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US National Practice Patterns in Ambulatory Operative Management of Lateral Epicondylitis

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US National Practice Patterns in Ambulatory Operative Management of Lateral Epicondylitis

First described by Runge1 in 1873 and later termed lawn-tennis arm by Major2 in 1883, lateral epicondylitis is a common cause of elbow pain, affecting 1% to 3% of the general population each year.3,4 Given that prevalence estimates are up to 15% among workers in repetitive hand task industries,5-7 symptoms of lateral epicondylitis are thought to be related to recurring wrist extension and alternating forearm pronation and supination.8 Between 80% and 90% of patients with lateral epicondylitis experience symptomatic improvement with conservative therapy,9-11 including rest and use of nonsteroidal anti-inflammatory medications,12 physical therapy,13,14 corticosteroid injections,10,15,16 orthoses,17,18 and shock wave therapy.19 However, between 4% and 11% of patients with newly diagnosed lateral epicondylitis do not respond to prolonged (6- to 12-month) conservative treatment and then require operative intervention,11,20,21 with some referral practices reporting rates as high as 25%.22

Traditionally, operative management of lateral epicondylitis involved open débridement of the extensor carpi radialis brevis (ECRB).11,20 More recently, the spectrum of operations for lateral epicondylitis has expanded to include procedures that repair the extensor origin after débridement of the torn tendon and angiofibroblastic dysplasia; procedures that use fasciotomy or direct release of the extensor origin from the epicondyle to relieve tension on the common extensor; procedures directed at the radial or posterior interosseous nerve; and procedures that use arthroscopic techniques to divide the orbicular ligament, reshape the radial head, or release the extensor origin.23 There has been debate about the value of repairing the ECRB, lengthening the ECRB, simultaneously decompressing the radial nerve or resecting epicondylar bone, and performing the procedures percutaneously, endoscopically, or arthroscopically.24-28 Despite multiple studies of the outcomes of these procedures,11,29-31 little is known regarding US national trends for operative treatment of lateral epicondylitis. Understanding national practice patterns and disease burden is essential to allocation of limited health care resources.

We conducted a study to determine US national trends in use of ambulatory surgery for lateral epicondylitis. We focused on age, sex, surgical setting, anesthetic type, and payment method.

Methods

As the National Survey of Ambulatory Surgery32 (NSAS) is an administrative dataset in which all data are deidentified and available for public use, this study was exempt from requiring institutional review board approval.

NSAS data were used to analyze trends in treatment of lateral epicondylitis between 1994 and 2006. NSAS was undertaken by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC) to obtain information about the use of ambulatory surgery in the United States. Since the early 1980s, ambulatory surgery has increased in the United States because of advances in medical technology and cost-containment initiatives.33 The number of procedures being performed in ambulatory surgery centers increased from 31.5 million in 1996 to 53.3 million in 2006.34 Funded by the CDC, NSAS is a national study that involves both hospital-based and freestanding ambulatory surgery centers and provides the most recent and comprehensive overview of ambulatory surgery in the United States.35 Because of budgetary limitations, 2006 was the last year in which data for NSAS were collected. Data for NSAS come from Medicare-participating, noninstitutional hospitals (excluding military hospitals, federal facilities, and Veteran Affairs hospitals) in all 50 states and the District of Columbia with a minimum of 6 beds staffed for patient use. NSAS used only short-stay hospitals (hospitals with an average length of stay for all patients of less than 30 days) or hospitals that had a specialty of general (medical or surgical) or children’s general. NSAS was conducted in 1994, 1996, and 2006 with medical information recorded on patient abstracts coded by contract staff. NSAS selected a sample of ambulatory surgery visits using a systematic random sampling procedure, and selection of visits within each facility was done separately for each location where ambulatory surgery was performed. In 1994, 751 facilities were sampled, and 88% of hospitals responded. In 1996, 750 facilities were sampled, and 91% of hospitals responded. In 2006, 696 facilities were sampled, and 75% responded. The surveys used International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes36 to classify medical diagnoses and procedures. To produce an unbiased national estimate, NCHS used multistage estimate procedures, including inflation by reciprocals of the probabilities of sample selection, population-weighting ratio adjustments, and adjustment for no response.37

Demographic and medical information was obtained for people with an ICD-9-CM diagnosis code of lateral epicondylitis (726.32), using previously described techniques.38 Data were then recorded for age, sex, facility type, insurance type, anesthesia type, diagnoses, and procedures.

Descriptive statistics consisted of means and standard deviations for continuous variables and frequency and percentages for discrete variables. Because NSAS data were collected on the basis of a probabilistic sample scheme, they were analyzed using a sampling weighting method. Sampling weights (inverse of selection probability) provided by the CDC were used to account for unequal sampling probabilities and to produce estimates for all visits in the United States. A Taylor linearization model provided by the CDC estimates was used to calculate standard error and confidence intervals (CIs) of the data. Standard error is a measure of sampling variability that occurs by chance because only a sample rather than the entire universe is surveyed. To define population parameters, NCHS chose 95% CIs along with a point estimate. Direct statistical comparison between years cannot be performed because of sampling differences in the database compared between years. The CIs, however, can suggest statistical differences if the data are nonoverlapping. US census data were used to obtain national population estimates for each year of the study (1994, 1996, 2006).39 Rates were presented as number of procedures per 100,000 standard population. For age, a direct adjustment procedure was used, and the US population in 2000 was selected as the standard population. Applying sex-specific rates to the standard population and dividing by the total in the standard population, we calculated sex-adjusted rates for each year. All data were analyzed using SPSS Version 20 software.

 

 

Results

A total of 30,311 ambulatory surgical procedures (95% CI, 27,292-33,330) or 10.44 per 100,000 capita were recorded by NSAS for the treatment of lateral epicondylitis in 2006 (Table 1). This represents a large increase in the total number of ambulatory procedures, from 21,852 in 1994 (95% CI, 19,981-23,722; 7.29/100,000) and 20,372 in 1996 (95% CI, 18,660-22,083; 6.73/100,000).

Between 1994 and 2006, the sex-adjusted rate of ambulatory surgery for lateral epicondylitis increased by 85% among females (7.74/100,000 to 14.31/100,000), whereas the rate decreased by 31% among males (8.07/100,000 to 5.59/100,000) (Table 1). The age-adjusted rate of ambulatory surgery for lateral epicondylitis increased among all age groups except the 30–39 years group (Table 2). The largest increase in age-adjusted rates was found for patients older than 50 years (275%) between 1994 and 2006.

During the study period, use of regional anesthesia nearly doubled, from 17% to 30%, whereas use of general anesthesia decreased, from 69% to 57% (Table 3). At all time points, the most common procedure performed for lateral epicondylitis in ambulatory surgery centers was division/release of the joint capsule of the elbow (Table 4). Private insurance remained the most common source of payment for all study years, ranging from 52% to 60% (Table 5). The Figure shows that, between 1994 and 2006, the proportion of surgeries performed in a freestanding ambulatory center increased.

 
 
 

Discussion

In this descriptive epidemiologic study, we used NSAS data to investigate trends in ambulatory surgery for lateral epicondylitis between 1994 and 2006.32 Our results showed that total number of procedures and the population-adjusted rate of procedures for lateral epicondylitis increased during the study period. The largest increase in age-adjusted rates of surgery for lateral epicondylitis was found among patients older than 50 years, whereas the highest age-adjusted rate of ambulatory surgery for lateral epicondylitis was found among patients between ages 40 and 49 years. These findings are similar to those of previous studies, which have shown that most patients with lateral epicondylitis present in the fourth and fifth decades of life.22 Prior reports have suggested that the incidence of lateral epicondylitis in men and women is equal.22 The present study found a change in sex-adjusted rates of ambulatory surgery for lateral epicondylitis between 1994 and 2006. Specifically, in 1994, surgery rates for men and women were similar (8.07/100,000 and 7.74/100,000), but in 2006 the sex-adjusted rate of surgery for lateral epicondylitis was almost 3 times higher for women than for men (14.31/100,000 vs 5.59/100,000).

We also found that the population-adjusted rate of lateral epicondylectomy increased drastically, from 0.4 per 100,000 in 1994 to 3.53 per 100,000 in 2006. Lateral epicondylectomy involves excision of the tip of the lateral epicondyle (typically, 0.5 cm) to produce a cancellous bone surface to which the edges of the débrided extensor tendon can be approximated without tension.23 It is possible that the increased rate of lateral epicondylectomy reflects evidence-based practice changes during the study period,27 though denervation was found more favorable than epicondylectomy in a recent study by Berry and colleagues.40 Future studies should investigate whether rates of epicondylectomy have changed since 2006. In addition, the present study showed a correlation between the introduction of arthroscopic techniques for the treatment of lateral epicondylitis and the period when much research was being conducted on the topic.24,25,28 As arthroscopic techniques improve, their rates are likely to continue to increase.

Our results also showed an increase in procedures performed in freestanding facilities. The rise in ambulatory surgical volume, speculated to result from more procedures being performed in freestanding facilities,34 has been reported with knee and shoulder arthroscopy.41 In addition, though general anesthesia remained the most used technique, our results showed a shift toward peripheral nerve blocks. The increase in regional anesthesia, which has also been noted in joint arthroscopy, is thought to stem from the advent of nerve-localizing technology, such as nerve stimulation and ultrasound guidance.41 Peripheral nerve blocks are favorable on both economic and quality measures, are associated with fewer opioid-related side effects, and overall provide better analgesia in comparison with opioids, highlighting their importance in the ambulatory setting.42

Although large, national databases are well suited to epidemiologic research,43 our study had limitations. As with all databases, NSAS is subject to data entry errors and coding errors.44,45 However, the database administrators corrected for this by using a multistage estimate procedure with weighting adjustments for no response and population-weighting ratio adjustments.35 Another limitation of this study is its lack of clinical detail, as procedure codes are general and do not allow differentiation between specific patients. Because of the retrospective nature of the analysis and the heterogeneity of the data, assessment of specific surgeries for lateral epicondylitis was limited. Although a strength of using NSAS to perform epidemiologic analyses is its large sample size, this also sacrifices specificity in terms of clinical insight. The results of this study may influence investigations to distinguish differences between procedures used in the treatment of lateral epicondylitis. Furthermore, the results of this study are limited to ambulatory surgery practice patterns in the United States between 1996 and 2006. Last, our ability to perform economic analyses was limited, as data on total hospital cost were not recorded by the surveys.

 

 

Conclusion

The increase in ambulatory surgery for lateral epicondylitis, demonstrated in this study, emphasizes the importance of national funding for surveys such as NSAS beyond 2006, as utilization trends may have considerable effects on health care policies that influence the quality of patient care.

References

1.    Runge F. Zur genese und behandlung des schreibekramfes. Berl Klin Wochenschr. 1873;10:245.

2.    Major HP. Lawn-tennis elbow. Br Med J. 1883;2:557.

3.    Allander E. Prevalence, incidence, and remission rates of some common rheumatic diseases or syndromes. Scand J Rheumatol. 1974;3(3):145-153.

4.    Verhaar JA. Tennis elbow. Anatomical, epidemiological and therapeutic aspects. Int Orthop. 1994;18(5):263-267.

5.    Kurppa K, Viikari-Juntura E, Kuosma E, Huuskonen M, Kivi P. Incidence of tenosynovitis or peritendinitis and epicondylitis in a meat-processing factory. Scand J Work Environ Health. 1991;17(1):32-37.

6.    Ranney D, Wells R, Moore A. Upper limb musculoskeletal disorders in highly repetitive industries: precise anatomical physical findings. Ergonomics. 1995;38(7):1408-1423.

7.    Haahr JP, Andersen JH. Physical and psychosocial risk factors for lateral epicondylitis: a population based case-referent study. Occup Environ Med. 2003;60(5):322-329.

8.    Goldie I. Epicondylitis lateralis humeri (epicondylalgia or tennis elbow). A pathogenetical study. Acta Chir Scand Suppl. 1964;57(suppl 399):1+.

9.    Binder AI, Hazleman BL. Lateral humeral epicondylitis—a study of natural history and the effect of conservative therapy. Br J Rheumatol. 1983;22(2):73-76.

10.  Smidt N, van der Windt DA, Assendelft WJ, Devillé WL, Korthals-de Bos IB, Bouter LM. Corticosteroid injections, physiotherapy, or a wait-and-see policy for lateral epicondylitis: a randomised controlled trial. Lancet. 2002;359(9307):657-662.

11.  Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979;61(6):832-839.

12.  Burnham R, Gregg R, Healy P, Steadward R. The effectiveness of topical diclofenac for lateral epicondylitis. Clin J Sport Med. 1998;8(2):78-81.

13.  Martinez-Silvestrini JA, Newcomer KL, Gay RE, Schaefer MP, Kortebein P, Arendt KW. Chronic lateral epicondylitis: comparative effectiveness of a home exercise program including stretching alone versus stretching supplemented with eccentric or concentric strengthening. J Hand Ther. 2005;18(4):411-419.

14.  Svernlöv B, Adolfsson L. Non-operative treatment regime including eccentric training for lateral humeral epicondylalgia. Scand J Med Sci Sports. 2001;11(6):328-334.

15.  Hay EM, Paterson SM, Lewis M, Hosie G, Croft P. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ. 1999;319(7215):964-968.

16.  Lewis M, Hay EM, Paterson SM, Croft P. Local steroid injections for tennis elbow: does the pain get worse before it gets better? Results from a randomized controlled trial. Clin J Pain. 2005;21(4):330-334.

17.  Van De Streek MD, Van Der Schans CP, De Greef MH, Postema K. The effect of a forearm/hand splint compared with an elbow band as a treatment for lateral epicondylitis. Prosthet Orthot Int. 2004;28(2):183-189.

18.  Struijs PA, Smidt N, Arola H, Dijk vC, Buchbinder R, Assendelft WJ. Orthotic devices for the treatment of tennis elbow. Cochrane Database Syst Rev. 2002;(1):CD001821.

19.  Buchbinder R, Green SE, Youd JM, Assendelft WJ, Barnsley L, Smidt N. Shock wave therapy for lateral elbow pain. Cochrane Database Syst Rev. 2005;(4):CD003524.

20.  Boyd HB, McLeod AC Jr. Tennis elbow. J Bone Joint Surg Am. 1973;55(6):1183-1187.

21.  Coonrad RW, Hooper WR. Tennis elbow: its course, natural history, conservative and surgical management. J Bone Joint Surg Am. 1973;55(6):1177-1182.

22.  Calfee RP, Patel A, DaSilva MF, Akelman E. Management of lateral epicondylitis: current concepts. J Am Acad Orthop Surg. 2008;16(1):19-29.

23.  Plancher KD, Bishai SK. Open lateral epicondylectomy: a simple technique update for the 21st century. Tech Orthop. 2006;21(4):276-282.

24.  Peart RE, Strickler SS, Schweitzer KM Jr. Lateral epicondylitis: a comparative study of open and arthroscopic lateral release. Am J Orthop. 2004;33(11):565-567.

25.  Dunkow PD, Jatti M, Muddu BN. A comparison of open and percutaneous techniques in the surgical treatment of tennis elbow. J Bone Joint Surg Br. 2004;86(5):701-704.

26.  Rosenberg N, Henderson I. Surgical treatment of resistant lateral epicondylitis. Follow-up study of 19 patients after excision, release and repair of proximal common extensor tendon origin. Arch Orthop Trauma Surg. 2002;122(9-10):514-517.

27.  Almquist EE, Necking L, Bach AW. Epicondylar resection with anconeus muscle transfer for chronic lateral epicondylitis. J Hand Surg Am. 1998;23(4):723-731.

28.  Smith AM, Castle JA, Ruch DS. Arthroscopic resection of the common extensor origin: anatomic considerations. J Shoulder Elbow Surg. 2003;12(4):375-379.

29.  Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J Shoulder Elbow Surg. 2000;9(6):475-482.

30.  Owens BD, Murphy KP, Kuklo TR. Arthroscopic release for lateral epicondylitis. Arthroscopy. 2001;17(6):582-587.

31.  Mullett H, Sprague M, Brown G, Hausman M. Arthroscopic treatment of lateral epicondylitis: clinical and cadaveric studies. Clin Orthop Relat Res. 2005;(439):123-128.

32.  National Survey of Ambulatory Surgery. Centers for Disease Control and Prevention website. http://www.cdc.gov/nchs/nsas/nsas_questionnaires.htm. Published May 4, 2010. Accessed November 10, 2015.

33.  Leader S, Moon M. Medicare trends in ambulatory surgery. Health Aff. 1989;8(1):158-170.

34.  Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;(11):1-25.

35.  Kim S, Bosque J, Meehan JP, Jamali A, Marder R. Increase in outpatient knee arthroscopy in the United States: a comparison of National Surveys of Ambulatory Surgery, 1996 and 2006. J Bone Joint Surg Am. 2011;93(11):994-1000.

36.  Centers for Disease Control and Prevention, National Center for Health Statistics. International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). http://www.cdc.gov/nchs/icd/icd9cm.htm. Updated June 18, 2013. Accessed October 28, 2015.

37.  Dennison C, Pokras R. Design and operation of the National Hospital Discharge Survey: 1988 redesign. Vital Health Stat 1. 2000;(39):1-42.

38.  Stundner O, Kirksey M, Chiu YL, et al. Demographics and perioperative outcome in patients with depression and anxiety undergoing total joint arthroplasty: a population-based study. Psychosomatics. 2013;54(2):149-157.

39.  Population estimates. US Department of Commerce, United States Census Bureau website. http://www.census.gov/popest/index.html. Accessed November 16, 2015.

40.  Berry N, Neumeister MW, Russell RC, Dellon AL. Epicondylectomy versus denervation for lateral humeral epicondylitis. Hand. 2011;6(2):174-178.

41.  Memtsoudis SG, Kuo C, Ma Y, Edwards A, Mazumdar M, Liguori G. Changes in anesthesia-related factors in ambulatory knee and shoulder surgery: United States 1996–2006. Reg Anesth Pain Med. 2011;36(4):327-331.

42.  Richman JM, Liu SS, Courpas G, et al. Does continuous peripheral nerve block provide superior pain control to opioids? A meta-analysis. Anesth Analg. 2006;102(1):248-257.

43.  Bohl DD, Basques BA, Golinvaux NS, Baumgaertner MR, Grauer JN. Nationwide Inpatient Sample and National Surgical Quality Improvement Program give different results in hip fracture studies. Clin Orthop Relat Res. 2014;472(6):1672-1680.

44.    Gray DT, Hodge DO, Ilstrup DM, Butterfield LC, Baratz KH, Concordance of Medicare data and population-based clinical data on cataract surgery utilization in Olmsted County, Minnesota. Am J Epidemiol. 1997;145(12):1123-1126.

45.  Memtsoudis SG. Limitations associated with the analysis of data from administrative databases. Anesthesiology. 2009;111(2):449.

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Author and Disclosure Information

Leonard T. Buller, MD, Matthew J. Best, MD, David Nigen, MD, Marc Ialenti, MD, and Michael G. Baraga, MD

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

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The American Journal of Orthopedics - 44(12)
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E508-E512
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american journal of orthopedics, AJO, original study, online exclusive, study, ambulatory, operative management, practice management, lateral epicondylitis, elbow, elbow pain, pain management, operative techniques, practice patterns, surgery, buller, best, nigen, ialenti, baraga
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Leonard T. Buller, MD, Matthew J. Best, MD, David Nigen, MD, Marc Ialenti, MD, and Michael G. Baraga, MD

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

Author and Disclosure Information

Leonard T. Buller, MD, Matthew J. Best, MD, David Nigen, MD, Marc Ialenti, MD, and Michael G. Baraga, MD

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

Article PDF
Article PDF

First described by Runge1 in 1873 and later termed lawn-tennis arm by Major2 in 1883, lateral epicondylitis is a common cause of elbow pain, affecting 1% to 3% of the general population each year.3,4 Given that prevalence estimates are up to 15% among workers in repetitive hand task industries,5-7 symptoms of lateral epicondylitis are thought to be related to recurring wrist extension and alternating forearm pronation and supination.8 Between 80% and 90% of patients with lateral epicondylitis experience symptomatic improvement with conservative therapy,9-11 including rest and use of nonsteroidal anti-inflammatory medications,12 physical therapy,13,14 corticosteroid injections,10,15,16 orthoses,17,18 and shock wave therapy.19 However, between 4% and 11% of patients with newly diagnosed lateral epicondylitis do not respond to prolonged (6- to 12-month) conservative treatment and then require operative intervention,11,20,21 with some referral practices reporting rates as high as 25%.22

Traditionally, operative management of lateral epicondylitis involved open débridement of the extensor carpi radialis brevis (ECRB).11,20 More recently, the spectrum of operations for lateral epicondylitis has expanded to include procedures that repair the extensor origin after débridement of the torn tendon and angiofibroblastic dysplasia; procedures that use fasciotomy or direct release of the extensor origin from the epicondyle to relieve tension on the common extensor; procedures directed at the radial or posterior interosseous nerve; and procedures that use arthroscopic techniques to divide the orbicular ligament, reshape the radial head, or release the extensor origin.23 There has been debate about the value of repairing the ECRB, lengthening the ECRB, simultaneously decompressing the radial nerve or resecting epicondylar bone, and performing the procedures percutaneously, endoscopically, or arthroscopically.24-28 Despite multiple studies of the outcomes of these procedures,11,29-31 little is known regarding US national trends for operative treatment of lateral epicondylitis. Understanding national practice patterns and disease burden is essential to allocation of limited health care resources.

We conducted a study to determine US national trends in use of ambulatory surgery for lateral epicondylitis. We focused on age, sex, surgical setting, anesthetic type, and payment method.

Methods

As the National Survey of Ambulatory Surgery32 (NSAS) is an administrative dataset in which all data are deidentified and available for public use, this study was exempt from requiring institutional review board approval.

NSAS data were used to analyze trends in treatment of lateral epicondylitis between 1994 and 2006. NSAS was undertaken by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC) to obtain information about the use of ambulatory surgery in the United States. Since the early 1980s, ambulatory surgery has increased in the United States because of advances in medical technology and cost-containment initiatives.33 The number of procedures being performed in ambulatory surgery centers increased from 31.5 million in 1996 to 53.3 million in 2006.34 Funded by the CDC, NSAS is a national study that involves both hospital-based and freestanding ambulatory surgery centers and provides the most recent and comprehensive overview of ambulatory surgery in the United States.35 Because of budgetary limitations, 2006 was the last year in which data for NSAS were collected. Data for NSAS come from Medicare-participating, noninstitutional hospitals (excluding military hospitals, federal facilities, and Veteran Affairs hospitals) in all 50 states and the District of Columbia with a minimum of 6 beds staffed for patient use. NSAS used only short-stay hospitals (hospitals with an average length of stay for all patients of less than 30 days) or hospitals that had a specialty of general (medical or surgical) or children’s general. NSAS was conducted in 1994, 1996, and 2006 with medical information recorded on patient abstracts coded by contract staff. NSAS selected a sample of ambulatory surgery visits using a systematic random sampling procedure, and selection of visits within each facility was done separately for each location where ambulatory surgery was performed. In 1994, 751 facilities were sampled, and 88% of hospitals responded. In 1996, 750 facilities were sampled, and 91% of hospitals responded. In 2006, 696 facilities were sampled, and 75% responded. The surveys used International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes36 to classify medical diagnoses and procedures. To produce an unbiased national estimate, NCHS used multistage estimate procedures, including inflation by reciprocals of the probabilities of sample selection, population-weighting ratio adjustments, and adjustment for no response.37

Demographic and medical information was obtained for people with an ICD-9-CM diagnosis code of lateral epicondylitis (726.32), using previously described techniques.38 Data were then recorded for age, sex, facility type, insurance type, anesthesia type, diagnoses, and procedures.

Descriptive statistics consisted of means and standard deviations for continuous variables and frequency and percentages for discrete variables. Because NSAS data were collected on the basis of a probabilistic sample scheme, they were analyzed using a sampling weighting method. Sampling weights (inverse of selection probability) provided by the CDC were used to account for unequal sampling probabilities and to produce estimates for all visits in the United States. A Taylor linearization model provided by the CDC estimates was used to calculate standard error and confidence intervals (CIs) of the data. Standard error is a measure of sampling variability that occurs by chance because only a sample rather than the entire universe is surveyed. To define population parameters, NCHS chose 95% CIs along with a point estimate. Direct statistical comparison between years cannot be performed because of sampling differences in the database compared between years. The CIs, however, can suggest statistical differences if the data are nonoverlapping. US census data were used to obtain national population estimates for each year of the study (1994, 1996, 2006).39 Rates were presented as number of procedures per 100,000 standard population. For age, a direct adjustment procedure was used, and the US population in 2000 was selected as the standard population. Applying sex-specific rates to the standard population and dividing by the total in the standard population, we calculated sex-adjusted rates for each year. All data were analyzed using SPSS Version 20 software.

 

 

Results

A total of 30,311 ambulatory surgical procedures (95% CI, 27,292-33,330) or 10.44 per 100,000 capita were recorded by NSAS for the treatment of lateral epicondylitis in 2006 (Table 1). This represents a large increase in the total number of ambulatory procedures, from 21,852 in 1994 (95% CI, 19,981-23,722; 7.29/100,000) and 20,372 in 1996 (95% CI, 18,660-22,083; 6.73/100,000).

Between 1994 and 2006, the sex-adjusted rate of ambulatory surgery for lateral epicondylitis increased by 85% among females (7.74/100,000 to 14.31/100,000), whereas the rate decreased by 31% among males (8.07/100,000 to 5.59/100,000) (Table 1). The age-adjusted rate of ambulatory surgery for lateral epicondylitis increased among all age groups except the 30–39 years group (Table 2). The largest increase in age-adjusted rates was found for patients older than 50 years (275%) between 1994 and 2006.

During the study period, use of regional anesthesia nearly doubled, from 17% to 30%, whereas use of general anesthesia decreased, from 69% to 57% (Table 3). At all time points, the most common procedure performed for lateral epicondylitis in ambulatory surgery centers was division/release of the joint capsule of the elbow (Table 4). Private insurance remained the most common source of payment for all study years, ranging from 52% to 60% (Table 5). The Figure shows that, between 1994 and 2006, the proportion of surgeries performed in a freestanding ambulatory center increased.

 
 
 

Discussion

In this descriptive epidemiologic study, we used NSAS data to investigate trends in ambulatory surgery for lateral epicondylitis between 1994 and 2006.32 Our results showed that total number of procedures and the population-adjusted rate of procedures for lateral epicondylitis increased during the study period. The largest increase in age-adjusted rates of surgery for lateral epicondylitis was found among patients older than 50 years, whereas the highest age-adjusted rate of ambulatory surgery for lateral epicondylitis was found among patients between ages 40 and 49 years. These findings are similar to those of previous studies, which have shown that most patients with lateral epicondylitis present in the fourth and fifth decades of life.22 Prior reports have suggested that the incidence of lateral epicondylitis in men and women is equal.22 The present study found a change in sex-adjusted rates of ambulatory surgery for lateral epicondylitis between 1994 and 2006. Specifically, in 1994, surgery rates for men and women were similar (8.07/100,000 and 7.74/100,000), but in 2006 the sex-adjusted rate of surgery for lateral epicondylitis was almost 3 times higher for women than for men (14.31/100,000 vs 5.59/100,000).

We also found that the population-adjusted rate of lateral epicondylectomy increased drastically, from 0.4 per 100,000 in 1994 to 3.53 per 100,000 in 2006. Lateral epicondylectomy involves excision of the tip of the lateral epicondyle (typically, 0.5 cm) to produce a cancellous bone surface to which the edges of the débrided extensor tendon can be approximated without tension.23 It is possible that the increased rate of lateral epicondylectomy reflects evidence-based practice changes during the study period,27 though denervation was found more favorable than epicondylectomy in a recent study by Berry and colleagues.40 Future studies should investigate whether rates of epicondylectomy have changed since 2006. In addition, the present study showed a correlation between the introduction of arthroscopic techniques for the treatment of lateral epicondylitis and the period when much research was being conducted on the topic.24,25,28 As arthroscopic techniques improve, their rates are likely to continue to increase.

Our results also showed an increase in procedures performed in freestanding facilities. The rise in ambulatory surgical volume, speculated to result from more procedures being performed in freestanding facilities,34 has been reported with knee and shoulder arthroscopy.41 In addition, though general anesthesia remained the most used technique, our results showed a shift toward peripheral nerve blocks. The increase in regional anesthesia, which has also been noted in joint arthroscopy, is thought to stem from the advent of nerve-localizing technology, such as nerve stimulation and ultrasound guidance.41 Peripheral nerve blocks are favorable on both economic and quality measures, are associated with fewer opioid-related side effects, and overall provide better analgesia in comparison with opioids, highlighting their importance in the ambulatory setting.42

Although large, national databases are well suited to epidemiologic research,43 our study had limitations. As with all databases, NSAS is subject to data entry errors and coding errors.44,45 However, the database administrators corrected for this by using a multistage estimate procedure with weighting adjustments for no response and population-weighting ratio adjustments.35 Another limitation of this study is its lack of clinical detail, as procedure codes are general and do not allow differentiation between specific patients. Because of the retrospective nature of the analysis and the heterogeneity of the data, assessment of specific surgeries for lateral epicondylitis was limited. Although a strength of using NSAS to perform epidemiologic analyses is its large sample size, this also sacrifices specificity in terms of clinical insight. The results of this study may influence investigations to distinguish differences between procedures used in the treatment of lateral epicondylitis. Furthermore, the results of this study are limited to ambulatory surgery practice patterns in the United States between 1996 and 2006. Last, our ability to perform economic analyses was limited, as data on total hospital cost were not recorded by the surveys.

 

 

Conclusion

The increase in ambulatory surgery for lateral epicondylitis, demonstrated in this study, emphasizes the importance of national funding for surveys such as NSAS beyond 2006, as utilization trends may have considerable effects on health care policies that influence the quality of patient care.

First described by Runge1 in 1873 and later termed lawn-tennis arm by Major2 in 1883, lateral epicondylitis is a common cause of elbow pain, affecting 1% to 3% of the general population each year.3,4 Given that prevalence estimates are up to 15% among workers in repetitive hand task industries,5-7 symptoms of lateral epicondylitis are thought to be related to recurring wrist extension and alternating forearm pronation and supination.8 Between 80% and 90% of patients with lateral epicondylitis experience symptomatic improvement with conservative therapy,9-11 including rest and use of nonsteroidal anti-inflammatory medications,12 physical therapy,13,14 corticosteroid injections,10,15,16 orthoses,17,18 and shock wave therapy.19 However, between 4% and 11% of patients with newly diagnosed lateral epicondylitis do not respond to prolonged (6- to 12-month) conservative treatment and then require operative intervention,11,20,21 with some referral practices reporting rates as high as 25%.22

Traditionally, operative management of lateral epicondylitis involved open débridement of the extensor carpi radialis brevis (ECRB).11,20 More recently, the spectrum of operations for lateral epicondylitis has expanded to include procedures that repair the extensor origin after débridement of the torn tendon and angiofibroblastic dysplasia; procedures that use fasciotomy or direct release of the extensor origin from the epicondyle to relieve tension on the common extensor; procedures directed at the radial or posterior interosseous nerve; and procedures that use arthroscopic techniques to divide the orbicular ligament, reshape the radial head, or release the extensor origin.23 There has been debate about the value of repairing the ECRB, lengthening the ECRB, simultaneously decompressing the radial nerve or resecting epicondylar bone, and performing the procedures percutaneously, endoscopically, or arthroscopically.24-28 Despite multiple studies of the outcomes of these procedures,11,29-31 little is known regarding US national trends for operative treatment of lateral epicondylitis. Understanding national practice patterns and disease burden is essential to allocation of limited health care resources.

We conducted a study to determine US national trends in use of ambulatory surgery for lateral epicondylitis. We focused on age, sex, surgical setting, anesthetic type, and payment method.

Methods

As the National Survey of Ambulatory Surgery32 (NSAS) is an administrative dataset in which all data are deidentified and available for public use, this study was exempt from requiring institutional review board approval.

NSAS data were used to analyze trends in treatment of lateral epicondylitis between 1994 and 2006. NSAS was undertaken by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC) to obtain information about the use of ambulatory surgery in the United States. Since the early 1980s, ambulatory surgery has increased in the United States because of advances in medical technology and cost-containment initiatives.33 The number of procedures being performed in ambulatory surgery centers increased from 31.5 million in 1996 to 53.3 million in 2006.34 Funded by the CDC, NSAS is a national study that involves both hospital-based and freestanding ambulatory surgery centers and provides the most recent and comprehensive overview of ambulatory surgery in the United States.35 Because of budgetary limitations, 2006 was the last year in which data for NSAS were collected. Data for NSAS come from Medicare-participating, noninstitutional hospitals (excluding military hospitals, federal facilities, and Veteran Affairs hospitals) in all 50 states and the District of Columbia with a minimum of 6 beds staffed for patient use. NSAS used only short-stay hospitals (hospitals with an average length of stay for all patients of less than 30 days) or hospitals that had a specialty of general (medical or surgical) or children’s general. NSAS was conducted in 1994, 1996, and 2006 with medical information recorded on patient abstracts coded by contract staff. NSAS selected a sample of ambulatory surgery visits using a systematic random sampling procedure, and selection of visits within each facility was done separately for each location where ambulatory surgery was performed. In 1994, 751 facilities were sampled, and 88% of hospitals responded. In 1996, 750 facilities were sampled, and 91% of hospitals responded. In 2006, 696 facilities were sampled, and 75% responded. The surveys used International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes36 to classify medical diagnoses and procedures. To produce an unbiased national estimate, NCHS used multistage estimate procedures, including inflation by reciprocals of the probabilities of sample selection, population-weighting ratio adjustments, and adjustment for no response.37

Demographic and medical information was obtained for people with an ICD-9-CM diagnosis code of lateral epicondylitis (726.32), using previously described techniques.38 Data were then recorded for age, sex, facility type, insurance type, anesthesia type, diagnoses, and procedures.

Descriptive statistics consisted of means and standard deviations for continuous variables and frequency and percentages for discrete variables. Because NSAS data were collected on the basis of a probabilistic sample scheme, they were analyzed using a sampling weighting method. Sampling weights (inverse of selection probability) provided by the CDC were used to account for unequal sampling probabilities and to produce estimates for all visits in the United States. A Taylor linearization model provided by the CDC estimates was used to calculate standard error and confidence intervals (CIs) of the data. Standard error is a measure of sampling variability that occurs by chance because only a sample rather than the entire universe is surveyed. To define population parameters, NCHS chose 95% CIs along with a point estimate. Direct statistical comparison between years cannot be performed because of sampling differences in the database compared between years. The CIs, however, can suggest statistical differences if the data are nonoverlapping. US census data were used to obtain national population estimates for each year of the study (1994, 1996, 2006).39 Rates were presented as number of procedures per 100,000 standard population. For age, a direct adjustment procedure was used, and the US population in 2000 was selected as the standard population. Applying sex-specific rates to the standard population and dividing by the total in the standard population, we calculated sex-adjusted rates for each year. All data were analyzed using SPSS Version 20 software.

 

 

Results

A total of 30,311 ambulatory surgical procedures (95% CI, 27,292-33,330) or 10.44 per 100,000 capita were recorded by NSAS for the treatment of lateral epicondylitis in 2006 (Table 1). This represents a large increase in the total number of ambulatory procedures, from 21,852 in 1994 (95% CI, 19,981-23,722; 7.29/100,000) and 20,372 in 1996 (95% CI, 18,660-22,083; 6.73/100,000).

Between 1994 and 2006, the sex-adjusted rate of ambulatory surgery for lateral epicondylitis increased by 85% among females (7.74/100,000 to 14.31/100,000), whereas the rate decreased by 31% among males (8.07/100,000 to 5.59/100,000) (Table 1). The age-adjusted rate of ambulatory surgery for lateral epicondylitis increased among all age groups except the 30–39 years group (Table 2). The largest increase in age-adjusted rates was found for patients older than 50 years (275%) between 1994 and 2006.

During the study period, use of regional anesthesia nearly doubled, from 17% to 30%, whereas use of general anesthesia decreased, from 69% to 57% (Table 3). At all time points, the most common procedure performed for lateral epicondylitis in ambulatory surgery centers was division/release of the joint capsule of the elbow (Table 4). Private insurance remained the most common source of payment for all study years, ranging from 52% to 60% (Table 5). The Figure shows that, between 1994 and 2006, the proportion of surgeries performed in a freestanding ambulatory center increased.

 
 
 

Discussion

In this descriptive epidemiologic study, we used NSAS data to investigate trends in ambulatory surgery for lateral epicondylitis between 1994 and 2006.32 Our results showed that total number of procedures and the population-adjusted rate of procedures for lateral epicondylitis increased during the study period. The largest increase in age-adjusted rates of surgery for lateral epicondylitis was found among patients older than 50 years, whereas the highest age-adjusted rate of ambulatory surgery for lateral epicondylitis was found among patients between ages 40 and 49 years. These findings are similar to those of previous studies, which have shown that most patients with lateral epicondylitis present in the fourth and fifth decades of life.22 Prior reports have suggested that the incidence of lateral epicondylitis in men and women is equal.22 The present study found a change in sex-adjusted rates of ambulatory surgery for lateral epicondylitis between 1994 and 2006. Specifically, in 1994, surgery rates for men and women were similar (8.07/100,000 and 7.74/100,000), but in 2006 the sex-adjusted rate of surgery for lateral epicondylitis was almost 3 times higher for women than for men (14.31/100,000 vs 5.59/100,000).

We also found that the population-adjusted rate of lateral epicondylectomy increased drastically, from 0.4 per 100,000 in 1994 to 3.53 per 100,000 in 2006. Lateral epicondylectomy involves excision of the tip of the lateral epicondyle (typically, 0.5 cm) to produce a cancellous bone surface to which the edges of the débrided extensor tendon can be approximated without tension.23 It is possible that the increased rate of lateral epicondylectomy reflects evidence-based practice changes during the study period,27 though denervation was found more favorable than epicondylectomy in a recent study by Berry and colleagues.40 Future studies should investigate whether rates of epicondylectomy have changed since 2006. In addition, the present study showed a correlation between the introduction of arthroscopic techniques for the treatment of lateral epicondylitis and the period when much research was being conducted on the topic.24,25,28 As arthroscopic techniques improve, their rates are likely to continue to increase.

Our results also showed an increase in procedures performed in freestanding facilities. The rise in ambulatory surgical volume, speculated to result from more procedures being performed in freestanding facilities,34 has been reported with knee and shoulder arthroscopy.41 In addition, though general anesthesia remained the most used technique, our results showed a shift toward peripheral nerve blocks. The increase in regional anesthesia, which has also been noted in joint arthroscopy, is thought to stem from the advent of nerve-localizing technology, such as nerve stimulation and ultrasound guidance.41 Peripheral nerve blocks are favorable on both economic and quality measures, are associated with fewer opioid-related side effects, and overall provide better analgesia in comparison with opioids, highlighting their importance in the ambulatory setting.42

Although large, national databases are well suited to epidemiologic research,43 our study had limitations. As with all databases, NSAS is subject to data entry errors and coding errors.44,45 However, the database administrators corrected for this by using a multistage estimate procedure with weighting adjustments for no response and population-weighting ratio adjustments.35 Another limitation of this study is its lack of clinical detail, as procedure codes are general and do not allow differentiation between specific patients. Because of the retrospective nature of the analysis and the heterogeneity of the data, assessment of specific surgeries for lateral epicondylitis was limited. Although a strength of using NSAS to perform epidemiologic analyses is its large sample size, this also sacrifices specificity in terms of clinical insight. The results of this study may influence investigations to distinguish differences between procedures used in the treatment of lateral epicondylitis. Furthermore, the results of this study are limited to ambulatory surgery practice patterns in the United States between 1996 and 2006. Last, our ability to perform economic analyses was limited, as data on total hospital cost were not recorded by the surveys.

 

 

Conclusion

The increase in ambulatory surgery for lateral epicondylitis, demonstrated in this study, emphasizes the importance of national funding for surveys such as NSAS beyond 2006, as utilization trends may have considerable effects on health care policies that influence the quality of patient care.

References

1.    Runge F. Zur genese und behandlung des schreibekramfes. Berl Klin Wochenschr. 1873;10:245.

2.    Major HP. Lawn-tennis elbow. Br Med J. 1883;2:557.

3.    Allander E. Prevalence, incidence, and remission rates of some common rheumatic diseases or syndromes. Scand J Rheumatol. 1974;3(3):145-153.

4.    Verhaar JA. Tennis elbow. Anatomical, epidemiological and therapeutic aspects. Int Orthop. 1994;18(5):263-267.

5.    Kurppa K, Viikari-Juntura E, Kuosma E, Huuskonen M, Kivi P. Incidence of tenosynovitis or peritendinitis and epicondylitis in a meat-processing factory. Scand J Work Environ Health. 1991;17(1):32-37.

6.    Ranney D, Wells R, Moore A. Upper limb musculoskeletal disorders in highly repetitive industries: precise anatomical physical findings. Ergonomics. 1995;38(7):1408-1423.

7.    Haahr JP, Andersen JH. Physical and psychosocial risk factors for lateral epicondylitis: a population based case-referent study. Occup Environ Med. 2003;60(5):322-329.

8.    Goldie I. Epicondylitis lateralis humeri (epicondylalgia or tennis elbow). A pathogenetical study. Acta Chir Scand Suppl. 1964;57(suppl 399):1+.

9.    Binder AI, Hazleman BL. Lateral humeral epicondylitis—a study of natural history and the effect of conservative therapy. Br J Rheumatol. 1983;22(2):73-76.

10.  Smidt N, van der Windt DA, Assendelft WJ, Devillé WL, Korthals-de Bos IB, Bouter LM. Corticosteroid injections, physiotherapy, or a wait-and-see policy for lateral epicondylitis: a randomised controlled trial. Lancet. 2002;359(9307):657-662.

11.  Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979;61(6):832-839.

12.  Burnham R, Gregg R, Healy P, Steadward R. The effectiveness of topical diclofenac for lateral epicondylitis. Clin J Sport Med. 1998;8(2):78-81.

13.  Martinez-Silvestrini JA, Newcomer KL, Gay RE, Schaefer MP, Kortebein P, Arendt KW. Chronic lateral epicondylitis: comparative effectiveness of a home exercise program including stretching alone versus stretching supplemented with eccentric or concentric strengthening. J Hand Ther. 2005;18(4):411-419.

14.  Svernlöv B, Adolfsson L. Non-operative treatment regime including eccentric training for lateral humeral epicondylalgia. Scand J Med Sci Sports. 2001;11(6):328-334.

15.  Hay EM, Paterson SM, Lewis M, Hosie G, Croft P. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ. 1999;319(7215):964-968.

16.  Lewis M, Hay EM, Paterson SM, Croft P. Local steroid injections for tennis elbow: does the pain get worse before it gets better? Results from a randomized controlled trial. Clin J Pain. 2005;21(4):330-334.

17.  Van De Streek MD, Van Der Schans CP, De Greef MH, Postema K. The effect of a forearm/hand splint compared with an elbow band as a treatment for lateral epicondylitis. Prosthet Orthot Int. 2004;28(2):183-189.

18.  Struijs PA, Smidt N, Arola H, Dijk vC, Buchbinder R, Assendelft WJ. Orthotic devices for the treatment of tennis elbow. Cochrane Database Syst Rev. 2002;(1):CD001821.

19.  Buchbinder R, Green SE, Youd JM, Assendelft WJ, Barnsley L, Smidt N. Shock wave therapy for lateral elbow pain. Cochrane Database Syst Rev. 2005;(4):CD003524.

20.  Boyd HB, McLeod AC Jr. Tennis elbow. J Bone Joint Surg Am. 1973;55(6):1183-1187.

21.  Coonrad RW, Hooper WR. Tennis elbow: its course, natural history, conservative and surgical management. J Bone Joint Surg Am. 1973;55(6):1177-1182.

22.  Calfee RP, Patel A, DaSilva MF, Akelman E. Management of lateral epicondylitis: current concepts. J Am Acad Orthop Surg. 2008;16(1):19-29.

23.  Plancher KD, Bishai SK. Open lateral epicondylectomy: a simple technique update for the 21st century. Tech Orthop. 2006;21(4):276-282.

