockey players found that 68% of players had concomitant meniscal tears (32 out of 47 players).41
Continue to: The presence of...
The presence of a meniscal tear on MRI is typically a surgical problem, especially if it occurred with an ACL injury. Meniscal repair is preferable, if possible, because there is a known association of increased cartilage contact pressures associated with meniscal debridement. Return to sport following meniscus injury hinges upon whether it is an isolated injury and how it is treated. If the meniscus injury occurs in isolation and can be treated with a debridement and partial resection alone, there is obviously a quicker return to sport as the player can be weight-bearing immediately following surgery. Return to skating after meniscal debridement and partial resection is usually 4 to 6 weeks, whereas meniscal repair protocols vary depending on surgeon; players may need 3 months to 4 months to return to the ice.
Quadriceps contusions are contact injuries that are not unique to ice hockey (Figure 3). They may result from player collision but also from direct blows from a hockey puck. A high velocity puck is known to cause immense trauma to the quadriceps muscles, which may result in localized bleeding and hematoma formation. If the player is able to anticipate the event, active contraction of the quadriceps muscle has been shown to absorb some of the energy and result in a less traumatic injury, but in a fast paced ice hockey game, the player’s anticipation is less likely than in other sports such as baseball.44Interestingly, the degree of knee flexion after injury is predictive of injury severity with milder injuries associated with angles >90 and more severe injuries resulting in knee flexion angles <45° and typically an antalgic gait.45 It is important to treat these injuries during the first 24 hours with the knee maintained in 120°of flexion, plus ice and compression, which can be achieved using a locked knee brace or elastic compression wrap. Quadriceps stretching and isometric strengthening should immediately follow the period of immobilization. The addition of NSAIDs may help prevent the formation of myositis ossificans. A study from West Point suggests that the average return to sport or activity ranges from 13 days (mild contusion) to 21 days (severe contusions), while others8 have indicated that if the injury is treated acutely and a player is able to regain motion and strength, return to ice hockey within a few days is possible.
FOOT AND ANKLE
Ice hockey has some unique injuries that can be attributed to the use of ice skates for play. One such injury is boot-top lacerations, which are fortunately rare as they can be a career-ending injury.47 The spectrum of injury ranges from superficial abrasions to more severe soft tissue disruption, including the extensor tendons and neurovascular structures. The actual mechanism of injury involves an opponent’s skate blade cutting across the anterior ankle. One early case report described a protective method of having players place their skate tongues deep to their protective shin pads, instead of turning the tongues down.47 Kevlar socks have also been shown to help prevent or minimize the damage from a skate blade.48
Injury to the lateral ankle ligaments, anterior talofibular ligament or calcaneofibular ligament, are usually more common than the higher ankle sprains involving the syndesmosis. However, this is not the case in ice hockey. The rigidity of the ice skate at the level of the lateral ligaments seems to impart a protective mechanism to the lower ligaments, but this results in a higher incidence of syndesmotic injuries. These high ankle injuries are unfortunately more debilitating and often require a longer recovery period. In a study of these injuries in NHL players, syndesmotic sprains made up 74% of all ankle sprains, whereas only 18.4% of ankle sprains involved the syndesmosis in American football players..49,50 The average number of days between injury and return to play is 45 days, and some authors believe that defensemen may have a harder time recovering because of the demands on their ankles by having to switch continuously between forward and backward skating.49
Most patients are treated conservatively when their ankle plain radiographs show a congruent mortise and no evidence of syndesmotic widening. If the player expresses pain when squeezing the syndesmosis, it is helpful to obtain stress radiographs to further evaluate for syndesmotic injury. Nonoperative management includes RICE, immobilization in a rigid boot with crutches to protect weight-bearing with gradual advancements and eventually physical therapy to address any ankle stiffness, followed by dynamic functional activities. Treatment options for syndesmotic widening and failed conservative management includes both screw and plate options as well as suture buttons.49,51,52
Ankle and foot fractures were historically a rare injury in ice hockey players based on radiograph evaluation; however, the recent study by Baker and colleagues4 demonstrated that MRI can be helpful in detecting subradiographic fractures. Most of the injuries detected after MRI were from being hit by a hockey puck; this was a novel mechanism that had not been previously reported in the literature.4 Of the injuries that resulted from a direct blow, 14 of 17 occurred on the medial aspect of the foot and ankle, which is believed to result another word? from a defender skating towards an offensive player and attempting to block shots on goal. In this study, all occult fractures involving the medial malleolus were eventually treated with open reduction and internal fixation and underwent routine healing.4 The navicular bone and base of the first metatarsal accounted for the remaining medial-sided fractures. In a recent analysis of risk factors for reoperation following operative fixation of foot fractures across the National Basketball Association, the National Football Leagues, Major League Baseball, and the National Hockey League only a total of 3 fractures involving the foot (1 navicular and 2 first metatarsal) were identified in NHL players over a 30-year period.53 The study acknowledged a major limitation being a public source for identifying players with fractures.
Lace bite is another common ice hockey injury. It typically occurs at the beginning of a season or whenever a player is breaking in a new pair of skates. The cause of the lace bite is the rigid tongue in the skate that rubs against the anterior ankle. Skating causes inflammation in the area of the tibialis anterior tendon, and the player will complain of significant anterior ankle pain. First line treatment for lace bite is ice (Figure 4A), NSAID gel (eg, diclofenac 1%), and a Bunga lace-bite pad (Absolute Athletics). (Figure 4B).
SUMMARY
Lower extremity injuries are common in ice hockey players, and a covering physician should be comfortable managing these injuries from breezers to skate. Proper evaluation and work-up is critical for early diagnosis and identification of pathology, which can minimize the impact of the injury and expedite a treatment plan to return the player safely to the ice and in the game.
1. 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.
2. Popkin CA, Nelson BJ, Park CN, et al. Head, neck, and shoulder injuries in ice hockey: current concepts. Am J Orthop (Belle Mead NJ). 2017;46(3):123-134.
3. Popkin CA, Schulz BM, Park CN, Bottiglieri TS, Lynch TS. Evaluation, management and prevention of lower extremity youth ice hockey injuries. Open Access J Sports Med. 534 2016;7:167-176.
4. Baker JC, Hoover EG, Hillen TJ, Smith MV, Wright RW, Rubin DA. Subradiographic foot and ankle fractures and bone contusions detected by MRI in elite ice hockey players. Am J Sports Med. 2016;44(5):1317-1323.
5. Philippon MJ, Ho CP, Briggs KK, Stull J, LaPrade RF. Prevalence of increased alpha angles as a measure of cam-type femoroacetabular impingement in youth ice hockey players. Am J Sports Med. 2013;41(6):1357-1362.
6. 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.
7. Jorgensen U, Schmidt-Olsen S. The epidemiology of ice hockey injuries. Br J Sports Med. 1986;20(1):7-9.
8. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. BrJ Sports Med. 2014;48(1):4-10.
9. Mosenthal W, Kim M, Holzshu R, Hanypsiak B, Athiviraham A. Common ice hockey injuries and treatment: a current concepts review. Curr Sports Med Rep. 2017;16(5):357-362.
10. Tyler TF, Silvers HJ, Gerhardt MB, Nicholas SJ. Groin injuries in sports medicine. Sports Health. 2010;2(3):231-236.
11. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521-533.
12. Dalton SL, Zupon AB, Gardner EC, Djoko A, Dompier TP, Kerr ZY. The epidemiology of hip/groin injuries in National Collegiate Athletic Association men's and women's ice hockey: 2009-2010 through 2014-2015 academic years. Orthop J Sports Med. 2016;4(3):2325967116632692.
13. Epstein DM, McHugh M, Yorio M, Neri B. Intra-articular hip injuries in national hockey league players: a descriptive epidemiological study. Am J Sports Med. 2013;41(2):343-348.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Ross JR, Bedi A, Stone RM, Sibilsky Enselman E, Kelly BT, Larson CM. Characterization of symptomatic hip impingement in butterfly ice hockey goalies. Arthroscopy. 2015;31(4):635-642.
16. Bedi A, Dolan M, Hetsroni I, et al. Surgical treatment of femoroacetabular impingement improves hip kinematics: a computer-assisted model. Am J Sports Med. 2011;39(Suppl):43S-49S.
17. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
18. Nepple JJ, Goljan P, Briggs KK, Garvey SE, Ryan M, Philippon MJ. Hip strength deficits in patients with symptomatic femoroacetabular impingement and labral ears. Arthroscopy. 2015;31(11):2106-2111.
19. Audenaert EA, Peeters I, Vigneron L, Baelde N, Pattyn C. Hip morphological characteristics and range of internal rotation in femoroacetabular impingement. Am J Sports Med. 2012;40(6):1329-1336.
20. Notzli HP, Wyss TF, Stoecklin CH, Schmid MR, Treiber K, Hodler J. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br. 2002;84(4):556-560.
21. Kuhn AW, Ross JR, Bedi A. Three-dimensional imaging and computer navigation in planning for hip preservation surgery. Sports Med Arthrosc Rev. 2015;23(4):e31-e38.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Kuhn AW, Noonan BC, Kelly BT, Larson CM, Bedi A. The hip in ice hockey: a current concepts review. Arthroscopy. 2016;32(9):1928-1938.
24. O'Connor M, Minkara AA, Westermann RW, Rosneck J, Lynch TS. Return to play after hip arthroscopy: a systematic review and meta-analysis. Am J Sports Med. 2018:46(11):2780-2788.
25. Minkara AA, Westermann RW, Rosneck J, Lynch TS. Systematic review and meta-analysis of outcomes after hip arthroscopy in femoroacetabular impingement. Am J Sports Med. 2018:363546517749475.
26. Philippon MJ, Weiss DR, Kuppersmith DA, Briggs KK, Hay CJ. Arthroscopic labral repair and treatment of femoroacetabular impingement in professional hockey players. Am J Sports Med. 2010;38(1):99-104.
27. Pierce CM, Laprade RF, Wahoff M, O'Brien L, Philippon MJ. Ice hockey goaltender rehabilitation, including on-ice progression, after arthroscopic hip surgery for femoroacetabular impingement. J Orthop Sports Phys Ther. 2013;43(3):129-141.
28. MacLeod DA, Gibbon WW. The sportsman's groin. Br J Surg. 1999;86(7):849-850.
29. Irshad K, Feldman LS, Lavoie C, Lacroix VJ, Mulder DS, Brown RA. Operative management of "hockey groin syndrome": 12 years of experience in National Hockey League players. Surgery. 2001;130(4):759-764; discussion 764-756.
30. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
31. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the "sports hernia": MR imaging findings. Radiology. 2008;247(3):797-807.
32. Jakoi A, O'Neill C, Damsgaard C, Fehring K, Tom J. Sports hernia in National Hockey League players: does surgery affect performance? Am J Sports Med. 2013;41(1):107-110.
33. Larson CM, Pierce BR, Giveans MR. Treatment of athletes with symptomatic intra-articular hip pathology and athletic pubalgia/sports hernia: a case series. Arthroscopy.2011;27(6):768-775.
34. Lorentzon R, Wedren H, Pietila 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.
35. Holmich P, Uhrskou P, Ulnits L, et al. Effectiveness of active physical training as treatment for long-standing adductor-related groin pain in athletes: randomised trial. Lancet. 1999;353(9151):439-443.
36. Sim FH, Chao EY. Injury potential in modern ice hockey. Am J Sports Med. 1978;6(6):378-384.
37. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
38. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. BrJ Sports Med. 2009;43(13):1000-1005.
39. Grant JA, Bedi A, Kurz J, Bancroft R, Miller BS. Incidence and injury characteristics of medial collateral ligament injuries in male collegiate ice hockey players. Sports Health. 2013;5(3):270-272.
40. Erickson BJ, Harris JD, Cole BJ, et al. Performance and return to sport after anterior cruciate ligament reconstruction in National Hockey League players. Orthop J Sports Med. 2014;2(9):2325967114548831.
41. Sikka R, Kurtenbach C, Steubs JT, Boyd JL, Nelson BJ. Anterior Cruciate Ligament Injuries in Professional Hockey Players. Am J Sports Med. 2016;44(2):378-383.
42. Friden T, Erlandsson T, Zatterstrom R, Lindstrand A, Moritz U. Compression or distraction of the anterior cruciate injured knee: variations in injury pattern in contact sports and downhill skiing. Knee Surg Sports Traumatol Arthrosc. 1995;3(3):144-147.
43. Kluczynski MA, Kang JV, Marzo JM, Bisson LJ. Magnetic resonance imaging and intra-articular findings after anterior cruciate ligament injuries in ice hockey versus other sports. Orthop J Sports Med. 2016;4(5):2325967116646534. 44. Beiner JM, Jokl P. Muscle contusion injuries: current treatment options. J Am Acad Orthop Surg. 2001;9(4):227-237.
45. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.
46. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.
47. Johnson PN, Mark; Green, Eric. Boot-top lacerations in ice hockey players: a new injury. Clin J Sports Med. 1991:205-208.
48. Nauth A, Aziz M, Tsuji M, Whalen DB, Theodoropoulos JS, Zdero R. The protective effect of Kevlar socks against hockey skate blade injuries: a biomechanical study. Orthop J Sports Med. 2014;2(Suppl 2):7.
49. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
50. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.
51. Marymont JV, Lynch MA, Henning CE. Acute ligamentous diastasis of the ankle without fracture. Evaluation by radionuclide imaging. Am J Sports Med. 1986;14(5):407-409.
52. Miller CD, Shelton WR, Barrett GR, Savoie FH, Dukes AD. Deltoid and syndesmosis ligament injury of the ankle without fracture. Am J Sports Med. 1995;23(6):746-750.
53. Singh SK, Larkin KE, Kadakia AR, Hsu WK. Risk factors for reoperation and performance-based outcomes after operative fixation of foot fractures in the professional athlete: a cross-sport analysis. Sports Health. 2018;10(1):70-74.
54. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.
55. Elattar O, Choi HR, Dills VD, Busconi B. Groin injuries (athletic pubalgia) and return to play. Sports Health. 2016;8(4):313-323.
1. 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.
2. Popkin CA, Nelson BJ, Park CN, et al. Head, neck, and shoulder injuries in ice hockey: current concepts. Am J Orthop (Belle Mead NJ). 2017;46(3):123-134.
3. Popkin CA, Schulz BM, Park CN, Bottiglieri TS, Lynch TS. Evaluation, management and prevention of lower extremity youth ice hockey injuries. Open Access J Sports Med. 534 2016;7:167-176.
4. Baker JC, Hoover EG, Hillen TJ, Smith MV, Wright RW, Rubin DA. Subradiographic foot and ankle fractures and bone contusions detected by MRI in elite ice hockey players. Am J Sports Med. 2016;44(5):1317-1323.
5. Philippon MJ, Ho CP, Briggs KK, Stull J, LaPrade RF. Prevalence of increased alpha angles as a measure of cam-type femoroacetabular impingement in youth ice hockey players. Am J Sports Med. 2013;41(6):1357-1362.
6. 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.
7. Jorgensen U, Schmidt-Olsen S. The epidemiology of ice hockey injuries. Br J Sports Med. 1986;20(1):7-9.
8. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. BrJ Sports Med. 2014;48(1):4-10.
9. Mosenthal W, Kim M, Holzshu R, Hanypsiak B, Athiviraham A. Common ice hockey injuries and treatment: a current concepts review. Curr Sports Med Rep. 2017;16(5):357-362.