24.  Peart RE, Strickler SS, Schweitzer KM Jr. Lateral epicondylitis: a comparative study of open and arthroscopic lateral release. Am J Orthop. 2004;33(11):565-567.

25.  Dunkow PD, Jatti M, Muddu BN. A comparison of open and percutaneous techniques in the surgical treatment of tennis elbow. J Bone Joint Surg Br. 2004;86(5):701-704.

26.  Rosenberg N, Henderson I. Surgical treatment of resistant lateral epicondylitis. Follow-up study of 19 patients after excision, release and repair of proximal common extensor tendon origin. Arch Orthop Trauma Surg. 2002;122(9-10):514-517.

27.  Almquist EE, Necking L, Bach AW. Epicondylar resection with anconeus muscle transfer for chronic lateral epicondylitis. J Hand Surg Am. 1998;23(4):723-731.

28.  Smith AM, Castle JA, Ruch DS. Arthroscopic resection of the common extensor origin: anatomic considerations. J Shoulder Elbow Surg. 2003;12(4):375-379.

29.  Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J Shoulder Elbow Surg. 2000;9(6):475-482.

30.  Owens BD, Murphy KP, Kuklo TR. Arthroscopic release for lateral epicondylitis. Arthroscopy. 2001;17(6):582-587.

31.  Mullett H, Sprague M, Brown G, Hausman M. Arthroscopic treatment of lateral epicondylitis: clinical and cadaveric studies. Clin Orthop Relat Res. 2005;(439):123-128.

32.  National Survey of Ambulatory Surgery. Centers for Disease Control and Prevention website. http://www.cdc.gov/nchs/nsas/nsas_questionnaires.htm. Published May 4, 2010. Accessed November 10, 2015.

33.  Leader S, Moon M. Medicare trends in ambulatory surgery. Health Aff. 1989;8(1):158-170.

34.  Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;(11):1-25.

35.  Kim S, Bosque J, Meehan JP, Jamali A, Marder R. Increase in outpatient knee arthroscopy in the United States: a comparison of National Surveys of Ambulatory Surgery, 1996 and 2006. J Bone Joint Surg Am. 2011;93(11):994-1000.

36.  Centers for Disease Control and Prevention, National Center for Health Statistics. International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). http://www.cdc.gov/nchs/icd/icd9cm.htm. Updated June 18, 2013. Accessed October 28, 2015.

37.  Dennison C, Pokras R. Design and operation of the National Hospital Discharge Survey: 1988 redesign. Vital Health Stat 1. 2000;(39):1-42.

38.  Stundner O, Kirksey M, Chiu YL, et al. Demographics and perioperative outcome in patients with depression and anxiety undergoing total joint arthroplasty: a population-based study. Psychosomatics. 2013;54(2):149-157.

39.  Population estimates. US Department of Commerce, United States Census Bureau website. http://www.census.gov/popest/index.html. Accessed November 16, 2015.

40.  Berry N, Neumeister MW, Russell RC, Dellon AL. Epicondylectomy versus denervation for lateral humeral epicondylitis. Hand. 2011;6(2):174-178.

41.  Memtsoudis SG, Kuo C, Ma Y, Edwards A, Mazumdar M, Liguori G. Changes in anesthesia-related factors in ambulatory knee and shoulder surgery: United States 1996–2006. Reg Anesth Pain Med. 2011;36(4):327-331.

42.  Richman JM, Liu SS, Courpas G, et al. Does continuous peripheral nerve block provide superior pain control to opioids? A meta-analysis. Anesth Analg. 2006;102(1):248-257.

43.  Bohl DD, Basques BA, Golinvaux NS, Baumgaertner MR, Grauer JN. Nationwide Inpatient Sample and National Surgical Quality Improvement Program give different results in hip fracture studies. Clin Orthop Relat Res. 2014;472(6):1672-1680.

44.    Gray DT, Hodge DO, Ilstrup DM, Butterfield LC, Baratz KH, Concordance of Medicare data and population-based clinical data on cataract surgery utilization in Olmsted County, Minnesota. Am J Epidemiol. 1997;145(12):1123-1126.

45.  Memtsoudis SG. Limitations associated with the analysis of data from administrative databases. Anesthesiology. 2009;111(2):449.

References

1.    Runge F. Zur genese und behandlung des schreibekramfes. Berl Klin Wochenschr. 1873;10:245.

2.    Major HP. Lawn-tennis elbow. Br Med J. 1883;2:557.

3.    Allander E. Prevalence, incidence, and remission rates of some common rheumatic diseases or syndromes. Scand J Rheumatol. 1974;3(3):145-153.

4.    Verhaar JA. Tennis elbow. Anatomical, epidemiological and therapeutic aspects. Int Orthop. 1994;18(5):263-267.

5.    Kurppa K, Viikari-Juntura E, Kuosma E, Huuskonen M, Kivi P. Incidence of tenosynovitis or peritendinitis and epicondylitis in a meat-processing factory. Scand J Work Environ Health. 1991;17(1):32-37.

6.    Ranney D, Wells R, Moore A. Upper limb musculoskeletal disorders in highly repetitive industries: precise anatomical physical findings. Ergonomics. 1995;38(7):1408-1423.

7.    Haahr JP, Andersen JH. Physical and psychosocial risk factors for lateral epicondylitis: a population based case-referent study. Occup Environ Med. 2003;60(5):322-329.

8.    Goldie I. Epicondylitis lateralis humeri (epicondylalgia or tennis elbow). A pathogenetical study. Acta Chir Scand Suppl. 1964;57(suppl 399):1+.

9.    Binder AI, Hazleman BL. Lateral humeral epicondylitis—a study of natural history and the effect of conservative therapy. Br J Rheumatol. 1983;22(2):73-76.

10.  Smidt N, van der Windt DA, Assendelft WJ, Devillé WL, Korthals-de Bos IB, Bouter LM. Corticosteroid injections, physiotherapy, or a wait-and-see policy for lateral epicondylitis: a randomised controlled trial. Lancet. 2002;359(9307):657-662.

11.  Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979;61(6):832-839.

12.  Burnham R, Gregg R, Healy P, Steadward R. The effectiveness of topical diclofenac for lateral epicondylitis. Clin J Sport Med. 1998;8(2):78-81.

13.  Martinez-Silvestrini JA, Newcomer KL, Gay RE, Schaefer MP, Kortebein P, Arendt KW. Chronic lateral epicondylitis: comparative effectiveness of a home exercise program including stretching alone versus stretching supplemented with eccentric or concentric strengthening. J Hand Ther. 2005;18(4):411-419.

14.  Svernlöv B, Adolfsson L. Non-operative treatment regime including eccentric training for lateral humeral epicondylalgia. Scand J Med Sci Sports. 2001;11(6):328-334.

15.  Hay EM, Paterson SM, Lewis M, Hosie G, Croft P. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ. 1999;319(7215):964-968.

16.  Lewis M, Hay EM, Paterson SM, Croft P. Local steroid injections for tennis elbow: does the pain get worse before it gets better? Results from a randomized controlled trial. Clin J Pain. 2005;21(4):330-334.

17.  Van De Streek MD, Van Der Schans CP, De Greef MH, Postema K. The effect of a forearm/hand splint compared with an elbow band as a treatment for lateral epicondylitis. Prosthet Orthot Int. 2004;28(2):183-189.

18.  Struijs PA, Smidt N, Arola H, Dijk vC, Buchbinder R, Assendelft WJ. Orthotic devices for the treatment of tennis elbow. Cochrane Database Syst Rev. 2002;(1):CD001821.

19.  Buchbinder R, Green SE, Youd JM, Assendelft WJ, Barnsley L, Smidt N. Shock wave therapy for lateral elbow pain. Cochrane Database Syst Rev. 2005;(4):CD003524.

20.  Boyd HB, McLeod AC Jr. Tennis elbow. J Bone Joint Surg Am. 1973;55(6):1183-1187.

21.  Coonrad RW, Hooper WR. Tennis elbow: its course, natural history, conservative and surgical management. J Bone Joint Surg Am. 1973;55(6):1177-1182.

22.  Calfee RP, Patel A, DaSilva MF, Akelman E. Management of lateral epicondylitis: current concepts. J Am Acad Orthop Surg. 2008;16(1):19-29.

23.  Plancher KD, Bishai SK. Open lateral epicondylectomy: a simple technique update for the 21st century. Tech Orthop. 2006;21(4):276-282.

24.  Peart RE, Strickler SS, Schweitzer KM Jr. Lateral epicondylitis: a comparative study of open and arthroscopic lateral release. Am J Orthop. 2004;33(11):565-567.

25.  Dunkow PD, Jatti M, Muddu BN. A comparison of open and percutaneous techniques in the surgical treatment of tennis elbow. J Bone Joint Surg Br. 2004;86(5):701-704.

26.  Rosenberg N, Henderson I. Surgical treatment of resistant lateral epicondylitis. Follow-up study of 19 patients after excision, release and repair of proximal common extensor tendon origin. Arch Orthop Trauma Surg. 2002;122(9-10):514-517.

27.  Almquist EE, Necking L, Bach AW. Epicondylar resection with anconeus muscle transfer for chronic lateral epicondylitis. J Hand Surg Am. 1998;23(4):723-731.

28.  Smith AM, Castle JA, Ruch DS. Arthroscopic resection of the common extensor origin: anatomic considerations. J Shoulder Elbow Surg. 2003;12(4):375-379.

29.  Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J Shoulder Elbow Surg. 2000;9(6):475-482.

30.  Owens BD, Murphy KP, Kuklo TR. Arthroscopic release for lateral epicondylitis. Arthroscopy. 2001;17(6):582-587.

31.  Mullett H, Sprague M, Brown G, Hausman M. Arthroscopic treatment of lateral epicondylitis: clinical and cadaveric studies. Clin Orthop Relat Res. 2005;(439):123-128.

32.  National Survey of Ambulatory Surgery. Centers for Disease Control and Prevention website. http://www.cdc.gov/nchs/nsas/nsas_questionnaires.htm. Published May 4, 2010. Accessed November 10, 2015.

33.  Leader S, Moon M. Medicare trends in ambulatory surgery. Health Aff. 1989;8(1):158-170.

34.  Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;(11):1-25.

35.  Kim S, Bosque J, Meehan JP, Jamali A, Marder R. Increase in outpatient knee arthroscopy in the United States: a comparison of National Surveys of Ambulatory Surgery, 1996 and 2006. J Bone Joint Surg Am. 2011;93(11):994-1000.

36.  Centers for Disease Control and Prevention, National Center for Health Statistics. International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). http://www.cdc.gov/nchs/icd/icd9cm.htm. Updated June 18, 2013. Accessed October 28, 2015.

37.  Dennison C, Pokras R. Design and operation of the National Hospital Discharge Survey: 1988 redesign. Vital Health Stat 1. 2000;(39):1-42.

38.  Stundner O, Kirksey M, Chiu YL, et al. Demographics and perioperative outcome in patients with depression and anxiety undergoing total joint arthroplasty: a population-based study. Psychosomatics. 2013;54(2):149-157.

39.  Population estimates. US Department of Commerce, United States Census Bureau website. http://www.census.gov/popest/index.html. Accessed November 16, 2015.

40.  Berry N, Neumeister MW, Russell RC, Dellon AL. Epicondylectomy versus denervation for lateral humeral epicondylitis. Hand. 2011;6(2):174-178.

41.  Memtsoudis SG, Kuo C, Ma Y, Edwards A, Mazumdar M, Liguori G. Changes in anesthesia-related factors in ambulatory knee and shoulder surgery: United States 1996–2006. Reg Anesth Pain Med. 2011;36(4):327-331.

42.  Richman JM, Liu SS, Courpas G, et al. Does continuous peripheral nerve block provide superior pain control to opioids? A meta-analysis. Anesth Analg. 2006;102(1):248-257.

43.  Bohl DD, Basques BA, Golinvaux NS, Baumgaertner MR, Grauer JN. Nationwide Inpatient Sample and National Surgical Quality Improvement Program give different results in hip fracture studies. Clin Orthop Relat Res. 2014;472(6):1672-1680.

44.    Gray DT, Hodge DO, Ilstrup DM, Butterfield LC, Baratz KH, Concordance of Medicare data and population-based clinical data on cataract surgery utilization in Olmsted County, Minnesota. Am J Epidemiol. 1997;145(12):1123-1126.

45.  Memtsoudis SG. Limitations associated with the analysis of data from administrative databases. Anesthesiology. 2009;111(2):449.

Issue
The American Journal of Orthopedics - 44(12)
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The American Journal of Orthopedics - 44(12)
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US National Practice Patterns in Ambulatory Operative Management of Lateral Epicondylitis
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US National Practice Patterns in Ambulatory Operative Management of Lateral Epicondylitis
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american journal of orthopedics, AJO, original study, online exclusive, study, ambulatory, operative management, practice management, lateral epicondylitis, elbow, elbow pain, pain management, operative techniques, practice patterns, surgery, buller, best, nigen, ialenti, baraga
Legacy Keywords
american journal of orthopedics, AJO, original study, online exclusive, study, ambulatory, operative management, practice management, lateral epicondylitis, elbow, elbow pain, pain management, operative techniques, practice patterns, surgery, buller, best, nigen, ialenti, baraga
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Total Knee Arthroplasty in Hemophilic Arthropathy

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Total Knee Arthroplasty in Hemophilic Arthropathy

Chronic hemophilic arthropathy, a well-known complication of hemophilia, develops as a long-term consequence of recurrent joint bleeds resulting in synovial hypertrophy (chronic proliferative synovitis) and joint cartilage destruction. Hemophilic arthropathy mostly affects the knees, ankles, and elbows and causes chronic joint pain and functional impairment in relatively young patients who have not received adequate primary prophylactic replacement therapy with factor concentrates from early childhood.1-3

In the late stages of hemophilic arthropathy of the knee, total knee arthroplasty (TKA) provides dramatic joint pain relief, improves knee functional status, and reduces rebleeding into the joint.4-8 TKA performed on a patient with hemophilia was first reported in the mid-1970s.9,10 In these cases, the surgical procedure itself is often complicated by severe fibrosis developing in the joint soft tissues, flexion joint contracture, and poor quality of the joint bone structures. Even though TKA significantly reduces joint pain in patients with chronic hemophilic arthropathy, some authors have achieved only modest functional outcomes and experienced a high rate of complications (infection, prosthetic loosening).11-13 Data on TKA outcomes are still scarce, and most studies have enrolled a limited number of patients.

We retrospectively evaluated the outcomes of 88 primary TKAs performed on patients with severe hemophilia at a single institution. Clinical outcomes and complications were assessed with a special focus on prosthetic survival and infection.

Patients and Methods

Ninety-one primary TKAs were performed in 77 patients with severe hemophilia A and B (factor VIII [FVIII] and factor IX plasma concentration, <1% each) between January 1, 1999, and December 31, 2011, and the medical records of all these patients were thoroughly reviewed in 2013. The cases of 3 patients who died shortly after surgery were excluded from analysis. Thus, 88 TKAs and 74 patients (74 males) were finally available for evaluation. Fourteen patients underwent bilateral TKAs but none concurrently. The patients provided written informed consent for print and electronic publication of their outcomes.

We recorded demographic data, type and severity of hemophilia, human immunodeficiency virus (HIV) status, hepatitis C virus (HCV) status, and Knee Society Scale (KSS) scores.14 KSS scores include Knee score (pain, range of motion [ROM], stability) and Function score (walking, stairs), both of which range from 0 (normal knee) to 100 (most affected knee). Prosthetic infection was classified (Segawa and colleagues15) as early or late, depending on timing of symptom onset (4 weeks after replacement surgery was the threshold used).

Patients received an intravenous bolus infusion of the deficient factor concentrate followed by continuous infusion to reach a plasma factor level of 100% just before surgery and during the first 7 postoperative days and 50% over the next 7 days (Table 1). Patients with a circulating inhibitor (3 overall) received bypassing agents FEIBA (FVIII inhibitor bypassing agent) or rFVIIa (recombinant factor VII activated) (Table 2). Patients were not given any antifibrinolytic treatment or thromboprophylaxis.

 

Surgery was performed in a standard surgical room. Patients were placed on the operating table in decubitus supinus position. A parapatellar medial incision was made on a bloodless surgical field (achieved with tourniquet ischemia). The prosthesis model used was always the cemented (gentamicin bone cement) NexGen (Zimmer). Patellar resurfacing was done in all cases (Figures 1A–1D). All TKAs were performed by Dr. Rodríguez-Merchán. Intravenous antibiotic prophylaxis was administered at anesthetic induction and during the first 48 hours after surgery (3 further doses). Active exercises were started on postoperative day 1. Joint load aided with 2 crutches was allowed starting on postoperative day 2.

Mean patient age was 38.2 years (range, 24-73 years). Of the 74 patients, 55 had a diagnosis of severe hemophilia A, and 19 had a diagnosis of severe hemophilia B. During the follow-up period, 23 patients died (mean time, 6.4 years; range, 4-9 years). Causes of death were acquired immune deficiency syndrome (AIDS), liver cirrhosis, and intracranial bleeding. Mean follow-up for the full series of patients was 8 years (range, 1-13 years).

Descriptive statistical analysis was performed with SPSS Windows Version 18.0. Prosthetic failure was regarded as implant removal for any reason. Student t test was used to compare continuous variables, and either χ2 test or Fisher exact test was used to compare categorical variables. P < .05 (2-sided) was considered significant.

Results

Prosthetic survival rates with implant removal for any reason regarded as final endpoint was 92%. Causes of failure were prosthetic infection (6 cases, 6.8%) and loosening (2 cases, 2.2%). Of the 6 prosthetic infections, 5 were regarded as late and 1 as early. Late infections were successfully sorted by performing 2-stage revision TKA with the Constrained Condylar Knee (Zimmer). Acute infections were managed by open joint débridement and polyethylene exchange. Both cases of aseptic loosening of the TKA were successfully managed with 1-stage revision TKA using the same implant model (Figures 2A–2D).

 

 

Mean KSS Knee score improved from 79 before surgery to 36 after surgery, and mean KSS Function score improved from 63 to 33. KSS Pain score, which is included in the Knee score, 0 (no pain) to 50 (most severe pain), improved from 47 to 8. Patients receiving inhibitors and patients who were HIV- or HCV-positive did not have poorer outcomes relative to those of patients not receiving inhibitors and patients who were HIV- or HCV-negative. Patients with liver cirrhosis had a lower prosthetic survival rate and lower Knee scores.

Discussion

The prosthetic survival rate found in this study compares well with other reported rates for patients with hemophilia and other bleeding disorders. However, evidence regarding long-term prosthesis survival in TKAs performed for patients with hemophilia is limited. Table 3 summarizes the main reported series of patients with hemophilia with 10-year prosthetic survival rates, number of TKAs performed, and mean follow-up period; in all these series, implant removal for any reason was regarded as the final endpoint.5-8,16,17 Mean follow-up in our study was 8 years. Clinical outcomes of TKA in patients with severe hemophilia and related disorders are expected to be inferior to those achieved in patients without a bleeding condition. The overall 10-year prosthetic survival rate for cemented TKA implants, as reported by the Norwegian Arthroplasty Register, was on the order of 93%.18 Mean age of our patients at time of surgery was only 38.2 years. TKAs performed in younger patients without a bleeding disorder have been associated with shorter implant survival times relative to those of elderly patients.19 Thus, Diduch and colleagues20 reported a prosthetic survival rate of 87% at 18 years in 108 TKAs performed on patients under age 55 years. Lonner and colleagues21 reported a better implant survival rate (90% at 8 years) in a series of patients under age 40 years (32 TKAs). In a study by Duffy and colleagues,22 the implant survival rate was 85% at 15 years in patients under age 55 years (74 TKAs). The results from our retrospective case assessment are quite similar to the overall prosthetic survival rates reported for TKAs performed on patients without hemophilia.

Rates of periprosthetic infection after primary TKA in patients with hemophilia and other bleeding conditions are much higher (up to 11%), with a mean infection rate of 6.2% (range, 1% to 11%), consistent with the rate found in our series of patients (6.8%)7,16,17,23,24 (Table 4). This rate is much higher than that reported after primary TKA in patients without hemophilia but is similar to some rates reported for patients with hemophilia. In our experience, most periprosthetic infections (5/6) were sorted as late.

Late infection is a major concern after TKA in patients with hemophilia, and various factors have been hypothesized as contributing to the high prevalence. An important factor is the high rate of HIV-positive patients among patients with hemophilia—which acts as a strong predisposing factor because of the often low CD4 counts and associated immune deficiency,25 but different reports have provided conflicting results in this respect.5,6,12 We found no relationship between HIV status and risk for periprosthetic infection, but conclusions are limited by the low number of HIV-positive patients in our series (14/74, 18.9%). Our patients’ late periprosthetic infections were diagnosed several years after TKA, suggesting hematogenous spread of infection. Most of these patients either were on regular prophylactic factor infusions or were being treated on demand, which might entail a risk for contamination of infusions by skin bacteria from the puncture site. Therefore, having an aseptic technique for administering coagulation factor concentrates is of paramount importance for patients with hemophilia and a knee implant.

Another important complication of TKA surgery is aseptic loosening of the prosthesis. Aseptic loosening occurred in 2.2% of our patients, but higher rates have been reported elsewhere.11,26 Rates of this complication increase over follow-up, and some authors have linked this complication to TKA polyethylene wear.27 Development of a reactive and destructive bone–cement interface and microhemorrhages into such interface might be implicated in the higher rate of loosening observed among patients with hemophilia.28

In the present study, preoperative and postoperative functional outcomes differed significantly. A modest postoperative total ROM of 69º to 79º has been reported by several authors.5,6 Postoperative ROM may vary—may be slightly increased, remain unchanged, or may even be reduced.4,23,26 Even though little improvement in total ROM is achieved after TKA, many authors have reported reduced flexion contracture and hence an easier gait. However, along with functional improvement, dramatic pain relief after TKA is perhaps the most remarkable aspect, and it has a strong effect on patient satisfaction after surgery.5,7,8,18,23

 

 

Our study had 2 main limitations. First, it was a retrospective case series evaluation with the usual issues of potential inaccuracy of medical records and information bias. Second, the study did not include a control group.

Conclusion

The primary TKAs performed in our patients with hemophilia have had a good prosthetic survival rate. Even though such a result is slightly inferior to results in patients without hemophilia, our prosthetic survival rate is not significantly different from the rates reported in other, younger patient subsets. Late periprosthetic infections are a major concern, and taking precautions to avoid hematogenous spread of infections during factor concentrate infusions is strongly encouraged.

References

1.    Arnold WD, Hilgartner MW. Hemophilic arthropathy. Current concepts of pathogenesis and management. J Bone Joint Surg Am. 1977;59(3):287-305.

2.    Rodriguez-Merchan EC. Common orthopaedic problems in haemophilia. Haemophilia. 1999;5(suppl 1):53-60.

3.    Steen Carlsson K, Höjgård S, Glomstein A, et al. On-demand vs. prophylactic treatment for severe haemophilia in Norway and Sweden: differences in treatment characteristics and outcome. Haemophilia. 2003;9(5):555-566.

4.    Teigland JC, Tjønnfjord GE, Evensen SA, Charania B. Knee arthroplasty in hemophilia. 5-12 year follow-up of 15 patients. Acta Orthop Scand. 1993;64(2):153-156.

5.    Silva M, Luck JV Jr. Long-term results of primary total knee replacement in patients with hemophilia. J Bone Joint Surg Am. 2005;87(1):85-91.

6.    Wang K, Street A, Dowrick A, Liew S. Clinical outcomes and patient satisfaction following total joint replacement in haemophilia—23-year experience in knees, hips and elbows. Haemophilia. 2012;18(1):86-93.

7.    Chevalier Y, Dargaud Y, Lienhart A, Chamouard V, Negrier C. Seventy-two total knee arthroplasties performed in patients with haemophilia using continuous infusion. Vox Sang. 2013;104(2):135-143.

8.    Zingg PO, Fucentese SF, Lutz W, Brand B, Mamisch N, Koch PP. Haemophilic knee arthropathy: long-term outcome after total knee replacement. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2465-2470.

9.    Kjaersgaard-Andersen P, Christiansen SE, Ingerslev J, Sneppen O. Total knee arthroplasty in classic hemophilia. Clin Orthop Relat Res. 1990;(256):137-146.

10.  Cohen I, Heim M, Martinowitz U, Chechick A. Orthopaedic outcome of total knee replacement in haemophilia A. Haemophilia. 2000;6(2):104-109.

11.  Fehily M, Fleming P, O’Shea E, Smith O, Smyth H. Total knee arthroplasty in patients with severe haemophilia. Int Orthop. 2002;26(2):89-91.

12.  Legroux-Gérot I, Strouk G, Parquet A, Goodemand J, Gougeon F, Duquesnoy B. Total knee arthroplasty in hemophilic arthropathy. Joint Bone Spine. 2003;70(1):22-32.

13.  Sheth DS, Oldfield D, Ambrose C, Clyburn T. Total knee arthroplasty in hemophilic arthropathy. J Arthroplasty. 2004;19(1):56-60.

14.  Insall JN, Dorr LD, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989;(248):13-14.

15.  Segawa H, Tsukayama DT, Kyle RF, Becker DA, Gustilo RB. Infection after total knee arthroplasty. A retrospective study of the treatment of eighty-one infections. J Bone Joint Surg Am. 1999;81(10):1434-1445.

16.  Goddard NJ, Mann HA, Lee CA. Total knee replacement in patients with end-stage haemophilic arthropathy. 25-year results. J Bone Joint Surg Br. 2010;92(8):1085-1089.

17.  Westberg M, Paus AC, Holme PA, Tjønnfjord GE. Haemophilic arthropathy: long-term outcomes in 107 primary total knee arthroplasties. Knee. 2014;21(1):147-150.

18.  Lygre SH, Espehaug B, Havelin LI, Vollset SE, Furnes O. Failure of total knee arthroplasty with or without patella resurfacing. A study from the Norwegian Arthroplasty Register with 0-15 years of follow-up. Acta Orthop. 2011;82(3):282-292.

19.  Post M, Telfer MC. Surgery in hemophilic patients. J Bone Joint Surg Am. 1975;57(8):1136-1145.

20.  Diduch DR, Insall JN, Scott WN, Scuderi GR, Font-Rodriguez D. Total knee replacement in young, active patients. Long-term follow-up and functional outcome. J Bone Joint Surg Am. 1997;79(4):575-582.

21.  Lonner JH, Hershman S, Mont M, Lotke PA. Total knee arthroplasty in patients 40 years of age and younger with osteoarthritis. Clin Orthop Relat Res. 2000;(380):85-90.

22.  Duffy GP, Crowder AR, Trousdale RR, Berry DJ. Cemented total knee arthroplasty using a modern prosthesis in young patients with osteoarthritis. J Arthroplasty. 2007;22(6 suppl 2):67-70.

23.  Chiang CC, Chen PQ, Shen MC, Tsai W. Total knee arthroplasty for severe haemophilic arthropathy: long-term experience in Taiwan. Haemophilia. 2008;14(4):828-834.

24.  Solimeno LP, Mancuso ME, Pasta G, Santagostino E, Perfetto S, Mannucci PM. Factors influencing the long-term outcome of primary total knee replacement in haemophiliacs: a review of 116 procedures at a single institution. Br J Haematol. 2009;145(2):227-234.

25.  Jämsen E, Varonen M, Huhtala H, et al. Incidence of prosthetic joint infections after primary knee arthroplasty. J Arthroplasty. 2010;25(1):87-92.

26.  Ragni MV, Crossett LS, Herndon JH. Postoperative infection following orthopaedic surgery in human immunodeficiency virus–infected hemophiliacs with CD4 counts < or = 200/mm3. J Arthroplasty. 1995;10(6):716-721.

27.    Hicks JL, Ribbans WJ, Buzzard B, et al. Infected joint replacements in HIV-positive patients with haemophilia. J Bone Joint Surg Br. 2001;83(7):1050-1054.

28.  Figgie MP, Goldberg VM, Figgie HE 3rd, Heiple KG, Sobel M. Total knee arthroplasty for the treatment of chronic hemophilic arthropathy. Clin Orthop Relat Res. 1989;(248):98-107.

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E. Carlos Rodríguez-Merchán, MD, PhD

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The American Journal of Orthopedics - 44(12)
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E503-E507
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american journal of orthopedics, AJO, original study, online exclusive, study, total knee arthroplasty, TKA, knee, arthroplasty, hemophilic, arthropathy, joint, pain, pain management, rodriguez-merchan, joint bleeding, blood
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E. Carlos Rodríguez-Merchán, MD, PhD

Author’s Disclosure Statement: The author reports no actual or potential conflict of interest in relation to this article.

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E. Carlos Rodríguez-Merchán, MD, PhD

Author’s Disclosure Statement: The author reports no actual or potential conflict of interest in relation to this article.

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Chronic hemophilic arthropathy, a well-known complication of hemophilia, develops as a long-term consequence of recurrent joint bleeds resulting in synovial hypertrophy (chronic proliferative synovitis) and joint cartilage destruction. Hemophilic arthropathy mostly affects the knees, ankles, and elbows and causes chronic joint pain and functional impairment in relatively young patients who have not received adequate primary prophylactic replacement therapy with factor concentrates from early childhood.1-3

In the late stages of hemophilic arthropathy of the knee, total knee arthroplasty (TKA) provides dramatic joint pain relief, improves knee functional status, and reduces rebleeding into the joint.4-8 TKA performed on a patient with hemophilia was first reported in the mid-1970s.9,10 In these cases, the surgical procedure itself is often complicated by severe fibrosis developing in the joint soft tissues, flexion joint contracture, and poor quality of the joint bone structures. Even though TKA significantly reduces joint pain in patients with chronic hemophilic arthropathy, some authors have achieved only modest functional outcomes and experienced a high rate of complications (infection, prosthetic loosening).11-13 Data on TKA outcomes are still scarce, and most studies have enrolled a limited number of patients.

We retrospectively evaluated the outcomes of 88 primary TKAs performed on patients with severe hemophilia at a single institution. Clinical outcomes and complications were assessed with a special focus on prosthetic survival and infection.

Patients and Methods

Ninety-one primary TKAs were performed in 77 patients with severe hemophilia A and B (factor VIII [FVIII] and factor IX plasma concentration, <1% each) between January 1, 1999, and December 31, 2011, and the medical records of all these patients were thoroughly reviewed in 2013. The cases of 3 patients who died shortly after surgery were excluded from analysis. Thus, 88 TKAs and 74 patients (74 males) were finally available for evaluation. Fourteen patients underwent bilateral TKAs but none concurrently. The patients provided written informed consent for print and electronic publication of their outcomes.

We recorded demographic data, type and severity of hemophilia, human immunodeficiency virus (HIV) status, hepatitis C virus (HCV) status, and Knee Society Scale (KSS) scores.14 KSS scores include Knee score (pain, range of motion [ROM], stability) and Function score (walking, stairs), both of which range from 0 (normal knee) to 100 (most affected knee). Prosthetic infection was classified (Segawa and colleagues15) as early or late, depending on timing of symptom onset (4 weeks after replacement surgery was the threshold used).

Patients received an intravenous bolus infusion of the deficient factor concentrate followed by continuous infusion to reach a plasma factor level of 100% just before surgery and during the first 7 postoperative days and 50% over the next 7 days (Table 1). Patients with a circulating inhibitor (3 overall) received bypassing agents FEIBA (FVIII inhibitor bypassing agent) or rFVIIa (recombinant factor VII activated) (Table 2). Patients were not given any antifibrinolytic treatment or thromboprophylaxis.

 

Surgery was performed in a standard surgical room. Patients were placed on the operating table in decubitus supinus position. A parapatellar medial incision was made on a bloodless surgical field (achieved with tourniquet ischemia). The prosthesis model used was always the cemented (gentamicin bone cement) NexGen (Zimmer). Patellar resurfacing was done in all cases (Figures 1A–1D). All TKAs were performed by Dr. Rodríguez-Merchán. Intravenous antibiotic prophylaxis was administered at anesthetic induction and during the first 48 hours after surgery (3 further doses). Active exercises were started on postoperative day 1. Joint load aided with 2 crutches was allowed starting on postoperative day 2.

Mean patient age was 38.2 years (range, 24-73 years). Of the 74 patients, 55 had a diagnosis of severe hemophilia A, and 19 had a diagnosis of severe hemophilia B. During the follow-up period, 23 patients died (mean time, 6.4 years; range, 4-9 years). Causes of death were acquired immune deficiency syndrome (AIDS), liver cirrhosis, and intracranial bleeding. Mean follow-up for the full series of patients was 8 years (range, 1-13 years).

Descriptive statistical analysis was performed with SPSS Windows Version 18.0. Prosthetic failure was regarded as implant removal for any reason. Student t test was used to compare continuous variables, and either χ2 test or Fisher exact test was used to compare categorical variables. P < .05 (2-sided) was considered significant.

Results

Prosthetic survival rates with implant removal for any reason regarded as final endpoint was 92%. Causes of failure were prosthetic infection (6 cases, 6.8%) and loosening (2 cases, 2.2%). Of the 6 prosthetic infections, 5 were regarded as late and 1 as early. Late infections were successfully sorted by performing 2-stage revision TKA with the Constrained Condylar Knee (Zimmer). Acute infections were managed by open joint débridement and polyethylene exchange. Both cases of aseptic loosening of the TKA were successfully managed with 1-stage revision TKA using the same implant model (Figures 2A–2D).

 

 

Mean KSS Knee score improved from 79 before surgery to 36 after surgery, and mean KSS Function score improved from 63 to 33. KSS Pain score, which is included in the Knee score, 0 (no pain) to 50 (most severe pain), improved from 47 to 8. Patients receiving inhibitors and patients who were HIV- or HCV-positive did not have poorer outcomes relative to those of patients not receiving inhibitors and patients who were HIV- or HCV-negative. Patients with liver cirrhosis had a lower prosthetic survival rate and lower Knee scores.

Discussion

The prosthetic survival rate found in this study compares well with other reported rates for patients with hemophilia and other bleeding disorders. However, evidence regarding long-term prosthesis survival in TKAs performed for patients with hemophilia is limited. Table 3 summarizes the main reported series of patients with hemophilia with 10-year prosthetic survival rates, number of TKAs performed, and mean follow-up period; in all these series, implant removal for any reason was regarded as the final endpoint.5-8,16,17 Mean follow-up in our study was 8 years. Clinical outcomes of TKA in patients with severe hemophilia and related disorders are expected to be inferior to those achieved in patients without a bleeding condition. The overall 10-year prosthetic survival rate for cemented TKA implants, as reported by the Norwegian Arthroplasty Register, was on the order of 93%.18 Mean age of our patients at time of surgery was only 38.2 years. TKAs performed in younger patients without a bleeding disorder have been associated with shorter implant survival times relative to those of elderly patients.19 Thus, Diduch and colleagues20 reported a prosthetic survival rate of 87% at 18 years in 108 TKAs performed on patients under age 55 years. Lonner and colleagues21 reported a better implant survival rate (90% at 8 years) in a series of patients under age 40 years (32 TKAs). In a study by Duffy and colleagues,22 the implant survival rate was 85% at 15 years in patients under age 55 years (74 TKAs). The results from our retrospective case assessment are quite similar to the overall prosthetic survival rates reported for TKAs performed on patients without hemophilia.

Rates of periprosthetic infection after primary TKA in patients with hemophilia and other bleeding conditions are much higher (up to 11%), with a mean infection rate of 6.2% (range, 1% to 11%), consistent with the rate found in our series of patients (6.8%)7,16,17,23,24 (Table 4). This rate is much higher than that reported after primary TKA in patients without hemophilia but is similar to some rates reported for patients with hemophilia. In our experience, most periprosthetic infections (5/6) were sorted as late.

Late infection is a major concern after TKA in patients with hemophilia, and various factors have been hypothesized as contributing to the high prevalence. An important factor is the high rate of HIV-positive patients among patients with hemophilia—which acts as a strong predisposing factor because of the often low CD4 counts and associated immune deficiency,25 but different reports have provided conflicting results in this respect.5,6,12 We found no relationship between HIV status and risk for periprosthetic infection, but conclusions are limited by the low number of HIV-positive patients in our series (14/74, 18.9%). Our patients’ late periprosthetic infections were diagnosed several years after TKA, suggesting hematogenous spread of infection. Most of these patients either were on regular prophylactic factor infusions or were being treated on demand, which might entail a risk for contamination of infusions by skin bacteria from the puncture site. Therefore, having an aseptic technique for administering coagulation factor concentrates is of paramount importance for patients with hemophilia and a knee implant.

Another important complication of TKA surgery is aseptic loosening of the prosthesis. Aseptic loosening occurred in 2.2% of our patients, but higher rates have been reported elsewhere.11,26 Rates of this complication increase over follow-up, and some authors have linked this complication to TKA polyethylene wear.27 Development of a reactive and destructive bone–cement interface and microhemorrhages into such interface might be implicated in the higher rate of loosening observed among patients with hemophilia.28

In the present study, preoperative and postoperative functional outcomes differed significantly. A modest postoperative total ROM of 69º to 79º has been reported by several authors.5,6 Postoperative ROM may vary—may be slightly increased, remain unchanged, or may even be reduced.4,23,26 Even though little improvement in total ROM is achieved after TKA, many authors have reported reduced flexion contracture and hence an easier gait. However, along with functional improvement, dramatic pain relief after TKA is perhaps the most remarkable aspect, and it has a strong effect on patient satisfaction after surgery.5,7,8,18,23

 

 

Our study had 2 main limitations. First, it was a retrospective case series evaluation with the usual issues of potential inaccuracy of medical records and information bias. Second, the study did not include a control group.

Conclusion

The primary TKAs performed in our patients with hemophilia have had a good prosthetic survival rate. Even though such a result is slightly inferior to results in patients without hemophilia, our prosthetic survival rate is not significantly different from the rates reported in other, younger patient subsets. Late periprosthetic infections are a major concern, and taking precautions to avoid hematogenous spread of infections during factor concentrate infusions is strongly encouraged.

Chronic hemophilic arthropathy, a well-known complication of hemophilia, develops as a long-term consequence of recurrent joint bleeds resulting in synovial hypertrophy (chronic proliferative synovitis) and joint cartilage destruction. Hemophilic arthropathy mostly affects the knees, ankles, and elbows and causes chronic joint pain and functional impairment in relatively young patients who have not received adequate primary prophylactic replacement therapy with factor concentrates from early childhood.1-3

In the late stages of hemophilic arthropathy of the knee, total knee arthroplasty (TKA) provides dramatic joint pain relief, improves knee functional status, and reduces rebleeding into the joint.4-8 TKA performed on a patient with hemophilia was first reported in the mid-1970s.9,10 In these cases, the surgical procedure itself is often complicated by severe fibrosis developing in the joint soft tissues, flexion joint contracture, and poor quality of the joint bone structures. Even though TKA significantly reduces joint pain in patients with chronic hemophilic arthropathy, some authors have achieved only modest functional outcomes and experienced a high rate of complications (infection, prosthetic loosening).11-13 Data on TKA outcomes are still scarce, and most studies have enrolled a limited number of patients.

We retrospectively evaluated the outcomes of 88 primary TKAs performed on patients with severe hemophilia at a single institution. Clinical outcomes and complications were assessed with a special focus on prosthetic survival and infection.

Patients and Methods

Ninety-one primary TKAs were performed in 77 patients with severe hemophilia A and B (factor VIII [FVIII] and factor IX plasma concentration, <1% each) between January 1, 1999, and December 31, 2011, and the medical records of all these patients were thoroughly reviewed in 2013. The cases of 3 patients who died shortly after surgery were excluded from analysis. Thus, 88 TKAs and 74 patients (74 males) were finally available for evaluation. Fourteen patients underwent bilateral TKAs but none concurrently. The patients provided written informed consent for print and electronic publication of their outcomes.

We recorded demographic data, type and severity of hemophilia, human immunodeficiency virus (HIV) status, hepatitis C virus (HCV) status, and Knee Society Scale (KSS) scores.14 KSS scores include Knee score (pain, range of motion [ROM], stability) and Function score (walking, stairs), both of which range from 0 (normal knee) to 100 (most affected knee). Prosthetic infection was classified (Segawa and colleagues15) as early or late, depending on timing of symptom onset (4 weeks after replacement surgery was the threshold used).

Patients received an intravenous bolus infusion of the deficient factor concentrate followed by continuous infusion to reach a plasma factor level of 100% just before surgery and during the first 7 postoperative days and 50% over the next 7 days (Table 1). Patients with a circulating inhibitor (3 overall) received bypassing agents FEIBA (FVIII inhibitor bypassing agent) or rFVIIa (recombinant factor VII activated) (Table 2). Patients were not given any antifibrinolytic treatment or thromboprophylaxis.

 

Surgery was performed in a standard surgical room. Patients were placed on the operating table in decubitus supinus position. A parapatellar medial incision was made on a bloodless surgical field (achieved with tourniquet ischemia). The prosthesis model used was always the cemented (gentamicin bone cement) NexGen (Zimmer). Patellar resurfacing was done in all cases (Figures 1A–1D). All TKAs were performed by Dr. Rodríguez-Merchán. Intravenous antibiotic prophylaxis was administered at anesthetic induction and during the first 48 hours after surgery (3 further doses). Active exercises were started on postoperative day 1. Joint load aided with 2 crutches was allowed starting on postoperative day 2.

Mean patient age was 38.2 years (range, 24-73 years). Of the 74 patients, 55 had a diagnosis of severe hemophilia A, and 19 had a diagnosis of severe hemophilia B. During the follow-up period, 23 patients died (mean time, 6.4 years; range, 4-9 years). Causes of death were acquired immune deficiency syndrome (AIDS), liver cirrhosis, and intracranial bleeding. Mean follow-up for the full series of patients was 8 years (range, 1-13 years).

Descriptive statistical analysis was performed with SPSS Windows Version 18.0. Prosthetic failure was regarded as implant removal for any reason. Student t test was used to compare continuous variables, and either χ2 test or Fisher exact test was used to compare categorical variables. P < .05 (2-sided) was considered significant.

Results

Prosthetic survival rates with implant removal for any reason regarded as final endpoint was 92%. Causes of failure were prosthetic infection (6 cases, 6.8%) and loosening (2 cases, 2.2%). Of the 6 prosthetic infections, 5 were regarded as late and 1 as early. Late infections were successfully sorted by performing 2-stage revision TKA with the Constrained Condylar Knee (Zimmer). Acute infections were managed by open joint débridement and polyethylene exchange. Both cases of aseptic loosening of the TKA were successfully managed with 1-stage revision TKA using the same implant model (Figures 2A–2D).

 

 

Mean KSS Knee score improved from 79 before surgery to 36 after surgery, and mean KSS Function score improved from 63 to 33. KSS Pain score, which is included in the Knee score, 0 (no pain) to 50 (most severe pain), improved from 47 to 8. Patients receiving inhibitors and patients who were HIV- or HCV-positive did not have poorer outcomes relative to those of patients not receiving inhibitors and patients who were HIV- or HCV-negative. Patients with liver cirrhosis had a lower prosthetic survival rate and lower Knee scores.

Discussion

The prosthetic survival rate found in this study compares well with other reported rates for patients with hemophilia and other bleeding disorders. However, evidence regarding long-term prosthesis survival in TKAs performed for patients with hemophilia is limited. Table 3 summarizes the main reported series of patients with hemophilia with 10-year prosthetic survival rates, number of TKAs performed, and mean follow-up period; in all these series, implant removal for any reason was regarded as the final endpoint.5-8,16,17 Mean follow-up in our study was 8 years. Clinical outcomes of TKA in patients with severe hemophilia and related disorders are expected to be inferior to those achieved in patients without a bleeding condition. The overall 10-year prosthetic survival rate for cemented TKA implants, as reported by the Norwegian Arthroplasty Register, was on the order of 93%.18 Mean age of our patients at time of surgery was only 38.2 years. TKAs performed in younger patients without a bleeding disorder have been associated with shorter implant survival times relative to those of elderly patients.19 Thus, Diduch and colleagues20 reported a prosthetic survival rate of 87% at 18 years in 108 TKAs performed on patients under age 55 years. Lonner and colleagues21 reported a better implant survival rate (90% at 8 years) in a series of patients under age 40 years (32 TKAs). In a study by Duffy and colleagues,22 the implant survival rate was 85% at 15 years in patients under age 55 years (74 TKAs). The results from our retrospective case assessment are quite similar to the overall prosthetic survival rates reported for TKAs performed on patients without hemophilia.