10. Tyler TF, Silvers HJ, Gerhardt MB, Nicholas SJ. Groin injuries in sports medicine. Sports Health. 2010;2(3):231-236.
11. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521-533.
12. Dalton SL, Zupon AB, Gardner EC, Djoko A, Dompier TP, Kerr ZY. The epidemiology of hip/groin injuries in National Collegiate Athletic Association men's and women's ice hockey: 2009-2010 through 2014-2015 academic years. Orthop J Sports Med. 2016;4(3):2325967116632692.
13. Epstein DM, McHugh M, Yorio M, Neri B. Intra-articular hip injuries in national hockey league players: a descriptive epidemiological study. Am J Sports Med. 2013;41(2):343-348.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Ross JR, Bedi A, Stone RM, Sibilsky Enselman E, Kelly BT, Larson CM. Characterization of symptomatic hip impingement in butterfly ice hockey goalies. Arthroscopy. 2015;31(4):635-642.
16. Bedi A, Dolan M, Hetsroni I, et al. Surgical treatment of femoroacetabular impingement improves hip kinematics: a computer-assisted model. Am J Sports Med. 2011;39(Suppl):43S-49S.
17. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
18. Nepple JJ, Goljan P, Briggs KK, Garvey SE, Ryan M, Philippon MJ. Hip strength deficits in patients with symptomatic femoroacetabular impingement and labral ears. Arthroscopy. 2015;31(11):2106-2111.
19. Audenaert EA, Peeters I, Vigneron L, Baelde N, Pattyn C. Hip morphological characteristics and range of internal rotation in femoroacetabular impingement. Am J Sports Med. 2012;40(6):1329-1336.
20. Notzli HP, Wyss TF, Stoecklin CH, Schmid MR, Treiber K, Hodler J. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br. 2002;84(4):556-560.
21. Kuhn AW, Ross JR, Bedi A. Three-dimensional imaging and computer navigation in planning for hip preservation surgery. Sports Med Arthrosc Rev. 2015;23(4):e31-e38.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. Kuhn AW, Noonan BC, Kelly BT, Larson CM, Bedi A. The hip in ice hockey: a current concepts review. Arthroscopy. 2016;32(9):1928-1938.
24. O'Connor M, Minkara AA, Westermann RW, Rosneck J, Lynch TS. Return to play after hip arthroscopy: a systematic review and meta-analysis. Am J Sports Med. 2018:46(11):2780-2788.
25. Minkara AA, Westermann RW, Rosneck J, Lynch TS. Systematic review and meta-analysis of outcomes after hip arthroscopy in femoroacetabular impingement. Am J Sports Med. 2018:363546517749475.
26. Philippon MJ, Weiss DR, Kuppersmith DA, Briggs KK, Hay CJ. Arthroscopic labral repair and treatment of femoroacetabular impingement in professional hockey players. Am J Sports Med. 2010;38(1):99-104.
27. Pierce CM, Laprade RF, Wahoff M, O'Brien L, Philippon MJ. Ice hockey goaltender rehabilitation, including on-ice progression, after arthroscopic hip surgery for femoroacetabular impingement. J Orthop Sports Phys Ther. 2013;43(3):129-141.
28. MacLeod DA, Gibbon WW. The sportsman's groin. Br J Surg. 1999;86(7):849-850.
29. Irshad K, Feldman LS, Lavoie C, Lacroix VJ, Mulder DS, Brown RA. Operative management of "hockey groin syndrome": 12 years of experience in National Hockey League players. Surgery. 2001;130(4):759-764; discussion 764-756.
30. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
31. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the "sports hernia": MR imaging findings. Radiology. 2008;247(3):797-807.
32. Jakoi A, O'Neill C, Damsgaard C, Fehring K, Tom J. Sports hernia in National Hockey League players: does surgery affect performance? Am J Sports Med. 2013;41(1):107-110.
33. Larson CM, Pierce BR, Giveans MR. Treatment of athletes with symptomatic intra-articular hip pathology and athletic pubalgia/sports hernia: a case series. Arthroscopy.2011;27(6):768-775.
34. Lorentzon R, Wedren H, Pietila 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.
35. Holmich P, Uhrskou P, Ulnits L, et al. Effectiveness of active physical training as treatment for long-standing adductor-related groin pain in athletes: randomised trial. Lancet. 1999;353(9151):439-443.
36. Sim FH, Chao EY. Injury potential in modern ice hockey. Am J Sports Med. 1978;6(6):378-384.
37. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
38. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. BrJ Sports Med. 2009;43(13):1000-1005.
39. Grant JA, Bedi A, Kurz J, Bancroft R, Miller BS. Incidence and injury characteristics of medial collateral ligament injuries in male collegiate ice hockey players. Sports Health. 2013;5(3):270-272.
40. Erickson BJ, Harris JD, Cole BJ, et al. Performance and return to sport after anterior cruciate ligament reconstruction in National Hockey League players. Orthop J Sports Med. 2014;2(9):2325967114548831.
41. Sikka R, Kurtenbach C, Steubs JT, Boyd JL, Nelson BJ. Anterior Cruciate Ligament Injuries in Professional Hockey Players. Am J Sports Med. 2016;44(2):378-383.
42. Friden T, Erlandsson T, Zatterstrom R, Lindstrand A, Moritz U. Compression or distraction of the anterior cruciate injured knee: variations in injury pattern in contact sports and downhill skiing. Knee Surg Sports Traumatol Arthrosc. 1995;3(3):144-147.
43. Kluczynski MA, Kang JV, Marzo JM, Bisson LJ. Magnetic resonance imaging and intra-articular findings after anterior cruciate ligament injuries in ice hockey versus other sports. Orthop J Sports Med. 2016;4(5):2325967116646534. 44. Beiner JM, Jokl P. Muscle contusion injuries: current treatment options. J Am Acad Orthop Surg. 2001;9(4):227-237.
45. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am. 1973;55(1):95-105.
46. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am J Sports Med. 1991;19(3):299-304.
47. Johnson PN, Mark; Green, Eric. Boot-top lacerations in ice hockey players: a new injury. Clin J Sports Med. 1991:205-208.
48. Nauth A, Aziz M, Tsuji M, Whalen DB, Theodoropoulos JS, Zdero R. The protective effect of Kevlar socks against hockey skate blade injuries: a biomechanical study. Orthop J Sports Med. 2014;2(Suppl 2):7.
49. Wright RW, Barile RJ, Surprenant DA, Matava MJ. Ankle syndesmosis sprains in national hockey league players. Am J Sports Med. 2004;32(8):1941-1945.
50. Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med. 1991;19(3):294-298.
51. Marymont JV, Lynch MA, Henning CE. Acute ligamentous diastasis of the ankle without fracture. Evaluation by radionuclide imaging. Am J Sports Med. 1986;14(5):407-409.
52. Miller CD, Shelton WR, Barrett GR, Savoie FH, Dukes AD. Deltoid and syndesmosis ligament injury of the ankle without fracture. Am J Sports Med. 1995;23(6):746-750.
53. Singh SK, Larkin KE, Kadakia AR, Hsu WK. Risk factors for reoperation and performance-based outcomes after operative fixation of foot fractures in the professional athlete: a cross-sport analysis. Sports Health. 2018;10(1):70-74.
54. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.
55. Elattar O, Choi HR, Dills VD, Busconi B. Groin injuries (athletic pubalgia) and return to play. Sports Health. 2016;8(4):313-323.
TAKE-HOME POINTS:
Ice hockey is a high-speed, collision sport with one of the highest injury rates in all of sports.
Femoroacetabular impingement is a cause of hip pain at all levels of ice hockey; studies indicate goaltenders are at high risk—particularly those who utilize the butterfly, as opposed to hybrid or stand-up, goaltending style.
Medial collateral ligament (MCL) tears are common in ice hockey and are usually the result of a collision with another player.
Use of Kevlar socks and placement of skate tongues deep to the shin pads can help reduce the chance of a boot-top laceration.
High-ankle sprains are more prevalent in ice hockey because of the rigidity of hockey skates and can be a cause of significant loss of time away from the rink.
Total knee replacement risk soars after arthroscopic surgery for meniscal tear
CHICAGO – A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.
At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.
“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.
Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.
Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.
At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.
The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.
“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.
He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.
“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.
Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.
Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.
SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.
CHICAGO – A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.
At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.
“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.
Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.
Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.
At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.
The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.
“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.
He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.
“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.
Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.
Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.
SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.
CHICAGO – A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.
At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.
“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.
Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.
Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.
At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.
The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.
“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.
He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.
“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.
Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.
Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.
SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.
REPORTING FROM THE ACR ANNUAL MEETING
Key clinical point: Risk of total knee replacement is five times higher after arthroscopic partial meniscectomy.
Major finding: Patients randomized to arthroscopic partial meniscectomy were 400% more likely to subsequently undergo total knee replacement than were those randomized to physical therapy alone.
Study details: This was a presentation of the 5-year follow-up results in 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy.
Disclosures: The presenter reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.
Source: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.
Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees
ABSTRACT
The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.
When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.
This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
Continue to: Knee OA is...
Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.
Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.2 Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2
However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3
Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5
Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10 This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11
The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.
Continue to: This report details...
STUDY PRESENTATION
This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.
TABLE. Patient Demographics | |
Male n (%) | 10 (58.8) |
Age, mean ± SD (range) | 68.27 ± 7.43 |
BMI, mean ± SD (range) | 28.98 ± 4.50 |
Kellgren–Lawrence grade 3 (n) | 7 |
Kellgren–Lawrence grade 4 (n) | 19 |
Abbreviation: BMI, body mass index.
The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.
METHODS
After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.
After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.
STATISTICAL ANALYSIS
Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.
Continue to: No significant adverse...
RESULTS
No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.
Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).
DISCUSSION
Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.
A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14
Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15
In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16
In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17
Continue to: The results of...
The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.
In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.
The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.
A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.
CONCLUSION
The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
- Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
- Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
- Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
- Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
- Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
- Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
- Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
- Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
- Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
- Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
- Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
- Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
- Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
- Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
- Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
- Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
- Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
- Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
ABSTRACT
The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.
When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.
This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
Continue to: Knee OA is...
Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.
Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.2 Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2
However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3
Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5
Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10 This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11
The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.
Continue to: This report details...
STUDY PRESENTATION
This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.
TABLE. Patient Demographics | |
Male n (%) | 10 (58.8) |
Age, mean ± SD (range) | 68.27 ± 7.43 |
BMI, mean ± SD (range) | 28.98 ± 4.50 |
Kellgren–Lawrence grade 3 (n) | 7 |
Kellgren–Lawrence grade 4 (n) | 19 |
Abbreviation: BMI, body mass index.
The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.
METHODS
After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.
After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.
STATISTICAL ANALYSIS
Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.
Continue to: No significant adverse...
RESULTS
No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.
Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).
DISCUSSION
Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.
A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14
Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15
In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16
In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17
Continue to: The results of...
The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.
In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.
The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.
A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.
CONCLUSION
The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
ABSTRACT
The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.
When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.
This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
Continue to: Knee OA is...
Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.
Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.2 Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2
However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3
Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5
Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10 This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11
The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.
Continue to: This report details...
STUDY PRESENTATION
This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.
TABLE. Patient Demographics | |
Male n (%) | 10 (58.8) |
Age, mean ± SD (range) | 68.27 ± 7.43 |
BMI, mean ± SD (range) | 28.98 ± 4.50 |
Kellgren–Lawrence grade 3 (n) | 7 |
Kellgren–Lawrence grade 4 (n) | 19 |
Abbreviation: BMI, body mass index.
The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.
METHODS
After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.
After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.
STATISTICAL ANALYSIS
Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.
Continue to: No significant adverse...
RESULTS
No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.
Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).
DISCUSSION
Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.
A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14
Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15
In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16
In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17
Continue to: The results of...
The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.
In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.
The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.
A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.
CONCLUSION
The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.
- Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
- Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
- Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
- Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
- Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
- Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
- Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
- Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
- Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
- Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
- Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
- Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
- Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
- Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
- Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
- Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
- Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
- Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
- Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
- Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
- Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
- Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
- Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
- Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
- Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
- Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
- Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
- Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
- Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
- Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
- Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
- Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
- Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
- Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
- Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
- Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
TAKE-HOME POINTS
- Severe knee osteoarthritis causes pain and limits functions in a substantial proportion of the aging population.
- Total knee arthroplasty is often recommended in this group of patients when conservative management has failed.
- Many patients in this group continue to seek a nonsurgical option for this process.
- Autologous, micro-fractured, minimally manipulated adipose tissue is easy to harvest, and injection into a knee joint resulted in significant improvement in pain and function for at least 12 months in this study population.
- This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population.
The Unintended Off-road Experience
ANSWER
A moderate amount of soft-tissue swelling is evident. There is also a fracture of the distal radius and an avulsion fracture of the triquetrum. The latter is the second most commonly fractured carpal bone after the scaphoid. Triquetral fractures usually result from a hyperflexion injury.
The patient’s wrist was immobilized in a splint, and referral to a hand surgeon was coordinated.
ANSWER
A moderate amount of soft-tissue swelling is evident. There is also a fracture of the distal radius and an avulsion fracture of the triquetrum. The latter is the second most commonly fractured carpal bone after the scaphoid. Triquetral fractures usually result from a hyperflexion injury.
The patient’s wrist was immobilized in a splint, and referral to a hand surgeon was coordinated.
ANSWER
A moderate amount of soft-tissue swelling is evident. There is also a fracture of the distal radius and an avulsion fracture of the triquetrum. The latter is the second most commonly fractured carpal bone after the scaphoid. Triquetral fractures usually result from a hyperflexion injury.
The patient’s wrist was immobilized in a splint, and referral to a hand surgeon was coordinated.
A 70-year-old woman is brought to the emergency department by EMS after being involved in a motor vehicle collision. She was a restrained driver in a vehicle that was hit by a tractor-trailer, causing her vehicle to go off the road and hit the guardrail. She does not recall if the airbag deployed, and she believes she momentarily lost consciousness. She is complaining of pain in the head and the right wrist.
Her medical history is significant for mild (controlled) hypertension. Primary survey reveals an elderly female who is awake, alert, and oriented and in mild distress. Her vital signs are stable.
The patient has a small laceration on her face. Her right wrist is moderately swollen, and she has decreased range of motion. There is also moderate tenderness to palpation. Pulses are good, as is capillary refill time in the fingernail bed.
Radiograph of the right wrist is obtained (oblique view shown). What is your impression?
Osteoporosis: Breaking Down the Treatment Options
Ms. B, a 72-year-old woman, presents with new-onset low back pain. A comprehensive workup is performed, and a radiograph reveals compression fractures of the L1 and L2 vertebral bodies. The patient recalls no trauma to account for her fractures. Dual-energy x-ray absorptiometry (DXA) is ordered; the results show evidence of osteoporosis. Ms. B asks about initiating longterm treatment.
Osteoporosis is a disease of significant public health concern.1 According to the NIH Osteoporosis and Related Bone Diseases National Resource Center, more than 53 million people in the United States either have osteoporosis or are at high risk for it.2 The total cost of osteoporosis-related fractures is expected to reach $25.3 billion by 2025.3 It is estimated that one in three women (and one in five men) older than 50 will sustain osteoporotic fractures.4 The morbidity and mortality associated with these fractures must be recognized by health care providers in all medical specialties. Appropriate preventive and treatment modalities should be employed when providing care to persons with or at risk for osteoporosis. Advances in medical science have yielded multiple options for the prevention and treatment of osteoporosis.