Rates of periprosthetic infection after primary TKA in patients with hemophilia and other bleeding conditions are much higher (up to 11%), with a mean infection rate of 6.2% (range, 1% to 11%), consistent with the rate found in our series of patients (6.8%)7,16,17,23,24 (Table 4). This rate is much higher than that reported after primary TKA in patients without hemophilia but is similar to some rates reported for patients with hemophilia. In our experience, most periprosthetic infections (5/6) were sorted as late.

Late infection is a major concern after TKA in patients with hemophilia, and various factors have been hypothesized as contributing to the high prevalence. An important factor is the high rate of HIV-positive patients among patients with hemophilia—which acts as a strong predisposing factor because of the often low CD4 counts and associated immune deficiency,25 but different reports have provided conflicting results in this respect.5,6,12 We found no relationship between HIV status and risk for periprosthetic infection, but conclusions are limited by the low number of HIV-positive patients in our series (14/74, 18.9%). Our patients’ late periprosthetic infections were diagnosed several years after TKA, suggesting hematogenous spread of infection. Most of these patients either were on regular prophylactic factor infusions or were being treated on demand, which might entail a risk for contamination of infusions by skin bacteria from the puncture site. Therefore, having an aseptic technique for administering coagulation factor concentrates is of paramount importance for patients with hemophilia and a knee implant.

Another important complication of TKA surgery is aseptic loosening of the prosthesis. Aseptic loosening occurred in 2.2% of our patients, but higher rates have been reported elsewhere.11,26 Rates of this complication increase over follow-up, and some authors have linked this complication to TKA polyethylene wear.27 Development of a reactive and destructive bone–cement interface and microhemorrhages into such interface might be implicated in the higher rate of loosening observed among patients with hemophilia.28

In the present study, preoperative and postoperative functional outcomes differed significantly. A modest postoperative total ROM of 69º to 79º has been reported by several authors.5,6 Postoperative ROM may vary—may be slightly increased, remain unchanged, or may even be reduced.4,23,26 Even though little improvement in total ROM is achieved after TKA, many authors have reported reduced flexion contracture and hence an easier gait. However, along with functional improvement, dramatic pain relief after TKA is perhaps the most remarkable aspect, and it has a strong effect on patient satisfaction after surgery.5,7,8,18,23

 

 

Our study had 2 main limitations. First, it was a retrospective case series evaluation with the usual issues of potential inaccuracy of medical records and information bias. Second, the study did not include a control group.

Conclusion

The primary TKAs performed in our patients with hemophilia have had a good prosthetic survival rate. Even though such a result is slightly inferior to results in patients without hemophilia, our prosthetic survival rate is not significantly different from the rates reported in other, younger patient subsets. Late periprosthetic infections are a major concern, and taking precautions to avoid hematogenous spread of infections during factor concentrate infusions is strongly encouraged.

References

1.    Arnold WD, Hilgartner MW. Hemophilic arthropathy. Current concepts of pathogenesis and management. J Bone Joint Surg Am. 1977;59(3):287-305.

2.    Rodriguez-Merchan EC. Common orthopaedic problems in haemophilia. Haemophilia. 1999;5(suppl 1):53-60.

3.    Steen Carlsson K, Höjgård S, Glomstein A, et al. On-demand vs. prophylactic treatment for severe haemophilia in Norway and Sweden: differences in treatment characteristics and outcome. Haemophilia. 2003;9(5):555-566.

4.    Teigland JC, Tjønnfjord GE, Evensen SA, Charania B. Knee arthroplasty in hemophilia. 5-12 year follow-up of 15 patients. Acta Orthop Scand. 1993;64(2):153-156.

5.    Silva M, Luck JV Jr. Long-term results of primary total knee replacement in patients with hemophilia. J Bone Joint Surg Am. 2005;87(1):85-91.

6.    Wang K, Street A, Dowrick A, Liew S. Clinical outcomes and patient satisfaction following total joint replacement in haemophilia—23-year experience in knees, hips and elbows. Haemophilia. 2012;18(1):86-93.

7.    Chevalier Y, Dargaud Y, Lienhart A, Chamouard V, Negrier C. Seventy-two total knee arthroplasties performed in patients with haemophilia using continuous infusion. Vox Sang. 2013;104(2):135-143.

8.    Zingg PO, Fucentese SF, Lutz W, Brand B, Mamisch N, Koch PP. Haemophilic knee arthropathy: long-term outcome after total knee replacement. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2465-2470.

9.    Kjaersgaard-Andersen P, Christiansen SE, Ingerslev J, Sneppen O. Total knee arthroplasty in classic hemophilia. Clin Orthop Relat Res. 1990;(256):137-146.

10.  Cohen I, Heim M, Martinowitz U, Chechick A. Orthopaedic outcome of total knee replacement in haemophilia A. Haemophilia. 2000;6(2):104-109.

11.  Fehily M, Fleming P, O’Shea E, Smith O, Smyth H. Total knee arthroplasty in patients with severe haemophilia. Int Orthop. 2002;26(2):89-91.

12.  Legroux-Gérot I, Strouk G, Parquet A, Goodemand J, Gougeon F, Duquesnoy B. Total knee arthroplasty in hemophilic arthropathy. Joint Bone Spine. 2003;70(1):22-32.

13.  Sheth DS, Oldfield D, Ambrose C, Clyburn T. Total knee arthroplasty in hemophilic arthropathy. J Arthroplasty. 2004;19(1):56-60.

14.  Insall JN, Dorr LD, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989;(248):13-14.

15.  Segawa H, Tsukayama DT, Kyle RF, Becker DA, Gustilo RB. Infection after total knee arthroplasty. A retrospective study of the treatment of eighty-one infections. J Bone Joint Surg Am. 1999;81(10):1434-1445.

16.  Goddard NJ, Mann HA, Lee CA. Total knee replacement in patients with end-stage haemophilic arthropathy. 25-year results. J Bone Joint Surg Br. 2010;92(8):1085-1089.

17.  Westberg M, Paus AC, Holme PA, Tjønnfjord GE. Haemophilic arthropathy: long-term outcomes in 107 primary total knee arthroplasties. Knee. 2014;21(1):147-150.

18.  Lygre SH, Espehaug B, Havelin LI, Vollset SE, Furnes O. Failure of total knee arthroplasty with or without patella resurfacing. A study from the Norwegian Arthroplasty Register with 0-15 years of follow-up. Acta Orthop. 2011;82(3):282-292.

19.  Post M, Telfer MC. Surgery in hemophilic patients. J Bone Joint Surg Am. 1975;57(8):1136-1145.

20.  Diduch DR, Insall JN, Scott WN, Scuderi GR, Font-Rodriguez D. Total knee replacement in young, active patients. Long-term follow-up and functional outcome. J Bone Joint Surg Am. 1997;79(4):575-582.

21.  Lonner JH, Hershman S, Mont M, Lotke PA. Total knee arthroplasty in patients 40 years of age and younger with osteoarthritis. Clin Orthop Relat Res. 2000;(380):85-90.

22.  Duffy GP, Crowder AR, Trousdale RR, Berry DJ. Cemented total knee arthroplasty using a modern prosthesis in young patients with osteoarthritis. J Arthroplasty. 2007;22(6 suppl 2):67-70.

23.  Chiang CC, Chen PQ, Shen MC, Tsai W. Total knee arthroplasty for severe haemophilic arthropathy: long-term experience in Taiwan. Haemophilia. 2008;14(4):828-834.

24.  Solimeno LP, Mancuso ME, Pasta G, Santagostino E, Perfetto S, Mannucci PM. Factors influencing the long-term outcome of primary total knee replacement in haemophiliacs: a review of 116 procedures at a single institution. Br J Haematol. 2009;145(2):227-234.

25.  Jämsen E, Varonen M, Huhtala H, et al. Incidence of prosthetic joint infections after primary knee arthroplasty. J Arthroplasty. 2010;25(1):87-92.

26.  Ragni MV, Crossett LS, Herndon JH. Postoperative infection following orthopaedic surgery in human immunodeficiency virus–infected hemophiliacs with CD4 counts < or = 200/mm3. J Arthroplasty. 1995;10(6):716-721.

27.    Hicks JL, Ribbans WJ, Buzzard B, et al. Infected joint replacements in HIV-positive patients with haemophilia. J Bone Joint Surg Br. 2001;83(7):1050-1054.

28.  Figgie MP, Goldberg VM, Figgie HE 3rd, Heiple KG, Sobel M. Total knee arthroplasty for the treatment of chronic hemophilic arthropathy. Clin Orthop Relat Res. 1989;(248):98-107.

References

1.    Arnold WD, Hilgartner MW. Hemophilic arthropathy. Current concepts of pathogenesis and management. J Bone Joint Surg Am. 1977;59(3):287-305.

2.    Rodriguez-Merchan EC. Common orthopaedic problems in haemophilia. Haemophilia. 1999;5(suppl 1):53-60.

3.    Steen Carlsson K, Höjgård S, Glomstein A, et al. On-demand vs. prophylactic treatment for severe haemophilia in Norway and Sweden: differences in treatment characteristics and outcome. Haemophilia. 2003;9(5):555-566.

4.    Teigland JC, Tjønnfjord GE, Evensen SA, Charania B. Knee arthroplasty in hemophilia. 5-12 year follow-up of 15 patients. Acta Orthop Scand. 1993;64(2):153-156.

5.    Silva M, Luck JV Jr. Long-term results of primary total knee replacement in patients with hemophilia. J Bone Joint Surg Am. 2005;87(1):85-91.

6.    Wang K, Street A, Dowrick A, Liew S. Clinical outcomes and patient satisfaction following total joint replacement in haemophilia—23-year experience in knees, hips and elbows. Haemophilia. 2012;18(1):86-93.

7.    Chevalier Y, Dargaud Y, Lienhart A, Chamouard V, Negrier C. Seventy-two total knee arthroplasties performed in patients with haemophilia using continuous infusion. Vox Sang. 2013;104(2):135-143.

8.    Zingg PO, Fucentese SF, Lutz W, Brand B, Mamisch N, Koch PP. Haemophilic knee arthropathy: long-term outcome after total knee replacement. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2465-2470.

9.    Kjaersgaard-Andersen P, Christiansen SE, Ingerslev J, Sneppen O. Total knee arthroplasty in classic hemophilia. Clin Orthop Relat Res. 1990;(256):137-146.

10.  Cohen I, Heim M, Martinowitz U, Chechick A. Orthopaedic outcome of total knee replacement in haemophilia A. Haemophilia. 2000;6(2):104-109.

11.  Fehily M, Fleming P, O’Shea E, Smith O, Smyth H. Total knee arthroplasty in patients with severe haemophilia. Int Orthop. 2002;26(2):89-91.

12.  Legroux-Gérot I, Strouk G, Parquet A, Goodemand J, Gougeon F, Duquesnoy B. Total knee arthroplasty in hemophilic arthropathy. Joint Bone Spine. 2003;70(1):22-32.

13.  Sheth DS, Oldfield D, Ambrose C, Clyburn T. Total knee arthroplasty in hemophilic arthropathy. J Arthroplasty. 2004;19(1):56-60.

14.  Insall JN, Dorr LD, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989;(248):13-14.

15.  Segawa H, Tsukayama DT, Kyle RF, Becker DA, Gustilo RB. Infection after total knee arthroplasty. A retrospective study of the treatment of eighty-one infections. J Bone Joint Surg Am. 1999;81(10):1434-1445.

16.  Goddard NJ, Mann HA, Lee CA. Total knee replacement in patients with end-stage haemophilic arthropathy. 25-year results. J Bone Joint Surg Br. 2010;92(8):1085-1089.

17.  Westberg M, Paus AC, Holme PA, Tjønnfjord GE. Haemophilic arthropathy: long-term outcomes in 107 primary total knee arthroplasties. Knee. 2014;21(1):147-150.

18.  Lygre SH, Espehaug B, Havelin LI, Vollset SE, Furnes O. Failure of total knee arthroplasty with or without patella resurfacing. A study from the Norwegian Arthroplasty Register with 0-15 years of follow-up. Acta Orthop. 2011;82(3):282-292.

19.  Post M, Telfer MC. Surgery in hemophilic patients. J Bone Joint Surg Am. 1975;57(8):1136-1145.

20.  Diduch DR, Insall JN, Scott WN, Scuderi GR, Font-Rodriguez D. Total knee replacement in young, active patients. Long-term follow-up and functional outcome. J Bone Joint Surg Am. 1997;79(4):575-582.

21.  Lonner JH, Hershman S, Mont M, Lotke PA. Total knee arthroplasty in patients 40 years of age and younger with osteoarthritis. Clin Orthop Relat Res. 2000;(380):85-90.

22.  Duffy GP, Crowder AR, Trousdale RR, Berry DJ. Cemented total knee arthroplasty using a modern prosthesis in young patients with osteoarthritis. J Arthroplasty. 2007;22(6 suppl 2):67-70.

23.  Chiang CC, Chen PQ, Shen MC, Tsai W. Total knee arthroplasty for severe haemophilic arthropathy: long-term experience in Taiwan. Haemophilia. 2008;14(4):828-834.

24.  Solimeno LP, Mancuso ME, Pasta G, Santagostino E, Perfetto S, Mannucci PM. Factors influencing the long-term outcome of primary total knee replacement in haemophiliacs: a review of 116 procedures at a single institution. Br J Haematol. 2009;145(2):227-234.

25.  Jämsen E, Varonen M, Huhtala H, et al. Incidence of prosthetic joint infections after primary knee arthroplasty. J Arthroplasty. 2010;25(1):87-92.

26.  Ragni MV, Crossett LS, Herndon JH. Postoperative infection following orthopaedic surgery in human immunodeficiency virus–infected hemophiliacs with CD4 counts < or = 200/mm3. J Arthroplasty. 1995;10(6):716-721.

27.    Hicks JL, Ribbans WJ, Buzzard B, et al. Infected joint replacements in HIV-positive patients with haemophilia. J Bone Joint Surg Br. 2001;83(7):1050-1054.

28.  Figgie MP, Goldberg VM, Figgie HE 3rd, Heiple KG, Sobel M. Total knee arthroplasty for the treatment of chronic hemophilic arthropathy. Clin Orthop Relat Res. 1989;(248):98-107.

Issue
The American Journal of Orthopedics - 44(12)
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The American Journal of Orthopedics - 44(12)
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E503-E507
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Total Knee Arthroplasty in Hemophilic Arthropathy
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Total Knee Arthroplasty in Hemophilic Arthropathy
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american journal of orthopedics, AJO, original study, online exclusive, study, total knee arthroplasty, TKA, knee, arthroplasty, hemophilic, arthropathy, joint, pain, pain management, rodriguez-merchan, joint bleeding, blood
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american journal of orthopedics, AJO, original study, online exclusive, study, total knee arthroplasty, TKA, knee, arthroplasty, hemophilic, arthropathy, joint, pain, pain management, rodriguez-merchan, joint bleeding, blood
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Effects of Tranexamic Acid Cytotoxicity on In Vitro Chondrocytes

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Effects of Tranexamic Acid Cytotoxicity on In Vitro Chondrocytes

For decades, tranexamic acid (TXA) has been used off-label to reduce perioperative blood loss in various surgical procedures, including orthopedic surgery, neurosurgery, urologic surgery, obstetrics and gynecology, and trauma surgery.1 TXA, a synthetic derivative of the amino acid lysine, produces antifibrinolytic activity by competitively inhibiting lysine-binding sites on plasminogen molecules—inhibiting the activation of plasmin and thus preserving the function of fibrin in clot formation. It is believed that, through this method, TXA retains blood clots more effectively, thereby reducing bleeding. Although intravenous delivery of TXA is generally accepted as safe, some studies have indicated that it may contribute to postoperative seizure activity as well as increased thromboembolic events.2,3 For these and other reasons, interest in topical (intra-articular) administration of TXA has increased.

Use of topical TXA in surgery has been expanding over the past several years, with reports of significant reductions in perioperative blood loss and transfusion requirements.4 Orthopedic surgeons specifically have explored the topical use of TXA, especially in total joint arthroplasty (TJA).5 The benefits are increased concentration at the operative site with reduced systemic exposure; cost reduction; and surgeon control.6,7 Several recent studies have yielded significant reductions in perioperative blood loss and transfusions with use of topical TXA.8-10 In the literature, effective dosing for topical TXA in TJA ranges from 250 mg to 3 g.11 The concentration of topical TXA is not consistently described but appears to fall between 15 and 100 mg/mL.12,13 Our institutions14 and several investigators15,16 have used topical TXA in TJA at a concentration of 100 mg/mL, so this was the initial TXA concentration we decided to study. We selected certain time points to allow for relatively early detection of cartilage damage and then followed it to 48 hours of exposure. In cases in which TXA is injected after capsular closure, it is unclear how rapidly the TXA diffuses out of the joint or to what degree it becomes diluted by bleeding or synovial fluid. Certainly, this varies from patient to patient. Clearly, TXA generally passes through the body unmodified when injected intravenously1 and therefore is unlikely to be chemically modified while in the joint.

Very little has been published on use of topical TXA in other orthopedic surgeries, such as intra-articular fracture fixation, ligament reconstruction, hemiarthroplasty, and unicompartmental arthroplasty. Unlike TJA, which removes all native cartilage, these procedures retain and depend on the viability of the native cartilage. Sitek and colleagues17 noted the effect of TXA on chondrocytes within the context of creating an extracellular fibrin matrix for chondrocyte transplant. There was no decrease in chondrocyte viability with TXA 10 mg/mL or 20 mg/mL. Use of fresh bovine cartilage explants as a model for the in vitro study of cartilage damage is well established, including chondrocyte viability and glycosaminoglycan (GAG) release as outcome measures.18,19 Human cartilage has also been studied in vitro using this model.20

In the present study, the primary goal was to test the hypothesis that TXA could be safely used in the presence of native cartilage. The secondary goal was to identify a safe concentration for intra-articular use if toxic characteristics were noted.

Materials and Methods

Young bovine stifle joints were obtained within 3 hours of slaughter at a local abattoir. The joint was disarticulated under sterile conditions, and the distal femoral articular surface was evaluated for any signs of damage or arthritis. All specimens contained healthy, undamaged articular surfaces. Full-thickness cartilage explants (excluding subchondral bone) were then immediately harvested—with use of a scalpel blade and a dermatologic biopsy punch 4 mm in diameter—from the distal, weight-bearing femur. The explants were placed in 24-well tissue-culture plates (USA Scientific), incubated in culture media (high-glucose Dulbecco’s Modified Eagle Medium, 10% fetal bovine serum, 1% penicillin/streptomycin, 1% fungizone; Life Technologies), and kept at 37°C and 5% CO2. Explants were allowed to rest in culture media for a minimum of 24 hours after harvest. The pH of the medium was not altered by the addition of TXA.

Bovine explants were randomly assigned to either TXA-exposure or control groups at several time points in replicates of 6. Culture medium was aspirated, and each explant was washed twice with sterile phosphate-buffered saline (PBS). Explants were then incubated at 37°C in culture medium as previously described, or in the same culture medium containing dissolved TXA at a concentration of 100 mg/mL. The explants were incubated at 37°C until harvest at 8, 24, or 48 hours after media addition. For harvest, the media were aspirated and stored at –20°C for GAG content analysis, and the explants were then harvested for LIVE/DEAD assay (Life Technologies) and GAG content analysis.

 

 

Explants were washed once in 75% ethanol and then digested in 0.5 mL papain digestion buffer (100 mM sodium phosphate, 10 mM EDTA, 10 mM L-cysteine, 0.125 mg/mL papain; Sigma-Aldrich) at 60°C for 24 hours. Digested samples were then diluted and subjected to GAG analysis.

Murine chondrocytes were harvested from the freshly harvested rib cages and sternums of mice (1-4 days old) as previously described.21 In brief, rib cages were washed twice in D-PBS and then incubated at 37°C for 60 min in 5 mL of 0.25% Trypsin-EDTA (Life Technologies). They were then washed in DMEM with 10% FBS, centrifuged at 1500 rpm for 5 min to remove the supernatant, and washed in sterile PBS. After removal of the PBS wash, the ribs were incubated in 2 mg/mL hyaluronidase in plain DMEM on a shaker at 37°C for 2 hours. Once soft tissue was removed, the rib cages were discarded, and the remaining soft tissue was incubated in a collagenase D/hyaluronidase digestion solution (collagenase D, 1 mg/mL; hyaluronidase, 1 mg/mL; BSA, 40 mg/mL in plain DMEM; Life Technologies) for 8 hours. The resultant cell suspension was filtered through a 40-µm cell strainer (BD Falcon). Isolated chondrocytes were then plated on culture slides (0.5×x106 cells; BD Falcon) and incubated in DMEM/F12 (1:1) complete media at 37°C and 5% CO2. Before experimental treatment, all cultures were visualized under phase microscopy to verify viability and morphology.

Murine chondrocytes were incubated in media (described above) containing TXA 0, 25, 50, or 100 mg/mL and were harvested 8, 24, or 48 hours after initial exposure. Cultures were maintained at 37°C and 5% CO2 until harvest. Culture medium was aspirated, and each sample was washed twice in sterile PBS before analysis with the LIVE/DEAD assay.

The amount of GAG released into the culture media was measured with a 1,9-dimethyl-methylene blue colorimetric assay (DMMB; 38.5 µM 1,9-dimethylmethylene blue, 40 mM glycine, 40.5 mM sodium chloride, 9.5 mM hydrochloric acid; Sigma-Aldrich) based on the method of Farndale and colleagues.22 In brief, 20 µL of media was mixed with the DMMB assay solution in a 96-well plate, and absorbance was read immediately at 530 nm on a microplate reader. Chondroitin 4-sulfate was used to produce a standard curve. Total GAG released into the media was then calculated based on the standard curve and calculated as a percentage of the total GAG content of each explant. Each sample time point and concentration had a replicate of 3.

Chondrocyte viability was assessed with use of the LIVE/DEAD Viability/Cytotoxicity Kit (Life Technologies) following the protocol. Cartilage explants were sectioned orthogonally to the articular surface at 100 µm per section. Four sections were obtained from each explant. Sections were then incubated in 60 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at room temperature in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 3 digital photographs (magnification ×4) were taken per sample with use of a fluorescein filter and a Texas red filter. The live and dead cells in an area were quantified with use of ImageJ, freely available image analysis software.23 This software was verified initially by blinded, manual count for accuracy. Each sample time point and concentration had a replicate of 3 or 4 explants.

Chondrocyte viability was assessed with the LIVE/DEAD Viability/Cytotoxicity Kit following the protocol. Slides were incubated in 200 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at 37°C in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 4 digital photographs (magnification ×4) were taken with use of a fluorescein filter and a Texas red filter. Live and dead cells in an area were quantified with use of ImageJ. Each sample time point and concentration had a replicate of 4 plates.

Statistical analyses were performed in the statistical environment R.24 Data were analyzed with a 2-tailed Student t test with Holm-Bonferroni correction made for multiple comparisons, and a family-wise error rate was set at α = 0.05.

Results

GAG release was notably higher in the explants exposed to TXA 100 mg/mL at all time points (Figure 1). Beginning 8 hours after initial incubation, there was a small but significant (P = .01) loss of GAG in TXA-treated explants (mean, 1.86%; SD, 0.44%) versus control explants (mean, 0.31%; SD, 0.24%). There was a trend of increasing loss with increasing time after initial incubation through 24 hours, GAG (mean, 3.92%; SD, 0.83%) versus control (mean, 1.63%; SD, 0.65%) (P = .02), reaching a peak at 48 hours, GAG (mean, 8.29%; SD, 1.82%) versus control (mean, 3.19%; SD, 0.53%) (P = .03).

 

 

Cell viability was notably higher in the control groups 24 and 48 hours after initial incubation (Figure 2), with a visually observable (Figure 3) but variable and nonsignificant (P = .33) difference in viability at 8 hours, control (mean, 63.87%; SD, 13.63%) versus TXA (mean, 46.08%; SD, 22.51%). As incubation time increased from 8 hours, there were significant decreases in cell viability at 24 hours (mean, 39.28%; SD, 4.12%; P = .024) and 48 hours (mean, 21.98%; SD, 2.15%; P = .0005) relative to controls.

After results of exposing murine cells to TXA at different concentrations were obtained, bovine explants were exposed to TXA 25 mg/mL, and viability was recorded 24 and 48 hours after exposure (Figure 4). There was no significant difference in viability between samples.

Cell viability was similar between the TXA 25 mg/mL and control samples at all time points (Figure 5). The TXA 50 mg/mL sample dropped from 66.51% viability at 8 hours to 6.81% viability at 24 hours and complete cell death by 48 hours. The TXA 100 mg/mL samples had no observable viable cells at 8, 24, and 48 hours (Figure 6, confirmed with light microscopy). The TXA 0 mg/mL and 25 mg/mL samples remained largely unchanged: 78.28% and 92.99% viable at 8 hours, 97.29% and 90.22% viable at 24 hours, and 91.62% and 91.35% viable at 48 hours, respectively. See Figures 4 and 5 for viability at all time points and concentrations. Statistical analyses were not performed on these data because the zero values obtained for all samples incubated in TXA 100 mg/mL and the 48-hour TXA 50 mg/mL samples prevented accurate estimation of P values and thus meaningful comparisons of the treatment groups.

Discussion

The results of this study showed that TXA is cytotoxic to both bovine and murine chondrocytes at a concentration of 100 mg/mL. There is a time-dependent increase in GAG release as well as a decrease in chondrocyte viability in intact bovine cartilage. These data suggest that topical or intra-articular administration of TXA at this concentration in the setting of native cartilage may have unintended, detrimental effects.

Murine chondrocyte monolayer cultures exposed to TXA at lower concentrations did not exhibit a concentration-dependent curve with respect to viability. Chondrocytes exposed to TXA 25 mg/mL had no reduction in viability relative to control samples. When the concentration was doubled to 50 mg/mL, however, viability was reduced to 6.81% by 24 hours (Figure 5). These data suggest that, between 25 mg/mL and 50 mg/mL, there is a concentration at which TXA becomes cytotoxic to murine chondrocytes. It should be cautioned that, though TXA was cytotoxic to chondrocytes in this study, the effects are still unknown and indeed may be similar to effects on other types of cells that are present in a replaced joint—such as synovial cells, inflammatory cells, and osteoblasts.

The unaffected viability of murine chondrocytes with TXA 25 mg/mL indicated that this may be a cutoff concentration for safety in the presence of cartilage. To confirm these results, we exposed the bovine explants to TXA 25 mg/mL as well. Consistent with the prior study, chondrocyte viability was unaffected at 48 hours. Some clinical studies have effectively used topical TXA at this concentration, or at a lower concentration, to reduce blood loss in TJA,25 which suggests that 25 mg/mL may be a safe yet effective dose for clinical use of topical TXA.

As the methods used in this study did not distinguish between late-apoptotic and necrotic cell death, we could not determine which mechanism of death led to the viability loss observed. If apoptosis is occurring, how TXA initiates this sequence is unclear. There have been no studies directly linking TXA to apoptotic events, though some studies have indicated that TXA interacts with several molecules other than plasminogen, including GABA (γ-aminobutyric acid) receptors, glycine receptors, and tachykinin neurokinin 1 receptors.26-28 According to these studies, these interactions may be responsible for seizure activity and increased emesis caused by TXA use. In addition, TXA-containing compounds, such as trans-aminomethylcyclohexanecarbonyl-l-(O-picolyl)tyrosine-octylamide, have been shown to induce apoptosis.29

It appears that the extracellular matrix (ECM) of native cartilage explants has a protective effect on chondrocytes. With exposure to TXA 100 mg/mL, the explants retained 52% viability at 24 hours, whereas the monolayer cultures were nonviable at that point. The weak negative charge of the molecule may retard its penetration into the ECM, though there was an inconsistent presentation of cell death at explant superficial zones in treated samples (Figure 3). Consistent surface layer cell death would be expected if slowed penetration were the only protective mechanism. It is possible that the ECM acts as a buffer or solvent, effectively reducing the concentration of TXA directly interacting with the chondrocytes. Further exploration is needed to elucidate the significance of the ECM in protecting chondrocytes from TXA.

 

 

Although its findings were highly reproducible, the present study had several limitations, including its in vitro nature and its use of a bovine and murine model rather than a human cell and tissue platform. It may be prudent to expose chondrocytes to TXA for a shorter time to try to mimic what theoretically occurs in vivo. In vivo studies may be a reasonable direction for experimentation. Clarifying the mechanism of cell death is of experimental interest as well. As the first of its kind, the present study provides an important initial database for exploration.

This study is the first to show that TXA has a cytotoxic effect on chondrocytes and that it damages cartilage at clinically used concentrations. Although more studies are needed to verify a safe concentration of TXA for topical use with human cartilage, our data indicate that TXA 25 mg/mL may be an effective yet safe dose for intra-articular use in native joints.

References

1.    McCormack PL. Tranexamic acid: a review of its use in the treatment of hyperfibrinolysis. Drugs. 2012;72(5):585-617.

2.    Murkin JM, Falter F, Granton J, Young B, Burt C, Chu M. High-dose tranexamic acid is associated with nonischemic clinical seizures in cardiac surgical patients. Anesth Analg. 2010;110(2):350-353.

3.    Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study. Arch Surg. 2012;147(2):113-119.

4.    Ker K, Prieto‐Merino D, Roberts I. Systematic review, meta‐analysis and meta‐regression of the effect of tranexamic acid on surgical blood loss. Br J Surg. 2013;100(10):1271-1279.

5.    Panteli M, Papakostidis C, Dahabreh Z, Giannoudis PV. Topical tranexamic acid in total knee replacement: a systematic review and meta-analysis. Knee. 2013;20(5):300-309.

6.    Alshryda S, Mason J, Vaghela M, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total knee replacement: a randomized controlled trial (TRANX-K). J Bone Joint Surg Am. 2013;95(21):1961-1968.

7.    Alshryda S, Mason J, Sarda P, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total hip replacement: a randomized controlled trial (TRANX-H). J Bone Joint Surg Am. 2013;95(21):1969-1974.

8.    Konig G, Hamlin BR, Waters JH. Topical tranexamic acid reduces blood loss and transfusion rates in total hip and total knee arthroplasty. J Arthroplasty. 2013;28(9):1473-1476.

9.    Lee SH, Cho KY, Khurana S, Kim KI. Less blood loss under concomitant administration of tranexamic acid and indirect factor Xa inhibitor following total knee arthroplasty: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2611-2617.

10. Chimento GF, Huff T, Ochsner JL Jr, Meyer M, Brandner L, Babin S. An evaluation of the use of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):74-77.

11. Aguilera-Roig X, Jordán-Sales M, Natera-Cisneros L, Monllau-García JC, Martínez-Zapata MJ. Tranexamic acid in orthopedic surgery [in Spanish]. Rev Esp Cir Ortop Traumatol. 2014;58(1):52-56.

12. Wong J, Abrishami A, El Beheiry H, et al. Topical application of tranexamic acid reduces postoperative blood loss in total knee arthroplasty: a randomized, controlled trial. J Bone Joint Surg Am. 2010;92(15):2503-2513.

13. Georgiadis AG, Muh SJ, Silverton CD, Weir RM, Laker MW. A prospective double-blind placebo controlled trial of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):78-82.

14. Tuttle JR, Ritterman SA, Cassidy DB, Anazonwu WA, Froehlich JA, Rubin LE. Cost benefit analysis of topical tranexamic acid in primary total hip and knee arthroplasty. J Arthroplasty. 2014;29(8):1512-1515.

15. Roy SP, Tanki UF, Dutta A, Jain SK, Nagi ON. Efficacy of intra-articular tranexamic acid in blood loss reduction following primary unilateral total knee arthroplasty. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2494-2501.

16. Ishida K, Tsumura N, Kitagawa A, et al. Intra-articular injection of tranexamic acid reduces not only blood loss but also knee joint swelling after total knee arthroplasty. Int Orthop. 2011;35(11):1639-1645.

17. Sitek P, Wysocka-Wycisk A, Kępski F, Król D, Bursig H, Dyląg S. PRP-fibrinogen gel-like chondrocyte carrier stabilized by TXA-preliminary study. Cell Tissue Bank. 2013;14(1):133-140.

18. Lo IK, Sciore P, Chung M, et al. Local anesthetics induce chondrocyte death in bovine articular cartilage disks in a dose- and duration-dependent manner. Arthroscopy. 2009;25(7):707-715.

19. Blumberg TJ, Natoli RM, Athanasiou KA. Effects of doxycycline on articular cartilage GAG release and mechanical properties following impact. Biotechnol Bioeng. 2008;100(3):506-515.

20. Piper SL, Kim HT. Comparison of ropivacaine and bupivacaine toxicity in human articular chondrocytes. J Bone Joint Surg Am. 2008;90(5):986-991.

21. Lefebvre V, Garofalo S, Zhou G, Metsäranta M, Vuorio E, De Crombrugghe B. Characterization of primary cultures of chondrocytes from type II collagen/beta-galactosidase transgenic mice. Matrix Biol. 1994;14(4):329-335.

22. Farndale RW, Buttle DJ, Barrett AJ. Improved quantitation and discrimination of sulphated glycosaminoglycans by use of dimethylmethylene blue. Biochim Biophys Acta. 1986;833(2):173-177.

23. Schneider CA, Rasband WS, Eliceiri KW. NIH Image to ImageJ: 25 years of image analysis. Nat Methods. 2012;9(7):671-675.

24. R Development Core Team. R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2008.

25. Sa-Ngasoongsong P, Channoom T, Kawinwonggowit V, et al. Postoperative blood loss reduction in computer-assisted surgery total knee replacement by low dose intra-articular tranexamic acid injection together with 2-hour clamp drain: a prospective triple-blinded randomized controlled trial. Orthop Rev. 2011;3(2):e12.

26. Lecker I, Wang DS, Romaschin AD, Peterson M, Mazer CD, Orser BA. Tranexamic acid concentrations associated with human seizures inhibit glycine receptors. J Clin Invest. 2012;122(12):4654-4666.

27. Kakiuchi H, Kawarai-Shimamura A, Kuwagata M, Orito K. Tranexamic acid induces kaolin intake stimulating a pathway involving tachykinin neurokinin 1 receptors in rats. Eur J Pharmacol. 2014;723:1-6.

28. Kratzer S, Irl H, Mattusch C, et al. Tranexamic acid impairs γ-aminobutyric acid receptor type A–mediated synaptic transmission in the murine amygdala: a potential mechanism for drug-induced seizures? Anesthesiology. 2014;120(3):639-649.

29. Lee E, Enomoto R, Takemura K, Tsuda Y, Okada Y. A selective plasmin inhibitor, trans-aminomethylcyclohexanecarbonyl-L-(O-picolyl)tyrosine-octylamide (YO-2), induces thymocyte apoptosis. Biochem Pharmacol. 2002;63(7):1315-1323.

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John R. Tuttle, MD, MS, Peter R. Feltman, MS, Scott A. Ritterman, MD, and Michael G. Ehrlich, MD

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The American Journal of Orthopedics - 44(12)
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E497-E502
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american journal of orthopedics, AJO, original study, online exclusive, study, tranexamic acid cytotoxicity, acid, chondrocytes, in vitro, TXA, topical tranexamic acid, transfusion, blood, cell, joints, blood loss, surgery, tuttle, feltman, ritterman, ehrlich
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John R. Tuttle, MD, MS, Peter R. Feltman, MS, Scott A. Ritterman, MD, and Michael G. Ehrlich, MD

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

Author and Disclosure Information

John R. Tuttle, MD, MS, Peter R. Feltman, MS, Scott A. Ritterman, MD, and Michael G. Ehrlich, MD

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

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For decades, tranexamic acid (TXA) has been used off-label to reduce perioperative blood loss in various surgical procedures, including orthopedic surgery, neurosurgery, urologic surgery, obstetrics and gynecology, and trauma surgery.1 TXA, a synthetic derivative of the amino acid lysine, produces antifibrinolytic activity by competitively inhibiting lysine-binding sites on plasminogen molecules—inhibiting the activation of plasmin and thus preserving the function of fibrin in clot formation. It is believed that, through this method, TXA retains blood clots more effectively, thereby reducing bleeding. Although intravenous delivery of TXA is generally accepted as safe, some studies have indicated that it may contribute to postoperative seizure activity as well as increased thromboembolic events.2,3 For these and other reasons, interest in topical (intra-articular) administration of TXA has increased.

Use of topical TXA in surgery has been expanding over the past several years, with reports of significant reductions in perioperative blood loss and transfusion requirements.4 Orthopedic surgeons specifically have explored the topical use of TXA, especially in total joint arthroplasty (TJA).5 The benefits are increased concentration at the operative site with reduced systemic exposure; cost reduction; and surgeon control.6,7 Several recent studies have yielded significant reductions in perioperative blood loss and transfusions with use of topical TXA.8-10 In the literature, effective dosing for topical TXA in TJA ranges from 250 mg to 3 g.11 The concentration of topical TXA is not consistently described but appears to fall between 15 and 100 mg/mL.12,13 Our institutions14 and several investigators15,16 have used topical TXA in TJA at a concentration of 100 mg/mL, so this was the initial TXA concentration we decided to study. We selected certain time points to allow for relatively early detection of cartilage damage and then followed it to 48 hours of exposure. In cases in which TXA is injected after capsular closure, it is unclear how rapidly the TXA diffuses out of the joint or to what degree it becomes diluted by bleeding or synovial fluid. Certainly, this varies from patient to patient. Clearly, TXA generally passes through the body unmodified when injected intravenously1 and therefore is unlikely to be chemically modified while in the joint.

Very little has been published on use of topical TXA in other orthopedic surgeries, such as intra-articular fracture fixation, ligament reconstruction, hemiarthroplasty, and unicompartmental arthroplasty. Unlike TJA, which removes all native cartilage, these procedures retain and depend on the viability of the native cartilage. Sitek and colleagues17 noted the effect of TXA on chondrocytes within the context of creating an extracellular fibrin matrix for chondrocyte transplant. There was no decrease in chondrocyte viability with TXA 10 mg/mL or 20 mg/mL. Use of fresh bovine cartilage explants as a model for the in vitro study of cartilage damage is well established, including chondrocyte viability and glycosaminoglycan (GAG) release as outcome measures.18,19 Human cartilage has also been studied in vitro using this model.20

In the present study, the primary goal was to test the hypothesis that TXA could be safely used in the presence of native cartilage. The secondary goal was to identify a safe concentration for intra-articular use if toxic characteristics were noted.

Materials and Methods

Young bovine stifle joints were obtained within 3 hours of slaughter at a local abattoir. The joint was disarticulated under sterile conditions, and the distal femoral articular surface was evaluated for any signs of damage or arthritis. All specimens contained healthy, undamaged articular surfaces. Full-thickness cartilage explants (excluding subchondral bone) were then immediately harvested—with use of a scalpel blade and a dermatologic biopsy punch 4 mm in diameter—from the distal, weight-bearing femur. The explants were placed in 24-well tissue-culture plates (USA Scientific), incubated in culture media (high-glucose Dulbecco’s Modified Eagle Medium, 10% fetal bovine serum, 1% penicillin/streptomycin, 1% fungizone; Life Technologies), and kept at 37°C and 5% CO2. Explants were allowed to rest in culture media for a minimum of 24 hours after harvest. The pH of the medium was not altered by the addition of TXA.

Bovine explants were randomly assigned to either TXA-exposure or control groups at several time points in replicates of 6. Culture medium was aspirated, and each explant was washed twice with sterile phosphate-buffered saline (PBS). Explants were then incubated at 37°C in culture medium as previously described, or in the same culture medium containing dissolved TXA at a concentration of 100 mg/mL. The explants were incubated at 37°C until harvest at 8, 24, or 48 hours after media addition. For harvest, the media were aspirated and stored at –20°C for GAG content analysis, and the explants were then harvested for LIVE/DEAD assay (Life Technologies) and GAG content analysis.

 

 

Explants were washed once in 75% ethanol and then digested in 0.5 mL papain digestion buffer (100 mM sodium phosphate, 10 mM EDTA, 10 mM L-cysteine, 0.125 mg/mL papain; Sigma-Aldrich) at 60°C for 24 hours. Digested samples were then diluted and subjected to GAG analysis.

Murine chondrocytes were harvested from the freshly harvested rib cages and sternums of mice (1-4 days old) as previously described.21 In brief, rib cages were washed twice in D-PBS and then incubated at 37°C for 60 min in 5 mL of 0.25% Trypsin-EDTA (Life Technologies). They were then washed in DMEM with 10% FBS, centrifuged at 1500 rpm for 5 min to remove the supernatant, and washed in sterile PBS. After removal of the PBS wash, the ribs were incubated in 2 mg/mL hyaluronidase in plain DMEM on a shaker at 37°C for 2 hours. Once soft tissue was removed, the rib cages were discarded, and the remaining soft tissue was incubated in a collagenase D/hyaluronidase digestion solution (collagenase D, 1 mg/mL; hyaluronidase, 1 mg/mL; BSA, 40 mg/mL in plain DMEM; Life Technologies) for 8 hours. The resultant cell suspension was filtered through a 40-µm cell strainer (BD Falcon). Isolated chondrocytes were then plated on culture slides (0.5×x106 cells; BD Falcon) and incubated in DMEM/F12 (1:1) complete media at 37°C and 5% CO2. Before experimental treatment, all cultures were visualized under phase microscopy to verify viability and morphology.

Murine chondrocytes were incubated in media (described above) containing TXA 0, 25, 50, or 100 mg/mL and were harvested 8, 24, or 48 hours after initial exposure. Cultures were maintained at 37°C and 5% CO2 until harvest. Culture medium was aspirated, and each sample was washed twice in sterile PBS before analysis with the LIVE/DEAD assay.

The amount of GAG released into the culture media was measured with a 1,9-dimethyl-methylene blue colorimetric assay (DMMB; 38.5 µM 1,9-dimethylmethylene blue, 40 mM glycine, 40.5 mM sodium chloride, 9.5 mM hydrochloric acid; Sigma-Aldrich) based on the method of Farndale and colleagues.22 In brief, 20 µL of media was mixed with the DMMB assay solution in a 96-well plate, and absorbance was read immediately at 530 nm on a microplate reader. Chondroitin 4-sulfate was used to produce a standard curve. Total GAG released into the media was then calculated based on the standard curve and calculated as a percentage of the total GAG content of each explant. Each sample time point and concentration had a replicate of 3.

Chondrocyte viability was assessed with use of the LIVE/DEAD Viability/Cytotoxicity Kit (Life Technologies) following the protocol. Cartilage explants were sectioned orthogonally to the articular surface at 100 µm per section. Four sections were obtained from each explant. Sections were then incubated in 60 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at room temperature in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 3 digital photographs (magnification ×4) were taken per sample with use of a fluorescein filter and a Texas red filter. The live and dead cells in an area were quantified with use of ImageJ, freely available image analysis software.23 This software was verified initially by blinded, manual count for accuracy. Each sample time point and concentration had a replicate of 3 or 4 explants.

Chondrocyte viability was assessed with the LIVE/DEAD Viability/Cytotoxicity Kit following the protocol. Slides were incubated in 200 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at 37°C in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 4 digital photographs (magnification ×4) were taken with use of a fluorescein filter and a Texas red filter. Live and dead cells in an area were quantified with use of ImageJ. Each sample time point and concentration had a replicate of 4 plates.

Statistical analyses were performed in the statistical environment R.24 Data were analyzed with a 2-tailed Student t test with Holm-Bonferroni correction made for multiple comparisons, and a family-wise error rate was set at α = 0.05.

Results

GAG release was notably higher in the explants exposed to TXA 100 mg/mL at all time points (Figure 1). Beginning 8 hours after initial incubation, there was a small but significant (P = .01) loss of GAG in TXA-treated explants (mean, 1.86%; SD, 0.44%) versus control explants (mean, 0.31%; SD, 0.24%). There was a trend of increasing loss with increasing time after initial incubation through 24 hours, GAG (mean, 3.92%; SD, 0.83%) versus control (mean, 1.63%; SD, 0.65%) (P = .02), reaching a peak at 48 hours, GAG (mean, 8.29%; SD, 1.82%) versus control (mean, 3.19%; SD, 0.53%) (P = .03).