CASE CONTINUED Ms. B’s medical history includes hypertension and GERD, for which she uses twice-daily dosing of a proton pump inhibitor (PPI). At age 53, she was diagnosed with left breast cancer, which required surgical excision and radiation therapy. She took tamoxifen for a total of five years, and the cancer did not recur. She takes no OTC products, including vitamins. She has no history of systemic inflammatory conditions, kidney stones, or extended treatment with corticosteroids. No history of gastrointestinal surgeries is reported. Ms. B has never smoked cigarettes and has never consumed two or more alcoholic beverages a day. She has no family history of osteoporosis in first-degree relatives. She is otherwise healthy but is physically inactive, with no regular weight-bearing exercise routine. It is also notable that she experienced an uneventful early menopause at age 41 and did not take estrogen replacement therapy.
NONPHARMACOLOGIC OPTIONS
Regular weight-bearing exercise, adequate calcium and vitamin D intake, smoking cessation, avoidance of heavy alcohol use, and education in fall prevention are vital. Recommended calcium intake varies by age, ranging from 1,000 mg/d to 1,200 mg/d in divided doses.2 Vitamin D intake is recommended at 600 IU/d until age 70; 800 IU/d after age 70;and additional units if deficiency is noted.2 Avoidance of medications that contribute to bone loss (eg, corticosteroids) is also encouraged, if possible. Patient education should include balance training and a home safety assessment.
CASE POINT Nonpharmacologic strategies should be encouraged for every patient to promote optimal bone health and to prevent or treat osteoporosis.
PHARMACOLOGIC OPTIONS
Oral bisphosphonates are considered firstline treatment for osteoporosis; currently available options include alendronate, risedronate, and ibandronate. Bisphosphonates work by inhibiting osteoclast function, thereby reducing bone resorption.5
Oral bisphosphonates have been clinically available since the 1990s and have demonstrated their efficacy, safety, and cost-effectiveness.6-8 However, a thoughtful approach should be taken to their use in specific patient populations: those with esophageal disorders, chronic kidney disease, and/or a history of bariatric gastrointestinal procedures. Bisphosphonates of any form should be avoided in a patient with chronic kidney disease with a glomerular filtration rate ≤ 30 mL/min or ≤ 35 mL/min (based on the package insert for the specific product).7 Patients with a recent or upcoming tooth extraction should also avoid using bisphosphonates until they have healed, due to concerns for osteonecrosis of the jaw.
Continue to: Administration of oral bisphosphonates requires...
Administration of oral bisphosphonates requires special attention. Oral bisphosphonates must be taken first thing in the morning with water; for the next 30 to 60 minutes, the patient must stay upright and not have any food, drink, or additional medications by mouth. These specifications may affect patient adherence to treatment.
Intravenous bisphosphonates. Depending on the IV bisphosphonate chosen—ibandronate and zoledronic acid are the currently available options—administration is recommended either every three or 12 months. A common adverse effect of IV bisphosphonates is flulike symptoms, which are generally brief in duration. Hypocalcemia has also been associated with IV administration, more so than with oral bisphosphonate use. Osteonecrosis of the jaw, while rare, must also be considered.
CASE POINT Because of Ms. B’s GERD requiring PPI use, oral bisphosphonates are not the most ideal treatment for her osteoporosis; they could exacerbate her gastrointestinal symptoms. IV bisphosphonates are a potential option for her, as this method of administration would eliminate the gastrointestinal risk associated with oral bisphosphonates.
Selective estrogen receptor modulators (SERMs), which are administered orally, are another option for osteoporosis treatment for vertebral fractures. One medication in this class, raloxifene, selectively acts on estrogen receptors—it works as an agonist in bone estrogen receptors (preventing bone loss) and an estrogen antagonist in other tissue (eg, breast, uterine). SERMs are not considered firstline treatment for osteoporosis because they appear to be less potent than other currently available agents. However, a postmenopausal patient with a high risk for invasive breast cancer without a history of fragility fracture might consider this option, as raloxifene can reduce the risk for invasive breast cancer.9 SERMs have been associated with an increase in thromboembolic events and hot flashes.
Calcitonin nasal spray is used much less commonly now because its effect on bone mineral density is weaker than other currently available options. Calcitonin nasal spray is administered as one spray in one nostril each day. There has been some concern regarding calcitonin use and its association with malignancy.10
Continue to: CASE POINT
CASE POINT Ms. B’s history of compression fractures suggests the need for potent pharmacologic options to treat her osteoporosis. SERMS and calcitonin nasal spray are felt to be less potent and therefore are not the preferred treatment recommendations for her
Parathyroid hormone analogs. The availability of the parathyroid hormone analogs teriparatide and abaloparatide gives patients and health care providers another treatment option for osteoporosis.11 These potent stimulators of bone remodeling help reduce future fracture risk. Teriparatide and abaloparatide are considered anabolic bone agents, rather than antiresorptive medications. These medications are administered subcutaneously daily for no more than two years. Many health care providers use parathyroid hormone analogs for patients with severe osteoporosis (T score, ≤ –3.5 without fragility fracture history or ≤ –2.5 with fragility fracture history).12 The cost of these agents must be considered when recommending them to eligible patients.8
Parathyroid hormone analogs do carry a black box warning because of an increased risk for osteosarcoma observed in rat studies.13,14 These products should therefore be avoided in patients with increased risk for osteosarcoma: those who have Paget disease of the bone or unexplained elevations of alkaline phosphatase; pediatric and young adult patients with open epiphyses; or those who have had external beam or implant radiation therapy involving the skeleton.13,14
CASE POINT Because of Ms. B’s prior history of breast cancer requiring radiation treatment, parathyroid hormone analogs are not recommended.
Denosumab is a human monoclonal antibody, a RANKL inhibitor, that works by preventing the development of osteoclasts. This medication is administered subcutaneously every six months. There are no dosing adjustments recommended for hepatic impairment.11 The denosumab package insert does not specify a dosage adjustment for patients with renal impairment; however, clinical studies have indicated that patients who have a creatine clearance < 30 mL/min or who are on dialysis are more likely to experience hypocalcemia with denosumab use.15 As with other newer osteoporosis treatments, cost considerations should be discussed with patients.
Continue to: One unique consideration...
One unique consideration is that clinical trials have shown an increased fracture risk and the return of bone mineral density to predenosumab treatment levels within 18 months of discontinuing the medication.15 Health care providers should be prepared to recommend alternative treatment options if denosumab is discontinued.
CASE CONCLUDED After a discussion of the risks, benefits, and expectations associated with each of the available treatment options, Ms. B and her health care provider narrow down her options to use of an IV bisphosphonate or denosumab for her osteoporosis. She ultimately chooses denosumab, based on her preference for an injectable medication.
CONCLUSION
The morbidity and mortality associated with osteoporosis can be improved with an appropriate balance of nonpharmacologic and pharmacologic approaches. The varying mechanisms of action, administration methods, and documented efficacy of the available medications provide an opportunity for patient education and informed decision-making when choosing treatment. For additional guidance, the American College of Physicians, the American Association of Clinical Endocrinologists, and American College of Endocrinology have published guidelines that can help in the decision-making process.16,17
1. Cauley JA. Public health impact of osteoporosis. J Gerontol A Biol Sci Med Sci. 2013;68(10):1243-1251.
2. NIH Osteoporosis and Related Bone Diseases National Resource Center. Osteoporosis overview. February 2017. www.bones.nih.gov/health-info/bone/osteoporosis/overview. Accessed October 1, 2018.
3. Dempster DW. Osteoporosis and the burden of osteoporosis-related fractures. Am J Manag Care. 2011;17: S164-S169.
4. International Osteoporosis Foundation. Osteoporosis facts and statistics. www.iofbonehealth.org/facts-and-statistics/calcium-studies-map. Accessed October 1, 2018.
5. Weinstein RS, Roberson PK, Manolagas SC. Giant osteoclast formation and long-term oral bisphosphonate therapy. N Engl J Med. 2009;360(1):53-62.
6. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2):S14-S21.
7. Miller PD. Long-term extension trials to prove the efficacy of and safety of bisphosphonates. Clin Invest. 2014;4(1):35-43.
8. Hiligsmann M, Evers SM, Sedrine B, et al. A systematic review of cost-effectiveness analyses of drugs for postmenopausal osteoporosis. Pharmacoeconomics. 2015;33(3):205-224.
9. Raloxifene [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
10. Wells G, Chernoff J, Gilligan JP, Krause DS. Does salmon calcitonin cause cancer? A review and meta-analysis. Osteoporos Int. 2016;27(1):13-19.
11. Leder BZ. Parathyroid hormone and parathyroid hormone-related protein analogs in osteoporosis therapy. Curr Osteoporos Rep. 2017;15:110-119.
12. Kendler DL, Marin F, Zerbini CAF, et al. Effects of teriparatide and risedronate on new fractures in post-menopausal women with severe osteoporosis (VERO): a multicentre, double-blind, double-dummy, randomised controlled trial. Lancet. 2018;391:230-240.
13. Teriparatide [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
14. Abaloparatide [package insert]. Waltham, MA: Radius Health, Inc; 2017.
15. Denosumab [package insert]. Thousand Oaks, CA: Amgen Inc; 2018.
16. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis—2016. Endocr Pract. 2016;22(4):1-42.
17. Qaseem A, Forciea MA, McLean RM, et al; Clinical Guidelines Committee of the American College of Physicians. Treatment of low bone density or osteoporosis to prevent fractures in men and women: a clinical practice guideline update from the American College of Physicians. Ann Intern Med. 2017;166(11):818-839.
Ms. B, a 72-year-old woman, presents with new-onset low back pain. A comprehensive workup is performed, and a radiograph reveals compression fractures of the L1 and L2 vertebral bodies. The patient recalls no trauma to account for her fractures. Dual-energy x-ray absorptiometry (DXA) is ordered; the results show evidence of osteoporosis. Ms. B asks about initiating longterm treatment.
Osteoporosis is a disease of significant public health concern.1 According to the NIH Osteoporosis and Related Bone Diseases National Resource Center, more than 53 million people in the United States either have osteoporosis or are at high risk for it.2 The total cost of osteoporosis-related fractures is expected to reach $25.3 billion by 2025.3 It is estimated that one in three women (and one in five men) older than 50 will sustain osteoporotic fractures.4 The morbidity and mortality associated with these fractures must be recognized by health care providers in all medical specialties. Appropriate preventive and treatment modalities should be employed when providing care to persons with or at risk for osteoporosis. Advances in medical science have yielded multiple options for the prevention and treatment of osteoporosis.
CASE CONTINUED Ms. B’s medical history includes hypertension and GERD, for which she uses twice-daily dosing of a proton pump inhibitor (PPI). At age 53, she was diagnosed with left breast cancer, which required surgical excision and radiation therapy. She took tamoxifen for a total of five years, and the cancer did not recur. She takes no OTC products, including vitamins. She has no history of systemic inflammatory conditions, kidney stones, or extended treatment with corticosteroids. No history of gastrointestinal surgeries is reported. Ms. B has never smoked cigarettes and has never consumed two or more alcoholic beverages a day. She has no family history of osteoporosis in first-degree relatives. She is otherwise healthy but is physically inactive, with no regular weight-bearing exercise routine. It is also notable that she experienced an uneventful early menopause at age 41 and did not take estrogen replacement therapy.
NONPHARMACOLOGIC OPTIONS
Regular weight-bearing exercise, adequate calcium and vitamin D intake, smoking cessation, avoidance of heavy alcohol use, and education in fall prevention are vital. Recommended calcium intake varies by age, ranging from 1,000 mg/d to 1,200 mg/d in divided doses.2 Vitamin D intake is recommended at 600 IU/d until age 70; 800 IU/d after age 70;and additional units if deficiency is noted.2 Avoidance of medications that contribute to bone loss (eg, corticosteroids) is also encouraged, if possible. Patient education should include balance training and a home safety assessment.
CASE POINT Nonpharmacologic strategies should be encouraged for every patient to promote optimal bone health and to prevent or treat osteoporosis.
PHARMACOLOGIC OPTIONS
Oral bisphosphonates are considered firstline treatment for osteoporosis; currently available options include alendronate, risedronate, and ibandronate. Bisphosphonates work by inhibiting osteoclast function, thereby reducing bone resorption.5
Oral bisphosphonates have been clinically available since the 1990s and have demonstrated their efficacy, safety, and cost-effectiveness.6-8 However, a thoughtful approach should be taken to their use in specific patient populations: those with esophageal disorders, chronic kidney disease, and/or a history of bariatric gastrointestinal procedures. Bisphosphonates of any form should be avoided in a patient with chronic kidney disease with a glomerular filtration rate ≤ 30 mL/min or ≤ 35 mL/min (based on the package insert for the specific product).7 Patients with a recent or upcoming tooth extraction should also avoid using bisphosphonates until they have healed, due to concerns for osteonecrosis of the jaw.
Continue to: Administration of oral bisphosphonates requires...
Administration of oral bisphosphonates requires special attention. Oral bisphosphonates must be taken first thing in the morning with water; for the next 30 to 60 minutes, the patient must stay upright and not have any food, drink, or additional medications by mouth. These specifications may affect patient adherence to treatment.
Intravenous bisphosphonates. Depending on the IV bisphosphonate chosen—ibandronate and zoledronic acid are the currently available options—administration is recommended either every three or 12 months. A common adverse effect of IV bisphosphonates is flulike symptoms, which are generally brief in duration. Hypocalcemia has also been associated with IV administration, more so than with oral bisphosphonate use. Osteonecrosis of the jaw, while rare, must also be considered.
CASE POINT Because of Ms. B’s GERD requiring PPI use, oral bisphosphonates are not the most ideal treatment for her osteoporosis; they could exacerbate her gastrointestinal symptoms. IV bisphosphonates are a potential option for her, as this method of administration would eliminate the gastrointestinal risk associated with oral bisphosphonates.
Selective estrogen receptor modulators (SERMs), which are administered orally, are another option for osteoporosis treatment for vertebral fractures. One medication in this class, raloxifene, selectively acts on estrogen receptors—it works as an agonist in bone estrogen receptors (preventing bone loss) and an estrogen antagonist in other tissue (eg, breast, uterine). SERMs are not considered firstline treatment for osteoporosis because they appear to be less potent than other currently available agents. However, a postmenopausal patient with a high risk for invasive breast cancer without a history of fragility fracture might consider this option, as raloxifene can reduce the risk for invasive breast cancer.9 SERMs have been associated with an increase in thromboembolic events and hot flashes.
Calcitonin nasal spray is used much less commonly now because its effect on bone mineral density is weaker than other currently available options. Calcitonin nasal spray is administered as one spray in one nostril each day. There has been some concern regarding calcitonin use and its association with malignancy.10
Continue to: CASE POINT
CASE POINT Ms. B’s history of compression fractures suggests the need for potent pharmacologic options to treat her osteoporosis. SERMS and calcitonin nasal spray are felt to be less potent and therefore are not the preferred treatment recommendations for her
Parathyroid hormone analogs. The availability of the parathyroid hormone analogs teriparatide and abaloparatide gives patients and health care providers another treatment option for osteoporosis.11 These potent stimulators of bone remodeling help reduce future fracture risk. Teriparatide and abaloparatide are considered anabolic bone agents, rather than antiresorptive medications. These medications are administered subcutaneously daily for no more than two years. Many health care providers use parathyroid hormone analogs for patients with severe osteoporosis (T score, ≤ –3.5 without fragility fracture history or ≤ –2.5 with fragility fracture history).12 The cost of these agents must be considered when recommending them to eligible patients.8
Parathyroid hormone analogs do carry a black box warning because of an increased risk for osteosarcoma observed in rat studies.13,14 These products should therefore be avoided in patients with increased risk for osteosarcoma: those who have Paget disease of the bone or unexplained elevations of alkaline phosphatase; pediatric and young adult patients with open epiphyses; or those who have had external beam or implant radiation therapy involving the skeleton.13,14
CASE POINT Because of Ms. B’s prior history of breast cancer requiring radiation treatment, parathyroid hormone analogs are not recommended.