 

 

Cell viability was notably higher in the control groups 24 and 48 hours after initial incubation (Figure 2), with a visually observable (Figure 3) but variable and nonsignificant (P = .33) difference in viability at 8 hours, control (mean, 63.87%; SD, 13.63%) versus TXA (mean, 46.08%; SD, 22.51%). As incubation time increased from 8 hours, there were significant decreases in cell viability at 24 hours (mean, 39.28%; SD, 4.12%; P = .024) and 48 hours (mean, 21.98%; SD, 2.15%; P = .0005) relative to controls.

After results of exposing murine cells to TXA at different concentrations were obtained, bovine explants were exposed to TXA 25 mg/mL, and viability was recorded 24 and 48 hours after exposure (Figure 4). There was no significant difference in viability between samples.

Cell viability was similar between the TXA 25 mg/mL and control samples at all time points (Figure 5). The TXA 50 mg/mL sample dropped from 66.51% viability at 8 hours to 6.81% viability at 24 hours and complete cell death by 48 hours. The TXA 100 mg/mL samples had no observable viable cells at 8, 24, and 48 hours (Figure 6, confirmed with light microscopy). The TXA 0 mg/mL and 25 mg/mL samples remained largely unchanged: 78.28% and 92.99% viable at 8 hours, 97.29% and 90.22% viable at 24 hours, and 91.62% and 91.35% viable at 48 hours, respectively. See Figures 4 and 5 for viability at all time points and concentrations. Statistical analyses were not performed on these data because the zero values obtained for all samples incubated in TXA 100 mg/mL and the 48-hour TXA 50 mg/mL samples prevented accurate estimation of P values and thus meaningful comparisons of the treatment groups.

Discussion

The results of this study showed that TXA is cytotoxic to both bovine and murine chondrocytes at a concentration of 100 mg/mL. There is a time-dependent increase in GAG release as well as a decrease in chondrocyte viability in intact bovine cartilage. These data suggest that topical or intra-articular administration of TXA at this concentration in the setting of native cartilage may have unintended, detrimental effects.

Murine chondrocyte monolayer cultures exposed to TXA at lower concentrations did not exhibit a concentration-dependent curve with respect to viability. Chondrocytes exposed to TXA 25 mg/mL had no reduction in viability relative to control samples. When the concentration was doubled to 50 mg/mL, however, viability was reduced to 6.81% by 24 hours (Figure 5). These data suggest that, between 25 mg/mL and 50 mg/mL, there is a concentration at which TXA becomes cytotoxic to murine chondrocytes. It should be cautioned that, though TXA was cytotoxic to chondrocytes in this study, the effects are still unknown and indeed may be similar to effects on other types of cells that are present in a replaced joint—such as synovial cells, inflammatory cells, and osteoblasts.

The unaffected viability of murine chondrocytes with TXA 25 mg/mL indicated that this may be a cutoff concentration for safety in the presence of cartilage. To confirm these results, we exposed the bovine explants to TXA 25 mg/mL as well. Consistent with the prior study, chondrocyte viability was unaffected at 48 hours. Some clinical studies have effectively used topical TXA at this concentration, or at a lower concentration, to reduce blood loss in TJA,25 which suggests that 25 mg/mL may be a safe yet effective dose for clinical use of topical TXA.

As the methods used in this study did not distinguish between late-apoptotic and necrotic cell death, we could not determine which mechanism of death led to the viability loss observed. If apoptosis is occurring, how TXA initiates this sequence is unclear. There have been no studies directly linking TXA to apoptotic events, though some studies have indicated that TXA interacts with several molecules other than plasminogen, including GABA (γ-aminobutyric acid) receptors, glycine receptors, and tachykinin neurokinin 1 receptors.26-28 According to these studies, these interactions may be responsible for seizure activity and increased emesis caused by TXA use. In addition, TXA-containing compounds, such as trans-aminomethylcyclohexanecarbonyl-l-(O-picolyl)tyrosine-octylamide, have been shown to induce apoptosis.29

It appears that the extracellular matrix (ECM) of native cartilage explants has a protective effect on chondrocytes. With exposure to TXA 100 mg/mL, the explants retained 52% viability at 24 hours, whereas the monolayer cultures were nonviable at that point. The weak negative charge of the molecule may retard its penetration into the ECM, though there was an inconsistent presentation of cell death at explant superficial zones in treated samples (Figure 3). Consistent surface layer cell death would be expected if slowed penetration were the only protective mechanism. It is possible that the ECM acts as a buffer or solvent, effectively reducing the concentration of TXA directly interacting with the chondrocytes. Further exploration is needed to elucidate the significance of the ECM in protecting chondrocytes from TXA.

 

 

Although its findings were highly reproducible, the present study had several limitations, including its in vitro nature and its use of a bovine and murine model rather than a human cell and tissue platform. It may be prudent to expose chondrocytes to TXA for a shorter time to try to mimic what theoretically occurs in vivo. In vivo studies may be a reasonable direction for experimentation. Clarifying the mechanism of cell death is of experimental interest as well. As the first of its kind, the present study provides an important initial database for exploration.

This study is the first to show that TXA has a cytotoxic effect on chondrocytes and that it damages cartilage at clinically used concentrations. Although more studies are needed to verify a safe concentration of TXA for topical use with human cartilage, our data indicate that TXA 25 mg/mL may be an effective yet safe dose for intra-articular use in native joints.

For decades, tranexamic acid (TXA) has been used off-label to reduce perioperative blood loss in various surgical procedures, including orthopedic surgery, neurosurgery, urologic surgery, obstetrics and gynecology, and trauma surgery.1 TXA, a synthetic derivative of the amino acid lysine, produces antifibrinolytic activity by competitively inhibiting lysine-binding sites on plasminogen molecules—inhibiting the activation of plasmin and thus preserving the function of fibrin in clot formation. It is believed that, through this method, TXA retains blood clots more effectively, thereby reducing bleeding. Although intravenous delivery of TXA is generally accepted as safe, some studies have indicated that it may contribute to postoperative seizure activity as well as increased thromboembolic events.2,3 For these and other reasons, interest in topical (intra-articular) administration of TXA has increased.

Use of topical TXA in surgery has been expanding over the past several years, with reports of significant reductions in perioperative blood loss and transfusion requirements.4 Orthopedic surgeons specifically have explored the topical use of TXA, especially in total joint arthroplasty (TJA).5 The benefits are increased concentration at the operative site with reduced systemic exposure; cost reduction; and surgeon control.6,7 Several recent studies have yielded significant reductions in perioperative blood loss and transfusions with use of topical TXA.8-10 In the literature, effective dosing for topical TXA in TJA ranges from 250 mg to 3 g.11 The concentration of topical TXA is not consistently described but appears to fall between 15 and 100 mg/mL.12,13 Our institutions14 and several investigators15,16 have used topical TXA in TJA at a concentration of 100 mg/mL, so this was the initial TXA concentration we decided to study. We selected certain time points to allow for relatively early detection of cartilage damage and then followed it to 48 hours of exposure. In cases in which TXA is injected after capsular closure, it is unclear how rapidly the TXA diffuses out of the joint or to what degree it becomes diluted by bleeding or synovial fluid. Certainly, this varies from patient to patient. Clearly, TXA generally passes through the body unmodified when injected intravenously1 and therefore is unlikely to be chemically modified while in the joint.

Very little has been published on use of topical TXA in other orthopedic surgeries, such as intra-articular fracture fixation, ligament reconstruction, hemiarthroplasty, and unicompartmental arthroplasty. Unlike TJA, which removes all native cartilage, these procedures retain and depend on the viability of the native cartilage. Sitek and colleagues17 noted the effect of TXA on chondrocytes within the context of creating an extracellular fibrin matrix for chondrocyte transplant. There was no decrease in chondrocyte viability with TXA 10 mg/mL or 20 mg/mL. Use of fresh bovine cartilage explants as a model for the in vitro study of cartilage damage is well established, including chondrocyte viability and glycosaminoglycan (GAG) release as outcome measures.18,19 Human cartilage has also been studied in vitro using this model.20

In the present study, the primary goal was to test the hypothesis that TXA could be safely used in the presence of native cartilage. The secondary goal was to identify a safe concentration for intra-articular use if toxic characteristics were noted.

Materials and Methods

Young bovine stifle joints were obtained within 3 hours of slaughter at a local abattoir. The joint was disarticulated under sterile conditions, and the distal femoral articular surface was evaluated for any signs of damage or arthritis. All specimens contained healthy, undamaged articular surfaces. Full-thickness cartilage explants (excluding subchondral bone) were then immediately harvested—with use of a scalpel blade and a dermatologic biopsy punch 4 mm in diameter—from the distal, weight-bearing femur. The explants were placed in 24-well tissue-culture plates (USA Scientific), incubated in culture media (high-glucose Dulbecco’s Modified Eagle Medium, 10% fetal bovine serum, 1% penicillin/streptomycin, 1% fungizone; Life Technologies), and kept at 37°C and 5% CO2. Explants were allowed to rest in culture media for a minimum of 24 hours after harvest. The pH of the medium was not altered by the addition of TXA.

Bovine explants were randomly assigned to either TXA-exposure or control groups at several time points in replicates of 6. Culture medium was aspirated, and each explant was washed twice with sterile phosphate-buffered saline (PBS). Explants were then incubated at 37°C in culture medium as previously described, or in the same culture medium containing dissolved TXA at a concentration of 100 mg/mL. The explants were incubated at 37°C until harvest at 8, 24, or 48 hours after media addition. For harvest, the media were aspirated and stored at –20°C for GAG content analysis, and the explants were then harvested for LIVE/DEAD assay (Life Technologies) and GAG content analysis.

 

 

Explants were washed once in 75% ethanol and then digested in 0.5 mL papain digestion buffer (100 mM sodium phosphate, 10 mM EDTA, 10 mM L-cysteine, 0.125 mg/mL papain; Sigma-Aldrich) at 60°C for 24 hours. Digested samples were then diluted and subjected to GAG analysis.

Murine chondrocytes were harvested from the freshly harvested rib cages and sternums of mice (1-4 days old) as previously described.21 In brief, rib cages were washed twice in D-PBS and then incubated at 37°C for 60 min in 5 mL of 0.25% Trypsin-EDTA (Life Technologies). They were then washed in DMEM with 10% FBS, centrifuged at 1500 rpm for 5 min to remove the supernatant, and washed in sterile PBS. After removal of the PBS wash, the ribs were incubated in 2 mg/mL hyaluronidase in plain DMEM on a shaker at 37°C for 2 hours. Once soft tissue was removed, the rib cages were discarded, and the remaining soft tissue was incubated in a collagenase D/hyaluronidase digestion solution (collagenase D, 1 mg/mL; hyaluronidase, 1 mg/mL; BSA, 40 mg/mL in plain DMEM; Life Technologies) for 8 hours. The resultant cell suspension was filtered through a 40-µm cell strainer (BD Falcon). Isolated chondrocytes were then plated on culture slides (0.5×x106 cells; BD Falcon) and incubated in DMEM/F12 (1:1) complete media at 37°C and 5% CO2. Before experimental treatment, all cultures were visualized under phase microscopy to verify viability and morphology.

Murine chondrocytes were incubated in media (described above) containing TXA 0, 25, 50, or 100 mg/mL and were harvested 8, 24, or 48 hours after initial exposure. Cultures were maintained at 37°C and 5% CO2 until harvest. Culture medium was aspirated, and each sample was washed twice in sterile PBS before analysis with the LIVE/DEAD assay.

The amount of GAG released into the culture media was measured with a 1,9-dimethyl-methylene blue colorimetric assay (DMMB; 38.5 µM 1,9-dimethylmethylene blue, 40 mM glycine, 40.5 mM sodium chloride, 9.5 mM hydrochloric acid; Sigma-Aldrich) based on the method of Farndale and colleagues.22 In brief, 20 µL of media was mixed with the DMMB assay solution in a 96-well plate, and absorbance was read immediately at 530 nm on a microplate reader. Chondroitin 4-sulfate was used to produce a standard curve. Total GAG released into the media was then calculated based on the standard curve and calculated as a percentage of the total GAG content of each explant. Each sample time point and concentration had a replicate of 3.

Chondrocyte viability was assessed with use of the LIVE/DEAD Viability/Cytotoxicity Kit (Life Technologies) following the protocol. Cartilage explants were sectioned orthogonally to the articular surface at 100 µm per section. Four sections were obtained from each explant. Sections were then incubated in 60 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at room temperature in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 3 digital photographs (magnification ×4) were taken per sample with use of a fluorescein filter and a Texas red filter. The live and dead cells in an area were quantified with use of ImageJ, freely available image analysis software.23 This software was verified initially by blinded, manual count for accuracy. Each sample time point and concentration had a replicate of 3 or 4 explants.

Chondrocyte viability was assessed with the LIVE/DEAD Viability/Cytotoxicity Kit following the protocol. Slides were incubated in 200 µL of 1-µM calcein AM/1-µM ethidium homodimer-1 solution at 37°C in the dark for 30 minutes. Sections were then viewed with a fluorescent microscope, and 4 digital photographs (magnification ×4) were taken with use of a fluorescein filter and a Texas red filter. Live and dead cells in an area were quantified with use of ImageJ. Each sample time point and concentration had a replicate of 4 plates.

Statistical analyses were performed in the statistical environment R.24 Data were analyzed with a 2-tailed Student t test with Holm-Bonferroni correction made for multiple comparisons, and a family-wise error rate was set at α = 0.05.

Results

GAG release was notably higher in the explants exposed to TXA 100 mg/mL at all time points (Figure 1). Beginning 8 hours after initial incubation, there was a small but significant (P = .01) loss of GAG in TXA-treated explants (mean, 1.86%; SD, 0.44%) versus control explants (mean, 0.31%; SD, 0.24%). There was a trend of increasing loss with increasing time after initial incubation through 24 hours, GAG (mean, 3.92%; SD, 0.83%) versus control (mean, 1.63%; SD, 0.65%) (P = .02), reaching a peak at 48 hours, GAG (mean, 8.29%; SD, 1.82%) versus control (mean, 3.19%; SD, 0.53%) (P = .03).

 

 

Cell viability was notably higher in the control groups 24 and 48 hours after initial incubation (Figure 2), with a visually observable (Figure 3) but variable and nonsignificant (P = .33) difference in viability at 8 hours, control (mean, 63.87%; SD, 13.63%) versus TXA (mean, 46.08%; SD, 22.51%). As incubation time increased from 8 hours, there were significant decreases in cell viability at 24 hours (mean, 39.28%; SD, 4.12%; P = .024) and 48 hours (mean, 21.98%; SD, 2.15%; P = .0005) relative to controls.

After results of exposing murine cells to TXA at different concentrations were obtained, bovine explants were exposed to TXA 25 mg/mL, and viability was recorded 24 and 48 hours after exposure (Figure 4). There was no significant difference in viability between samples.

Cell viability was similar between the TXA 25 mg/mL and control samples at all time points (Figure 5). The TXA 50 mg/mL sample dropped from 66.51% viability at 8 hours to 6.81% viability at 24 hours and complete cell death by 48 hours. The TXA 100 mg/mL samples had no observable viable cells at 8, 24, and 48 hours (Figure 6, confirmed with light microscopy). The TXA 0 mg/mL and 25 mg/mL samples remained largely unchanged: 78.28% and 92.99% viable at 8 hours, 97.29% and 90.22% viable at 24 hours, and 91.62% and 91.35% viable at 48 hours, respectively. See Figures 4 and 5 for viability at all time points and concentrations. Statistical analyses were not performed on these data because the zero values obtained for all samples incubated in TXA 100 mg/mL and the 48-hour TXA 50 mg/mL samples prevented accurate estimation of P values and thus meaningful comparisons of the treatment groups.

Discussion

The results of this study showed that TXA is cytotoxic to both bovine and murine chondrocytes at a concentration of 100 mg/mL. There is a time-dependent increase in GAG release as well as a decrease in chondrocyte viability in intact bovine cartilage. These data suggest that topical or intra-articular administration of TXA at this concentration in the setting of native cartilage may have unintended, detrimental effects.

Murine chondrocyte monolayer cultures exposed to TXA at lower concentrations did not exhibit a concentration-dependent curve with respect to viability. Chondrocytes exposed to TXA 25 mg/mL had no reduction in viability relative to control samples. When the concentration was doubled to 50 mg/mL, however, viability was reduced to 6.81% by 24 hours (Figure 5). These data suggest that, between 25 mg/mL and 50 mg/mL, there is a concentration at which TXA becomes cytotoxic to murine chondrocytes. It should be cautioned that, though TXA was cytotoxic to chondrocytes in this study, the effects are still unknown and indeed may be similar to effects on other types of cells that are present in a replaced joint—such as synovial cells, inflammatory cells, and osteoblasts.

The unaffected viability of murine chondrocytes with TXA 25 mg/mL indicated that this may be a cutoff concentration for safety in the presence of cartilage. To confirm these results, we exposed the bovine explants to TXA 25 mg/mL as well. Consistent with the prior study, chondrocyte viability was unaffected at 48 hours. Some clinical studies have effectively used topical TXA at this concentration, or at a lower concentration, to reduce blood loss in TJA,25 which suggests that 25 mg/mL may be a safe yet effective dose for clinical use of topical TXA.

As the methods used in this study did not distinguish between late-apoptotic and necrotic cell death, we could not determine which mechanism of death led to the viability loss observed. If apoptosis is occurring, how TXA initiates this sequence is unclear. There have been no studies directly linking TXA to apoptotic events, though some studies have indicated that TXA interacts with several molecules other than plasminogen, including GABA (γ-aminobutyric acid) receptors, glycine receptors, and tachykinin neurokinin 1 receptors.26-28 According to these studies, these interactions may be responsible for seizure activity and increased emesis caused by TXA use. In addition, TXA-containing compounds, such as trans-aminomethylcyclohexanecarbonyl-l-(O-picolyl)tyrosine-octylamide, have been shown to induce apoptosis.29

It appears that the extracellular matrix (ECM) of native cartilage explants has a protective effect on chondrocytes. With exposure to TXA 100 mg/mL, the explants retained 52% viability at 24 hours, whereas the monolayer cultures were nonviable at that point. The weak negative charge of the molecule may retard its penetration into the ECM, though there was an inconsistent presentation of cell death at explant superficial zones in treated samples (Figure 3). Consistent surface layer cell death would be expected if slowed penetration were the only protective mechanism. It is possible that the ECM acts as a buffer or solvent, effectively reducing the concentration of TXA directly interacting with the chondrocytes. Further exploration is needed to elucidate the significance of the ECM in protecting chondrocytes from TXA.

 

 

Although its findings were highly reproducible, the present study had several limitations, including its in vitro nature and its use of a bovine and murine model rather than a human cell and tissue platform. It may be prudent to expose chondrocytes to TXA for a shorter time to try to mimic what theoretically occurs in vivo. In vivo studies may be a reasonable direction for experimentation. Clarifying the mechanism of cell death is of experimental interest as well. As the first of its kind, the present study provides an important initial database for exploration.

This study is the first to show that TXA has a cytotoxic effect on chondrocytes and that it damages cartilage at clinically used concentrations. Although more studies are needed to verify a safe concentration of TXA for topical use with human cartilage, our data indicate that TXA 25 mg/mL may be an effective yet safe dose for intra-articular use in native joints.

References

1.    McCormack PL. Tranexamic acid: a review of its use in the treatment of hyperfibrinolysis. Drugs. 2012;72(5):585-617.

2.    Murkin JM, Falter F, Granton J, Young B, Burt C, Chu M. High-dose tranexamic acid is associated with nonischemic clinical seizures in cardiac surgical patients. Anesth Analg. 2010;110(2):350-353.

3.    Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study. Arch Surg. 2012;147(2):113-119.

4.    Ker K, Prieto‐Merino D, Roberts I. Systematic review, meta‐analysis and meta‐regression of the effect of tranexamic acid on surgical blood loss. Br J Surg. 2013;100(10):1271-1279.

5.    Panteli M, Papakostidis C, Dahabreh Z, Giannoudis PV. Topical tranexamic acid in total knee replacement: a systematic review and meta-analysis. Knee. 2013;20(5):300-309.

6.    Alshryda S, Mason J, Vaghela M, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total knee replacement: a randomized controlled trial (TRANX-K). J Bone Joint Surg Am. 2013;95(21):1961-1968.

7.    Alshryda S, Mason J, Sarda P, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total hip replacement: a randomized controlled trial (TRANX-H). J Bone Joint Surg Am. 2013;95(21):1969-1974.

8.    Konig G, Hamlin BR, Waters JH. Topical tranexamic acid reduces blood loss and transfusion rates in total hip and total knee arthroplasty. J Arthroplasty. 2013;28(9):1473-1476.

9.    Lee SH, Cho KY, Khurana S, Kim KI. Less blood loss under concomitant administration of tranexamic acid and indirect factor Xa inhibitor following total knee arthroplasty: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2611-2617.

10. Chimento GF, Huff T, Ochsner JL Jr, Meyer M, Brandner L, Babin S. An evaluation of the use of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):74-77.

11. Aguilera-Roig X, Jordán-Sales M, Natera-Cisneros L, Monllau-García JC, Martínez-Zapata MJ. Tranexamic acid in orthopedic surgery [in Spanish]. Rev Esp Cir Ortop Traumatol. 2014;58(1):52-56.

12. Wong J, Abrishami A, El Beheiry H, et al. Topical application of tranexamic acid reduces postoperative blood loss in total knee arthroplasty: a randomized, controlled trial. J Bone Joint Surg Am. 2010;92(15):2503-2513.

13. Georgiadis AG, Muh SJ, Silverton CD, Weir RM, Laker MW. A prospective double-blind placebo controlled trial of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):78-82.

14. Tuttle JR, Ritterman SA, Cassidy DB, Anazonwu WA, Froehlich JA, Rubin LE. Cost benefit analysis of topical tranexamic acid in primary total hip and knee arthroplasty. J Arthroplasty. 2014;29(8):1512-1515.

15. Roy SP, Tanki UF, Dutta A, Jain SK, Nagi ON. Efficacy of intra-articular tranexamic acid in blood loss reduction following primary unilateral total knee arthroplasty. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2494-2501.

16. Ishida K, Tsumura N, Kitagawa A, et al. Intra-articular injection of tranexamic acid reduces not only blood loss but also knee joint swelling after total knee arthroplasty. Int Orthop. 2011;35(11):1639-1645.

17. Sitek P, Wysocka-Wycisk A, Kępski F, Król D, Bursig H, Dyląg S. PRP-fibrinogen gel-like chondrocyte carrier stabilized by TXA-preliminary study. Cell Tissue Bank. 2013;14(1):133-140.

18. Lo IK, Sciore P, Chung M, et al. Local anesthetics induce chondrocyte death in bovine articular cartilage disks in a dose- and duration-dependent manner. Arthroscopy. 2009;25(7):707-715.

19. Blumberg TJ, Natoli RM, Athanasiou KA. Effects of doxycycline on articular cartilage GAG release and mechanical properties following impact. Biotechnol Bioeng. 2008;100(3):506-515.

20. Piper SL, Kim HT. Comparison of ropivacaine and bupivacaine toxicity in human articular chondrocytes. J Bone Joint Surg Am. 2008;90(5):986-991.

21. Lefebvre V, Garofalo S, Zhou G, Metsäranta M, Vuorio E, De Crombrugghe B. Characterization of primary cultures of chondrocytes from type II collagen/beta-galactosidase transgenic mice. Matrix Biol. 1994;14(4):329-335.

22. Farndale RW, Buttle DJ, Barrett AJ. Improved quantitation and discrimination of sulphated glycosaminoglycans by use of dimethylmethylene blue. Biochim Biophys Acta. 1986;833(2):173-177.

23. Schneider CA, Rasband WS, Eliceiri KW. NIH Image to ImageJ: 25 years of image analysis. Nat Methods. 2012;9(7):671-675.

24. R Development Core Team. R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2008.

25. Sa-Ngasoongsong P, Channoom T, Kawinwonggowit V, et al. Postoperative blood loss reduction in computer-assisted surgery total knee replacement by low dose intra-articular tranexamic acid injection together with 2-hour clamp drain: a prospective triple-blinded randomized controlled trial. Orthop Rev. 2011;3(2):e12.

26. Lecker I, Wang DS, Romaschin AD, Peterson M, Mazer CD, Orser BA. Tranexamic acid concentrations associated with human seizures inhibit glycine receptors. J Clin Invest. 2012;122(12):4654-4666.

27. Kakiuchi H, Kawarai-Shimamura A, Kuwagata M, Orito K. Tranexamic acid induces kaolin intake stimulating a pathway involving tachykinin neurokinin 1 receptors in rats. Eur J Pharmacol. 2014;723:1-6.

28. Kratzer S, Irl H, Mattusch C, et al. Tranexamic acid impairs γ-aminobutyric acid receptor type A–mediated synaptic transmission in the murine amygdala: a potential mechanism for drug-induced seizures? Anesthesiology. 2014;120(3):639-649.

29. Lee E, Enomoto R, Takemura K, Tsuda Y, Okada Y. A selective plasmin inhibitor, trans-aminomethylcyclohexanecarbonyl-L-(O-picolyl)tyrosine-octylamide (YO-2), induces thymocyte apoptosis. Biochem Pharmacol. 2002;63(7):1315-1323.

References

1.    McCormack PL. Tranexamic acid: a review of its use in the treatment of hyperfibrinolysis. Drugs. 2012;72(5):585-617.

2.    Murkin JM, Falter F, Granton J, Young B, Burt C, Chu M. High-dose tranexamic acid is associated with nonischemic clinical seizures in cardiac surgical patients. Anesth Analg. 2010;110(2):350-353.

3.    Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study. Arch Surg. 2012;147(2):113-119.

4.    Ker K, Prieto‐Merino D, Roberts I. Systematic review, meta‐analysis and meta‐regression of the effect of tranexamic acid on surgical blood loss. Br J Surg. 2013;100(10):1271-1279.

5.    Panteli M, Papakostidis C, Dahabreh Z, Giannoudis PV. Topical tranexamic acid in total knee replacement: a systematic review and meta-analysis. Knee. 2013;20(5):300-309.

6.    Alshryda S, Mason J, Vaghela M, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total knee replacement: a randomized controlled trial (TRANX-K). J Bone Joint Surg Am. 2013;95(21):1961-1968.

7.    Alshryda S, Mason J, Sarda P, et al. Topical (intra-articular) tranexamic acid reduces blood loss and transfusion rates following total hip replacement: a randomized controlled trial (TRANX-H). J Bone Joint Surg Am. 2013;95(21):1969-1974.

8.    Konig G, Hamlin BR, Waters JH. Topical tranexamic acid reduces blood loss and transfusion rates in total hip and total knee arthroplasty. J Arthroplasty. 2013;28(9):1473-1476.

9.    Lee SH, Cho KY, Khurana S, Kim KI. Less blood loss under concomitant administration of tranexamic acid and indirect factor Xa inhibitor following total knee arthroplasty: a prospective randomized controlled trial. Knee Surg Sports Traumatol Arthrosc. 2013;21(11):2611-2617.

10. Chimento GF, Huff T, Ochsner JL Jr, Meyer M, Brandner L, Babin S. An evaluation of the use of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):74-77.

11. Aguilera-Roig X, Jordán-Sales M, Natera-Cisneros L, Monllau-García JC, Martínez-Zapata MJ. Tranexamic acid in orthopedic surgery [in Spanish]. Rev Esp Cir Ortop Traumatol. 2014;58(1):52-56.

12. Wong J, Abrishami A, El Beheiry H, et al. Topical application of tranexamic acid reduces postoperative blood loss in total knee arthroplasty: a randomized, controlled trial. J Bone Joint Surg Am. 2010;92(15):2503-2513.

13. Georgiadis AG, Muh SJ, Silverton CD, Weir RM, Laker MW. A prospective double-blind placebo controlled trial of topical tranexamic acid in total knee arthroplasty. J Arthroplasty. 2013;28(8 suppl):78-82.

14. Tuttle JR, Ritterman SA, Cassidy DB, Anazonwu WA, Froehlich JA, Rubin LE. Cost benefit analysis of topical tranexamic acid in primary total hip and knee arthroplasty. J Arthroplasty. 2014;29(8):1512-1515.

15. Roy SP, Tanki UF, Dutta A, Jain SK, Nagi ON. Efficacy of intra-articular tranexamic acid in blood loss reduction following primary unilateral total knee arthroplasty. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2494-2501.

16. Ishida K, Tsumura N, Kitagawa A, et al. Intra-articular injection of tranexamic acid reduces not only blood loss but also knee joint swelling after total knee arthroplasty. Int Orthop. 2011;35(11):1639-1645.

17. Sitek P, Wysocka-Wycisk A, Kępski F, Król D, Bursig H, Dyląg S. PRP-fibrinogen gel-like chondrocyte carrier stabilized by TXA-preliminary study. Cell Tissue Bank. 2013;14(1):133-140.

18. Lo IK, Sciore P, Chung M, et al. Local anesthetics induce chondrocyte death in bovine articular cartilage disks in a dose- and duration-dependent manner. Arthroscopy. 2009;25(7):707-715.

19. Blumberg TJ, Natoli RM, Athanasiou KA. Effects of doxycycline on articular cartilage GAG release and mechanical properties following impact. Biotechnol Bioeng. 2008;100(3):506-515.

20. Piper SL, Kim HT. Comparison of ropivacaine and bupivacaine toxicity in human articular chondrocytes. J Bone Joint Surg Am. 2008;90(5):986-991.

21. Lefebvre V, Garofalo S, Zhou G, Metsäranta M, Vuorio E, De Crombrugghe B. Characterization of primary cultures of chondrocytes from type II collagen/beta-galactosidase transgenic mice. Matrix Biol. 1994;14(4):329-335.

22. Farndale RW, Buttle DJ, Barrett AJ. Improved quantitation and discrimination of sulphated glycosaminoglycans by use of dimethylmethylene blue. Biochim Biophys Acta. 1986;833(2):173-177.

23. Schneider CA, Rasband WS, Eliceiri KW. NIH Image to ImageJ: 25 years of image analysis. Nat Methods. 2012;9(7):671-675.

24. R Development Core Team. R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2008.

25. Sa-Ngasoongsong P, Channoom T, Kawinwonggowit V, et al. Postoperative blood loss reduction in computer-assisted surgery total knee replacement by low dose intra-articular tranexamic acid injection together with 2-hour clamp drain: a prospective triple-blinded randomized controlled trial. Orthop Rev. 2011;3(2):e12.

26. Lecker I, Wang DS, Romaschin AD, Peterson M, Mazer CD, Orser BA. Tranexamic acid concentrations associated with human seizures inhibit glycine receptors. J Clin Invest. 2012;122(12):4654-4666.

27. Kakiuchi H, Kawarai-Shimamura A, Kuwagata M, Orito K. Tranexamic acid induces kaolin intake stimulating a pathway involving tachykinin neurokinin 1 receptors in rats. Eur J Pharmacol. 2014;723:1-6.

28. Kratzer S, Irl H, Mattusch C, et al. Tranexamic acid impairs γ-aminobutyric acid receptor type A–mediated synaptic transmission in the murine amygdala: a potential mechanism for drug-induced seizures? Anesthesiology. 2014;120(3):639-649.

29. Lee E, Enomoto R, Takemura K, Tsuda Y, Okada Y. A selective plasmin inhibitor, trans-aminomethylcyclohexanecarbonyl-L-(O-picolyl)tyrosine-octylamide (YO-2), induces thymocyte apoptosis. Biochem Pharmacol. 2002;63(7):1315-1323.

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The American Journal of Orthopedics - 44(12)
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Effects of Tranexamic Acid Cytotoxicity on In Vitro Chondrocytes
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Effects of Tranexamic Acid Cytotoxicity on In Vitro Chondrocytes
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Prevalence of Low Bone Mineral Density in Younger Versus Older Women With Distal Radius Fractures

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Prevalence of Low Bone Mineral Density in Younger Versus Older Women With Distal Radius Fractures

Many organizations and work groups have issued recommendations regarding which patients should undergo bone densitometry. In 2004, the US Surgeon General recommended bone mineral density (BMD) evaluation for all women over age 65 years and for women and men with fragility fractures.1 The Centers for Medicare & Medicaid Services recommended BMD assessment for estrogen-deficient patients, for patients with vertebral abnormalities or hyperparathyroidism, and for patients receiving either steroid therapy or osteoporosis medications approved by the US Food and Drug Administration.2 The US Preventive Services Task Force and the National Osteoporosis Foundation each recommended screening for all women age 65 years or older and for postmenopausal women (age, 60-64 years) at high risk.3,4 The International Society for Clinical Densitometry (ISCD) recommended screening for all women age 65 years or older, all men age 70 years or older, and high-risk women under age 65 years.5

These current recommendations for BMD evaluation focus on women over age 65 years. More recent studies of postmenopausal women with distal radius fractures (DRFs) have found that both younger women (age, 45-65 years) and older women (age, ≥65 years) can have lower BMD and increased risk for hip and spine fracture.6,7 The authors of those studies recommended that all postmenopausal women with DRFs be evaluated for low BMD and that fracture prevention treatment be initiated. Earnshaw and colleagues8 and Oyen and colleagues9 found that men and women (age, ≥50 years) with DRFs had low BMD and elevated 10-year fracture rates. They concluded that BMD should be evaluated and treated in all DRF patients age 50 years or older. Other studies have shown low BMD in the contralateral distal radius of patients of all ages who presented with Colles fractures.10,11 These 2 studies did not measure spine or hip BMD.

The literature on BMD of younger women with DRFs is limited, relying solely on data collected for the contralateral distal radius.10,11 The ISCD recommended measuring both hip and spine BMD in premenopausal women. They also stated that z scores, not t scores, should be used for premenopausal women.5 The causes of low BMD in women over age 55 years are primarily nutritional deficiency and normal aging.1 In younger females, low BMD results from secondary causes, such as diet, medications, medical conditions, and endocrine disorders. When the secondary cause of low BMD can be identified and treated, osteoporosis can be stopped and even reversed in younger patients.12-14 Low BMD is more amenable to treatment in younger patients than in postmenopausal women. Younger patients with low BMD carry a higher lifetime fracture risk because they have more years of life with low BMD; therefore, early identification and treatment have a more significant impact on fracture prevention in these patients.

In the present study, we determined the prevalence of osteoporosis and osteopenia in younger women (age, 35-50 years) with DRFs and compared BMD measurements from younger women (age, 35-50 years) and older women (age, >50 years) with DRFs. The main goal was to determine which patients should be referred for bone densitometry and subsequent treatment.

Patients and Methods

This study received institutional review board approval. During a 5-year period (January 2005–August 2010), we prospectively collected dual-energy x-ray absorptiometry (DXA) scans for 128 women (age, >35 years) who presented with DRFs to our level I trauma center. Age ranged from 35 to 86 years. Data on mechanism of injury, treatment, and body mass index (BMI) were collected. The 128 patients were divided into a younger group (47 women; age range, 35-50 years; mean age, 44 years) and an older group (81 women; age, ≥51 years; mean age, 61 years). Mean BMI was 29.3 in the younger group and 28.8 in the older group (P = .88) (Table).

BMD was measured with a General Electric Lunar Prodigy Advance scanner that was tested annually for accuracy and precision. BMD of hips and lumbar spines was measured with a 76-Kv x-ray source. All DXA scans were analyzed by the same physician. BMD was omitted in cases of patients with a history of lumbar spine or hip fracture.

Two-sample Student t test was used to compare the 2 groups’ data. When multiple groups were being compared, analysis of variance was used. Spearman rank-order test was used to calculate a correlation coefficient for evaluation of the relationships between age and BMD.

Results

Mean lumbar spine (L1–L4) BMD was 1.12 in the younger group and 1.063 in the older group (P = .02); t scores were –0.63 and –1.132, respectively (P = .02); and mean z scores were –0.69 and –0.61, respectively (P = .81). Mean femoral neck BMD was 0.91 in the younger group and 0.80 in the older group (P < .05); t scores were –0.87 and –1.65, respectively (P < .01), and mean femoral neck z scores were –0.69 and –0.67, respectively (P = .92).

 

 

To further analyze BMD of specific age groups, we divided patients by decade: 35-39, 40-49, 50-59, 60-69, 70-79, 80-89 years. Among all 6 decades, there were no statistically significant differences between hip z scores (P = .83) (Figure 1). Spearman rank-order correlation test showed a moderate inverse correlation between age and femoral neck BMD (R = –0.42) and t score (R = –0.43). There was a weak correlation between increasing age and decreasing spine BMD, t score, and z score (Rs = –0.27, –0.31, 0.03). There was no correlation between age and femoral neck z score (R = –0.04).

According to the WHO classification system, 11 (23%) of the 47 women in the younger group were osteopenic, and 8 (17%) were osteoporotic, based on spine BMD. Hip BMD values indicated that 20 patients (43%) were osteopenic, and 3 (6%) were osteoporotic. One patient in the younger group had a hip z score of less than –2, and 14 patients (39%) had a hip z score between –2 and –1. Six patients (18%) had a spine z score of less than –2, and 6 patients (18%) had a spine z score between –2 and –1. Of the 81 older patients, 22 (27%) were osteopenic, and 21 (26%) were osteoporotic, according to spine measurements. The femoral neck data indicated that 39 (48%) of the older patients were osteopenic, and 22 (27%) were osteoporotic.

In both groups, mechanisms of injury were identified. Of the 47 younger patients, 26 fell from standing, 7 fell from a height of more than 6 feet, and 14 were injured in motor vehicle collisions (MVCs). Of the 81 older patients, 2 sustained a direct blow, 64 fell from standing, 4 fell from a height of more than 6 feet, and 11 were injured in MVCs. The differences in z scores based on mechanism of injury were not statistically significant (P = .22) (Figure 2).

Discussion

Several studies have shown that older women with DRFs have low BMD in the spine and femoral neck.8,9 These studies focused on older women who sustained low-energy fractures caused by a fall from a standing height. Studies of younger women with DRFs focused on BMD of the contralateral distal radius, not the spine or femoral neck.10,11 Those study groups also had low BMD. Findings from a multitude of studies have established that patients who are older than 50 years when they sustain distal radius fragility fractures should be referred for bone densitometry studies, and there is increasing evidence that younger patients with fragility fractures should undergo this evaluation as well.

The present study was designed to expand the range of patients and mechanisms of injury. Women in this study were 35 years or older. In addition to collecting data from patients injured in a fall from standing, we examined the medical records of women injured in MVCs, in falls from heights of more than 6 feet, and from direct trauma to the wrist. We measured the BMD of the spine and femoral neck and of the contralateral distal radius.

For this discussion, several key points should be made about BMD evaluation in younger versus older women. Most organizations caution against using spine BMD in older women. The ISCD, however, recommended measuring both hip and spine BMD; whereas BMD can be falsely elevated by spine osteoarthritis in older patients, spine BMD measurements are accurate in younger patients not affected by osteoarthritis. The ISCD also stipulated that z scores should be used in examining BMD in younger patients. The z score is a value of how many standard deviations BMD differs from a matched population of the same age, sex, ethnicity, and weight. The t score, which is useful in evaluating older patients, compares a patient’s BMD with that of an average 30-year-old.12

According to the WHO classification system (intended for older women), osteopenia is indicated by a t score between –1.0 and –2.5, and osteoporosis is indicated by a t score of less than –2.5. In the present study, about 43% of the younger patients (age, 35-50 years) with DRFs were osteopenic, and 6% of these patients were osteoporotic. In concert with previous studies,9 48% of our older women (age, >50 years) with DRFs were osteopenic, and 27% were osteoporotic. The difference in mean spinal z scores between the younger and older groups was not statistically significant (P = .81).

As mentioned, when examining BMD of younger patients, it is imperative to use spine z scores. About 18% of our younger patients had a z score of less than –2, and 18% had a z score between –2 and –1. In our comparison of patients from 5 different age decades (range, 35-79 years), there was no statistically significant difference in z scores (P = .83). In addition, there was no correlation between increasing age and decreasing z score (R = –0.04).

 

 

Secondary causes of osteoporosis have been documented in 30% of premenopausal women and 55% of men with vertebral fractures.13-15 Primary osteoporosis results from the normal aging process; secondary osteoporosis results from reversible causes, including medications, gastrointestinal disorders, renal disease, endocrine disorders, and sedentary lifestyle.15,16 When a secondary cause of osteoporosis is identified, treatment can be initiated to increase BMD. As younger patients can reverse bone loss and even increase BMD, it is important to identify reversible causes of osteopenia and osteoporosis in this age group. It is well documented that both younger and older patients with DRFs are at increased risk for subsequent fractures.6 Preventing further bone loss at a younger age may drastically decrease lifetime fracture risk.12,17

Most previous studies of BMD in women were limited to patients with DRFs caused by a low-energy mechanism or by a fall from standing. Current recommendations for BMD testing focus on postmenopausal women who have sustained a fragility or low-energy DRF. When an osteoporotic or osteopenic patient’s distal radius is subjected to a high-energy force, a fracture is likely. Therefore, we expanded our study to include high-energy mechanisms of injury. Our analysis of BMD in patients with DRFs sustained in MVCs indicated that 12% of this group were osteoporotic, and 44% were osteopenic. Forty-three percent of our younger patients with a DRF fractured in a MVC were osteopenic, and 6% were osteoporotic. Among 4 mechanisms of injury for DRFs, there was no statistically significant difference in z scores (P = .22) (Figure 2). This provides evidence that a significant portion of patients with DRFs from both high- and low-energy mechanisms are osteoporotic or osteopenic. Patients with DRFs sustained in MVCs or in falls from heights of more than 6 feet should be referred for BMD evaluation.         

Conclusion

A significant proportion of younger patients with DRFs are osteopenic or osteoporotic (43% and 6%, respectively), and their z scores are comparable to those of older patients with DRFs. There was no statistically significant difference in BMD z scores between younger and older patients and no difference in mechanisms of injury. This is evidence that younger patients with DRFs caused by a high- or low-energy mechanism of injury should undergo both DXA scan and BMD evaluation. If osteoporosis or osteopenia can be diagnosed at an earlier age, and if these patients can be properly treated, subsequent fractures could be prevented. The present study provides evidence supporting a simplification of the current recommendations for BMD evaluation: All women with DRFs should undergo bone densitometry.

References

1.    US Department of Health and Human Services. Bone Health and Osteoporosis: A Report of the Surgeon General. Rockville, MD: US Dept of Health and Human Services, Public Health Service, Office of the Surgeon General; 2004. http://www.ncbi.nlm.nih.gov/books/NBK45513/pdf/Bookshelf_NBK45513.pdf. Accessed November 3, 2015.

2.    Bone mass measurement (bone density). Medicare website. https://www.medicare.gov/coverage/bone-density.html. Accessed November 3, 2015.

3.    Final update summary: osteoporosis: screening. US Preventive Services Task Force website. http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/osteoporosis-screening. Updated July 2015. Accessed November 3, 2015.

4.    National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Washington, DC: National Osteoporosis Foundation; 2010. http://nof.org/files/nof/public/content/file/344/upload/159.pdf. Accessed November 3, 2015.

5.    Khan AA, Bachrach L, Brown JP, et al. Canadian Panel of International Society of Clinical Densitometry. Standards and guidelines for performing central dual-energy x-ray absorptiometry in premenopausal women, men, and children. J Clin Densitom. 2004;7(1):51-64.

6.    Barrett-Connor E, Sajjan SG, Siris ES, Miller PD, Chen YT, Markson LE. Wrist fracture as a predictor of future fractures in younger versus older postmenopausal women: results from the National Osteoporosis Risk Assessment (NORA). Osteoporos Int. 2008;19(5):607-613.

7.    Lauritzen JB, Schwarz P, Lund B, McNair P, Transbøl I. Changing incidence and residual lifetime risk of common osteoporosis-related fractures. Osteoporos Int. 1993;3(3):127-132.