Denosumab is a human monoclonal antibody, a RANKL inhibitor, that works by preventing the development of osteoclasts. This medication is administered subcutaneously every six months. There are no dosing adjustments recommended for hepatic impairment.11 The denosumab package insert does not specify a dosage adjustment for patients with renal impairment; however, clinical studies have indicated that patients who have a creatine clearance < 30 mL/min or who are on dialysis are more likely to experience hypocalcemia with denosumab use.15 As with other newer osteoporosis treatments, cost considerations should be discussed with patients.
Continue to: One unique consideration...
One unique consideration is that clinical trials have shown an increased fracture risk and the return of bone mineral density to predenosumab treatment levels within 18 months of discontinuing the medication.15 Health care providers should be prepared to recommend alternative treatment options if denosumab is discontinued.
CASE CONCLUDED After a discussion of the risks, benefits, and expectations associated with each of the available treatment options, Ms. B and her health care provider narrow down her options to use of an IV bisphosphonate or denosumab for her osteoporosis. She ultimately chooses denosumab, based on her preference for an injectable medication.
CONCLUSION
The morbidity and mortality associated with osteoporosis can be improved with an appropriate balance of nonpharmacologic and pharmacologic approaches. The varying mechanisms of action, administration methods, and documented efficacy of the available medications provide an opportunity for patient education and informed decision-making when choosing treatment. For additional guidance, the American College of Physicians, the American Association of Clinical Endocrinologists, and American College of Endocrinology have published guidelines that can help in the decision-making process.16,17
Ms. B, a 72-year-old woman, presents with new-onset low back pain. A comprehensive workup is performed, and a radiograph reveals compression fractures of the L1 and L2 vertebral bodies. The patient recalls no trauma to account for her fractures. Dual-energy x-ray absorptiometry (DXA) is ordered; the results show evidence of osteoporosis. Ms. B asks about initiating longterm treatment.
Osteoporosis is a disease of significant public health concern.1 According to the NIH Osteoporosis and Related Bone Diseases National Resource Center, more than 53 million people in the United States either have osteoporosis or are at high risk for it.2 The total cost of osteoporosis-related fractures is expected to reach $25.3 billion by 2025.3 It is estimated that one in three women (and one in five men) older than 50 will sustain osteoporotic fractures.4 The morbidity and mortality associated with these fractures must be recognized by health care providers in all medical specialties. Appropriate preventive and treatment modalities should be employed when providing care to persons with or at risk for osteoporosis. Advances in medical science have yielded multiple options for the prevention and treatment of osteoporosis.
CASE CONTINUED Ms. B’s medical history includes hypertension and GERD, for which she uses twice-daily dosing of a proton pump inhibitor (PPI). At age 53, she was diagnosed with left breast cancer, which required surgical excision and radiation therapy. She took tamoxifen for a total of five years, and the cancer did not recur. She takes no OTC products, including vitamins. She has no history of systemic inflammatory conditions, kidney stones, or extended treatment with corticosteroids. No history of gastrointestinal surgeries is reported. Ms. B has never smoked cigarettes and has never consumed two or more alcoholic beverages a day. She has no family history of osteoporosis in first-degree relatives. She is otherwise healthy but is physically inactive, with no regular weight-bearing exercise routine. It is also notable that she experienced an uneventful early menopause at age 41 and did not take estrogen replacement therapy.
NONPHARMACOLOGIC OPTIONS
Regular weight-bearing exercise, adequate calcium and vitamin D intake, smoking cessation, avoidance of heavy alcohol use, and education in fall prevention are vital. Recommended calcium intake varies by age, ranging from 1,000 mg/d to 1,200 mg/d in divided doses.2 Vitamin D intake is recommended at 600 IU/d until age 70; 800 IU/d after age 70;and additional units if deficiency is noted.2 Avoidance of medications that contribute to bone loss (eg, corticosteroids) is also encouraged, if possible. Patient education should include balance training and a home safety assessment.
CASE POINT Nonpharmacologic strategies should be encouraged for every patient to promote optimal bone health and to prevent or treat osteoporosis.
PHARMACOLOGIC OPTIONS
Oral bisphosphonates are considered firstline treatment for osteoporosis; currently available options include alendronate, risedronate, and ibandronate. Bisphosphonates work by inhibiting osteoclast function, thereby reducing bone resorption.5
Oral bisphosphonates have been clinically available since the 1990s and have demonstrated their efficacy, safety, and cost-effectiveness.6-8 However, a thoughtful approach should be taken to their use in specific patient populations: those with esophageal disorders, chronic kidney disease, and/or a history of bariatric gastrointestinal procedures. Bisphosphonates of any form should be avoided in a patient with chronic kidney disease with a glomerular filtration rate ≤ 30 mL/min or ≤ 35 mL/min (based on the package insert for the specific product).7 Patients with a recent or upcoming tooth extraction should also avoid using bisphosphonates until they have healed, due to concerns for osteonecrosis of the jaw.
Continue to: Administration of oral bisphosphonates requires...
Administration of oral bisphosphonates requires special attention. Oral bisphosphonates must be taken first thing in the morning with water; for the next 30 to 60 minutes, the patient must stay upright and not have any food, drink, or additional medications by mouth. These specifications may affect patient adherence to treatment.
Intravenous bisphosphonates. Depending on the IV bisphosphonate chosen—ibandronate and zoledronic acid are the currently available options—administration is recommended either every three or 12 months. A common adverse effect of IV bisphosphonates is flulike symptoms, which are generally brief in duration. Hypocalcemia has also been associated with IV administration, more so than with oral bisphosphonate use. Osteonecrosis of the jaw, while rare, must also be considered.
CASE POINT Because of Ms. B’s GERD requiring PPI use, oral bisphosphonates are not the most ideal treatment for her osteoporosis; they could exacerbate her gastrointestinal symptoms. IV bisphosphonates are a potential option for her, as this method of administration would eliminate the gastrointestinal risk associated with oral bisphosphonates.
Selective estrogen receptor modulators (SERMs), which are administered orally, are another option for osteoporosis treatment for vertebral fractures. One medication in this class, raloxifene, selectively acts on estrogen receptors—it works as an agonist in bone estrogen receptors (preventing bone loss) and an estrogen antagonist in other tissue (eg, breast, uterine). SERMs are not considered firstline treatment for osteoporosis because they appear to be less potent than other currently available agents. However, a postmenopausal patient with a high risk for invasive breast cancer without a history of fragility fracture might consider this option, as raloxifene can reduce the risk for invasive breast cancer.9 SERMs have been associated with an increase in thromboembolic events and hot flashes.