8.    Earnshaw SA, Cawte SA, Worley A, Hosking DJ. Colles’ fracture of the wrist as an indicator of underlying osteoporosis in postmenopausal women: a prospective study of bone mineral density and bone turnover rate. Osteoporos Int. 1998;8(1):53-60.

9.    Oyen J, Brudvik C, Gjesdal CG, Tell GS, Lie SA, Hove LM. Osteoporosis as a risk factor for distal radius fractures: a case–control study. J Bone Joint Surg Am. 2011;93(4):348-356.

10. Wigderowitz CA, Cunningham T, Rowley DI, Mole PA, Paterson CR. Peripheral bone mineral density in patients with distal radial fractures. J Bone Joint Surg Br. 2003;85(3):423-425.

11. Wigderowitz CA, Rowley DI, Mole PA, Paterson CR, Abel EW. Bone mineral density of the radius in patients with Colles’ fracture. J Bone Joint Surg Br. 2000;82(1):87-89.

12. Khan A, Syed Z. Bone mineral density assessment in premenopausal women. Womens Health. 2006;2(4):639-645.

13. Fitzpatrick LA. Secondary causes of osteoporosis. Mayo Clin Proc. 2002;77(5):453-468.

14. Hudec SM, Camacho PM. Secondary causes of osteoporosis. Endocr Pract. 2013;19(1):120-128.

15. Scane AC, Sutcliffe AM, Francis RM. Osteoporosis in men. Baillieres Clin Rheumatol. 1993;7(3):589-601.

16. Binkley N, Bilezikian JP, Kendler DL, Leib ES, Lewiecki EM, Petak SM. Summary of the International Society for Clinical Densitometry 2005 Position Development Conference. J Bone Miner Res. 2007;22(5):643-645.

17. Kelepouris N, Harper KD, Gannon F, Kaplan FS, Haddad JG. Severe osteoporosis in men. Ann Intern Med. 1995;123(6):452-460.

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Patrick A. Massey, MD, Jeremy R. James, MD, Joseph Bonvillain, MD, Bradley G. Nelson, MD, Stacey R. Massey, MD, and Anne Hollister, MD

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

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The American Journal of Orthopedics - 44(12)
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E493-E496
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american journal of orthopedics, AJO, original study, online exclusive, study, bone, bone mineral density, BMD, distal radius fractures, fracture, fracture management, fractures, DRF, osteoporosis, wrist, joint, massey, james, bonvillain, nelson, hollister
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Patrick A. Massey, MD, Jeremy R. James, MD, Joseph Bonvillain, MD, Bradley G. Nelson, MD, Stacey R. Massey, MD, and Anne Hollister, MD

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

Author and Disclosure Information

Patrick A. Massey, MD, Jeremy R. James, MD, Joseph Bonvillain, MD, Bradley G. Nelson, MD, Stacey R. Massey, MD, and Anne Hollister, MD

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

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Many organizations and work groups have issued recommendations regarding which patients should undergo bone densitometry. In 2004, the US Surgeon General recommended bone mineral density (BMD) evaluation for all women over age 65 years and for women and men with fragility fractures.1 The Centers for Medicare & Medicaid Services recommended BMD assessment for estrogen-deficient patients, for patients with vertebral abnormalities or hyperparathyroidism, and for patients receiving either steroid therapy or osteoporosis medications approved by the US Food and Drug Administration.2 The US Preventive Services Task Force and the National Osteoporosis Foundation each recommended screening for all women age 65 years or older and for postmenopausal women (age, 60-64 years) at high risk.3,4 The International Society for Clinical Densitometry (ISCD) recommended screening for all women age 65 years or older, all men age 70 years or older, and high-risk women under age 65 years.5

These current recommendations for BMD evaluation focus on women over age 65 years. More recent studies of postmenopausal women with distal radius fractures (DRFs) have found that both younger women (age, 45-65 years) and older women (age, ≥65 years) can have lower BMD and increased risk for hip and spine fracture.6,7 The authors of those studies recommended that all postmenopausal women with DRFs be evaluated for low BMD and that fracture prevention treatment be initiated. Earnshaw and colleagues8 and Oyen and colleagues9 found that men and women (age, ≥50 years) with DRFs had low BMD and elevated 10-year fracture rates. They concluded that BMD should be evaluated and treated in all DRF patients age 50 years or older. Other studies have shown low BMD in the contralateral distal radius of patients of all ages who presented with Colles fractures.10,11 These 2 studies did not measure spine or hip BMD.

The literature on BMD of younger women with DRFs is limited, relying solely on data collected for the contralateral distal radius.10,11 The ISCD recommended measuring both hip and spine BMD in premenopausal women. They also stated that z scores, not t scores, should be used for premenopausal women.5 The causes of low BMD in women over age 55 years are primarily nutritional deficiency and normal aging.1 In younger females, low BMD results from secondary causes, such as diet, medications, medical conditions, and endocrine disorders. When the secondary cause of low BMD can be identified and treated, osteoporosis can be stopped and even reversed in younger patients.12-14 Low BMD is more amenable to treatment in younger patients than in postmenopausal women. Younger patients with low BMD carry a higher lifetime fracture risk because they have more years of life with low BMD; therefore, early identification and treatment have a more significant impact on fracture prevention in these patients.

In the present study, we determined the prevalence of osteoporosis and osteopenia in younger women (age, 35-50 years) with DRFs and compared BMD measurements from younger women (age, 35-50 years) and older women (age, >50 years) with DRFs. The main goal was to determine which patients should be referred for bone densitometry and subsequent treatment.

Patients and Methods

This study received institutional review board approval. During a 5-year period (January 2005–August 2010), we prospectively collected dual-energy x-ray absorptiometry (DXA) scans for 128 women (age, >35 years) who presented with DRFs to our level I trauma center. Age ranged from 35 to 86 years. Data on mechanism of injury, treatment, and body mass index (BMI) were collected. The 128 patients were divided into a younger group (47 women; age range, 35-50 years; mean age, 44 years) and an older group (81 women; age, ≥51 years; mean age, 61 years). Mean BMI was 29.3 in the younger group and 28.8 in the older group (P = .88) (Table).

BMD was measured with a General Electric Lunar Prodigy Advance scanner that was tested annually for accuracy and precision. BMD of hips and lumbar spines was measured with a 76-Kv x-ray source. All DXA scans were analyzed by the same physician. BMD was omitted in cases of patients with a history of lumbar spine or hip fracture.

Two-sample Student t test was used to compare the 2 groups’ data. When multiple groups were being compared, analysis of variance was used. Spearman rank-order test was used to calculate a correlation coefficient for evaluation of the relationships between age and BMD.

Results

Mean lumbar spine (L1–L4) BMD was 1.12 in the younger group and 1.063 in the older group (P = .02); t scores were –0.63 and –1.132, respectively (P = .02); and mean z scores were –0.69 and –0.61, respectively (P = .81). Mean femoral neck BMD was 0.91 in the younger group and 0.80 in the older group (P < .05); t scores were –0.87 and –1.65, respectively (P < .01), and mean femoral neck z scores were –0.69 and –0.67, respectively (P = .92).

 

 

To further analyze BMD of specific age groups, we divided patients by decade: 35-39, 40-49, 50-59, 60-69, 70-79, 80-89 years. Among all 6 decades, there were no statistically significant differences between hip z scores (P = .83) (Figure 1). Spearman rank-order correlation test showed a moderate inverse correlation between age and femoral neck BMD (R = –0.42) and t score (R = –0.43). There was a weak correlation between increasing age and decreasing spine BMD, t score, and z score (Rs = –0.27, –0.31, 0.03). There was no correlation between age and femoral neck z score (R = –0.04).

According to the WHO classification system, 11 (23%) of the 47 women in the younger group were osteopenic, and 8 (17%) were osteoporotic, based on spine BMD. Hip BMD values indicated that 20 patients (43%) were osteopenic, and 3 (6%) were osteoporotic. One patient in the younger group had a hip z score of less than –2, and 14 patients (39%) had a hip z score between –2 and –1. Six patients (18%) had a spine z score of less than –2, and 6 patients (18%) had a spine z score between –2 and –1. Of the 81 older patients, 22 (27%) were osteopenic, and 21 (26%) were osteoporotic, according to spine measurements. The femoral neck data indicated that 39 (48%) of the older patients were osteopenic, and 22 (27%) were osteoporotic.

In both groups, mechanisms of injury were identified. Of the 47 younger patients, 26 fell from standing, 7 fell from a height of more than 6 feet, and 14 were injured in motor vehicle collisions (MVCs). Of the 81 older patients, 2 sustained a direct blow, 64 fell from standing, 4 fell from a height of more than 6 feet, and 11 were injured in MVCs. The differences in z scores based on mechanism of injury were not statistically significant (P = .22) (Figure 2).

Discussion

Several studies have shown that older women with DRFs have low BMD in the spine and femoral neck.8,9 These studies focused on older women who sustained low-energy fractures caused by a fall from a standing height. Studies of younger women with DRFs focused on BMD of the contralateral distal radius, not the spine or femoral neck.10,11 Those study groups also had low BMD. Findings from a multitude of studies have established that patients who are older than 50 years when they sustain distal radius fragility fractures should be referred for bone densitometry studies, and there is increasing evidence that younger patients with fragility fractures should undergo this evaluation as well.

The present study was designed to expand the range of patients and mechanisms of injury. Women in this study were 35 years or older. In addition to collecting data from patients injured in a fall from standing, we examined the medical records of women injured in MVCs, in falls from heights of more than 6 feet, and from direct trauma to the wrist. We measured the BMD of the spine and femoral neck and of the contralateral distal radius.

For this discussion, several key points should be made about BMD evaluation in younger versus older women. Most organizations caution against using spine BMD in older women. The ISCD, however, recommended measuring both hip and spine BMD; whereas BMD can be falsely elevated by spine osteoarthritis in older patients, spine BMD measurements are accurate in younger patients not affected by osteoarthritis. The ISCD also stipulated that z scores should be used in examining BMD in younger patients. The z score is a value of how many standard deviations BMD differs from a matched population of the same age, sex, ethnicity, and weight. The t score, which is useful in evaluating older patients, compares a patient’s BMD with that of an average 30-year-old.12

According to the WHO classification system (intended for older women), osteopenia is indicated by a t score between –1.0 and –2.5, and osteoporosis is indicated by a t score of less than –2.5. In the present study, about 43% of the younger patients (age, 35-50 years) with DRFs were osteopenic, and 6% of these patients were osteoporotic. In concert with previous studies,9 48% of our older women (age, >50 years) with DRFs were osteopenic, and 27% were osteoporotic. The difference in mean spinal z scores between the younger and older groups was not statistically significant (P = .81).

As mentioned, when examining BMD of younger patients, it is imperative to use spine z scores. About 18% of our younger patients had a z score of less than –2, and 18% had a z score between –2 and –1. In our comparison of patients from 5 different age decades (range, 35-79 years), there was no statistically significant difference in z scores (P = .83). In addition, there was no correlation between increasing age and decreasing z score (R = –0.04).

 

 

Secondary causes of osteoporosis have been documented in 30% of premenopausal women and 55% of men with vertebral fractures.13-15 Primary osteoporosis results from the normal aging process; secondary osteoporosis results from reversible causes, including medications, gastrointestinal disorders, renal disease, endocrine disorders, and sedentary lifestyle.15,16 When a secondary cause of osteoporosis is identified, treatment can be initiated to increase BMD. As younger patients can reverse bone loss and even increase BMD, it is important to identify reversible causes of osteopenia and osteoporosis in this age group. It is well documented that both younger and older patients with DRFs are at increased risk for subsequent fractures.6 Preventing further bone loss at a younger age may drastically decrease lifetime fracture risk.12,17

Most previous studies of BMD in women were limited to patients with DRFs caused by a low-energy mechanism or by a fall from standing. Current recommendations for BMD testing focus on postmenopausal women who have sustained a fragility or low-energy DRF. When an osteoporotic or osteopenic patient’s distal radius is subjected to a high-energy force, a fracture is likely. Therefore, we expanded our study to include high-energy mechanisms of injury. Our analysis of BMD in patients with DRFs sustained in MVCs indicated that 12% of this group were osteoporotic, and 44% were osteopenic. Forty-three percent of our younger patients with a DRF fractured in a MVC were osteopenic, and 6% were osteoporotic. Among 4 mechanisms of injury for DRFs, there was no statistically significant difference in z scores (P = .22) (Figure 2). This provides evidence that a significant portion of patients with DRFs from both high- and low-energy mechanisms are osteoporotic or osteopenic. Patients with DRFs sustained in MVCs or in falls from heights of more than 6 feet should be referred for BMD evaluation.         

Conclusion

A significant proportion of younger patients with DRFs are osteopenic or osteoporotic (43% and 6%, respectively), and their z scores are comparable to those of older patients with DRFs. There was no statistically significant difference in BMD z scores between younger and older patients and no difference in mechanisms of injury. This is evidence that younger patients with DRFs caused by a high- or low-energy mechanism of injury should undergo both DXA scan and BMD evaluation. If osteoporosis or osteopenia can be diagnosed at an earlier age, and if these patients can be properly treated, subsequent fractures could be prevented. The present study provides evidence supporting a simplification of the current recommendations for BMD evaluation: All women with DRFs should undergo bone densitometry.

Many organizations and work groups have issued recommendations regarding which patients should undergo bone densitometry. In 2004, the US Surgeon General recommended bone mineral density (BMD) evaluation for all women over age 65 years and for women and men with fragility fractures.1 The Centers for Medicare & Medicaid Services recommended BMD assessment for estrogen-deficient patients, for patients with vertebral abnormalities or hyperparathyroidism, and for patients receiving either steroid therapy or osteoporosis medications approved by the US Food and Drug Administration.2 The US Preventive Services Task Force and the National Osteoporosis Foundation each recommended screening for all women age 65 years or older and for postmenopausal women (age, 60-64 years) at high risk.3,4 The International Society for Clinical Densitometry (ISCD) recommended screening for all women age 65 years or older, all men age 70 years or older, and high-risk women under age 65 years.5

These current recommendations for BMD evaluation focus on women over age 65 years. More recent studies of postmenopausal women with distal radius fractures (DRFs) have found that both younger women (age, 45-65 years) and older women (age, ≥65 years) can have lower BMD and increased risk for hip and spine fracture.6,7 The authors of those studies recommended that all postmenopausal women with DRFs be evaluated for low BMD and that fracture prevention treatment be initiated. Earnshaw and colleagues8 and Oyen and colleagues9 found that men and women (age, ≥50 years) with DRFs had low BMD and elevated 10-year fracture rates. They concluded that BMD should be evaluated and treated in all DRF patients age 50 years or older. Other studies have shown low BMD in the contralateral distal radius of patients of all ages who presented with Colles fractures.10,11 These 2 studies did not measure spine or hip BMD.

The literature on BMD of younger women with DRFs is limited, relying solely on data collected for the contralateral distal radius.10,11 The ISCD recommended measuring both hip and spine BMD in premenopausal women. They also stated that z scores, not t scores, should be used for premenopausal women.5 The causes of low BMD in women over age 55 years are primarily nutritional deficiency and normal aging.1 In younger females, low BMD results from secondary causes, such as diet, medications, medical conditions, and endocrine disorders. When the secondary cause of low BMD can be identified and treated, osteoporosis can be stopped and even reversed in younger patients.12-14 Low BMD is more amenable to treatment in younger patients than in postmenopausal women. Younger patients with low BMD carry a higher lifetime fracture risk because they have more years of life with low BMD; therefore, early identification and treatment have a more significant impact on fracture prevention in these patients.

In the present study, we determined the prevalence of osteoporosis and osteopenia in younger women (age, 35-50 years) with DRFs and compared BMD measurements from younger women (age, 35-50 years) and older women (age, >50 years) with DRFs. The main goal was to determine which patients should be referred for bone densitometry and subsequent treatment.

Patients and Methods

This study received institutional review board approval. During a 5-year period (January 2005–August 2010), we prospectively collected dual-energy x-ray absorptiometry (DXA) scans for 128 women (age, >35 years) who presented with DRFs to our level I trauma center. Age ranged from 35 to 86 years. Data on mechanism of injury, treatment, and body mass index (BMI) were collected. The 128 patients were divided into a younger group (47 women; age range, 35-50 years; mean age, 44 years) and an older group (81 women; age, ≥51 years; mean age, 61 years). Mean BMI was 29.3 in the younger group and 28.8 in the older group (P = .88) (Table).

BMD was measured with a General Electric Lunar Prodigy Advance scanner that was tested annually for accuracy and precision. BMD of hips and lumbar spines was measured with a 76-Kv x-ray source. All DXA scans were analyzed by the same physician. BMD was omitted in cases of patients with a history of lumbar spine or hip fracture.

Two-sample Student t test was used to compare the 2 groups’ data. When multiple groups were being compared, analysis of variance was used. Spearman rank-order test was used to calculate a correlation coefficient for evaluation of the relationships between age and BMD.

Results

Mean lumbar spine (L1–L4) BMD was 1.12 in the younger group and 1.063 in the older group (P = .02); t scores were –0.63 and –1.132, respectively (P = .02); and mean z scores were –0.69 and –0.61, respectively (P = .81). Mean femoral neck BMD was 0.91 in the younger group and 0.80 in the older group (P < .05); t scores were –0.87 and –1.65, respectively (P < .01), and mean femoral neck z scores were –0.69 and –0.67, respectively (P = .92).

 

 

To further analyze BMD of specific age groups, we divided patients by decade: 35-39, 40-49, 50-59, 60-69, 70-79, 80-89 years. Among all 6 decades, there were no statistically significant differences between hip z scores (P = .83) (Figure 1). Spearman rank-order correlation test showed a moderate inverse correlation between age and femoral neck BMD (R = –0.42) and t score (R = –0.43). There was a weak correlation between increasing age and decreasing spine BMD, t score, and z score (Rs = –0.27, –0.31, 0.03). There was no correlation between age and femoral neck z score (R = –0.04).

According to the WHO classification system, 11 (23%) of the 47 women in the younger group were osteopenic, and 8 (17%) were osteoporotic, based on spine BMD. Hip BMD values indicated that 20 patients (43%) were osteopenic, and 3 (6%) were osteoporotic. One patient in the younger group had a hip z score of less than –2, and 14 patients (39%) had a hip z score between –2 and –1. Six patients (18%) had a spine z score of less than –2, and 6 patients (18%) had a spine z score between –2 and –1. Of the 81 older patients, 22 (27%) were osteopenic, and 21 (26%) were osteoporotic, according to spine measurements. The femoral neck data indicated that 39 (48%) of the older patients were osteopenic, and 22 (27%) were osteoporotic.

In both groups, mechanisms of injury were identified. Of the 47 younger patients, 26 fell from standing, 7 fell from a height of more than 6 feet, and 14 were injured in motor vehicle collisions (MVCs). Of the 81 older patients, 2 sustained a direct blow, 64 fell from standing, 4 fell from a height of more than 6 feet, and 11 were injured in MVCs. The differences in z scores based on mechanism of injury were not statistically significant (P = .22) (Figure 2).

Discussion

Several studies have shown that older women with DRFs have low BMD in the spine and femoral neck.8,9 These studies focused on older women who sustained low-energy fractures caused by a fall from a standing height. Studies of younger women with DRFs focused on BMD of the contralateral distal radius, not the spine or femoral neck.10,11 Those study groups also had low BMD. Findings from a multitude of studies have established that patients who are older than 50 years when they sustain distal radius fragility fractures should be referred for bone densitometry studies, and there is increasing evidence that younger patients with fragility fractures should undergo this evaluation as well.

The present study was designed to expand the range of patients and mechanisms of injury. Women in this study were 35 years or older. In addition to collecting data from patients injured in a fall from standing, we examined the medical records of women injured in MVCs, in falls from heights of more than 6 feet, and from direct trauma to the wrist. We measured the BMD of the spine and femoral neck and of the contralateral distal radius.

For this discussion, several key points should be made about BMD evaluation in younger versus older women. Most organizations caution against using spine BMD in older women. The ISCD, however, recommended measuring both hip and spine BMD; whereas BMD can be falsely elevated by spine osteoarthritis in older patients, spine BMD measurements are accurate in younger patients not affected by osteoarthritis. The ISCD also stipulated that z scores should be used in examining BMD in younger patients. The z score is a value of how many standard deviations BMD differs from a matched population of the same age, sex, ethnicity, and weight. The t score, which is useful in evaluating older patients, compares a patient’s BMD with that of an average 30-year-old.12

According to the WHO classification system (intended for older women), osteopenia is indicated by a t score between –1.0 and –2.5, and osteoporosis is indicated by a t score of less than –2.5. In the present study, about 43% of the younger patients (age, 35-50 years) with DRFs were osteopenic, and 6% of these patients were osteoporotic. In concert with previous studies,9 48% of our older women (age, >50 years) with DRFs were osteopenic, and 27% were osteoporotic. The difference in mean spinal z scores between the younger and older groups was not statistically significant (P = .81).

As mentioned, when examining BMD of younger patients, it is imperative to use spine z scores. About 18% of our younger patients had a z score of less than –2, and 18% had a z score between –2 and –1. In our comparison of patients from 5 different age decades (range, 35-79 years), there was no statistically significant difference in z scores (P = .83). In addition, there was no correlation between increasing age and decreasing z score (R = –0.04).

 

 

Secondary causes of osteoporosis have been documented in 30% of premenopausal women and 55% of men with vertebral fractures.13-15 Primary osteoporosis results from the normal aging process; secondary osteoporosis results from reversible causes, including medications, gastrointestinal disorders, renal disease, endocrine disorders, and sedentary lifestyle.15,16 When a secondary cause of osteoporosis is identified, treatment can be initiated to increase BMD. As younger patients can reverse bone loss and even increase BMD, it is important to identify reversible causes of osteopenia and osteoporosis in this age group. It is well documented that both younger and older patients with DRFs are at increased risk for subsequent fractures.6 Preventing further bone loss at a younger age may drastically decrease lifetime fracture risk.12,17

Most previous studies of BMD in women were limited to patients with DRFs caused by a low-energy mechanism or by a fall from standing. Current recommendations for BMD testing focus on postmenopausal women who have sustained a fragility or low-energy DRF. When an osteoporotic or osteopenic patient’s distal radius is subjected to a high-energy force, a fracture is likely. Therefore, we expanded our study to include high-energy mechanisms of injury. Our analysis of BMD in patients with DRFs sustained in MVCs indicated that 12% of this group were osteoporotic, and 44% were osteopenic. Forty-three percent of our younger patients with a DRF fractured in a MVC were osteopenic, and 6% were osteoporotic. Among 4 mechanisms of injury for DRFs, there was no statistically significant difference in z scores (P = .22) (Figure 2). This provides evidence that a significant portion of patients with DRFs from both high- and low-energy mechanisms are osteoporotic or osteopenic. Patients with DRFs sustained in MVCs or in falls from heights of more than 6 feet should be referred for BMD evaluation.         

Conclusion

A significant proportion of younger patients with DRFs are osteopenic or osteoporotic (43% and 6%, respectively), and their z scores are comparable to those of older patients with DRFs. There was no statistically significant difference in BMD z scores between younger and older patients and no difference in mechanisms of injury. This is evidence that younger patients with DRFs caused by a high- or low-energy mechanism of injury should undergo both DXA scan and BMD evaluation. If osteoporosis or osteopenia can be diagnosed at an earlier age, and if these patients can be properly treated, subsequent fractures could be prevented. The present study provides evidence supporting a simplification of the current recommendations for BMD evaluation: All women with DRFs should undergo bone densitometry.

References

1.    US Department of Health and Human Services. Bone Health and Osteoporosis: A Report of the Surgeon General. Rockville, MD: US Dept of Health and Human Services, Public Health Service, Office of the Surgeon General; 2004. http://www.ncbi.nlm.nih.gov/books/NBK45513/pdf/Bookshelf_NBK45513.pdf. Accessed November 3, 2015.

2.    Bone mass measurement (bone density). Medicare website. https://www.medicare.gov/coverage/bone-density.html. Accessed November 3, 2015.

3.    Final update summary: osteoporosis: screening. US Preventive Services Task Force website. http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/osteoporosis-screening. Updated July 2015. Accessed November 3, 2015.

4.    National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Washington, DC: National Osteoporosis Foundation; 2010. http://nof.org/files/nof/public/content/file/344/upload/159.pdf. Accessed November 3, 2015.

5.    Khan AA, Bachrach L, Brown JP, et al. Canadian Panel of International Society of Clinical Densitometry. Standards and guidelines for performing central dual-energy x-ray absorptiometry in premenopausal women, men, and children. J Clin Densitom. 2004;7(1):51-64.

6.    Barrett-Connor E, Sajjan SG, Siris ES, Miller PD, Chen YT, Markson LE. Wrist fracture as a predictor of future fractures in younger versus older postmenopausal women: results from the National Osteoporosis Risk Assessment (NORA). Osteoporos Int. 2008;19(5):607-613.

7.    Lauritzen JB, Schwarz P, Lund B, McNair P, Transbøl I. Changing incidence and residual lifetime risk of common osteoporosis-related fractures. Osteoporos Int. 1993;3(3):127-132.

8.    Earnshaw SA, Cawte SA, Worley A, Hosking DJ. Colles’ fracture of the wrist as an indicator of underlying osteoporosis in postmenopausal women: a prospective study of bone mineral density and bone turnover rate. Osteoporos Int. 1998;8(1):53-60.

9.    Oyen J, Brudvik C, Gjesdal CG, Tell GS, Lie SA, Hove LM. Osteoporosis as a risk factor for distal radius fractures: a case–control study. J Bone Joint Surg Am. 2011;93(4):348-356.

10. Wigderowitz CA, Cunningham T, Rowley DI, Mole PA, Paterson CR. Peripheral bone mineral density in patients with distal radial fractures. J Bone Joint Surg Br. 2003;85(3):423-425.

11. Wigderowitz CA, Rowley DI, Mole PA, Paterson CR, Abel EW. Bone mineral density of the radius in patients with Colles’ fracture. J Bone Joint Surg Br. 2000;82(1):87-89.

12. Khan A, Syed Z. Bone mineral density assessment in premenopausal women. Womens Health. 2006;2(4):639-645.

13. Fitzpatrick LA. Secondary causes of osteoporosis. Mayo Clin Proc. 2002;77(5):453-468.

14. Hudec SM, Camacho PM. Secondary causes of osteoporosis. Endocr Pract. 2013;19(1):120-128.

15. Scane AC, Sutcliffe AM, Francis RM. Osteoporosis in men. Baillieres Clin Rheumatol. 1993;7(3):589-601.

16. Binkley N, Bilezikian JP, Kendler DL, Leib ES, Lewiecki EM, Petak SM. Summary of the International Society for Clinical Densitometry 2005 Position Development Conference. J Bone Miner Res. 2007;22(5):643-645.

17. Kelepouris N, Harper KD, Gannon F, Kaplan FS, Haddad JG. Severe osteoporosis in men. Ann Intern Med. 1995;123(6):452-460.

References

1.    US Department of Health and Human Services. Bone Health and Osteoporosis: A Report of the Surgeon General. Rockville, MD: US Dept of Health and Human Services, Public Health Service, Office of the Surgeon General; 2004. http://www.ncbi.nlm.nih.gov/books/NBK45513/pdf/Bookshelf_NBK45513.pdf. Accessed November 3, 2015.

2.    Bone mass measurement (bone density). Medicare website. https://www.medicare.gov/coverage/bone-density.html. Accessed November 3, 2015.

3.    Final update summary: osteoporosis: screening. US Preventive Services Task Force website. http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/osteoporosis-screening. Updated July 2015. Accessed November 3, 2015.

4.    National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Washington, DC: National Osteoporosis Foundation; 2010. http://nof.org/files/nof/public/content/file/344/upload/159.pdf. Accessed November 3, 2015.

5.    Khan AA, Bachrach L, Brown JP, et al. Canadian Panel of International Society of Clinical Densitometry. Standards and guidelines for performing central dual-energy x-ray absorptiometry in premenopausal women, men, and children. J Clin Densitom. 2004;7(1):51-64.

6.    Barrett-Connor E, Sajjan SG, Siris ES, Miller PD, Chen YT, Markson LE. Wrist fracture as a predictor of future fractures in younger versus older postmenopausal women: results from the National Osteoporosis Risk Assessment (NORA). Osteoporos Int. 2008;19(5):607-613.

7.    Lauritzen JB, Schwarz P, Lund B, McNair P, Transbøl I. Changing incidence and residual lifetime risk of common osteoporosis-related fractures. Osteoporos Int. 1993;3(3):127-132.

8.    Earnshaw SA, Cawte SA, Worley A, Hosking DJ. Colles’ fracture of the wrist as an indicator of underlying osteoporosis in postmenopausal women: a prospective study of bone mineral density and bone turnover rate. Osteoporos Int. 1998;8(1):53-60.

9.    Oyen J, Brudvik C, Gjesdal CG, Tell GS, Lie SA, Hove LM. Osteoporosis as a risk factor for distal radius fractures: a case–control study. J Bone Joint Surg Am. 2011;93(4):348-356.

10. Wigderowitz CA, Cunningham T, Rowley DI, Mole PA, Paterson CR. Peripheral bone mineral density in patients with distal radial fractures. J Bone Joint Surg Br. 2003;85(3):423-425.

11. Wigderowitz CA, Rowley DI, Mole PA, Paterson CR, Abel EW. Bone mineral density of the radius in patients with Colles’ fracture. J Bone Joint Surg Br. 2000;82(1):87-89.

12. Khan A, Syed Z. Bone mineral density assessment in premenopausal women. Womens Health. 2006;2(4):639-645.

13. Fitzpatrick LA. Secondary causes of osteoporosis. Mayo Clin Proc. 2002;77(5):453-468.

14. Hudec SM, Camacho PM. Secondary causes of osteoporosis. Endocr Pract. 2013;19(1):120-128.

15. Scane AC, Sutcliffe AM, Francis RM. Osteoporosis in men. Baillieres Clin Rheumatol. 1993;7(3):589-601.

16. Binkley N, Bilezikian JP, Kendler DL, Leib ES, Lewiecki EM, Petak SM. Summary of the International Society for Clinical Densitometry 2005 Position Development Conference. J Bone Miner Res. 2007;22(5):643-645.

17. Kelepouris N, Harper KD, Gannon F, Kaplan FS, Haddad JG. Severe osteoporosis in men. Ann Intern Med. 1995;123(6):452-460.

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The American Journal of Orthopedics - 44(12)
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Prevalence of Low Bone Mineral Density in Younger Versus Older Women With Distal Radius Fractures
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Analysis of Predictors and Outcomes of Allogeneic Blood Transfusion After Shoulder Arthroplasty

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Analysis of Predictors and Outcomes of Allogeneic Blood Transfusion After Shoulder Arthroplasty

In shoulder arthroplasty, it is not uncommon for patients to receive postoperative blood transfusions; rates range from 7% to 43%.1-6 Allogeneic blood transfusions (ABTs) are costly and not entirely free of risks.7 The risk for infection has decreased because of improved screening and risk reduction strategies, but there are still significant risks associated with ABTs, such as clerical errors, acute and delayed hemolytic reactions, graft-versus-host reactions, transfusion-related acute lung injury, and anaphylaxis.8-10 As use of shoulder arthroplasty continues to increase, the importance of minimizing unnecessary transfusions is growing as well.7

Predictive factors for ABT have been explored in other orthopedic settings, yet little has been done in shoulder arthroplasty.1-6,11-15 Previous shoulder arthroplasty studies have shown that low preoperative hemoglobin (Hb) levels are independent risk factors for postoperative blood transfusion. However, there is debate over the significance of other variables, such as procedure type, age, sex, and medical comorbidities. Further, prior studies were limited by relatively small samples from single institutions; the largest series included fewer than 600 patients.1-6

We conducted a study to determine predictors of ABT in a large cohort of patients admitted to US hospitals for shoulder arthroplasty. We also wanted to evaluate the effect of ABT on postoperative outcomes, including inpatient mortality, adverse events, prolonged hospital stay, and nonroutine discharge. According to the null hypothesis, in shoulder arthroplasty there will be no difference in risk factors between patients who require ABT and those who did not, after accounting for confounding variables.

Materials and Methods

This study was exempt from institutional review board approval, as all data were appropriately deidentified before use in this project. We used the Nationwide Inpatient Sample (NIS) to retrospectively study the period 2002–2011, from which all demographic, clinical, and resource use data were derived.16 NIS, an annual survey conducted by the Agency for Healthcare Research and Quality (AHRQ) since 1988, has generated a huge amount of data, forming the largest all-payer inpatient care database in the United States. Yearly samples contain discharge data from about 8 million hospital stays at more than 1000 hospitals across 46 states, approximating a 20% random sample of all hospital discharges at participating institutions.17 These data are then weighted to generate statistically valid national estimates.

The NIS database uses International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM) codes to identify 15 medical diagnoses up to the year 2008 and a maximum of 25 medical diagnoses and 15 procedures thereafter. In addition, the database includes information on patient and hospital characteristics as well as inpatient outcomes such as length of stay, total hospitalization charges, and discharge disposition.18,19 Given its large sample size and data volume, NIS is a powerful tool in the analysis of data associated with a multitude of medical diagnoses and procedures.20

We used the NIS database to study a population of 422,371 patients (age, >18 years) who underwent total shoulder arthroplasty (TSA) or hemiarthroplasty (HSA) between 2002 and 2011. ICD-9-CM procedure codes for TSA (81.80, 81.88) and HSA (81.81) were used to identify this population. We also analyzed data for reverse TSA for the year 2011. Then we divided our target population into 2 different cohorts: patients who did not receive any blood transfusion products and patients who received a transfusion of allogeneic packed cells (ICD-9-CM code 99.04 was used to identify the latter cohort).

In this study, normal distribution of the dataset was assumed, given the large sample size. The 2 cohorts were evaluated through bivariate analysis using the Pearson χ2 test for categorical data and the independent-samples t test for continuous data. The extent to which diagnosis, age, race, sex, and medical comorbidities were predictive of blood transfusion after TSA or HSA was evaluated through multivariate binary logistic regression analysis. Statistical significance was set at P < .05. All statistical analyses and data modeling were performed with SPSS Version 22.0.

Results

Using the NIS database, we stratified an estimated 422,371 patients who presented for shoulder arthroplasty between January 1, 2002, and December 31, 2011, into a TSA cohort (59.3%) and an HSA cohort (40.7%). Eight percent (33,889) of all patients received an ABT; the proportion of patients who received ABT was higher (P < .001) for the HSA cohort (55.6%) than the TSA cohort (39.4%). Further, the rate of ABT after shoulder arthroplasty showed an upward inclination (Figure).

Demographically, patients who received ABT tended (P < .001) to be older (74±11 years vs 68±11 years) and of a minority race (black or Hispanic) and to fall in either the lowest range of median household income (21.5% vs 20.7%; ≤$38,999) or the highest (27.3% vs 25.4%; ≥$63,000). Shoulder arthroplasty with ABT occurred more often (P < .001) at hospitals that were urban (13.3% vs 11.3%), medium in size (27.3% vs 23.4%), and nonteaching (56.2% vs 54.3%). In addition, ABT was used more often (P < .001) in patients with a primary diagnosis of fracture (43.1% vs 14.3%) or fracture nonunion (4.4% vs 2.1%). These groups also had a longer (P < .001) hospital stay (5.0±4.3 days vs 2.5±2.2 days). Table 1 summarizes these findings.

 

 

The 2 cohorts were then analyzed for presence of medical comorbidities (Table 2). Patients who required ABT during shoulder arthroplasty had a significantly (P < .001) higher prevalence of congestive heart failure, chronic lung disease, hypertension, uncomplicated and complicated diabetes mellitus, liver disease, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, weight loss, coagulopathy, and deficiency anemia.

In multivariate regression modeling (Table 3), demographic predictors of ABT (P < .001) included increasing age (odds ratio [OR], 1.03 per year; 95% confidence interval [95% CI], 1.03-1.03), female sex (OR, 1.55; 95% CI, 1.51-1.60), and minority race (black or Hispanic). Odds of requiring ABT were higher for patients with Medicare (OR, 1.25; 95% CI, 1.20-1.30) and patients with Medicaid (OR, 1.63; 95% CI, 1.51-1.77) than for patients with private insurance.

ABT was more likely to be required (P < .001) in patients with a primary diagnosis of fracture (OR, 4.49; 95% CI, 4.34-4.65), avascular necrosis (OR, 2.06; 95% CI, 1.91-2.22), rheumatoid arthritis (OR, 1.91; 95% CI, 1.72-2.12), fracture nonunion (OR, 3.55; 95% CI, 3.33-3.79), or rotator cuff arthropathy (OR, 1.47; 95% CI, 1.41-1.54) than for patients with osteoarthritis. Moreover, compared with patients having HSA, patients having TSA were more likely to require ABT (OR, 1.20; 95% CI, 1.17-1.24). According to the analysis restricted to the year 2011, compared with patients having anatomical TSAs, patients having reverse TSAs were 1.6 times more likely (P < .001) to require ABT (OR, 1.63; 95% CI, 1.50-1.79).

With the exception of obesity, all comorbidities were significant (P < .001) independent predictors of ABT after shoulder arthroplasty: deficiency anemia (OR, 3.42; 95% CI, 3.32-3.52), coagulopathy (OR, 2.54; 95% CI, 2.36-2.73), fluid and electrolyte disorders (OR, 1.91; 95% CI, 1.84-1.97), and weight loss (OR, 1.78; 95% CI, 1.58-2.00).

Patients who received ABT were more likely to experience adverse events (OR, 1.74; 95% CI, 1.68-1.81), prolonged hospital stay (OR, 3.21; 95% CI, 3.12-3.30), and nonroutine discharge (OR, 1.77; 95% CI, 1.72-1.82) (Table 4). There was no difference in mortality between the 2 cohorts.

Discussion

There is an abundance of literature on blood transfusions in hip and knee arthroplasty, but there are few articles on ABT in shoulder arthroplasty, and they all report data from single institutions with relatively low caseloads.1,2,11-13,15,21 In the present study, we investigated ABT in shoulder arthroplasty from the perspective of a multi-institutional database with a caseload of more than 400,000. Given the rapidly increasing rates of shoulder arthroplasty, it is important to further examine this issue to minimize unnecessary blood transfusion and its associated risks and costs.7

We found that 8% of patients who had shoulder arthroplasty received ABT, which is consistent with previously reported transfusion rates (range, 7%-43%).1-6 Rates of ABT after shoulder arthroplasty have continued to rise. The exception, a decrease during the year 2010, can be explained by increased efforts to more rigidly follow transfusion indication guidelines to reduce the number of potentially unnecessary ABTs.21-24 Our study also identified numerous significant independent predictors of ABT in shoulder arthroplasty: age, sex, race, insurance status, procedure type, primary diagnoses, and multiple medical comorbidities.

Demographics

According to our analysis, more than 80% of patients who received ABT were over age 65 years, which aligns with what several other studies have demonstrated: Increasing age is a predictor of ABT, despite higher rates of comorbidities and lower preoperative Hb levels in this population.1,2,4,5,25-27 Consistent with previous work, female sex was predictive of ABT.2,5 It has been suggested that females are more likely predisposed to ABT because of lower preoperative Hb and smaller blood mass.2,5,28 Interestingly, our study showed a higher likelihood of ABT in both black and Hispanic populations. Further, patients with Medicare or Medicaid were more likely to receive ABT.

Primary Diagnosis

Although patients with a primary diagnosis of osteoarthritis constitute the majority of patients who undergo shoulder arthroplasty, our analysis showed that patients with a diagnosis of proximal humerus fracture were more likely to receive ABT. This finding is reasonable given studies showing the high prevalence of proximal humerus fractures in elderly women.29,30 Similarly, patients with a humerus fracture nonunion were more likely to receive a blood transfusion, which is unsurprising given the increased complexity associated with arthroplasty in this predominately elderly population.31 Interestingly, compared with patients with osteoarthritis, patients with any one of the other primary diagnoses were more likely to require a transfusion—proximal humerus fracture being the most significant, followed by humerus fracture nonunion, avascular necrosis, rheumatoid arthritis, and rotator cuff arthropathy.

 

 

Type of Arthroplasty

Bivariate analysis revealed that 55.6% of the patients who received ABT underwent HSA; the other 44.4% underwent TSA. The effect of primary diagnosis on procedure choice likely played a role in this finding. HSA indications include humerus fracture, which has been associated with increased ABT, whereas patients with osteoarthritis requiring TSA are significantly less likely to require ABT, as reflected in this analysis.7,32-34 Previous studies have failed to show a difference in blood transfusion rates between TSA and HSA.2,4-6,35 Conversely, with confounding factors controlled for, multivariate logistic regression analysis showed that TSA was 1.2 times more likely than HSA to require ABT, which could be explained by the increased operative time, case complexity, and blood loss that may be associated with the glenoid exposure.36,37 With analysis restricted to the year 2011, patients with reverse TSAs were 1.6 times more likely than patients with anatomical TSAs to receive a blood transfusion (OR, 1.63; 95% CI, 1.50-1.79). Although this finding differs from what was previously reported, it fits given that patients having reverse TSAs are often older and may present with a more significant comorbidity profile.3 In addition, there are the increased technical surgical aspects associated with “salvage surgery” for challenging indications such as cuff arthropathy and failed previous arthroplasty.38-41

Medical Comorbidities

Patients who received ABT were more likely to present with numerous medical comorbidities. Previous studies have indicated that the presence of multiple medical comorbidities significantly increased blood transfusion rates, possibly by working synergistically.42 All studies of blood transfusion in shoulder arthroplasty concluded that lower preoperative Hb was an independent predictor.1-6 Schumer and colleagues4 reported a 4-fold increase in likelihood of blood transfusion in patients with a preoperative Hb level less than 12.5 g/dL. In addition, Millett and colleagues6 showed a 20-fold increase in likelihood of transfusion in patients with a preoperative Hb level less than 11.0 g/dL compared with patients with a level higher than 13.0 g/dL. Patients with a Hb level between 11.0 and 13.0 g/dL showed a 5-fold increase in likelihood of transfusion.6 We should note that correction of preoperative anemia through various pharmacologic methods (eg, erythropoietin, intravenous iron supplementation) has been shown to decrease postoperative transfusion rates.43,44 Although we could not include preoperative Hb levels in the present study, given inherent limitations in using NIS, our multivariate analysis showed that preoperative deficiency anemia and coagulopathy were the most significant predictors of ABT.

In addition, the multivariate logistic regression model showed that both cardiac disease and diabetes were independent predictors of ABT, confirming data reported by Ahmadi and colleagues.1 Although not as well characterized in other studies, in the current analysis multiple other medical comorbidities, including fluid and electrolyte abnormalities, weight loss, liver disease, renal failure, and chronic lung disease, had significant predictive value. Contrarily, obesity significantly decreased the odds of ABT, likely because of higher baseline blood volume in obese patients.

Patient Outcomes

Patients who undergo shoulder arthroplasty with ABT are more likely to experience adverse events or a prolonged hospital stay and are more often discharged to a nursing home or an extended-care facility. In this population, however, deaths did not occur at a significantly higher rate—similar to what was found for patients who underwent hip or knee arthroplasty with blood transfusions.45

Little has been done to investigate the effect of pharmacologic agents on the need for perioperative ABT for orthopedic shoulder procedures. Aprotinin, tranexamic acid, epoetin-α, and aminocaproic acid have all been effective in limiting ABT during the perioperative period in various orthopedic hip, knee, and spine procedures.9,46-53 Given the increased morbidity associated with ABT, it may be beneficial to use similar methods to limit blood loss in high-risk patients undergoing shoulder arthroplasty.

Study Limitations

NIS has intrinsic limitations. Given its massive volume, it is subject to errors in both data entry and clinical coding. Moreover, the database lacks data that would have been useful in our study: preoperative Hb levels, intraoperative course, number of units transfused, total blood loss, use of blood conservation techniques, transfusion protocols, and severity of comorbidities. Reverse TSA was given a unique ICD-9-CM code in October 2010, so 2011 was the only year we were able to examine the relationship between reverse TSA and transfusions. Further, our analysis was unable to identify any medications, including chronic anticoagulants or postoperative prophylaxis, that have been shown to significantly affect blood transfusion rates.54 Yet, there are obvious advantages to using the NIS database, as previously outlined across the medical landscape.

 

 

Conclusion

Our results confirmed previous findings and identified new predictors of ABT in shoulder arthroplasty in a large cohort. We examined demographics and perioperative complications while identifying predictors of ABT use. Patients who received ABT were older, female, and nonwhite and were covered by Medicare or Medicaid insurance, and many had a primary diagnosis of proximal humerus fracture. The ABT cohort had numerous medical comorbidities, including deficiency anemia and coagulopathy. Identifying this patient population is a prerequisite to educating patients while minimizing unnecessary risks and costs.

Using NIS data on a population of 422,371 patients who underwent shoulder arthroplasty, we identified the 5 likeliest predictors of ABT: fracture, fracture nonunion, deficiency anemia, coagulopathy, and avascular necrosis. Of the identified variables associated with ABT, deficiency anemia may be the most amenable to treatment; therefore, there may be benefit in delaying elective shoulder arthroplasty in this cohort. Given these findings, it is important to identify at-risk patients before surgery, with the intent to provide education and minimize risk.

References

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2.    Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.

3.    Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.

4.    Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.

5.    Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.

6.    Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.

7.    Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.

8.    Ceccherini-Nelli L, Filipponi F, Mosca F, Campa M. The risk of contracting an infectious disease from blood transfusion. Transplantation Proc. 2004;36(3):680-682.

9.    Friedman R, Homering M, Holberg G, Berkowitz SD. Allogeneic blood transfusions and postoperative infections after total hip or knee arthroplasty. J Bone Joint Surg Am. 2014;96(4):272-278.

10. Hatzidakis AM, Mendlick RM, McKillip T, Reddy RL, Garvin KL. Preoperative autologous donation for total joint arthroplasty. An analysis of risk factors for allogenic transfusion. J Bone Joint Surg Am. 2000;82(1):89-100.

11. Park JH, Rasouli MR, Mortazavi SM, Tokarski AT, Maltenfort MG, Parvizi J. Predictors of perioperative blood loss in total joint arthroplasty. J Bone Joint Surg Am. 2013;95(19):1777-1783.

12. Aderinto J, Brenkel IJ. Pre-operative predictors of the requirement for blood transfusion following total hip replacement. J Bone Joint Surg Br. 2004;86(7):970-973.

13. Browne JA, Adib F, Brown TE, Novicoff WM. Transfusion rates are increasing following total hip arthroplasty: risk factors and outcomes. J Arthroplasty. 2013;28(8 suppl):34-37.

14. Yoshihara H, Yoneoka D. Predictors of allogeneic blood transfusion in spinal fusion in the United States, 2004–2009. Spine. 2014;39(4):304-310.

15. Noticewala MS, Nyce JD, Wang W, Geller JA, Macaulay W. Predicting need for allogeneic transfusion after total knee arthroplasty. J Arthroplasty. 2012;27(6):961-967.

16. Griffin JW, Novicoff WM, Browne JA, Brockmeier SF. Obstructive sleep apnea as a risk factor after shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(12):e6-e9.

17. Maynard C, Sales AE. Changes in the use of coronary artery revascularization procedures in the Department of Veterans Affairs, the National Hospital Discharge Survey, and the Nationwide Inpatient Sample, 1991–1999. BMC Health Serv Res. 2003;3(1):12.

18. Pereira BM, Chan PH, Weinstein PR, Fishman RA. Cerebral protection during reperfusion with superoxide dismutase in focal cerebral ischemia. Adv Neurol. 1990;52:97-103.

19. Hambright D, Henderson RA, Cook C, Worrell T, Moorman CT, Bolognesi MP. A comparison of perioperative outcomes in patients with and without rheumatoid arthritis after receiving a total shoulder replacement arthroplasty. J Shoulder Elbow Surg. 2011;20(1):77-85.

20. Ponce BA, Menendez ME, Oladeji LO, Soldado F. Diabetes as a risk factor for poorer early postoperative outcomes after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):671-678.

21. Pierson JL, Hannon TJ, Earles DR. A blood-conservation algorithm to reduce blood transfusions after total hip and knee arthroplasty. J Bone Joint Surg Am. 2004;86(7):1512-1518.

22. Martinez V, Monsaingeon-Lion A, Cherif K, Judet T, Chauvin M, Fletcher D. Transfusion strategy for primary knee and hip arthroplasty: impact of an algorithm to lower transfusion rates and hospital costs. Br J Anaesth. 2007;99(6):794-800.

23. Helm AT, Karski MT, Parsons SJ, Sampath JS, Bale RS. A strategy for reducing blood-transfusion requirements in elective orthopaedic surgery. Audit of an algorithm for arthroplasty of the lower limb. J Bone Joint Surg Br. 2003;85(4):484-489.

24. Watts CD, Pagnano MW. Minimising blood loss and transfusion in contemporary hip and knee arthroplasty. J Bone Joint Surg Br. 2012;94(11 suppl A):8-10.

25. Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104(8):2263-2268.

26. Rogers MA, Blumberg N, Heal JM, Langa KM. Utilization of blood transfusion among older adults in the United States. Transfusion. 2011;51(4):710-718.

27. Cobain TJ, Vamvakas EC, Wells A, Titlestad K. A survey of the demographics of blood use. Transfusion Med. 2007;17(1):1-15.

28. Fosco M, Di Fiore M. Factors predicting blood transfusion in different surgical procedures for degenerative spine disease. Eur Rev Med Pharmacol Sci. 2012;16(13):1853-1858.

29. Handoll HH, Ollivere BJ, Rollins KE. Interventions for treating proximal humeral fractures in adults. Cochrane Database Syst Rev. 2012;12:CD000434.

30. Neuhaus V, Swellengrebel CH, Bossen JK, Ring D. What are the factors influencing outcome among patients admitted to a hospital with a proximal humeral fracture? Clin Orthop Relat Res. 2013;471(5):1698-1706.

31. Volgas DA, Stannard JP, Alonso JE. Nonunions of the humerus. Clin Orthop Relat Res. 2004;(419):46-50.

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34.  Izquierdo R, Voloshin I, Edwards S, et al. Treatment of glenohumeral osteoarthritis. J Am Acad Orthop Surg. 2010;18(6):375-382.

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47. Chang CH, Chang Y, Chen DW, Ueng SW, Lee MS. Topical tranexamic acid reduces blood loss and transfusion rates associated with primary total hip arthroplasty. Clin Orthop Relat Res. 2014;472(5):1552-1557.

48. Delasotta LA, Orozco F, Jafari SM, Blair JL, Ong A. Should we use preoperative epoetin-alpha in the mildly anemic patient undergoing simultaneous total knee arthroplasty? Open Orthop J. 2013;7:47-50.

49. Delasotta LA, Rangavajjula A, Frank ML, Blair J, Orozco F, Ong A. The use of preoperative epoetin-alpha in revision hip arthroplasty. Open Orthop J. 2012;6:179-183.

50. Kelley TC, Tucker KK, Adams MJ, Dalury DF. Use of tranexamic acid results in decreased blood loss and decreased transfusions in patients undergoing staged bilateral total knee arthroplasty. Transfusion. 2014;54(1):26-30.

51. Martin JG, Cassatt KB, Kincaid-Cinnamon KA, Westendorf DS, Garton AS, Lemke JH. Topical administration of tranexamic acid in primary total hip and total knee arthroplasty. J Arthroplasty. 2014;29(5):889-894.

52. Tzortzopoulou A, Cepeda MS, Schumann R, Carr DB. Antifibrinolytic agents for reducing blood loss in scoliosis surgery in children. Cochrane Database Syst Rev. 2008(3):CD006883.

53. Zhang H, Chen J, Chen F, Que W. The effect of tranexamic acid on blood loss and use of blood products in total knee arthroplasty: a meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2012;20(9):1742-1752.

54. Bong MR, Patel V, Chang E, Issack PS, Hebert R, Di Cesare PE. Risks associated with blood transfusion after total knee arthroplasty. J Arthroplasty. 2004;19(3):281-287.

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Brent A. Ponce, MD, Jonathan C. Yu, MD, Mariano E. Menendez, MD, and Lasun O. Oladeji, MS

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The American Journal of Orthopedics - 44(12)
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american journal of orthopedics, AJO, original study, online exclusive, study, allogeneic, blood, transfusion, shoulder arthroplasty, shoulder, arthroplasty, total shoulder arthroplasty, TSA, ABT, ponce, yu, menendez, oladeji
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Brent A. Ponce, MD, Jonathan C. Yu, MD, Mariano E. Menendez, MD, and Lasun O. Oladeji, MS

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

Author and Disclosure Information

Brent A. Ponce, MD, Jonathan C. Yu, MD, Mariano E. Menendez, MD, and Lasun O. Oladeji, MS

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

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Article PDF

In shoulder arthroplasty, it is not uncommon for patients to receive postoperative blood transfusions; rates range from 7% to 43%.1-6 Allogeneic blood transfusions (ABTs) are costly and not entirely free of risks.7 The risk for infection has decreased because of improved screening and risk reduction strategies, but there are still significant risks associated with ABTs, such as clerical errors, acute and delayed hemolytic reactions, graft-versus-host reactions, transfusion-related acute lung injury, and anaphylaxis.8-10 As use of shoulder arthroplasty continues to increase, the importance of minimizing unnecessary transfusions is growing as well.7

Predictive factors for ABT have been explored in other orthopedic settings, yet little has been done in shoulder arthroplasty.1-6,11-15 Previous shoulder arthroplasty studies have shown that low preoperative hemoglobin (Hb) levels are independent risk factors for postoperative blood transfusion. However, there is debate over the significance of other variables, such as procedure type, age, sex, and medical comorbidities. Further, prior studies were limited by relatively small samples from single institutions; the largest series included fewer than 600 patients.1-6

We conducted a study to determine predictors of ABT in a large cohort of patients admitted to US hospitals for shoulder arthroplasty. We also wanted to evaluate the effect of ABT on postoperative outcomes, including inpatient mortality, adverse events, prolonged hospital stay, and nonroutine discharge. According to the null hypothesis, in shoulder arthroplasty there will be no difference in risk factors between patients who require ABT and those who did not, after accounting for confounding variables.

Materials and Methods

This study was exempt from institutional review board approval, as all data were appropriately deidentified before use in this project. We used the Nationwide Inpatient Sample (NIS) to retrospectively study the period 2002–2011, from which all demographic, clinical, and resource use data were derived.16 NIS, an annual survey conducted by the Agency for Healthcare Research and Quality (AHRQ) since 1988, has generated a huge amount of data, forming the largest all-payer inpatient care database in the United States. Yearly samples contain discharge data from about 8 million hospital stays at more than 1000 hospitals across 46 states, approximating a 20% random sample of all hospital discharges at participating institutions.17 These data are then weighted to generate statistically valid national estimates.

The NIS database uses International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM) codes to identify 15 medical diagnoses up to the year 2008 and a maximum of 25 medical diagnoses and 15 procedures thereafter. In addition, the database includes information on patient and hospital characteristics as well as inpatient outcomes such as length of stay, total hospitalization charges, and discharge disposition.18,19 Given its large sample size and data volume, NIS is a powerful tool in the analysis of data associated with a multitude of medical diagnoses and procedures.20

We used the NIS database to study a population of 422,371 patients (age, >18 years) who underwent total shoulder arthroplasty (TSA) or hemiarthroplasty (HSA) between 2002 and 2011. ICD-9-CM procedure codes for TSA (81.80, 81.88) and HSA (81.81) were used to identify this population. We also analyzed data for reverse TSA for the year 2011. Then we divided our target population into 2 different cohorts: patients who did not receive any blood transfusion products and patients who received a transfusion of allogeneic packed cells (ICD-9-CM code 99.04 was used to identify the latter cohort).

In this study, normal distribution of the dataset was assumed, given the large sample size. The 2 cohorts were evaluated through bivariate analysis using the Pearson χ2 test for categorical data and the independent-samples t test for continuous data. The extent to which diagnosis, age, race, sex, and medical comorbidities were predictive of blood transfusion after TSA or HSA was evaluated through multivariate binary logistic regression analysis. Statistical significance was set at P < .05. All statistical analyses and data modeling were performed with SPSS Version 22.0.

Results

Using the NIS database, we stratified an estimated 422,371 patients who presented for shoulder arthroplasty between January 1, 2002, and December 31, 2011, into a TSA cohort (59.3%) and an HSA cohort (40.7%). Eight percent (33,889) of all patients received an ABT; the proportion of patients who received ABT was higher (P < .001) for the HSA cohort (55.6%) than the TSA cohort (39.4%). Further, the rate of ABT after shoulder arthroplasty showed an upward inclination (Figure).

Demographically, patients who received ABT tended (P < .001) to be older (74±11 years vs 68±11 years) and of a minority race (black or Hispanic) and to fall in either the lowest range of median household income (21.5% vs 20.7%; ≤$38,999) or the highest (27.3% vs 25.4%; ≥$63,000). Shoulder arthroplasty with ABT occurred more often (P < .001) at hospitals that were urban (13.3% vs 11.3%), medium in size (27.3% vs 23.4%), and nonteaching (56.2% vs 54.3%). In addition, ABT was used more often (P < .001) in patients with a primary diagnosis of fracture (43.1% vs 14.3%) or fracture nonunion (4.4% vs 2.1%). These groups also had a longer (P < .001) hospital stay (5.0±4.3 days vs 2.5±2.2 days). Table 1 summarizes these findings.

 

 

The 2 cohorts were then analyzed for presence of medical comorbidities (Table 2). Patients who required ABT during shoulder arthroplasty had a significantly (P < .001) higher prevalence of congestive heart failure, chronic lung disease, hypertension, uncomplicated and complicated diabetes mellitus, liver disease, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, weight loss, coagulopathy, and deficiency anemia.

In multivariate regression modeling (Table 3), demographic predictors of ABT (P < .001) included increasing age (odds ratio [OR], 1.03 per year; 95% confidence interval [95% CI], 1.03-1.03), female sex (OR, 1.55; 95% CI, 1.51-1.60), and minority race (black or Hispanic). Odds of requiring ABT were higher for patients with Medicare (OR, 1.25; 95% CI, 1.20-1.30) and patients with Medicaid (OR, 1.63; 95% CI, 1.51-1.77) than for patients with private insurance.

ABT was more likely to be required (P < .001) in patients with a primary diagnosis of fracture (OR, 4.49; 95% CI, 4.34-4.65), avascular necrosis (OR, 2.06; 95% CI, 1.91-2.22), rheumatoid arthritis (OR, 1.91; 95% CI, 1.72-2.12), fracture nonunion (OR, 3.55; 95% CI, 3.33-3.79), or rotator cuff arthropathy (OR, 1.47; 95% CI, 1.41-1.54) than for patients with osteoarthritis. Moreover, compared with patients having HSA, patients having TSA were more likely to require ABT (OR, 1.20; 95% CI, 1.17-1.24). According to the analysis restricted to the year 2011, compared with patients having anatomical TSAs, patients having reverse TSAs were 1.6 times more likely (P < .001) to require ABT (OR, 1.63; 95% CI, 1.50-1.79).

With the exception of obesity, all comorbidities were significant (P < .001) independent predictors of ABT after shoulder arthroplasty: deficiency anemia (OR, 3.42; 95% CI, 3.32-3.52), coagulopathy (OR, 2.54; 95% CI, 2.36-2.73), fluid and electrolyte disorders (OR, 1.91; 95% CI, 1.84-1.97), and weight loss (OR, 1.78; 95% CI, 1.58-2.00).

Patients who received ABT were more likely to experience adverse events (OR, 1.74; 95% CI, 1.68-1.81), prolonged hospital stay (OR, 3.21; 95% CI, 3.12-3.30), and nonroutine discharge (OR, 1.77; 95% CI, 1.72-1.82) (Table 4). There was no difference in mortality between the 2 cohorts.

Discussion

There is an abundance of literature on blood transfusions in hip and knee arthroplasty, but there are few articles on ABT in shoulder arthroplasty, and they all report data from single institutions with relatively low caseloads.1,2,11-13,15,21 In the present study, we investigated ABT in shoulder arthroplasty from the perspective of a multi-institutional database with a caseload of more than 400,000. Given the rapidly increasing rates of shoulder arthroplasty, it is important to further examine this issue to minimize unnecessary blood transfusion and its associated risks and costs.7

We found that 8% of patients who had shoulder arthroplasty received ABT, which is consistent with previously reported transfusion rates (range, 7%-43%).1-6 Rates of ABT after shoulder arthroplasty have continued to rise. The exception, a decrease during the year 2010, can be explained by increased efforts to more rigidly follow transfusion indication guidelines to reduce the number of potentially unnecessary ABTs.21-24 Our study also identified numerous significant independent predictors of ABT in shoulder arthroplasty: age, sex, race, insurance status, procedure type, primary diagnoses, and multiple medical comorbidities.

Demographics

According to our analysis, more than 80% of patients who received ABT were over age 65 years, which aligns with what several other studies have demonstrated: Increasing age is a predictor of ABT, despite higher rates of comorbidities and lower preoperative Hb levels in this population.1,2,4,5,25-27 Consistent with previous work, female sex was predictive of ABT.2,5 It has been suggested that females are more likely predisposed to ABT because of lower preoperative Hb and smaller blood mass.2,5,28 Interestingly, our study showed a higher likelihood of ABT in both black and Hispanic populations. Further, patients with Medicare or Medicaid were more likely to receive ABT.

Primary Diagnosis

Although patients with a primary diagnosis of osteoarthritis constitute the majority of patients who undergo shoulder arthroplasty, our analysis showed that patients with a diagnosis of proximal humerus fracture were more likely to receive ABT. This finding is reasonable given studies showing the high prevalence of proximal humerus fractures in elderly women.29,30 Similarly, patients with a humerus fracture nonunion were more likely to receive a blood transfusion, which is unsurprising given the increased complexity associated with arthroplasty in this predominately elderly population.31 Interestingly, compared with patients with osteoarthritis, patients with any one of the other primary diagnoses were more likely to require a transfusion—proximal humerus fracture being the most significant, followed by humerus fracture nonunion, avascular necrosis, rheumatoid arthritis, and rotator cuff arthropathy.

 

 

Type of Arthroplasty

Bivariate analysis revealed that 55.6% of the patients who received ABT underwent HSA; the other 44.4% underwent TSA. The effect of primary diagnosis on procedure choice likely played a role in this finding. HSA indications include humerus fracture, which has been associated with increased ABT, whereas patients with osteoarthritis requiring TSA are significantly less likely to require ABT, as reflected in this analysis.7,32-34 Previous studies have failed to show a difference in blood transfusion rates between TSA and HSA.2,4-6,35 Conversely, with confounding factors controlled for, multivariate logistic regression analysis showed that TSA was 1.2 times more likely than HSA to require ABT, which could be explained by the increased operative time, case complexity, and blood loss that may be associated with the glenoid exposure.36,37 With analysis restricted to the year 2011, patients with reverse TSAs were 1.6 times more likely than patients with anatomical TSAs to receive a blood transfusion (OR, 1.63; 95% CI, 1.50-1.79). Although this finding differs from what was previously reported, it fits given that patients having reverse TSAs are often older and may present with a more significant comorbidity profile.3 In addition, there are the increased technical surgical aspects associated with “salvage surgery” for challenging indications such as cuff arthropathy and failed previous arthroplasty.38-41

Medical Comorbidities

Patients who received ABT were more likely to present with numerous medical comorbidities. Previous studies have indicated that the presence of multiple medical comorbidities significantly increased blood transfusion rates, possibly by working synergistically.42 All studies of blood transfusion in shoulder arthroplasty concluded that lower preoperative Hb was an independent predictor.1-6 Schumer and colleagues4 reported a 4-fold increase in likelihood of blood transfusion in patients with a preoperative Hb level less than 12.5 g/dL. In addition, Millett and colleagues6 showed a 20-fold increase in likelihood of transfusion in patients with a preoperative Hb level less than 11.0 g/dL compared with patients with a level higher than 13.0 g/dL. Patients with a Hb level between 11.0 and 13.0 g/dL showed a 5-fold increase in likelihood of transfusion.6 We should note that correction of preoperative anemia through various pharmacologic methods (eg, erythropoietin, intravenous iron supplementation) has been shown to decrease postoperative transfusion rates.43,44 Although we could not include preoperative Hb levels in the present study, given inherent limitations in using NIS, our multivariate analysis showed that preoperative deficiency anemia and coagulopathy were the most significant predictors of ABT.

In addition, the multivariate logistic regression model showed that both cardiac disease and diabetes were independent predictors of ABT, confirming data reported by Ahmadi and colleagues.1 Although not as well characterized in other studies, in the current analysis multiple other medical comorbidities, including fluid and electrolyte abnormalities, weight loss, liver disease, renal failure, and chronic lung disease, had significant predictive value. Contrarily, obesity significantly decreased the odds of ABT, likely because of higher baseline blood volume in obese patients.

Patient Outcomes

Patients who undergo shoulder arthroplasty with ABT are more likely to experience adverse events or a prolonged hospital stay and are more often discharged to a nursing home or an extended-care facility. In this population, however, deaths did not occur at a significantly higher rate—similar to what was found for patients who underwent hip or knee arthroplasty with blood transfusions.45

Little has been done to investigate the effect of pharmacologic agents on the need for perioperative ABT for orthopedic shoulder procedures. Aprotinin, tranexamic acid, epoetin-α, and aminocaproic acid have all been effective in limiting ABT during the perioperative period in various orthopedic hip, knee, and spine procedures.9,46-53 Given the increased morbidity associated with ABT, it may be beneficial to use similar methods to limit blood loss in high-risk patients undergoing shoulder arthroplasty.

Study Limitations

NIS has intrinsic limitations. Given its massive volume, it is subject to errors in both data entry and clinical coding. Moreover, the database lacks data that would have been useful in our study: preoperative Hb levels, intraoperative course, number of units transfused, total blood loss, use of blood conservation techniques, transfusion protocols, and severity of comorbidities. Reverse TSA was given a unique ICD-9-CM code in October 2010, so 2011 was the only year we were able to examine the relationship between reverse TSA and transfusions. Further, our analysis was unable to identify any medications, including chronic anticoagulants or postoperative prophylaxis, that have been shown to significantly affect blood transfusion rates.54 Yet, there are obvious advantages to using the NIS database, as previously outlined across the medical landscape.

 

 

Conclusion

Our results confirmed previous findings and identified new predictors of ABT in shoulder arthroplasty in a large cohort. We examined demographics and perioperative complications while identifying predictors of ABT use. Patients who received ABT were older, female, and nonwhite and were covered by Medicare or Medicaid insurance, and many had a primary diagnosis of proximal humerus fracture. The ABT cohort had numerous medical comorbidities, including deficiency anemia and coagulopathy. Identifying this patient population is a prerequisite to educating patients while minimizing unnecessary risks and costs.

Using NIS data on a population of 422,371 patients who underwent shoulder arthroplasty, we identified the 5 likeliest predictors of ABT: fracture, fracture nonunion, deficiency anemia, coagulopathy, and avascular necrosis. Of the identified variables associated with ABT, deficiency anemia may be the most amenable to treatment; therefore, there may be benefit in delaying elective shoulder arthroplasty in this cohort. Given these findings, it is important to identify at-risk patients before surgery, with the intent to provide education and minimize risk.

In shoulder arthroplasty, it is not uncommon for patients to receive postoperative blood transfusions; rates range from 7% to 43%.1-6 Allogeneic blood transfusions (ABTs) are costly and not entirely free of risks.7 The risk for infection has decreased because of improved screening and risk reduction strategies, but there are still significant risks associated with ABTs, such as clerical errors, acute and delayed hemolytic reactions, graft-versus-host reactions, transfusion-related acute lung injury, and anaphylaxis.8-10 As use of shoulder arthroplasty continues to increase, the importance of minimizing unnecessary transfusions is growing as well.7

Predictive factors for ABT have been explored in other orthopedic settings, yet little has been done in shoulder arthroplasty.1-6,11-15 Previous shoulder arthroplasty studies have shown that low preoperative hemoglobin (Hb) levels are independent risk factors for postoperative blood transfusion. However, there is debate over the significance of other variables, such as procedure type, age, sex, and medical comorbidities. Further, prior studies were limited by relatively small samples from single institutions; the largest series included fewer than 600 patients.1-6

We conducted a study to determine predictors of ABT in a large cohort of patients admitted to US hospitals for shoulder arthroplasty. We also wanted to evaluate the effect of ABT on postoperative outcomes, including inpatient mortality, adverse events, prolonged hospital stay, and nonroutine discharge. According to the null hypothesis, in shoulder arthroplasty there will be no difference in risk factors between patients who require ABT and those who did not, after accounting for confounding variables.

Materials and Methods

This study was exempt from institutional review board approval, as all data were appropriately deidentified before use in this project. We used the Nationwide Inpatient Sample (NIS) to retrospectively study the period 2002–2011, from which all demographic, clinical, and resource use data were derived.16 NIS, an annual survey conducted by the Agency for Healthcare Research and Quality (AHRQ) since 1988, has generated a huge amount of data, forming the largest all-payer inpatient care database in the United States. Yearly samples contain discharge data from about 8 million hospital stays at more than 1000 hospitals across 46 states, approximating a 20% random sample of all hospital discharges at participating institutions.17 These data are then weighted to generate statistically valid national estimates.

The NIS database uses International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM) codes to identify 15 medical diagnoses up to the year 2008 and a maximum of 25 medical diagnoses and 15 procedures thereafter. In addition, the database includes information on patient and hospital characteristics as well as inpatient outcomes such as length of stay, total hospitalization charges, and discharge disposition.18,19 Given its large sample size and data volume, NIS is a powerful tool in the analysis of data associated with a multitude of medical diagnoses and procedures.20

We used the NIS database to study a population of 422,371 patients (age, >18 years) who underwent total shoulder arthroplasty (TSA) or hemiarthroplasty (HSA) between 2002 and 2011. ICD-9-CM procedure codes for TSA (81.80, 81.88) and HSA (81.81) were used to identify this population. We also analyzed data for reverse TSA for the year 2011. Then we divided our target population into 2 different cohorts: patients who did not receive any blood transfusion products and patients who received a transfusion of allogeneic packed cells (ICD-9-CM code 99.04 was used to identify the latter cohort).

In this study, normal distribution of the dataset was assumed, given the large sample size. The 2 cohorts were evaluated through bivariate analysis using the Pearson χ2 test for categorical data and the independent-samples t test for continuous data. The extent to which diagnosis, age, race, sex, and medical comorbidities were predictive of blood transfusion after TSA or HSA was evaluated through multivariate binary logistic regression analysis. Statistical significance was set at P < .05. All statistical analyses and data modeling were performed with SPSS Version 22.0.

Results

Using the NIS database, we stratified an estimated 422,371 patients who presented for shoulder arthroplasty between January 1, 2002, and December 31, 2011, into a TSA cohort (59.3%) and an HSA cohort (40.7%). Eight percent (33,889) of all patients received an ABT; the proportion of patients who received ABT was higher (P < .001) for the HSA cohort (55.6%) than the TSA cohort (39.4%). Further, the rate of ABT after shoulder arthroplasty showed an upward inclination (Figure).

Demographically, patients who received ABT tended (P < .001) to be older (74±11 years vs 68±11 years) and of a minority race (black or Hispanic) and to fall in either the lowest range of median household income (21.5% vs 20.7%; ≤$38,999) or the highest (27.3% vs 25.4%; ≥$63,000). Shoulder arthroplasty with ABT occurred more often (P < .001) at hospitals that were urban (13.3% vs 11.3%), medium in size (27.3% vs 23.4%), and nonteaching (56.2% vs 54.3%). In addition, ABT was used more often (P < .001) in patients with a primary diagnosis of fracture (43.1% vs 14.3%) or fracture nonunion (4.4% vs 2.1%). These groups also had a longer (P < .001) hospital stay (5.0±4.3 days vs 2.5±2.2 days). Table 1 summarizes these findings.

 

 

The 2 cohorts were then analyzed for presence of medical comorbidities (Table 2). Patients who required ABT during shoulder arthroplasty had a significantly (P < .001) higher prevalence of congestive heart failure, chronic lung disease, hypertension, uncomplicated and complicated diabetes mellitus, liver disease, renal failure, fluid and electrolyte disorders, pulmonary circulatory disease, weight loss, coagulopathy, and deficiency anemia.

In multivariate regression modeling (Table 3), demographic predictors of ABT (P < .001) included increasing age (odds ratio [OR], 1.03 per year; 95% confidence interval [95% CI], 1.03-1.03), female sex (OR, 1.55; 95% CI, 1.51-1.60), and minority race (black or Hispanic). Odds of requiring ABT were higher for patients with Medicare (OR, 1.25; 95% CI, 1.20-1.30) and patients with Medicaid (OR, 1.63; 95% CI, 1.51-1.77) than for patients with private insurance.

ABT was more likely to be required (P < .001) in patients with a primary diagnosis of fracture (OR, 4.49; 95% CI, 4.34-4.65), avascular necrosis (OR, 2.06; 95% CI, 1.91-2.22), rheumatoid arthritis (OR, 1.91; 95% CI, 1.72-2.12), fracture nonunion (OR, 3.55; 95% CI, 3.33-3.79), or rotator cuff arthropathy (OR, 1.47; 95% CI, 1.41-1.54) than for patients with osteoarthritis. Moreover, compared with patients having HSA, patients having TSA were more likely to require ABT (OR, 1.20; 95% CI, 1.17-1.24). According to the analysis restricted to the year 2011, compared with patients having anatomical TSAs, patients having reverse TSAs were 1.6 times more likely (P < .001) to require ABT (OR, 1.63; 95% CI, 1.50-1.79).

With the exception of obesity, all comorbidities were significant (P < .001) independent predictors of ABT after shoulder arthroplasty: deficiency anemia (OR, 3.42; 95% CI, 3.32-3.52), coagulopathy (OR, 2.54; 95% CI, 2.36-2.73), fluid and electrolyte disorders (OR, 1.91; 95% CI, 1.84-1.97), and weight loss (OR, 1.78; 95% CI, 1.58-2.00).

Patients who received ABT were more likely to experience adverse events (OR, 1.74; 95% CI, 1.68-1.81), prolonged hospital stay (OR, 3.21; 95% CI, 3.12-3.30), and nonroutine discharge (OR, 1.77; 95% CI, 1.72-1.82) (Table 4). There was no difference in mortality between the 2 cohorts.

Discussion

There is an abundance of literature on blood transfusions in hip and knee arthroplasty, but there are few articles on ABT in shoulder arthroplasty, and they all report data from single institutions with relatively low caseloads.1,2,11-13,15,21 In the present study, we investigated ABT in shoulder arthroplasty from the perspective of a multi-institutional database with a caseload of more than 400,000. Given the rapidly increasing rates of shoulder arthroplasty, it is important to further examine this issue to minimize unnecessary blood transfusion and its associated risks and costs.7

We found that 8% of patients who had shoulder arthroplasty received ABT, which is consistent with previously reported transfusion rates (range, 7%-43%).1-6 Rates of ABT after shoulder arthroplasty have continued to rise. The exception, a decrease during the year 2010, can be explained by increased efforts to more rigidly follow transfusion indication guidelines to reduce the number of potentially unnecessary ABTs.21-24 Our study also identified numerous significant independent predictors of ABT in shoulder arthroplasty: age, sex, race, insurance status, procedure type, primary diagnoses, and multiple medical comorbidities.

Demographics

According to our analysis, more than 80% of patients who received ABT were over age 65 years, which aligns with what several other studies have demonstrated: Increasing age is a predictor of ABT, despite higher rates of comorbidities and lower preoperative Hb levels in this population.1,2,4,5,25-27 Consistent with previous work, female sex was predictive of ABT.2,5 It has been suggested that females are more likely predisposed to ABT because of lower preoperative Hb and smaller blood mass.2,5,28 Interestingly, our study showed a higher likelihood of ABT in both black and Hispanic populations. Further, patients with Medicare or Medicaid were more likely to receive ABT.

Primary Diagnosis

Although patients with a primary diagnosis of osteoarthritis constitute the majority of patients who undergo shoulder arthroplasty, our analysis showed that patients with a diagnosis of proximal humerus fracture were more likely to receive ABT. This finding is reasonable given studies showing the high prevalence of proximal humerus fractures in elderly women.29,30 Similarly, patients with a humerus fracture nonunion were more likely to receive a blood transfusion, which is unsurprising given the increased complexity associated with arthroplasty in this predominately elderly population.31 Interestingly, compared with patients with osteoarthritis, patients with any one of the other primary diagnoses were more likely to require a transfusion—proximal humerus fracture being the most significant, followed by humerus fracture nonunion, avascular necrosis, rheumatoid arthritis, and rotator cuff arthropathy.

 

 

Type of Arthroplasty

Bivariate analysis revealed that 55.6% of the patients who received ABT underwent HSA; the other 44.4% underwent TSA. The effect of primary diagnosis on procedure choice likely played a role in this finding. HSA indications include humerus fracture, which has been associated with increased ABT, whereas patients with osteoarthritis requiring TSA are significantly less likely to require ABT, as reflected in this analysis.7,32-34 Previous studies have failed to show a difference in blood transfusion rates between TSA and HSA.2,4-6,35 Conversely, with confounding factors controlled for, multivariate logistic regression analysis showed that TSA was 1.2 times more likely than HSA to require ABT, which could be explained by the increased operative time, case complexity, and blood loss that may be associated with the glenoid exposure.36,37 With analysis restricted to the year 2011, patients with reverse TSAs were 1.6 times more likely than patients with anatomical TSAs to receive a blood transfusion (OR, 1.63; 95% CI, 1.50-1.79). Although this finding differs from what was previously reported, it fits given that patients having reverse TSAs are often older and may present with a more significant comorbidity profile.3 In addition, there are the increased technical surgical aspects associated with “salvage surgery” for challenging indications such as cuff arthropathy and failed previous arthroplasty.38-41

Medical Comorbidities

Patients who received ABT were more likely to present with numerous medical comorbidities. Previous studies have indicated that the presence of multiple medical comorbidities significantly increased blood transfusion rates, possibly by working synergistically.42 All studies of blood transfusion in shoulder arthroplasty concluded that lower preoperative Hb was an independent predictor.1-6 Schumer and colleagues4 reported a 4-fold increase in likelihood of blood transfusion in patients with a preoperative Hb level less than 12.5 g/dL. In addition, Millett and colleagues6 showed a 20-fold increase in likelihood of transfusion in patients with a preoperative Hb level less than 11.0 g/dL compared with patients with a level higher than 13.0 g/dL. Patients with a Hb level between 11.0 and 13.0 g/dL showed a 5-fold increase in likelihood of transfusion.6 We should note that correction of preoperative anemia through various pharmacologic methods (eg, erythropoietin, intravenous iron supplementation) has been shown to decrease postoperative transfusion rates.43,44 Although we could not include preoperative Hb levels in the present study, given inherent limitations in using NIS, our multivariate analysis showed that preoperative deficiency anemia and coagulopathy were the most significant predictors of ABT.

In addition, the multivariate logistic regression model showed that both cardiac disease and diabetes were independent predictors of ABT, confirming data reported by Ahmadi and colleagues.1 Although not as well characterized in other studies, in the current analysis multiple other medical comorbidities, including fluid and electrolyte abnormalities, weight loss, liver disease, renal failure, and chronic lung disease, had significant predictive value. Contrarily, obesity significantly decreased the odds of ABT, likely because of higher baseline blood volume in obese patients.

Patient Outcomes

Patients who undergo shoulder arthroplasty with ABT are more likely to experience adverse events or a prolonged hospital stay and are more often discharged to a nursing home or an extended-care facility. In this population, however, deaths did not occur at a significantly higher rate—similar to what was found for patients who underwent hip or knee arthroplasty with blood transfusions.45

Little has been done to investigate the effect of pharmacologic agents on the need for perioperative ABT for orthopedic shoulder procedures. Aprotinin, tranexamic acid, epoetin-α, and aminocaproic acid have all been effective in limiting ABT during the perioperative period in various orthopedic hip, knee, and spine procedures.9,46-53 Given the increased morbidity associated with ABT, it may be beneficial to use similar methods to limit blood loss in high-risk patients undergoing shoulder arthroplasty.

Study Limitations

NIS has intrinsic limitations. Given its massive volume, it is subject to errors in both data entry and clinical coding. Moreover, the database lacks data that would have been useful in our study: preoperative Hb levels, intraoperative course, number of units transfused, total blood loss, use of blood conservation techniques, transfusion protocols, and severity of comorbidities. Reverse TSA was given a unique ICD-9-CM code in October 2010, so 2011 was the only year we were able to examine the relationship between reverse TSA and transfusions. Further, our analysis was unable to identify any medications, including chronic anticoagulants or postoperative prophylaxis, that have been shown to significantly affect blood transfusion rates.54 Yet, there are obvious advantages to using the NIS database, as previously outlined across the medical landscape.

 

 

Conclusion

Our results confirmed previous findings and identified new predictors of ABT in shoulder arthroplasty in a large cohort. We examined demographics and perioperative complications while identifying predictors of ABT use. Patients who received ABT were older, female, and nonwhite and were covered by Medicare or Medicaid insurance, and many had a primary diagnosis of proximal humerus fracture. The ABT cohort had numerous medical comorbidities, including deficiency anemia and coagulopathy. Identifying this patient population is a prerequisite to educating patients while minimizing unnecessary risks and costs.

Using NIS data on a population of 422,371 patients who underwent shoulder arthroplasty, we identified the 5 likeliest predictors of ABT: fracture, fracture nonunion, deficiency anemia, coagulopathy, and avascular necrosis. Of the identified variables associated with ABT, deficiency anemia may be the most amenable to treatment; therefore, there may be benefit in delaying elective shoulder arthroplasty in this cohort. Given these findings, it is important to identify at-risk patients before surgery, with the intent to provide education and minimize risk.

References

1.    Ahmadi S, Lawrence TM, Sahota S, et al. The incidence and risk factors for blood transfusion in revision shoulder arthroplasty: our institution’s experience and review of the literature. J Shoulder Elbow Surg. 2014;23(1):43-48.

2.    Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.

3.    Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.

4.    Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.

5.    Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.

6.    Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.

7.    Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.

8.    Ceccherini-Nelli L, Filipponi F, Mosca F, Campa M. The risk of contracting an infectious disease from blood transfusion. Transplantation Proc. 2004;36(3):680-682.

9.    Friedman R, Homering M, Holberg G, Berkowitz SD. Allogeneic blood transfusions and postoperative infections after total hip or knee arthroplasty. J Bone Joint Surg Am. 2014;96(4):272-278.

10. Hatzidakis AM, Mendlick RM, McKillip T, Reddy RL, Garvin KL. Preoperative autologous donation for total joint arthroplasty. An analysis of risk factors for allogenic transfusion. J Bone Joint Surg Am. 2000;82(1):89-100.

11. Park JH, Rasouli MR, Mortazavi SM, Tokarski AT, Maltenfort MG, Parvizi J. Predictors of perioperative blood loss in total joint arthroplasty. J Bone Joint Surg Am. 2013;95(19):1777-1783.

12. Aderinto J, Brenkel IJ. Pre-operative predictors of the requirement for blood transfusion following total hip replacement. J Bone Joint Surg Br. 2004;86(7):970-973.

13. Browne JA, Adib F, Brown TE, Novicoff WM. Transfusion rates are increasing following total hip arthroplasty: risk factors and outcomes. J Arthroplasty. 2013;28(8 suppl):34-37.

14. Yoshihara H, Yoneoka D. Predictors of allogeneic blood transfusion in spinal fusion in the United States, 2004–2009. Spine. 2014;39(4):304-310.

15. Noticewala MS, Nyce JD, Wang W, Geller JA, Macaulay W. Predicting need for allogeneic transfusion after total knee arthroplasty. J Arthroplasty. 2012;27(6):961-967.

16. Griffin JW, Novicoff WM, Browne JA, Brockmeier SF. Obstructive sleep apnea as a risk factor after shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(12):e6-e9.

17. Maynard C, Sales AE. Changes in the use of coronary artery revascularization procedures in the Department of Veterans Affairs, the National Hospital Discharge Survey, and the Nationwide Inpatient Sample, 1991–1999. BMC Health Serv Res. 2003;3(1):12.

18. Pereira BM, Chan PH, Weinstein PR, Fishman RA. Cerebral protection during reperfusion with superoxide dismutase in focal cerebral ischemia. Adv Neurol. 1990;52:97-103.

19. Hambright D, Henderson RA, Cook C, Worrell T, Moorman CT, Bolognesi MP. A comparison of perioperative outcomes in patients with and without rheumatoid arthritis after receiving a total shoulder replacement arthroplasty. J Shoulder Elbow Surg. 2011;20(1):77-85.

20. Ponce BA, Menendez ME, Oladeji LO, Soldado F. Diabetes as a risk factor for poorer early postoperative outcomes after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):671-678.

21. Pierson JL, Hannon TJ, Earles DR. A blood-conservation algorithm to reduce blood transfusions after total hip and knee arthroplasty. J Bone Joint Surg Am. 2004;86(7):1512-1518.

22. Martinez V, Monsaingeon-Lion A, Cherif K, Judet T, Chauvin M, Fletcher D. Transfusion strategy for primary knee and hip arthroplasty: impact of an algorithm to lower transfusion rates and hospital costs. Br J Anaesth. 2007;99(6):794-800.

23. Helm AT, Karski MT, Parsons SJ, Sampath JS, Bale RS. A strategy for reducing blood-transfusion requirements in elective orthopaedic surgery. Audit of an algorithm for arthroplasty of the lower limb. J Bone Joint Surg Br. 2003;85(4):484-489.

24. Watts CD, Pagnano MW. Minimising blood loss and transfusion in contemporary hip and knee arthroplasty. J Bone Joint Surg Br. 2012;94(11 suppl A):8-10.

25. Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104(8):2263-2268.

26. Rogers MA, Blumberg N, Heal JM, Langa KM. Utilization of blood transfusion among older adults in the United States. Transfusion. 2011;51(4):710-718.

27. Cobain TJ, Vamvakas EC, Wells A, Titlestad K. A survey of the demographics of blood use. Transfusion Med. 2007;17(1):1-15.

28. Fosco M, Di Fiore M. Factors predicting blood transfusion in different surgical procedures for degenerative spine disease. Eur Rev Med Pharmacol Sci. 2012;16(13):1853-1858.

29. Handoll HH, Ollivere BJ, Rollins KE. Interventions for treating proximal humeral fractures in adults. Cochrane Database Syst Rev. 2012;12:CD000434.

30. Neuhaus V, Swellengrebel CH, Bossen JK, Ring D. What are the factors influencing outcome among patients admitted to a hospital with a proximal humeral fracture? Clin Orthop Relat Res. 2013;471(5):1698-1706.

31. Volgas DA, Stannard JP, Alonso JE. Nonunions of the humerus. Clin Orthop Relat Res. 2004;(419):46-50.

32. Chambers L, Dines JS, Lorich DG, Dines DM. Hemiarthroplasty for proximal humerus fractures. Curr Rev Musculoskeletal Med. 2013;6(1):57-62.

33. Jain NB, Hocker S, Pietrobon R, Guller U, Bathia N, Higgins LD. Total arthroplasty versus hemiarthroplasty for glenohumeral osteoarthritis: role of provider volume. J Shoulder Elbow Surg. 2005;14(4):361-367.

34.  Izquierdo R, Voloshin I, Edwards S, et al. Treatment of glenohumeral osteoarthritis. J Am Acad Orthop Surg. 2010;18(6):375-382.

35. Shields E, Iannuzzi JC, Thorsness R, Noyes K, Voloshin I. Perioperative complications after hemiarthroplasty and total shoulder arthroplasty are equivalent. J Shoulder Elbow Surg. 2014;23(10):1449-1453.

36. Gartsman GM, Roddey TS, Hammerman SM. Shoulder arthroplasty with or without resurfacing of the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am. 2000;82(1):26-34.

37. Singh A, Yian EH, Dillon MT, Takayanagi M, Burke MF, Navarro RA. The effect of surgeon and hospital volume on shoulder arthroplasty perioperative quality metrics. J Shoulder Elbow Surg. 2014;23(8):1187-1194.