Calcitonin nasal spray is used much less commonly now because its effect on bone mineral density is weaker than other currently available options. Calcitonin nasal spray is administered as one spray in one nostril each day. There has been some concern regarding calcitonin use and its association with malignancy.10
Continue to: CASE POINT
CASE POINT Ms. B’s history of compression fractures suggests the need for potent pharmacologic options to treat her osteoporosis. SERMS and calcitonin nasal spray are felt to be less potent and therefore are not the preferred treatment recommendations for her
Parathyroid hormone analogs. The availability of the parathyroid hormone analogs teriparatide and abaloparatide gives patients and health care providers another treatment option for osteoporosis.11 These potent stimulators of bone remodeling help reduce future fracture risk. Teriparatide and abaloparatide are considered anabolic bone agents, rather than antiresorptive medications. These medications are administered subcutaneously daily for no more than two years. Many health care providers use parathyroid hormone analogs for patients with severe osteoporosis (T score, ≤ –3.5 without fragility fracture history or ≤ –2.5 with fragility fracture history).12 The cost of these agents must be considered when recommending them to eligible patients.8
Parathyroid hormone analogs do carry a black box warning because of an increased risk for osteosarcoma observed in rat studies.13,14 These products should therefore be avoided in patients with increased risk for osteosarcoma: those who have Paget disease of the bone or unexplained elevations of alkaline phosphatase; pediatric and young adult patients with open epiphyses; or those who have had external beam or implant radiation therapy involving the skeleton.13,14
CASE POINT Because of Ms. B’s prior history of breast cancer requiring radiation treatment, parathyroid hormone analogs are not recommended.
Denosumab is a human monoclonal antibody, a RANKL inhibitor, that works by preventing the development of osteoclasts. This medication is administered subcutaneously every six months. There are no dosing adjustments recommended for hepatic impairment.11 The denosumab package insert does not specify a dosage adjustment for patients with renal impairment; however, clinical studies have indicated that patients who have a creatine clearance < 30 mL/min or who are on dialysis are more likely to experience hypocalcemia with denosumab use.15 As with other newer osteoporosis treatments, cost considerations should be discussed with patients.
Continue to: One unique consideration...
One unique consideration is that clinical trials have shown an increased fracture risk and the return of bone mineral density to predenosumab treatment levels within 18 months of discontinuing the medication.15 Health care providers should be prepared to recommend alternative treatment options if denosumab is discontinued.
CASE CONCLUDED After a discussion of the risks, benefits, and expectations associated with each of the available treatment options, Ms. B and her health care provider narrow down her options to use of an IV bisphosphonate or denosumab for her osteoporosis. She ultimately chooses denosumab, based on her preference for an injectable medication.
CONCLUSION
The morbidity and mortality associated with osteoporosis can be improved with an appropriate balance of nonpharmacologic and pharmacologic approaches. The varying mechanisms of action, administration methods, and documented efficacy of the available medications provide an opportunity for patient education and informed decision-making when choosing treatment. For additional guidance, the American College of Physicians, the American Association of Clinical Endocrinologists, and American College of Endocrinology have published guidelines that can help in the decision-making process.16,17
1. Cauley JA. Public health impact of osteoporosis. J Gerontol A Biol Sci Med Sci. 2013;68(10):1243-1251.
2. NIH Osteoporosis and Related Bone Diseases National Resource Center. Osteoporosis overview. February 2017. www.bones.nih.gov/health-info/bone/osteoporosis/overview. Accessed October 1, 2018.
3. Dempster DW. Osteoporosis and the burden of osteoporosis-related fractures. Am J Manag Care. 2011;17: S164-S169.
4. International Osteoporosis Foundation. Osteoporosis facts and statistics. www.iofbonehealth.org/facts-and-statistics/calcium-studies-map. Accessed October 1, 2018.
5. Weinstein RS, Roberson PK, Manolagas SC. Giant osteoclast formation and long-term oral bisphosphonate therapy. N Engl J Med. 2009;360(1):53-62.
6. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2):S14-S21.
7. Miller PD. Long-term extension trials to prove the efficacy of and safety of bisphosphonates. Clin Invest. 2014;4(1):35-43.
8. Hiligsmann M, Evers SM, Sedrine B, et al. A systematic review of cost-effectiveness analyses of drugs for postmenopausal osteoporosis. Pharmacoeconomics. 2015;33(3):205-224.
9. Raloxifene [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
10. Wells G, Chernoff J, Gilligan JP, Krause DS. Does salmon calcitonin cause cancer? A review and meta-analysis. Osteoporos Int. 2016;27(1):13-19.
11. Leder BZ. Parathyroid hormone and parathyroid hormone-related protein analogs in osteoporosis therapy. Curr Osteoporos Rep. 2017;15:110-119.
12. Kendler DL, Marin F, Zerbini CAF, et al. Effects of teriparatide and risedronate on new fractures in post-menopausal women with severe osteoporosis (VERO): a multicentre, double-blind, double-dummy, randomised controlled trial. Lancet. 2018;391:230-240.
13. Teriparatide [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
14. Abaloparatide [package insert]. Waltham, MA: Radius Health, Inc; 2017.
15. Denosumab [package insert]. Thousand Oaks, CA: Amgen Inc; 2018.
16. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis—2016. Endocr Pract. 2016;22(4):1-42.
17. Qaseem A, Forciea MA, McLean RM, et al; Clinical Guidelines Committee of the American College of Physicians. Treatment of low bone density or osteoporosis to prevent fractures in men and women: a clinical practice guideline update from the American College of Physicians. Ann Intern Med. 2017;166(11):818-839.
1. Cauley JA. Public health impact of osteoporosis. J Gerontol A Biol Sci Med Sci. 2013;68(10):1243-1251.
2. NIH Osteoporosis and Related Bone Diseases National Resource Center. Osteoporosis overview. February 2017. www.bones.nih.gov/health-info/bone/osteoporosis/overview. Accessed October 1, 2018.
3. Dempster DW. Osteoporosis and the burden of osteoporosis-related fractures. Am J Manag Care. 2011;17: S164-S169.
4. International Osteoporosis Foundation. Osteoporosis facts and statistics. www.iofbonehealth.org/facts-and-statistics/calcium-studies-map. Accessed October 1, 2018.
5. Weinstein RS, Roberson PK, Manolagas SC. Giant osteoclast formation and long-term oral bisphosphonate therapy. N Engl J Med. 2009;360(1):53-62.
6. Bilezikian JP. Efficacy of bisphosphonates in reducing fracture risk in postmenopausal osteoporosis. Am J Med. 2009;122(2):S14-S21.
7. Miller PD. Long-term extension trials to prove the efficacy of and safety of bisphosphonates. Clin Invest. 2014;4(1):35-43.
8. Hiligsmann M, Evers SM, Sedrine B, et al. A systematic review of cost-effectiveness analyses of drugs for postmenopausal osteoporosis. Pharmacoeconomics. 2015;33(3):205-224.
9. Raloxifene [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
10. Wells G, Chernoff J, Gilligan JP, Krause DS. Does salmon calcitonin cause cancer? A review and meta-analysis. Osteoporos Int. 2016;27(1):13-19.
11. Leder BZ. Parathyroid hormone and parathyroid hormone-related protein analogs in osteoporosis therapy. Curr Osteoporos Rep. 2017;15:110-119.
12. Kendler DL, Marin F, Zerbini CAF, et al. Effects of teriparatide and risedronate on new fractures in post-menopausal women with severe osteoporosis (VERO): a multicentre, double-blind, double-dummy, randomised controlled trial. Lancet. 2018;391:230-240.
13. Teriparatide [package insert]. Indianapolis, IN: Lilly USA, LLC; 2018.
14. Abaloparatide [package insert]. Waltham, MA: Radius Health, Inc; 2017.
15. Denosumab [package insert]. Thousand Oaks, CA: Amgen Inc; 2018.
16. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis—2016. Endocr Pract. 2016;22(4):1-42.
17. Qaseem A, Forciea MA, McLean RM, et al; Clinical Guidelines Committee of the American College of Physicians. Treatment of low bone density or osteoporosis to prevent fractures in men and women: a clinical practice guideline update from the American College of Physicians. Ann Intern Med. 2017;166(11):818-839.