38. Groh GI, Groh GM. Complications rates, reoperation rates, and the learning curve in reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(3):388-394.

39. Boileau P, Gonzalez JF, Chuinard C, Bicknell R, Walch G. Reverse total shoulder arthroplasty after failed rotator cuff surgery. J Shoulder Elbow Surg. 2009;18(4):600-606.

40.    Boileau P, Watkinson D, Hatzidakis AM, Hovorka I. Neer Award 2005: the Grammont reverse shoulder prosthesis: results in cuff tear arthritis, fracture sequelae, and revision arthroplasty. J Shoulder Elbow Surg. 2006;15(5):527-540.

41. Boileau P, Watkinson DJ, Hatzidakis AM, Balg F. Grammont reverse prosthesis: design, rationale, and biomechanics. J Shoulder Elbow Surg. 2005;14(1 suppl S):147S-161S.

42. Pola E, Papaleo P, Santoliquido A, Gasparini G, Aulisa L, De Santis E. Clinical factors associated with an increased risk of perioperative blood transfusion in nonanemic patients undergoing total hip arthroplasty. J Bone Joint Surg Am. 2004;86(1):57-61.

43. Lin DM, Lin ES, Tran MH. Efficacy and safety of erythropoietin and intravenous iron in perioperative blood management: a systematic review. Transfusion Med Rev. 2013;27(4):221-234.

44. Muñoz M, Gómez-Ramírez S, Cuenca J, et al. Very-short-term perioperative intravenous iron administration and postoperative outcome in major orthopedic surgery: a pooled analysis of observational data from 2547 patients. Transfusion. 2014;54(2):289-299.

45. Danninger T, Rasul R, Poeran J, et al. Blood transfusions in total hip and knee arthroplasty: an analysis of outcomes. ScientificWorldJournal. 2014;2014:623460.

46. Baldus CR, Bridwell KH, Lenke LG, Okubadejo GO. Can we safely reduce blood loss during lumbar pedicle subtraction osteotomy procedures using tranexamic acid or aprotinin? A comparative study with controls. Spine. 2010;35(2):235-239.

47. Chang CH, Chang Y, Chen DW, Ueng SW, Lee MS. Topical tranexamic acid reduces blood loss and transfusion rates associated with primary total hip arthroplasty. Clin Orthop Relat Res. 2014;472(5):1552-1557.

48. Delasotta LA, Orozco F, Jafari SM, Blair JL, Ong A. Should we use preoperative epoetin-alpha in the mildly anemic patient undergoing simultaneous total knee arthroplasty? Open Orthop J. 2013;7:47-50.

49. Delasotta LA, Rangavajjula A, Frank ML, Blair J, Orozco F, Ong A. The use of preoperative epoetin-alpha in revision hip arthroplasty. Open Orthop J. 2012;6:179-183.

50. Kelley TC, Tucker KK, Adams MJ, Dalury DF. Use of tranexamic acid results in decreased blood loss and decreased transfusions in patients undergoing staged bilateral total knee arthroplasty. Transfusion. 2014;54(1):26-30.

51. Martin JG, Cassatt KB, Kincaid-Cinnamon KA, Westendorf DS, Garton AS, Lemke JH. Topical administration of tranexamic acid in primary total hip and total knee arthroplasty. J Arthroplasty. 2014;29(5):889-894.

52. Tzortzopoulou A, Cepeda MS, Schumann R, Carr DB. Antifibrinolytic agents for reducing blood loss in scoliosis surgery in children. Cochrane Database Syst Rev. 2008(3):CD006883.

53. Zhang H, Chen J, Chen F, Que W. The effect of tranexamic acid on blood loss and use of blood products in total knee arthroplasty: a meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2012;20(9):1742-1752.

54. Bong MR, Patel V, Chang E, Issack PS, Hebert R, Di Cesare PE. Risks associated with blood transfusion after total knee arthroplasty. J Arthroplasty. 2004;19(3):281-287.

References

1.    Ahmadi S, Lawrence TM, Sahota S, et al. The incidence and risk factors for blood transfusion in revision shoulder arthroplasty: our institution’s experience and review of the literature. J Shoulder Elbow Surg. 2014;23(1):43-48.

2.    Sperling JW, Duncan SF, Cofield RH, Schleck CD, Harmsen WS. Incidence and risk factors for blood transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(6):599-601.

3.    Hardy JC, Hung M, Snow BJ, et al. Blood transfusion associated with shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(2):233-239.

4.    Schumer RA, Chae JS, Markert RJ, Sprott D, Crosby LA. Predicting transfusion in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):91-96.

5.    Gruson KI, Accousti KJ, Parsons BO, Pillai G, Flatow EL. Transfusion after shoulder arthroplasty: an analysis of rates and risk factors. J Shoulder Elbow Surg. 2009;18(2):225-230.

6.    Millett PJ, Porramatikul M, Chen N, Zurakowski D, Warner JJ. Analysis of transfusion predictors in shoulder arthroplasty. J Bone Joint Surg Am. 2006;88(6):1223-1230.

7.    Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254.

8.    Ceccherini-Nelli L, Filipponi F, Mosca F, Campa M. The risk of contracting an infectious disease from blood transfusion. Transplantation Proc. 2004;36(3):680-682.

9.    Friedman R, Homering M, Holberg G, Berkowitz SD. Allogeneic blood transfusions and postoperative infections after total hip or knee arthroplasty. J Bone Joint Surg Am. 2014;96(4):272-278.

10. Hatzidakis AM, Mendlick RM, McKillip T, Reddy RL, Garvin KL. Preoperative autologous donation for total joint arthroplasty. An analysis of risk factors for allogenic transfusion. J Bone Joint Surg Am. 2000;82(1):89-100.

11. Park JH, Rasouli MR, Mortazavi SM, Tokarski AT, Maltenfort MG, Parvizi J. Predictors of perioperative blood loss in total joint arthroplasty. J Bone Joint Surg Am. 2013;95(19):1777-1783.

12. Aderinto J, Brenkel IJ. Pre-operative predictors of the requirement for blood transfusion following total hip replacement. J Bone Joint Surg Br. 2004;86(7):970-973.

13. Browne JA, Adib F, Brown TE, Novicoff WM. Transfusion rates are increasing following total hip arthroplasty: risk factors and outcomes. J Arthroplasty. 2013;28(8 suppl):34-37.

14. Yoshihara H, Yoneoka D. Predictors of allogeneic blood transfusion in spinal fusion in the United States, 2004–2009. Spine. 2014;39(4):304-310.

15. Noticewala MS, Nyce JD, Wang W, Geller JA, Macaulay W. Predicting need for allogeneic transfusion after total knee arthroplasty. J Arthroplasty. 2012;27(6):961-967.

16. Griffin JW, Novicoff WM, Browne JA, Brockmeier SF. Obstructive sleep apnea as a risk factor after shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(12):e6-e9.

17. Maynard C, Sales AE. Changes in the use of coronary artery revascularization procedures in the Department of Veterans Affairs, the National Hospital Discharge Survey, and the Nationwide Inpatient Sample, 1991–1999. BMC Health Serv Res. 2003;3(1):12.

18. Pereira BM, Chan PH, Weinstein PR, Fishman RA. Cerebral protection during reperfusion with superoxide dismutase in focal cerebral ischemia. Adv Neurol. 1990;52:97-103.

19. Hambright D, Henderson RA, Cook C, Worrell T, Moorman CT, Bolognesi MP. A comparison of perioperative outcomes in patients with and without rheumatoid arthritis after receiving a total shoulder replacement arthroplasty. J Shoulder Elbow Surg. 2011;20(1):77-85.

20. Ponce BA, Menendez ME, Oladeji LO, Soldado F. Diabetes as a risk factor for poorer early postoperative outcomes after shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):671-678.

21. Pierson JL, Hannon TJ, Earles DR. A blood-conservation algorithm to reduce blood transfusions after total hip and knee arthroplasty. J Bone Joint Surg Am. 2004;86(7):1512-1518.

22. Martinez V, Monsaingeon-Lion A, Cherif K, Judet T, Chauvin M, Fletcher D. Transfusion strategy for primary knee and hip arthroplasty: impact of an algorithm to lower transfusion rates and hospital costs. Br J Anaesth. 2007;99(6):794-800.

23. Helm AT, Karski MT, Parsons SJ, Sampath JS, Bale RS. A strategy for reducing blood-transfusion requirements in elective orthopaedic surgery. Audit of an algorithm for arthroplasty of the lower limb. J Bone Joint Surg Br. 2003;85(4):484-489.

24. Watts CD, Pagnano MW. Minimising blood loss and transfusion in contemporary hip and knee arthroplasty. J Bone Joint Surg Br. 2012;94(11 suppl A):8-10.

25. Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia. Blood. 2004;104(8):2263-2268.

26. Rogers MA, Blumberg N, Heal JM, Langa KM. Utilization of blood transfusion among older adults in the United States. Transfusion. 2011;51(4):710-718.

27. Cobain TJ, Vamvakas EC, Wells A, Titlestad K. A survey of the demographics of blood use. Transfusion Med. 2007;17(1):1-15.

28. Fosco M, Di Fiore M. Factors predicting blood transfusion in different surgical procedures for degenerative spine disease. Eur Rev Med Pharmacol Sci. 2012;16(13):1853-1858.

29. Handoll HH, Ollivere BJ, Rollins KE. Interventions for treating proximal humeral fractures in adults. Cochrane Database Syst Rev. 2012;12:CD000434.

30. Neuhaus V, Swellengrebel CH, Bossen JK, Ring D. What are the factors influencing outcome among patients admitted to a hospital with a proximal humeral fracture? Clin Orthop Relat Res. 2013;471(5):1698-1706.

31. Volgas DA, Stannard JP, Alonso JE. Nonunions of the humerus. Clin Orthop Relat Res. 2004;(419):46-50.

32. Chambers L, Dines JS, Lorich DG, Dines DM. Hemiarthroplasty for proximal humerus fractures. Curr Rev Musculoskeletal Med. 2013;6(1):57-62.

33. Jain NB, Hocker S, Pietrobon R, Guller U, Bathia N, Higgins LD. Total arthroplasty versus hemiarthroplasty for glenohumeral osteoarthritis: role of provider volume. J Shoulder Elbow Surg. 2005;14(4):361-367.

34.  Izquierdo R, Voloshin I, Edwards S, et al. Treatment of glenohumeral osteoarthritis. J Am Acad Orthop Surg. 2010;18(6):375-382.

35. Shields E, Iannuzzi JC, Thorsness R, Noyes K, Voloshin I. Perioperative complications after hemiarthroplasty and total shoulder arthroplasty are equivalent. J Shoulder Elbow Surg. 2014;23(10):1449-1453.

36. Gartsman GM, Roddey TS, Hammerman SM. Shoulder arthroplasty with or without resurfacing of the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am. 2000;82(1):26-34.

37. Singh A, Yian EH, Dillon MT, Takayanagi M, Burke MF, Navarro RA. The effect of surgeon and hospital volume on shoulder arthroplasty perioperative quality metrics. J Shoulder Elbow Surg. 2014;23(8):1187-1194.

38. Groh GI, Groh GM. Complications rates, reoperation rates, and the learning curve in reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(3):388-394.

39. Boileau P, Gonzalez JF, Chuinard C, Bicknell R, Walch G. Reverse total shoulder arthroplasty after failed rotator cuff surgery. J Shoulder Elbow Surg. 2009;18(4):600-606.

40.    Boileau P, Watkinson D, Hatzidakis AM, Hovorka I. Neer Award 2005: the Grammont reverse shoulder prosthesis: results in cuff tear arthritis, fracture sequelae, and revision arthroplasty. J Shoulder Elbow Surg. 2006;15(5):527-540.

41. Boileau P, Watkinson DJ, Hatzidakis AM, Balg F. Grammont reverse prosthesis: design, rationale, and biomechanics. J Shoulder Elbow Surg. 2005;14(1 suppl S):147S-161S.

42. Pola E, Papaleo P, Santoliquido A, Gasparini G, Aulisa L, De Santis E. Clinical factors associated with an increased risk of perioperative blood transfusion in nonanemic patients undergoing total hip arthroplasty. J Bone Joint Surg Am. 2004;86(1):57-61.

43. Lin DM, Lin ES, Tran MH. Efficacy and safety of erythropoietin and intravenous iron in perioperative blood management: a systematic review. Transfusion Med Rev. 2013;27(4):221-234.

44. Muñoz M, Gómez-Ramírez S, Cuenca J, et al. Very-short-term perioperative intravenous iron administration and postoperative outcome in major orthopedic surgery: a pooled analysis of observational data from 2547 patients. Transfusion. 2014;54(2):289-299.

45. Danninger T, Rasul R, Poeran J, et al. Blood transfusions in total hip and knee arthroplasty: an analysis of outcomes. ScientificWorldJournal. 2014;2014:623460.

46. Baldus CR, Bridwell KH, Lenke LG, Okubadejo GO. Can we safely reduce blood loss during lumbar pedicle subtraction osteotomy procedures using tranexamic acid or aprotinin? A comparative study with controls. Spine. 2010;35(2):235-239.

47. Chang CH, Chang Y, Chen DW, Ueng SW, Lee MS. Topical tranexamic acid reduces blood loss and transfusion rates associated with primary total hip arthroplasty. Clin Orthop Relat Res. 2014;472(5):1552-1557.

48. Delasotta LA, Orozco F, Jafari SM, Blair JL, Ong A. Should we use preoperative epoetin-alpha in the mildly anemic patient undergoing simultaneous total knee arthroplasty? Open Orthop J. 2013;7:47-50.

49. Delasotta LA, Rangavajjula A, Frank ML, Blair J, Orozco F, Ong A. The use of preoperative epoetin-alpha in revision hip arthroplasty. Open Orthop J. 2012;6:179-183.

50. Kelley TC, Tucker KK, Adams MJ, Dalury DF. Use of tranexamic acid results in decreased blood loss and decreased transfusions in patients undergoing staged bilateral total knee arthroplasty. Transfusion. 2014;54(1):26-30.

51. Martin JG, Cassatt KB, Kincaid-Cinnamon KA, Westendorf DS, Garton AS, Lemke JH. Topical administration of tranexamic acid in primary total hip and total knee arthroplasty. J Arthroplasty. 2014;29(5):889-894.

52. Tzortzopoulou A, Cepeda MS, Schumann R, Carr DB. Antifibrinolytic agents for reducing blood loss in scoliosis surgery in children. Cochrane Database Syst Rev. 2008(3):CD006883.

53. Zhang H, Chen J, Chen F, Que W. The effect of tranexamic acid on blood loss and use of blood products in total knee arthroplasty: a meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2012;20(9):1742-1752.

54. Bong MR, Patel V, Chang E, Issack PS, Hebert R, Di Cesare PE. Risks associated with blood transfusion after total knee arthroplasty. J Arthroplasty. 2004;19(3):281-287.

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The American Journal of Orthopedics - 44(12)
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The American Journal of Orthopedics - 44(12)
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Analysis of Predictors and Outcomes of Allogeneic Blood Transfusion After Shoulder Arthroplasty
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Analysis of Predictors and Outcomes of Allogeneic Blood Transfusion After Shoulder Arthroplasty
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american journal of orthopedics, AJO, original study, online exclusive, study, allogeneic, blood, transfusion, shoulder arthroplasty, shoulder, arthroplasty, total shoulder arthroplasty, TSA, ABT, ponce, yu, menendez, oladeji
Legacy Keywords
american journal of orthopedics, AJO, original study, online exclusive, study, allogeneic, blood, transfusion, shoulder arthroplasty, shoulder, arthroplasty, total shoulder arthroplasty, TSA, ABT, ponce, yu, menendez, oladeji
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Orthopedic Practice Patterns Relating to Anterior Cruciate Ligament Reconstruction in Elite Athletes

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Orthopedic Practice Patterns Relating to Anterior Cruciate Ligament Reconstruction in Elite Athletes

National Hockey League (NHL), Major League Soccer (MLS), and US Olympic/World Cup Ski/Snowboard (Olympic) athletes receive orthopedic care from a select group of surgeons. There are 30 NHL teams, 19 MLS teams, 1 Olympic ski team, and 1 Olympic snowboard team, for a total of 51 teams and a rough total of 2229 athletes (1500 NHL, 570 MLS, 159 Olympic).1

Studies have shown that MLS athletes and X-Game skiers and snowboarders have performed well on return to sport (RTS) after anterior cruciate ligament (ACL) reconstruction.2,3 However, the techniques, graft choices, and rehabilitation protocols used to return these elite athletes to their preinjury level of performance have not been elucidated. It is unclear if the treatment given to these elite athletes differs from that given to recreational athletes and nonathletes. Bradley and colleagues4 examined how 32 NFL team orthopedists treated ACL tears, and Erickson and colleagues5 recently surveyed NFL and National Collegiate Athletic Association (NCAA) team physicians to determine practice patterns (eg, surgical techniques, graft choices, postoperative protocols) in treating ACL tears. Until now, however, no one has examined NHL, MLS, or Olympic team orthopedic surgeons’ practice patterns as they relate to ACL reconstruction.

We conducted an online survey of NHL, MLS, and Olympic team orthopedic surgeons to determine practice patterns relating to ACL reconstruction in elite athletes. Given the practice patterns of surgeons in our practice, we hypothesized that the surveyed surgeons treating these elite athletes would most commonly use bone–patellar tendon–bone (BPTB) autograft with a single-bundle technique. We also hypothesized that they would permit RTS without a brace at a minimum of 6 months after surgery, with a normal physical examination, and after successful completion of a structured battery of RTS tests.

Materials and Methods

On the SurveyMonkey website (http://www.surveymonkey.com), we created a 7-question base survey, with other questions added for the NHL and MLS surveys (Figure 1). We sent this survey to 94 team orthopedic surgeons (41 NHL, 26 MLS, 27 Olympic) identified through Internet searches and direct contact with team public relations departments. The survey was approved by MLS and NHL research committees. In 2013, each survey was sent out 5 times. The response rates for each round are shown in Figure 2. All responses remained confidential; we did not learn surgeons’ identities. Data were collected and analyzed through the SurveyMonkey website. Each surgeon was instructed to respond to all relevant questions in the survey. The survey was designed such that the participant could not submit the survey without answering all the questions. Descriptive statistics were calculated for each study and parameter analyzed. Continuous variable data are reported as means and standard deviations (weighted means where applicable). Categorical data are reported as frequencies with percentages.

Results

Of the 94 team orthopedic surgeons surveyed, 47 (50%) responded (NHL, 49%; MLS, 50%; Olympic, 52%). Mean (SD) experience as a team physician was 7.73 (5.33) years (range, 2-20 years) for NHL, 6.77 (6.64) years (range, 2-20 years) for MLS, and 1.14 (0.36) years (range, 1-10 years) for Olympic. Mean (SD) number of ACL reconstructions performed in 2012 was 101 (51) for NHL (range, 50-200), 78 (38) for MLS (range, 20-150), and 110 (105) for Olympic (range, 25-175) (Table 1). Of the 47 surgeons, 42 (89.4%) used autograft in the treatment of elite athletes, and 5 (10.6%) used allograft. Autograft choices were BPTB (n = 33; 70.2%), 4-strand semitendinosus (n = 7; 14.9%), and quadriceps (n = 2; 4.3%); allograft choices were 4-strand semitendinosus (n = 4; 8.5%) and BPTB (n = 1; 2.1%) (Table 2).

Of the 40 surgeons (85.1%) who indicated they would use autograft in 25-year-old recreational athletes, 25 (53.2%) would use BPTB, 13 (27.7%) would use 4-strand semitendinosus, and 2 (4.3%) would use quadriceps; of the 7 who indicated they would use allograft, 4 (8.5%) would use 4-strand semitendinosus, and 3 (6.4%) would use BPTB. In the NHL and MLS surveys, 19 surgeons (57.6%) indicated they would use autograft (6 would use BPTB, 13 would use 4-strand semitendinosus), and 14 (42.4%) would use allograft (7 would use BPTB, 5 would use Achilles, and 2 would use tibialis anterior) in 35-year-old recreational athletes.

Twenty-one surgeons (44.7%) were drilling the femoral tunnel through a transtibial portal, 36.2% through an anteromedial portal, and 12.8% using a 2-incision technique. All surgeons indicated they were using a single-bundle technique in ACL reconstruction. Thirty-three surgeons (70.2%) did not recommend a brace for their elite athletes on RTS. Olympic team surgeons had the highest rate of brace wear in RTS (50%, both skiers and snowboarders); NHL and MLS surgeons had significantly lower rates (25% and 15.4%, respectively) (Table 3).

 

 

Twenty (60.6%) of the NHL and MLS surgeons recommended waiting at least 6 months before RTS; 2 (6.1%) recommended waiting at least 9 months; no surgeon recommended waiting at least 12 months; and the others did not have a specific time frame for RTS. Twenty-seven surgeons (81.8%) recommended RTS after an athlete passed a series of RTS tests (eg, Vail, single-leg hop). Nineteen surgeons (57.6%) recommended waiting until the athlete had full range of motion, no pain, full strength, and subjective stability in the knee. Physicians could choose more than one answer for the previous question, allowing for a total percentage higher than 100%.

Discussion

The goal of this study was to determine how NHL, MLS, and Olympic team orthopedic surgeons manage ACL tears in elite and recreational athletes. Our study hypotheses were confirmed, as 70.2% of those surveyed used BPTB autograft for elite athletes, 100% used the single-bundle technique, 70.2% did not require a brace on RTS, 81.8% recommended RTS after the athlete passed a series of RTS tests (eg, Vail, single-leg hop), and 60.6% waited at least 6 months after surgery.

As soccer and skiing are the top 2 sports in which participants sustain ACL tears, it is necessary to report how surgeons obtain successful results in these patient populations.6 Using the US and Norwegian ACL reconstruction registries, Granan and colleagues6 found that, over a 7-year period, 5760 ACL tears occurred during soccer, and 2030 occurred during skiing. The scope of ACL injuries is broad, and treatment patterns must be elucidated. Although most surgeons do not treat elite athletes, many high school and college athletes compete at very high levels. Therefore, replicating the methods of the surgeons who treat elite athletes may be warranted.

In our survey, autograft (89.4%), particularly BPTB autograft (70.2%), was the most common graft choice for elite athletes. The rate of allograft use (42.4%) was higher for 35-year-old recreational athletes. As BPTB autograft produces reliable long-term results, this graft type is a reasonable choice.7 However, only 18% of our surveyed orthopedic surgeons indicated they would use BPTB autograft in older, recreational athletes. This stark difference is likely related to the more than 40% long-term side effects of anterior knee pain and graft harvest site morbidity with BPTB autograft as opposed to allograft and other types of autograft.8,9 Younger patients may be more willing to accept some anterior knee pain to ensure bone-to-bone healing with BPTB autograft. This shift in graft choice may also reflect the desire to minimize skin incisions and their resulting scars, especially in female recreational athletes.

In a meta-analysis of more than 5000 patients, Kraeutler and colleagues7 found that BPTB autograft outperformed allograft according to several knee scores, including Lysholm and Tegner, and had a lower re-rupture rate (4.3% vs 12.7%). However, despite the superior performance of BPTB autograft, graft choice cannot overcome surgeon error in graft placement.10 BPTB autograft appears to remain the gold standard for ACL reconstruction for many reasons, including low failure rates and decreased costs.11 Recently, investigators have tried to challenge the superiority of BPTB autograft. In a retrospective case–control study, Mascarenhas and colleagues12 found that hamstring autograft afforded patients better extension and higher subjective outcome scores. Bourke and colleagues13 found a higher rate of contralateral ACL rupture in patients treated with BPTB autograft compared with hamstring autograft.

According to this survey, 44.7% of surgeons indicated they drilled the femoral tunnel through a transtibial portal, 36.2% used an anteromedial portal, and 12.8% used the 2-incision technique. These methods were recently evaluated to determine if any is superior to the others, but the study results were not definitive.14 Franceschi and colleagues15 found improved rotational and anterior stability of the knee with use of an anteromedial approach, but their findings were not clinically or functionally significant. Wang and colleagues16 found an extension loss in the late-stance phase of gait with the anteromedial approach; the transtibial approach was correlated with inferior anterior-posterior stability during the stance phase of gait. Therefore, our results parallel those in the current literature in that the surveyed population is split on which technique to use and likely bases its practice on comfort level and residency/fellowship training.

Limitations

This study had several limitations. First, it provided level V evidence of team physicians in 3 major sports. Although some of these physicians were also treating athletes in other sports, our survey targeted NHL, MLS, and Olympic athletes. It did not address all ages and both sexes—which is significant, given the higher rate of ACL tears in females. All NHL and MLS players are male, and there was a high rate of BPTB graft use in these sports. However, recreational athletes include both males and females, and the fact that some surgeons would choose a hamstring graft for a female for cosmetic reasons must not be overlooked. Conversely, that there was no difference in the number of BPTB autografts chosen between NHL and MLS surgeons versus Olympic surgeons, where females are included (all chose about 60% BPTB autografts for their elite athletes), disputes this limitation. Our survey response rate was 50%. Other studies have had similar rates in relation to ACL practices,17 especially elite team physicians’ practices,5 and recent literature has confirmed that lower response rates in surveys did not alter results and may in fact have improved results.18,19 This percentage could be falsely low if some of our email addresses were incorrect. This rate also raises the possibility of selection bias, as surgeons who routinely used allograft in their athlete population may not have wanted to admit this. It is possible that some NHL, MLS, and Olympic athletes were treated by surgeons not included in this survey (in some cases, a non–team surgeon may have performed the athlete’s surgery). This survey did not address concomitant knee pathology or cover all possible technique variables.

 

 

Conclusion

Most of the NHL, MLS, and Olympic team orthopedic surgeons who were surveyed perform their ACL reconstructions using BPTB autograft, using a single-bundle technique, through a transtibial portal, and do not require bracing for their athletes returning to sport. Most required their athletes to complete a series of RTS tests before resuming competitive play.

References

1.    Team USA. 2013. US Olympic Committee website. http://www.teamusa.org/athletes?pg=1&seasonId=%7BCF2DC66A-C2B3-44A8-ABB8-A486F3FBFDDF%7D&ngbId=%7BB36167A0-2AC8-4B0F-876F-93D0A44DF60A%7D. Accessed October 23, 2015.

2.    Erickson BJ, Harris JD, Cvetanovich GL, et al. Performance and return to sport after anterior cruciate ligament reconstruction in male major league soccer players. Orthop J Sports Med. 2013;1(2):1-8.

3.    Erickson BJ, Harris JD, Fillingham YA, et al. Performance and return to sport after anterior cruciate ligament reconstruction in X-Games skiers and snowboarders. Orthop J Sports Med. 2013;1(6):1-5.

4.    Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

5.    Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

6.    Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

7.    Kraeutler MJ, Bravman JT, McCarty EC. Bone–patellar tendon–bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

8.    Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: allograft versus autograft. Arthroscopy. 2005;21(7):774-785.

9.    Kartus J, Magnusson L, Stener S, Brandsson S, Eriksson BI, Karlsson J. Complications following arthroscopic anterior cruciate ligament reconstruction. A 2-5-year follow-up of 604 patients with special emphasis on anterior knee pain. Knee Surg Sports Traumatol Arthrosc. 1999;7(1):2-8.

10.  Boszotta H. Arthroscopic anterior cruciate ligament reconstruction using a patellar tendon graft in press-fit technique: surgical technique and follow-up. Arthroscopy. 1997;13(3):332-339.

11.  Hospodar SJ, Miller MD. Controversies in ACL reconstruction: bone–patellar tendon–bone anterior cruciate ligament reconstruction remains the gold standard. Sports Med Arthrosc Rev. 2009;17(4):242-246.

12.  Mascarenhas R, Tranovich MJ, Kropf EJ, Fu FH, Harner CD. Bone–patellar tendon–bone autograft versus hamstring autograft anterior cruciate ligament reconstruction in the young athlete: a retrospective matched analysis with 2-10 year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1520-1527.

13.  Bourke HE, Salmon LJ, Waller A, Patterson V, Pinczewski LA. Survival of the anterior cruciate ligament graft and the contralateral ACL at a minimum of 15 years. Am J Sports Med. 2012;40(9):1985-1992.

14.  Chalmers PN, Mall NA, Cole BJ, Verma NN, Bush-Joseph CA, Bach BR Jr. Anteromedial versus transtibial tunnel drilling in anterior cruciate ligament reconstructions: a systematic review. Arthroscopy. 2013;29(7):1235-1242.

15.  Franceschi F, Papalia R, Rizzello G, Del Buono A, Maffulli N, Denaro V. Anteromedial portal versus transtibial drilling techniques in anterior cruciate ligament reconstruction: any clinical relevance? A retrospective comparative study. Arthroscopy. 2013;29(8):1330-1337.

16.  Wang H, Fleischli JE, Zheng NN. Transtibial versus anteromedial portal technique in single-bundle anterior cruciate ligament reconstruction: outcomes of knee joint kinematics during walking. Am J Sports Med. 2013;41(8):1847-1856.

17.  Chechik O, Amar E, Khashan M, Lador R, Eyal G, Gold A. An international survey on anterior cruciate ligament reconstruction practices. Int Orthop. 2013;37(2):201-206.

18.  Keeter S, Miller C, Kohut A, Groves RM, Presser S. Consequences of reducing nonresponse in a national telephone survey. Public Opin Q. 2000;64(2):125-148.

19.  Curtin R, Presser S, Singer E. The effects of response rate changes on the index of consumer sentiment. Public Opin Q. 2000;64(4):413-428.

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Brandon J. Erickson, MD, Joshua D. Harris, MD, Yale A. Fillingham, MD, Gregory L. Cvetanovich, MD, Charles Bush-Joseph, MD, Brian J. Cole, MD, MBA, Bernard R. Bach Jr, MD, and Nikhil N. Verma, MD

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

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The American Journal of Orthopedics - 44(12)
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E480-E485
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american journal of orthopedics, AJO, original study, online exclusive, study, practice, anterior cruciate ligament, ACL, reconstruction, athletes, sports medicine, athletic, sports, hockey, soccer, olympic, ski, snowboard, team, NHL, MLS, sport, erickson, harris, fillingham, cvetanovich, bush-joseph, cole, bach, verma
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Brandon J. Erickson, MD, Joshua D. Harris, MD, Yale A. Fillingham, MD, Gregory L. Cvetanovich, MD, Charles Bush-Joseph, MD, Brian J. Cole, MD, MBA, Bernard R. Bach Jr, MD, and Nikhil N. Verma, MD

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

Author and Disclosure Information

Brandon J. Erickson, MD, Joshua D. Harris, MD, Yale A. Fillingham, MD, Gregory L. Cvetanovich, MD, Charles Bush-Joseph, MD, Brian J. Cole, MD, MBA, Bernard R. Bach Jr, MD, and Nikhil N. Verma, MD

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

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National Hockey League (NHL), Major League Soccer (MLS), and US Olympic/World Cup Ski/Snowboard (Olympic) athletes receive orthopedic care from a select group of surgeons. There are 30 NHL teams, 19 MLS teams, 1 Olympic ski team, and 1 Olympic snowboard team, for a total of 51 teams and a rough total of 2229 athletes (1500 NHL, 570 MLS, 159 Olympic).1

Studies have shown that MLS athletes and X-Game skiers and snowboarders have performed well on return to sport (RTS) after anterior cruciate ligament (ACL) reconstruction.2,3 However, the techniques, graft choices, and rehabilitation protocols used to return these elite athletes to their preinjury level of performance have not been elucidated. It is unclear if the treatment given to these elite athletes differs from that given to recreational athletes and nonathletes. Bradley and colleagues4 examined how 32 NFL team orthopedists treated ACL tears, and Erickson and colleagues5 recently surveyed NFL and National Collegiate Athletic Association (NCAA) team physicians to determine practice patterns (eg, surgical techniques, graft choices, postoperative protocols) in treating ACL tears. Until now, however, no one has examined NHL, MLS, or Olympic team orthopedic surgeons’ practice patterns as they relate to ACL reconstruction.

We conducted an online survey of NHL, MLS, and Olympic team orthopedic surgeons to determine practice patterns relating to ACL reconstruction in elite athletes. Given the practice patterns of surgeons in our practice, we hypothesized that the surveyed surgeons treating these elite athletes would most commonly use bone–patellar tendon–bone (BPTB) autograft with a single-bundle technique. We also hypothesized that they would permit RTS without a brace at a minimum of 6 months after surgery, with a normal physical examination, and after successful completion of a structured battery of RTS tests.

Materials and Methods

On the SurveyMonkey website (http://www.surveymonkey.com), we created a 7-question base survey, with other questions added for the NHL and MLS surveys (Figure 1). We sent this survey to 94 team orthopedic surgeons (41 NHL, 26 MLS, 27 Olympic) identified through Internet searches and direct contact with team public relations departments. The survey was approved by MLS and NHL research committees. In 2013, each survey was sent out 5 times. The response rates for each round are shown in Figure 2. All responses remained confidential; we did not learn surgeons’ identities. Data were collected and analyzed through the SurveyMonkey website. Each surgeon was instructed to respond to all relevant questions in the survey. The survey was designed such that the participant could not submit the survey without answering all the questions. Descriptive statistics were calculated for each study and parameter analyzed. Continuous variable data are reported as means and standard deviations (weighted means where applicable). Categorical data are reported as frequencies with percentages.

Results

Of the 94 team orthopedic surgeons surveyed, 47 (50%) responded (NHL, 49%; MLS, 50%; Olympic, 52%). Mean (SD) experience as a team physician was 7.73 (5.33) years (range, 2-20 years) for NHL, 6.77 (6.64) years (range, 2-20 years) for MLS, and 1.14 (0.36) years (range, 1-10 years) for Olympic. Mean (SD) number of ACL reconstructions performed in 2012 was 101 (51) for NHL (range, 50-200), 78 (38) for MLS (range, 20-150), and 110 (105) for Olympic (range, 25-175) (Table 1). Of the 47 surgeons, 42 (89.4%) used autograft in the treatment of elite athletes, and 5 (10.6%) used allograft. Autograft choices were BPTB (n = 33; 70.2%), 4-strand semitendinosus (n = 7; 14.9%), and quadriceps (n = 2; 4.3%); allograft choices were 4-strand semitendinosus (n = 4; 8.5%) and BPTB (n = 1; 2.1%) (Table 2).

Of the 40 surgeons (85.1%) who indicated they would use autograft in 25-year-old recreational athletes, 25 (53.2%) would use BPTB, 13 (27.7%) would use 4-strand semitendinosus, and 2 (4.3%) would use quadriceps; of the 7 who indicated they would use allograft, 4 (8.5%) would use 4-strand semitendinosus, and 3 (6.4%) would use BPTB. In the NHL and MLS surveys, 19 surgeons (57.6%) indicated they would use autograft (6 would use BPTB, 13 would use 4-strand semitendinosus), and 14 (42.4%) would use allograft (7 would use BPTB, 5 would use Achilles, and 2 would use tibialis anterior) in 35-year-old recreational athletes.

Twenty-one surgeons (44.7%) were drilling the femoral tunnel through a transtibial portal, 36.2% through an anteromedial portal, and 12.8% using a 2-incision technique. All surgeons indicated they were using a single-bundle technique in ACL reconstruction. Thirty-three surgeons (70.2%) did not recommend a brace for their elite athletes on RTS. Olympic team surgeons had the highest rate of brace wear in RTS (50%, both skiers and snowboarders); NHL and MLS surgeons had significantly lower rates (25% and 15.4%, respectively) (Table 3).

 

 

Twenty (60.6%) of the NHL and MLS surgeons recommended waiting at least 6 months before RTS; 2 (6.1%) recommended waiting at least 9 months; no surgeon recommended waiting at least 12 months; and the others did not have a specific time frame for RTS. Twenty-seven surgeons (81.8%) recommended RTS after an athlete passed a series of RTS tests (eg, Vail, single-leg hop). Nineteen surgeons (57.6%) recommended waiting until the athlete had full range of motion, no pain, full strength, and subjective stability in the knee. Physicians could choose more than one answer for the previous question, allowing for a total percentage higher than 100%.

Discussion

The goal of this study was to determine how NHL, MLS, and Olympic team orthopedic surgeons manage ACL tears in elite and recreational athletes. Our study hypotheses were confirmed, as 70.2% of those surveyed used BPTB autograft for elite athletes, 100% used the single-bundle technique, 70.2% did not require a brace on RTS, 81.8% recommended RTS after the athlete passed a series of RTS tests (eg, Vail, single-leg hop), and 60.6% waited at least 6 months after surgery.

As soccer and skiing are the top 2 sports in which participants sustain ACL tears, it is necessary to report how surgeons obtain successful results in these patient populations.6 Using the US and Norwegian ACL reconstruction registries, Granan and colleagues6 found that, over a 7-year period, 5760 ACL tears occurred during soccer, and 2030 occurred during skiing. The scope of ACL injuries is broad, and treatment patterns must be elucidated. Although most surgeons do not treat elite athletes, many high school and college athletes compete at very high levels. Therefore, replicating the methods of the surgeons who treat elite athletes may be warranted.

In our survey, autograft (89.4%), particularly BPTB autograft (70.2%), was the most common graft choice for elite athletes. The rate of allograft use (42.4%) was higher for 35-year-old recreational athletes. As BPTB autograft produces reliable long-term results, this graft type is a reasonable choice.7 However, only 18% of our surveyed orthopedic surgeons indicated they would use BPTB autograft in older, recreational athletes. This stark difference is likely related to the more than 40% long-term side effects of anterior knee pain and graft harvest site morbidity with BPTB autograft as opposed to allograft and other types of autograft.8,9 Younger patients may be more willing to accept some anterior knee pain to ensure bone-to-bone healing with BPTB autograft. This shift in graft choice may also reflect the desire to minimize skin incisions and their resulting scars, especially in female recreational athletes.

In a meta-analysis of more than 5000 patients, Kraeutler and colleagues7 found that BPTB autograft outperformed allograft according to several knee scores, including Lysholm and Tegner, and had a lower re-rupture rate (4.3% vs 12.7%). However, despite the superior performance of BPTB autograft, graft choice cannot overcome surgeon error in graft placement.10 BPTB autograft appears to remain the gold standard for ACL reconstruction for many reasons, including low failure rates and decreased costs.11 Recently, investigators have tried to challenge the superiority of BPTB autograft. In a retrospective case–control study, Mascarenhas and colleagues12 found that hamstring autograft afforded patients better extension and higher subjective outcome scores. Bourke and colleagues13 found a higher rate of contralateral ACL rupture in patients treated with BPTB autograft compared with hamstring autograft.

According to this survey, 44.7% of surgeons indicated they drilled the femoral tunnel through a transtibial portal, 36.2% used an anteromedial portal, and 12.8% used the 2-incision technique. These methods were recently evaluated to determine if any is superior to the others, but the study results were not definitive.14 Franceschi and colleagues15 found improved rotational and anterior stability of the knee with use of an anteromedial approach, but their findings were not clinically or functionally significant. Wang and colleagues16 found an extension loss in the late-stance phase of gait with the anteromedial approach; the transtibial approach was correlated with inferior anterior-posterior stability during the stance phase of gait. Therefore, our results parallel those in the current literature in that the surveyed population is split on which technique to use and likely bases its practice on comfort level and residency/fellowship training.

Limitations

This study had several limitations. First, it provided level V evidence of team physicians in 3 major sports. Although some of these physicians were also treating athletes in other sports, our survey targeted NHL, MLS, and Olympic athletes. It did not address all ages and both sexes—which is significant, given the higher rate of ACL tears in females. All NHL and MLS players are male, and there was a high rate of BPTB graft use in these sports. However, recreational athletes include both males and females, and the fact that some surgeons would choose a hamstring graft for a female for cosmetic reasons must not be overlooked. Conversely, that there was no difference in the number of BPTB autografts chosen between NHL and MLS surgeons versus Olympic surgeons, where females are included (all chose about 60% BPTB autografts for their elite athletes), disputes this limitation. Our survey response rate was 50%. Other studies have had similar rates in relation to ACL practices,17 especially elite team physicians’ practices,5 and recent literature has confirmed that lower response rates in surveys did not alter results and may in fact have improved results.18,19 This percentage could be falsely low if some of our email addresses were incorrect. This rate also raises the possibility of selection bias, as surgeons who routinely used allograft in their athlete population may not have wanted to admit this. It is possible that some NHL, MLS, and Olympic athletes were treated by surgeons not included in this survey (in some cases, a non–team surgeon may have performed the athlete’s surgery). This survey did not address concomitant knee pathology or cover all possible technique variables.

 

 

Conclusion

Most of the NHL, MLS, and Olympic team orthopedic surgeons who were surveyed perform their ACL reconstructions using BPTB autograft, using a single-bundle technique, through a transtibial portal, and do not require bracing for their athletes returning to sport. Most required their athletes to complete a series of RTS tests before resuming competitive play.

National Hockey League (NHL), Major League Soccer (MLS), and US Olympic/World Cup Ski/Snowboard (Olympic) athletes receive orthopedic care from a select group of surgeons. There are 30 NHL teams, 19 MLS teams, 1 Olympic ski team, and 1 Olympic snowboard team, for a total of 51 teams and a rough total of 2229 athletes (1500 NHL, 570 MLS, 159 Olympic).1

Studies have shown that MLS athletes and X-Game skiers and snowboarders have performed well on return to sport (RTS) after anterior cruciate ligament (ACL) reconstruction.2,3 However, the techniques, graft choices, and rehabilitation protocols used to return these elite athletes to their preinjury level of performance have not been elucidated. It is unclear if the treatment given to these elite athletes differs from that given to recreational athletes and nonathletes. Bradley and colleagues4 examined how 32 NFL team orthopedists treated ACL tears, and Erickson and colleagues5 recently surveyed NFL and National Collegiate Athletic Association (NCAA) team physicians to determine practice patterns (eg, surgical techniques, graft choices, postoperative protocols) in treating ACL tears. Until now, however, no one has examined NHL, MLS, or Olympic team orthopedic surgeons’ practice patterns as they relate to ACL reconstruction.

We conducted an online survey of NHL, MLS, and Olympic team orthopedic surgeons to determine practice patterns relating to ACL reconstruction in elite athletes. Given the practice patterns of surgeons in our practice, we hypothesized that the surveyed surgeons treating these elite athletes would most commonly use bone–patellar tendon–bone (BPTB) autograft with a single-bundle technique. We also hypothesized that they would permit RTS without a brace at a minimum of 6 months after surgery, with a normal physical examination, and after successful completion of a structured battery of RTS tests.

Materials and Methods

On the SurveyMonkey website (http://www.surveymonkey.com), we created a 7-question base survey, with other questions added for the NHL and MLS surveys (Figure 1). We sent this survey to 94 team orthopedic surgeons (41 NHL, 26 MLS, 27 Olympic) identified through Internet searches and direct contact with team public relations departments. The survey was approved by MLS and NHL research committees. In 2013, each survey was sent out 5 times. The response rates for each round are shown in Figure 2. All responses remained confidential; we did not learn surgeons’ identities. Data were collected and analyzed through the SurveyMonkey website. Each surgeon was instructed to respond to all relevant questions in the survey. The survey was designed such that the participant could not submit the survey without answering all the questions. Descriptive statistics were calculated for each study and parameter analyzed. Continuous variable data are reported as means and standard deviations (weighted means where applicable). Categorical data are reported as frequencies with percentages.

Results

Of the 94 team orthopedic surgeons surveyed, 47 (50%) responded (NHL, 49%; MLS, 50%; Olympic, 52%). Mean (SD) experience as a team physician was 7.73 (5.33) years (range, 2-20 years) for NHL, 6.77 (6.64) years (range, 2-20 years) for MLS, and 1.14 (0.36) years (range, 1-10 years) for Olympic. Mean (SD) number of ACL reconstructions performed in 2012 was 101 (51) for NHL (range, 50-200), 78 (38) for MLS (range, 20-150), and 110 (105) for Olympic (range, 25-175) (Table 1). Of the 47 surgeons, 42 (89.4%) used autograft in the treatment of elite athletes, and 5 (10.6%) used allograft. Autograft choices were BPTB (n = 33; 70.2%), 4-strand semitendinosus (n = 7; 14.9%), and quadriceps (n = 2; 4.3%); allograft choices were 4-strand semitendinosus (n = 4; 8.5%) and BPTB (n = 1; 2.1%) (Table 2).

Of the 40 surgeons (85.1%) who indicated they would use autograft in 25-year-old recreational athletes, 25 (53.2%) would use BPTB, 13 (27.7%) would use 4-strand semitendinosus, and 2 (4.3%) would use quadriceps; of the 7 who indicated they would use allograft, 4 (8.5%) would use 4-strand semitendinosus, and 3 (6.4%) would use BPTB. In the NHL and MLS surveys, 19 surgeons (57.6%) indicated they would use autograft (6 would use BPTB, 13 would use 4-strand semitendinosus), and 14 (42.4%) would use allograft (7 would use BPTB, 5 would use Achilles, and 2 would use tibialis anterior) in 35-year-old recreational athletes.

Twenty-one surgeons (44.7%) were drilling the femoral tunnel through a transtibial portal, 36.2% through an anteromedial portal, and 12.8% using a 2-incision technique. All surgeons indicated they were using a single-bundle technique in ACL reconstruction. Thirty-three surgeons (70.2%) did not recommend a brace for their elite athletes on RTS. Olympic team surgeons had the highest rate of brace wear in RTS (50%, both skiers and snowboarders); NHL and MLS surgeons had significantly lower rates (25% and 15.4%, respectively) (Table 3).

 

 

Twenty (60.6%) of the NHL and MLS surgeons recommended waiting at least 6 months before RTS; 2 (6.1%) recommended waiting at least 9 months; no surgeon recommended waiting at least 12 months; and the others did not have a specific time frame for RTS. Twenty-seven surgeons (81.8%) recommended RTS after an athlete passed a series of RTS tests (eg, Vail, single-leg hop). Nineteen surgeons (57.6%) recommended waiting until the athlete had full range of motion, no pain, full strength, and subjective stability in the knee. Physicians could choose more than one answer for the previous question, allowing for a total percentage higher than 100%.

Discussion

The goal of this study was to determine how NHL, MLS, and Olympic team orthopedic surgeons manage ACL tears in elite and recreational athletes. Our study hypotheses were confirmed, as 70.2% of those surveyed used BPTB autograft for elite athletes, 100% used the single-bundle technique, 70.2% did not require a brace on RTS, 81.8% recommended RTS after the athlete passed a series of RTS tests (eg, Vail, single-leg hop), and 60.6% waited at least 6 months after surgery.

As soccer and skiing are the top 2 sports in which participants sustain ACL tears, it is necessary to report how surgeons obtain successful results in these patient populations.6 Using the US and Norwegian ACL reconstruction registries, Granan and colleagues6 found that, over a 7-year period, 5760 ACL tears occurred during soccer, and 2030 occurred during skiing. The scope of ACL injuries is broad, and treatment patterns must be elucidated. Although most surgeons do not treat elite athletes, many high school and college athletes compete at very high levels. Therefore, replicating the methods of the surgeons who treat elite athletes may be warranted.

In our survey, autograft (89.4%), particularly BPTB autograft (70.2%), was the most common graft choice for elite athletes. The rate of allograft use (42.4%) was higher for 35-year-old recreational athletes. As BPTB autograft produces reliable long-term results, this graft type is a reasonable choice.7 However, only 18% of our surveyed orthopedic surgeons indicated they would use BPTB autograft in older, recreational athletes. This stark difference is likely related to the more than 40% long-term side effects of anterior knee pain and graft harvest site morbidity with BPTB autograft as opposed to allograft and other types of autograft.8,9 Younger patients may be more willing to accept some anterior knee pain to ensure bone-to-bone healing with BPTB autograft. This shift in graft choice may also reflect the desire to minimize skin incisions and their resulting scars, especially in female recreational athletes.

In a meta-analysis of more than 5000 patients, Kraeutler and colleagues7 found that BPTB autograft outperformed allograft according to several knee scores, including Lysholm and Tegner, and had a lower re-rupture rate (4.3% vs 12.7%). However, despite the superior performance of BPTB autograft, graft choice cannot overcome surgeon error in graft placement.10 BPTB autograft appears to remain the gold standard for ACL reconstruction for many reasons, including low failure rates and decreased costs.11 Recently, investigators have tried to challenge the superiority of BPTB autograft. In a retrospective case–control study, Mascarenhas and colleagues12 found that hamstring autograft afforded patients better extension and higher subjective outcome scores. Bourke and colleagues13 found a higher rate of contralateral ACL rupture in patients treated with BPTB autograft compared with hamstring autograft.

According to this survey, 44.7% of surgeons indicated they drilled the femoral tunnel through a transtibial portal, 36.2% used an anteromedial portal, and 12.8% used the 2-incision technique. These methods were recently evaluated to determine if any is superior to the others, but the study results were not definitive.14 Franceschi and colleagues15 found improved rotational and anterior stability of the knee with use of an anteromedial approach, but their findings were not clinically or functionally significant. Wang and colleagues16 found an extension loss in the late-stance phase of gait with the anteromedial approach; the transtibial approach was correlated with inferior anterior-posterior stability during the stance phase of gait. Therefore, our results parallel those in the current literature in that the surveyed population is split on which technique to use and likely bases its practice on comfort level and residency/fellowship training.

Limitations

This study had several limitations. First, it provided level V evidence of team physicians in 3 major sports. Although some of these physicians were also treating athletes in other sports, our survey targeted NHL, MLS, and Olympic athletes. It did not address all ages and both sexes—which is significant, given the higher rate of ACL tears in females. All NHL and MLS players are male, and there was a high rate of BPTB graft use in these sports. However, recreational athletes include both males and females, and the fact that some surgeons would choose a hamstring graft for a female for cosmetic reasons must not be overlooked. Conversely, that there was no difference in the number of BPTB autografts chosen between NHL and MLS surgeons versus Olympic surgeons, where females are included (all chose about 60% BPTB autografts for their elite athletes), disputes this limitation. Our survey response rate was 50%. Other studies have had similar rates in relation to ACL practices,17 especially elite team physicians’ practices,5 and recent literature has confirmed that lower response rates in surveys did not alter results and may in fact have improved results.18,19 This percentage could be falsely low if some of our email addresses were incorrect. This rate also raises the possibility of selection bias, as surgeons who routinely used allograft in their athlete population may not have wanted to admit this. It is possible that some NHL, MLS, and Olympic athletes were treated by surgeons not included in this survey (in some cases, a non–team surgeon may have performed the athlete’s surgery). This survey did not address concomitant knee pathology or cover all possible technique variables.

 

 

Conclusion

Most of the NHL, MLS, and Olympic team orthopedic surgeons who were surveyed perform their ACL reconstructions using BPTB autograft, using a single-bundle technique, through a transtibial portal, and do not require bracing for their athletes returning to sport. Most required their athletes to complete a series of RTS tests before resuming competitive play.

References

1.    Team USA. 2013. US Olympic Committee website. http://www.teamusa.org/athletes?pg=1&seasonId=%7BCF2DC66A-C2B3-44A8-ABB8-A486F3FBFDDF%7D&ngbId=%7BB36167A0-2AC8-4B0F-876F-93D0A44DF60A%7D. Accessed October 23, 2015.

2.    Erickson BJ, Harris JD, Cvetanovich GL, et al. Performance and return to sport after anterior cruciate ligament reconstruction in male major league soccer players. Orthop J Sports Med. 2013;1(2):1-8.

3.    Erickson BJ, Harris JD, Fillingham YA, et al. Performance and return to sport after anterior cruciate ligament reconstruction in X-Games skiers and snowboarders. Orthop J Sports Med. 2013;1(6):1-5.

4.    Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

5.    Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

6.    Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

7.    Kraeutler MJ, Bravman JT, McCarty EC. Bone–patellar tendon–bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

8.    Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: allograft versus autograft. Arthroscopy. 2005;21(7):774-785.

9.    Kartus J, Magnusson L, Stener S, Brandsson S, Eriksson BI, Karlsson J. Complications following arthroscopic anterior cruciate ligament reconstruction. A 2-5-year follow-up of 604 patients with special emphasis on anterior knee pain. Knee Surg Sports Traumatol Arthrosc. 1999;7(1):2-8.

10.  Boszotta H. Arthroscopic anterior cruciate ligament reconstruction using a patellar tendon graft in press-fit technique: surgical technique and follow-up. Arthroscopy. 1997;13(3):332-339.

11.  Hospodar SJ, Miller MD. Controversies in ACL reconstruction: bone–patellar tendon–bone anterior cruciate ligament reconstruction remains the gold standard. Sports Med Arthrosc Rev. 2009;17(4):242-246.

12.  Mascarenhas R, Tranovich MJ, Kropf EJ, Fu FH, Harner CD. Bone–patellar tendon–bone autograft versus hamstring autograft anterior cruciate ligament reconstruction in the young athlete: a retrospective matched analysis with 2-10 year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1520-1527.

13.  Bourke HE, Salmon LJ, Waller A, Patterson V, Pinczewski LA. Survival of the anterior cruciate ligament graft and the contralateral ACL at a minimum of 15 years. Am J Sports Med. 2012;40(9):1985-1992.

14.  Chalmers PN, Mall NA, Cole BJ, Verma NN, Bush-Joseph CA, Bach BR Jr. Anteromedial versus transtibial tunnel drilling in anterior cruciate ligament reconstructions: a systematic review. Arthroscopy. 2013;29(7):1235-1242.

15.  Franceschi F, Papalia R, Rizzello G, Del Buono A, Maffulli N, Denaro V. Anteromedial portal versus transtibial drilling techniques in anterior cruciate ligament reconstruction: any clinical relevance? A retrospective comparative study. Arthroscopy. 2013;29(8):1330-1337.

16.  Wang H, Fleischli JE, Zheng NN. Transtibial versus anteromedial portal technique in single-bundle anterior cruciate ligament reconstruction: outcomes of knee joint kinematics during walking. Am J Sports Med. 2013;41(8):1847-1856.

17.  Chechik O, Amar E, Khashan M, Lador R, Eyal G, Gold A. An international survey on anterior cruciate ligament reconstruction practices. Int Orthop. 2013;37(2):201-206.

18.  Keeter S, Miller C, Kohut A, Groves RM, Presser S. Consequences of reducing nonresponse in a national telephone survey. Public Opin Q. 2000;64(2):125-148.

19.  Curtin R, Presser S, Singer E. The effects of response rate changes on the index of consumer sentiment. Public Opin Q. 2000;64(4):413-428.

References

1.    Team USA. 2013. US Olympic Committee website. http://www.teamusa.org/athletes?pg=1&seasonId=%7BCF2DC66A-C2B3-44A8-ABB8-A486F3FBFDDF%7D&ngbId=%7BB36167A0-2AC8-4B0F-876F-93D0A44DF60A%7D. Accessed October 23, 2015.

2.    Erickson BJ, Harris JD, Cvetanovich GL, et al. Performance and return to sport after anterior cruciate ligament reconstruction in male major league soccer players. Orthop J Sports Med. 2013;1(2):1-8.

3.    Erickson BJ, Harris JD, Fillingham YA, et al. Performance and return to sport after anterior cruciate ligament reconstruction in X-Games skiers and snowboarders. Orthop J Sports Med. 2013;1(6):1-5.

4.    Bradley JP, Klimkiewicz JJ, Rytel MJ, Powell JW. Anterior cruciate ligament injuries in the National Football League: epidemiology and current treatment trends among team physicians. Arthroscopy. 2002;18(5):502-509.

5.    Erickson BJ, Harris JD, Fillingham YA, et al. Anterior cruciate ligament reconstruction practice patterns by NFL and NCAA football team physicians. Arthroscopy. 2014;30(6):731-738.

6.    Granan LP, Inacio MC, Maletis GB, Funahashi TT, Engebretsen L. Sport-specific injury pattern recorded during anterior cruciate ligament reconstruction. Am J Sports Med. 2013;41(12):2814-2818.

7.    Kraeutler MJ, Bravman JT, McCarty EC. Bone–patellar tendon–bone autograft versus allograft in outcomes of anterior cruciate ligament reconstruction: a meta-analysis of 5182 patients. Am J Sports Med. 2013;41(10):2439-2448.

8.    Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: allograft versus autograft. Arthroscopy. 2005;21(7):774-785.

9.    Kartus J, Magnusson L, Stener S, Brandsson S, Eriksson BI, Karlsson J. Complications following arthroscopic anterior cruciate ligament reconstruction. A 2-5-year follow-up of 604 patients with special emphasis on anterior knee pain. Knee Surg Sports Traumatol Arthrosc. 1999;7(1):2-8.

10.  Boszotta H. Arthroscopic anterior cruciate ligament reconstruction using a patellar tendon graft in press-fit technique: surgical technique and follow-up. Arthroscopy. 1997;13(3):332-339.

11.  Hospodar SJ, Miller MD. Controversies in ACL reconstruction: bone–patellar tendon–bone anterior cruciate ligament reconstruction remains the gold standard. Sports Med Arthrosc Rev. 2009;17(4):242-246.

12.  Mascarenhas R, Tranovich MJ, Kropf EJ, Fu FH, Harner CD. Bone–patellar tendon–bone autograft versus hamstring autograft anterior cruciate ligament reconstruction in the young athlete: a retrospective matched analysis with 2-10 year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(8):1520-1527.

13.  Bourke HE, Salmon LJ, Waller A, Patterson V, Pinczewski LA. Survival of the anterior cruciate ligament graft and the contralateral ACL at a minimum of 15 years. Am J Sports Med. 2012;40(9):1985-1992.

14.  Chalmers PN, Mall NA, Cole BJ, Verma NN, Bush-Joseph CA, Bach BR Jr. Anteromedial versus transtibial tunnel drilling in anterior cruciate ligament reconstructions: a systematic review. Arthroscopy. 2013;29(7):1235-1242.

15.  Franceschi F, Papalia R, Rizzello G, Del Buono A, Maffulli N, Denaro V. Anteromedial portal versus transtibial drilling techniques in anterior cruciate ligament reconstruction: any clinical relevance? A retrospective comparative study. Arthroscopy. 2013;29(8):1330-1337.

16.  Wang H, Fleischli JE, Zheng NN. Transtibial versus anteromedial portal technique in single-bundle anterior cruciate ligament reconstruction: outcomes of knee joint kinematics during walking. Am J Sports Med. 2013;41(8):1847-1856.

17.  Chechik O, Amar E, Khashan M, Lador R, Eyal G, Gold A. An international survey on anterior cruciate ligament reconstruction practices. Int Orthop. 2013;37(2):201-206.

18.  Keeter S, Miller C, Kohut A, Groves RM, Presser S. Consequences of reducing nonresponse in a national telephone survey. Public Opin Q. 2000;64(2):125-148.

19.  Curtin R, Presser S, Singer E. The effects of response rate changes on the index of consumer sentiment. Public Opin Q. 2000;64(4):413-428.

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The Dilemma of the Racist Patient

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The Dilemma of the Racist Patient

Medicine is not immune from the pervasive grasp of racism. It spills from other dimensions into the realm of healing and poses challenges to those charged with care of the patient. The literature widely documents racist experiences of patients, and differential treatment and health care disparities based on race.1,2 As a field, medicine is overshadowed by infamous experiments, such as the Tuskegee and Guatemala experiments, and routine studies that demonstrate poor treatment of minority patients.3-5 Although much-needed discussion and research is being done on the unfair treatment of patients, little is written about racist patients and their subsequent effect on health care providers and institutions. Such interactions can cause significant distress to providers, damage the therapeutic physician–patient relationship, and threaten the collegial and structural framework of an institution.6 The silent acquiescence to patients’ racist demands in recent times has become a legal, ethical, and medical dilemma that deserves attention.

No specific example of patient-generated racism is needed because most minority physicians have experienced an overtly racist interaction with a patient. The true incidence of these interactions is unknown because of underreporting secondary to the tendency of physicians to disregard this behavior in the name of “professionalism,” and because reporting of these incidents can sometimes expose how poorly a provider has dealt with the issue and draw admonishment.7 In addition to the overt interactions, numerous examples of subtle racism may exist. Manifestations of such subtleties include failure to cooperate with a history and physical examination, use of hostile language, and aggressive body language. The New York Times gives the example of an Asian female physician tending to a burly, unreceptive, swastika-tattooed patient.8 Such racist interactions are concerning, especially as diversity among newly practicing physicians increases.9

Medical Training

In medical school, students are educated to embody compassion and caring. Their care of patients should rise above the fray of poverty, interpersonal conflict, and prejudice.10 To further this point, medical school curricula have recently introduced standardized patients to teach empathy and simulate difficult encounters in order to help students learn to navigate interactions with aggressive, racist patients. In these scenarios, the patient quickly relinquishes his/her views after an overly understanding student engages the patient in conversation and addresses the source of their angst. Rarely do real-life scenarios play out in such an idealistic manner. The expectation remains, however, that the physician model extreme patience and understanding and honor the patient’s autonomy.

The American Medical Association (AMA), a guiding force in medical education, outlines the patient–physician relationship.10 Such a relationship is a mutually trusting undertaking in which the provider is the patient’s advocate and holds the well-being of the patient supreme. The goal is to alleviate suffering, and it should be done without regard to self-interest.10 The AMA also offers clear instruction to the physician in its code of medical ethics that the physician may not discriminate based on race, color, religion, national origin, sexual orientation, gender identity, or any other basis that would constitute invidious discrimination. With regard to the discriminatory practices of patients, the AMA instructs that “patients who use derogatory language or otherwise act in a prejudicial manner toward physicians, other health care professionals, or others in the health care setting, seriously undermine the integrity of the patient–physician relationship. Such behavior, if unmodified, may constitute sufficient justification for the physician to arrange for the transfer of care.”10 The AMA has also recently launched an online ethics journal, AMA Journal of Ethics, which explores difficult patient interactions and continues to reiterate the supreme role of the physician. When dealing with patients, the anti-discrimination policy is clearly set forth for physicians.

The Dilemma

Anti-discrimination policies for patients are not as clear. Patients are allowed to pick their own provider, and most institutions allow selection based on gender. Most institutions have no guidelines prohibiting provider-selection based on race, and no published hospital policies explicitly restrict racist demands. Although a culture of respect is encouraged through many hospitals’ published slogans and on websites, at the authors’ institution, no published guidelines exist about the behavior of the patient. When no such policies exist, differential treatment of patients’ racist requests ensues and frustration results. Legally, Title VII of the Civil Rights Act of 1964 bars all employers from discriminating with respect to employment conditions or terms on the basis of race, color, religion, sex, or national origin.11 Honoring a patient’s racist demands that results in discrimination of employees is a violation of that law. Reports of hospitals acceding to racist requests have often resulted in upset staff and lawsuits.12-14 Legal language, however, may be foreign in cases of life and death, or scenarios involving significant illness. Physicians in such cases often grant racist requests; for example, a Korean patient underwent life-saving measures only after he was given a non-Japanese provider, and a surgeon granted the wish of a patient’s husband to prohibit African American providers and staff members from entering the operating suite when his wife was undergoing an operation.15 Some would argue that granting a patient’s bigoted request is akin to institutionalized racism.16

 

 

The doctor–patient relationship is a powerful cornerstone for medicine. Confidence in the physician results in higher satisfaction for both parties and adherence to the treatment regimen on the part of the patient. Prejudiced interactions threaten the therapeutic alliance between patient and provider. Research has investigated how race plays a role in the doctor–patient relationship. When permitted, patients more often pick a provider of their own race.17 One of 5 African American patients wishes to have an African American provider, and such a desire is often based on a previous negative racist encounter.18 A patient’s perceptions of discrimination in general correlate with preference for same-race providers, highlighting that a patient’s overall experience with discrimination leads them to prefer a same-race physician. Race-concordant relationships (ie, one in which the provider and patient are of the same race) not only show increased satisfaction, but patients also perceive that their interactions with a racially similar physician are more participatory.19-22 In non–English speaking groups, preferences for racially similar physicians are largely based on language similarity, but Latinos feel that Latino physicians are more empathetic to their complaints.23 Such views are felt not only by patients, but also by providers. One of 3 physicians feels that patients receiving care from a physician that is of the patient’s own race is superior to that provided by a race-discordant physician.24 Superior outcomes from race-concordant doctor–patient relationships have led some to argue in favor of granting a patient’s wishes for a provider of similar race because doing so can confer additional health benefits.25

Possible Solutions

The solution to such a complex and uncomfortable issue begins with addressing the problem. Patients who make racist remarks and racist demands should be courteously informed that their behavior is inappropriate and hurtful. Failure to voice such a concern results in passive, tacit approval of racist remarks and can be distressing to other patients and staff members in the vicinity.26 It is unfair for a physician, as the leader of the care team, to ignore such behavior because it places staff members, who spend much more time with the patient, in a potentially abusive situation and leaves them feeling helpless.27 Toward this end, appropriate training, beginning in medical school and continuing in residency, in confronting racist patients is needed to ease the too often felt sense of discomfort among providers.7,26

Medical school, although rightly placing patient comfort at the center of dialogue, too often drowns out the personality of the student in the name of professionalism, which becomes a problem as a young physician struggles to reconcile his or her personality with the newly ingrained teaching to remain professional. This internal conflict can lead to frustration. A necessary prerequisite to beginning dialogue is that the physician recognizes his or her own emotional baggage from prior racially charged events and continues to remain professional. Airing the issue can help establish dialogue that can identify underlying causes of the patient’s misplaced anger. An illness and its subsequent hospitalization can make a patient feel vulnerable and helpless, and in those with poor coping mechanisms, misdirection of emotion is not uncommon.

In more difficult scenarios where attempts at dialogue reach an impasse, an ethics team should be consulted. Most institutions have such help available. Their expertise and experience can help in addressing the needs of the patient judiciously. Some institutions have dedicated multidisciplinary teams to help providers deal with dangerous and difficult patients. The implementation of the teams has reduced confrontation and litigation.28 If the impasse remains despite intervention, the physician should step aside after the patient’s care is transitioned to a provider that satisfies the needs of the patient.

 In clinically emergent scenarios, ethics consultation or prolonged discussion may not be feasible. In such cases, the patient’s wishes should be honored and attempts should be made to receive permission for life-saving or limb-saving intervention. At large tertiary care centers, the wishes of the patient can be more easily granted than at an outlying facility or rural clinic. If the patient’s wishes cannot be respected in a life-or-death scenario and the patient continues to refuse care, the principle of patient autonomy dictates that no care can be provided. Much in the same way Jehovah’s Witnesses can refuse transfusion of blood products based upon their belief system, any patient can and should be allowed to freely refuse care from a provider.

Racism is a societal disease that is complex and multilayered, and it can be deeply entrenched in the minds of those afflicted and, thus, difficult to eradicate. The manifestations of bigotry in medical settings are only one example of a mindset that likely exists in multiple aspects of life. Hospitals and clinics can become a place to establish dialogue between racially intolerant patients and their providers, but they are not the venue where firmly held racist views can be expected to be wholly reversed. Having the objective to reverse prejudiced beliefs prior to providing care is discordant to the practice of medicine and can harm a patient if an unnecessary delay ensues. Although hospitals should try to avoid offending staff members, there should be an understanding that appropriate and timely patient care is the primary goal in medicine.29 As we move to a more multicultural society, it is the hope of the authors that these already infrequent racist encounters will continue to diminish, and that medical schools and residency programs will train physicians who are highly understanding and culturally competent.

References

1.    Dimick J, Ruhter J, Sarrazin MV, Birkmeyer JD. Black patients more likely than whites to undergo surgery at low-quality hospitals in segregated regions. Health Aff (Millwood). 2013;32(6):1046-1053.

2.    Kelaher MA, Ferdinand AS, Paradies Y. Experiencing racism in health care: the mental health impacts for Victorian Aboriginal communities. Med J Aust. 2014;201(1):44-47.

3.    Johnson RL, Roter D, Powe NR, Cooper LA. Patient race/ethnicity and quality of patient-physician communication during medical visits. Am J Public Health. 2004;94(12):2084-2090.

4.    US Public Health Service Syphilis Study at Tuskegee. Centers for Disease Control and Prevention website. http://www.cdc.gov/tuskegee. Updated December 30, 2013. Accessed October 27, 2015.

5.    Fact Sheet on the 1946-1948 US Public Health Service Sexually Transmitted Diseases (STD) Inoculation Study. US Department of Health and Human Services website. http://www.hhs.gov/1946inoculationstudy/factsheet.html. Accessed October 27, 2015.

6.    Inoue M, Tsukano K, Muraoka M, Kaneko F, Okamura H. Psychological impact of verbal abuse and violence by patients on nurses working in psychiatric departments. Psychiatry Clin Neurosci. 2006;60(1):29-36.

7.    Jain SH. The racist patient. Ann Intern Med. 2013;158(8):632.

8.    Chen PW. When the patient is racist. New York Times. July 25, 2013. http://well.blogs.nytimes.com/2013/07/25/when-the-patient-is-racist/?_php=true&_type=blogs&_php=true&_type=blogs&_r=1. Accessed October 27, 2015.

9.     Castillo-Page L. Diversity in Medical Education: Facts & Figures 2012. Washington, DC: Association of American Medical Colleges; 2012:26-32. https://members.aamc.org/eweb/upload/Diversity%20in%20Medical%20Education_Facts%20and%20Figures%202012.pdf. Accessed October 27, 2015.

10.  The patient-physician relationship. Opinion 10.015. Code of Medical Ethics. American Medical Association website. http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion10015.page?. Issued December 2001. Accessed October 27, 2015.

11.  Civil Rights Act of 1964, 42 US Code § 2000e (1964). US Government Printing Office website. http://www.gpo.gov/fdsys/pkg/USCODE-2011-title42/html/USCODE-2011-title42-chap21.htm. Accessed October 27, 2015.

12.  Some hospitals grant patients’ racist requests. Houston Chronicle. February 23, 2013. http://www.chron.com/life/healthzone/article/Some-hospitals-grant-patients-racist-requests-4302145.php. Accessed October 27, 2015.

13.  Prichard O. Three workers sue Abington Hospital over racist incident; supervisors obliged a 2003 demand for only white staff in a delivery. The suits follow a federal ruling. Philadelphia Inquirer. September 16, 2005. http://articles.philly.com/2005-09-16/news/25429798_1_nursing-racial-slur-obstetrical-resident. Accessed October 27, 2015.

14.  Nurses told not to touch white patient. WNEM website. http://www.wnem.com/story/22911660/nurses-told-not-to-touch-white-patient. Published July 23, 2013. Updated August 20, 2013. Accessed October 27, 2015.

15.  Kipnis K. Quality care and the wounds of diversity. In: Mappes T DD, ed. Biomedical Ethics. 6th ed. Boston, MA: McGraw-Hill; 2006.

16.  Moghal N. Allowing patients to choose the ethnicity of attending doctors is institutional racism. BMJ. 2014;348:g265.

17.  Saha S, Taggart SH, Komaromy M, Bindman AB. Do patients choose physicians of their own race? Health Aff (Millwood). 2000;19(4):76-83.

18.  Malat J, van Ryn M. African-American preference for same-race healthcare providers: the role of healthcare discrimination. Ethnicity Dis. 2005;15(4):740-747.

19.  LaVeist TA, Carroll T. Race of physician and satisfaction with care among African-American patients. J Natl Med Assoc. 2002;94(11):937-943.

20.  Saha S, Komaromy M, Koepsell TD, Bindman AB. Patient-physician racial concordance and the perceived quality and use of health care. Arch Intern Med. 1999;159(9):997-1004.

21.  Cooper-Patrick L, Gallo JJ, Gonzales JJ, et al. Race, gender, and partnership in the patient-physician relationship. JAMA. 1999;282(6):583-589.

22.  Cooper LA, Roter DL, Johnson RL, Ford DE, Steinwachs DM, Powe NR. Patient-centered communication, ratings of care, and concordance of patient and physician race. Ann Intern Med. 2003;139(11):907-915.

23.  Garcia JA, Paterniti DA, Romano PS, Kravitz RL. Patient p for physician characteristics in university-based primary care clinics. Ethnicity Dis. 2003;13(2):259-267.

24.  Padela AI, Schneider SM, He H, Ali Z, Richardson TM. Patient choice of provider type in the emergency department: perceptions and factors relating to accommodation of requests for care providers. Emerg Med J. 2010;27(6):465-469.

25.  Paul-Emile K. Patients’ racial p and the medical culture of accommodation. UCLA Law Rev. 2012;60(2):462-504.

26.  Selby M. Ethical dilemma: dealing with racist patients. BMJ. 1999;318(7191):1129.

27.  Warshafsky RJ. Lack of support for staff to combat racism. BMJ. 2014;348:g1716.

28.  Carlson MJ, Baker LH. Difficult, dangerous, and drug seeking: the 3D way to better patient care. Am J Public Health. 1998;88(8):1250-1252.

29.   Lane-Fall M. A piece of my mind. Accommodating bigotry. JAMA. 2014;311(2):139-140

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Authors’ Disclosure Statement: Dr. Mir wishes to report that he is a paid consultant for Smith & Nephew. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Mir wishes to report that he is a paid consultant for Smith & Nephew. The other authors report no actual or potential conflict of interest in relation to this article.

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Medicine is not immune from the pervasive grasp of racism. It spills from other dimensions into the realm of healing and poses challenges to those charged with care of the patient. The literature widely documents racist experiences of patients, and differential treatment and health care disparities based on race.1,2 As a field, medicine is overshadowed by infamous experiments, such as the Tuskegee and Guatemala experiments, and routine studies that demonstrate poor treatment of minority patients.3-5 Although much-needed discussion and research is being done on the unfair treatment of patients, little is written about racist patients and their subsequent effect on health care providers and institutions. Such interactions can cause significant distress to providers, damage the therapeutic physician–patient relationship, and threaten the collegial and structural framework of an institution.6 The silent acquiescence to patients’ racist demands in recent times has become a legal, ethical, and medical dilemma that deserves attention.

No specific example of patient-generated racism is needed because most minority physicians have experienced an overtly racist interaction with a patient. The true incidence of these interactions is unknown because of underreporting secondary to the tendency of physicians to disregard this behavior in the name of “professionalism,” and because reporting of these incidents can sometimes expose how poorly a provider has dealt with the issue and draw admonishment.7 In addition to the overt interactions, numerous examples of subtle racism may exist. Manifestations of such subtleties include failure to cooperate with a history and physical examination, use of hostile language, and aggressive body language. The New York Times gives the example of an Asian female physician tending to a burly, unreceptive, swastika-tattooed patient.8 Such racist interactions are concerning, especially as diversity among newly practicing physicians increases.9

Medical Training

In medical school, students are educated to embody compassion and caring. Their care of patients should rise above the fray of poverty, interpersonal conflict, and prejudice.10 To further this point, medical school curricula have recently introduced standardized patients to teach empathy and simulate difficult encounters in order to help students learn to navigate interactions with aggressive, racist patients. In these scenarios, the patient quickly relinquishes his/her views after an overly understanding student engages the patient in conversation and addresses the source of their angst. Rarely do real-life scenarios play out in such an idealistic manner. The expectation remains, however, that the physician model extreme patience and understanding and honor the patient’s autonomy.

The American Medical Association (AMA), a guiding force in medical education, outlines the patient–physician relationship.10 Such a relationship is a mutually trusting undertaking in which the provider is the patient’s advocate and holds the well-being of the patient supreme. The goal is to alleviate suffering, and it should be done without regard to self-interest.10 The AMA also offers clear instruction to the physician in its code of medical ethics that the physician may not discriminate based on race, color, religion, national origin, sexual orientation, gender identity, or any other basis that would constitute invidious discrimination. With regard to the discriminatory practices of patients, the AMA instructs that “patients who use derogatory language or otherwise act in a prejudicial manner toward physicians, other health care professionals, or others in the health care setting, seriously undermine the integrity of the patient–physician relationship. Such behavior, if unmodified, may constitute sufficient justification for the physician to arrange for the transfer of care.”10 The AMA has also recently launched an online ethics journal, AMA Journal of Ethics, which explores difficult patient interactions and continues to reiterate the supreme role of the physician. When dealing with patients, the anti-discrimination policy is clearly set forth for physicians.

The Dilemma

Anti-discrimination policies for patients are not as clear. Patients are allowed to pick their own provider, and most institutions allow selection based on gender. Most institutions have no guidelines prohibiting provider-selection based on race, and no published hospital policies explicitly restrict racist demands. Although a culture of respect is encouraged through many hospitals’ published slogans and on websites, at the authors’ institution, no published guidelines exist about the behavior of the patient. When no such policies exist, differential treatment of patients’ racist requests ensues and frustration results. Legally, Title VII of the Civil Rights Act of 1964 bars all employers from discriminating with respect to employment conditions or terms on the basis of race, color, religion, sex, or national origin.11 Honoring a patient’s racist demands that results in discrimination of employees is a violation of that law. Reports of hospitals acceding to racist requests have often resulted in upset staff and lawsuits.12-14 Legal language, however, may be foreign in cases of life and death, or scenarios involving significant illness. Physicians in such cases often grant racist requests; for example, a Korean patient underwent life-saving measures only after he was given a non-Japanese provider, and a surgeon granted the wish of a patient’s husband to prohibit African American providers and staff members from entering the operating suite when his wife was undergoing an operation.15 Some would argue that granting a patient’s bigoted request is akin to institutionalized racism.16

 

 

The doctor–patient relationship is a powerful cornerstone for medicine. Confidence in the physician results in higher satisfaction for both parties and adherence to the treatment regimen on the part of the patient. Prejudiced interactions threaten the therapeutic alliance between patient and provider. Research has investigated how race plays a role in the doctor–patient relationship. When permitted, patients more often pick a provider of their own race.17 One of 5 African American patients wishes to have an African American provider, and such a desire is often based on a previous negative racist encounter.18 A patient’s perceptions of discrimination in general correlate with preference for same-race providers, highlighting that a patient’s overall experience with discrimination leads them to prefer a same-race physician. Race-concordant relationships (ie, one in which the provider and patient are of the same race) not only show increased satisfaction, but patients also perceive that their interactions with a racially similar physician are more participatory.19-22 In non–English speaking groups, preferences for racially similar physicians are largely based on language similarity, but Latinos feel that Latino physicians are more empathetic to their complaints.23 Such views are felt not only by patients, but also by providers. One of 3 physicians feels that patients receiving care from a physician that is of the patient’s own race is superior to that provided by a race-discordant physician.24 Superior outcomes from race-concordant doctor–patient relationships have led some to argue in favor of granting a patient’s wishes for a provider of similar race because doing so can confer additional health benefits.25

Possible Solutions

The solution to such a complex and uncomfortable issue begins with addressing the problem. Patients who make racist remarks and racist demands should be courteously informed that their behavior is inappropriate and hurtful. Failure to voice such a concern results in passive, tacit approval of racist remarks and can be distressing to other patients and staff members in the vicinity.26 It is unfair for a physician, as the leader of the care team, to ignore such behavior because it places staff members, who spend much more time with the patient, in a potentially abusive situation and leaves them feeling helpless.27 Toward this end, appropriate training, beginning in medical school and continuing in residency, in confronting racist patients is needed to ease the too often felt sense of discomfort among providers.7,26

Medical school, although rightly placing patient comfort at the center of dialogue, too often drowns out the personality of the student in the name of professionalism, which becomes a problem as a young physician struggles to reconcile his or her personality with the newly ingrained teaching to remain professional. This internal conflict can lead to frustration. A necessary prerequisite to beginning dialogue is that the physician recognizes his or her own emotional baggage from prior racially charged events and continues to remain professional. Airing the issue can help establish dialogue that can identify underlying causes of the patient’s misplaced anger. An illness and its subsequent hospitalization can make a patient feel vulnerable and helpless, and in those with poor coping mechanisms, misdirection of emotion is not uncommon.

In more difficult scenarios where attempts at dialogue reach an impasse, an ethics team should be consulted. Most institutions have such help available. Their expertise and experience can help in addressing the needs of the patient judiciously. Some institutions have dedicated multidisciplinary teams to help providers deal with dangerous and difficult patients. The implementation of the teams has reduced confrontation and litigation.28 If the impasse remains despite intervention, the physician should step aside after the patient’s care is transitioned to a provider that satisfies the needs of the patient.

 In clinically emergent scenarios, ethics consultation or prolonged discussion may not be feasible. In such cases, the patient’s wishes should be honored and attempts should be made to receive permission for life-saving or limb-saving intervention. At large tertiary care centers, the wishes of the patient can be more easily granted than at an outlying facility or rural clinic. If the patient’s wishes cannot be respected in a life-or-death scenario and the patient continues to refuse care, the principle of patient autonomy dictates that no care can be provided. Much in the same way Jehovah’s Witnesses can refuse transfusion of blood products based upon their belief system, any patient can and should be allowed to freely refuse care from a provider.

Racism is a societal disease that is complex and multilayered, and it can be deeply entrenched in the minds of those afflicted and, thus, difficult to eradicate. The manifestations of bigotry in medical settings are only one example of a mindset that likely exists in multiple aspects of life. Hospitals and clinics can become a place to establish dialogue between racially intolerant patients and their providers, but they are not the venue where firmly held racist views can be expected to be wholly reversed. Having the objective to reverse prejudiced beliefs prior to providing care is discordant to the practice of medicine and can harm a patient if an unnecessary delay ensues. Although hospitals should try to avoid offending staff members, there should be an understanding that appropriate and timely patient care is the primary goal in medicine.29 As we move to a more multicultural society, it is the hope of the authors that these already infrequent racist encounters will continue to diminish, and that medical schools and residency programs will train physicians who are highly understanding and culturally competent.

Medicine is not immune from the pervasive grasp of racism. It spills from other dimensions into the realm of healing and poses challenges to those charged with care of the patient. The literature widely documents racist experiences of patients, and differential treatment and health care disparities based on race.1,2 As a field, medicine is overshadowed by infamous experiments, such as the Tuskegee and Guatemala experiments, and routine studies that demonstrate poor treatment of minority patients.3-5 Although much-needed discussion and research is being done on the unfair treatment of patients, little is written about racist patients and their subsequent effect on health care providers and institutions. Such interactions can cause significant distress to providers, damage the therapeutic physician–patient relationship, and threaten the collegial and structural framework of an institution.6 The silent acquiescence to patients’ racist demands in recent times has become a legal, ethical, and medical dilemma that deserves attention.

No specific example of patient-generated racism is needed because most minority physicians have experienced an overtly racist interaction with a patient. The true incidence of these interactions is unknown because of underreporting secondary to the tendency of physicians to disregard this behavior in the name of “professionalism,” and because reporting of these incidents can sometimes expose how poorly a provider has dealt with the issue and draw admonishment.7 In addition to the overt interactions, numerous examples of subtle racism may exist. Manifestations of such subtleties include failure to cooperate with a history and physical examination, use of hostile language, and aggressive body language. The New York Times gives the example of an Asian female physician tending to a burly, unreceptive, swastika-tattooed patient.8 Such racist interactions are concerning, especially as diversity among newly practicing physicians increases.9

Medical Training

In medical school, students are educated to embody compassion and caring. Their care of patients should rise above the fray of poverty, interpersonal conflict, and prejudice.10 To further this point, medical school curricula have recently introduced standardized patients to teach empathy and simulate difficult encounters in order to help students learn to navigate interactions with aggressive, racist patients. In these scenarios, the patient quickly relinquishes his/her views after an overly understanding student engages the patient in conversation and addresses the source of their angst. Rarely do real-life scenarios play out in such an idealistic manner. The expectation remains, however, that the physician model extreme patience and understanding and honor the patient’s autonomy.

The American Medical Association (AMA), a guiding force in medical education, outlines the patient–physician relationship.10 Such a relationship is a mutually trusting undertaking in which the provider is the patient’s advocate and holds the well-being of the patient supreme. The goal is to alleviate suffering, and it should be done without regard to self-interest.10 The AMA also offers clear instruction to the physician in its code of medical ethics that the physician may not discriminate based on race, color, religion, national origin, sexual orientation, gender identity, or any other basis that would constitute invidious discrimination. With regard to the discriminatory practices of patients, the AMA instructs that “patients who use derogatory language or otherwise act in a prejudicial manner toward physicians, other health care professionals, or others in the health care setting, seriously undermine the integrity of the patient–physician relationship. Such behavior, if unmodified, may constitute sufficient justification for the physician to arrange for the transfer of care.”10 The AMA has also recently launched an online ethics journal, AMA Journal of Ethics, which explores difficult patient interactions and continues to reiterate the supreme role of the physician. When dealing with patients, the anti-discrimination policy is clearly set forth for physicians.

The Dilemma

Anti-discrimination policies for patients are not as clear. Patients are allowed to pick their own provider, and most institutions allow selection based on gender. Most institutions have no guidelines prohibiting provider-selection based on race, and no published hospital policies explicitly restrict racist demands. Although a culture of respect is encouraged through many hospitals’ published slogans and on websites, at the authors’ institution, no published guidelines exist about the behavior of the patient. When no such policies exist, differential treatment of patients’ racist requests ensues and frustration results. Legally, Title VII of the Civil Rights Act of 1964 bars all employers from discriminating with respect to employment conditions or terms on the basis of race, color, religion, sex, or national origin.11 Honoring a patient’s racist demands that results in discrimination of employees is a violation of that law. Reports of hospitals acceding to racist requests have often resulted in upset staff and lawsuits.12-14 Legal language, however, may be foreign in cases of life and death, or scenarios involving significant illness. Physicians in such cases often grant racist requests; for example, a Korean patient underwent life-saving measures only after he was given a non-Japanese provider, and a surgeon granted the wish of a patient’s husband to prohibit African American providers and staff members from entering the operating suite when his wife was undergoing an operation.15 Some would argue that granting a patient’s bigoted request is akin to institutionalized racism.16

 

 

The doctor–patient relationship is a powerful cornerstone for medicine. Confidence in the physician results in higher satisfaction for both parties and adherence to the treatment regimen on the part of the patient. Prejudiced interactions threaten the therapeutic alliance between patient and provider. Research has investigated how race plays a role in the doctor–patient relationship. When permitted, patients more often pick a provider of their own race.17 One of 5 African American patients wishes to have an African American provider, and such a desire is often based on a previous negative racist encounter.18 A patient’s perceptions of discrimination in general correlate with preference for same-race providers, highlighting that a patient’s overall experience with discrimination leads them to prefer a same-race physician. Race-concordant relationships (ie, one in which the provider and patient are of the same race) not only show increased satisfaction, but patients also perceive that their interactions with a racially similar physician are more participatory.19-22 In non–English speaking groups, preferences for racially similar physicians are largely based on language similarity, but Latinos feel that Latino physicians are more empathetic to their complaints.23 Such views are felt not only by patients, but also by providers. One of 3 physicians feels that patients receiving care from a physician that is of the patient’s own race is superior to that provided by a race-discordant physician.24 Superior outcomes from race-concordant doctor–patient relationships have led some to argue in favor of granting a patient’s wishes for a provider of similar race because doing so can confer additional health benefits.25

Possible Solutions

The solution to such a complex and uncomfortable issue begins with addressing the problem. Patients who make racist remarks and racist demands should be courteously informed that their behavior is inappropriate and hurtful. Failure to voice such a concern results in passive, tacit approval of racist remarks and can be distressing to other patients and staff members in the vicinity.26 It is unfair for a physician, as the leader of the care team, to ignore such behavior because it places staff members, who spend much more time with the patient, in a potentially abusive situation and leaves them feeling helpless.27 Toward this end, appropriate training, beginning in medical school and continuing in residency, in confronting racist patients is needed to ease the too often felt sense of discomfort among providers.7,26

Medical school, although rightly placing patient comfort at the center of dialogue, too often drowns out the personality of the student in the name of professionalism, which becomes a problem as a young physician struggles to reconcile his or her personality with the newly ingrained teaching to remain professional. This internal conflict can lead to frustration. A necessary prerequisite to beginning dialogue is that the physician recognizes his or her own emotional baggage from prior racially charged events and continues to remain professional. Airing the issue can help establish dialogue that can identify underlying causes of the patient’s misplaced anger. An illness and its subsequent hospitalization can make a patient feel vulnerable and helpless, and in those with poor coping mechanisms, misdirection of emotion is not uncommon.

In more difficult scenarios where attempts at dialogue reach an impasse, an ethics team should be consulted. Most institutions have such help available. Their expertise and experience can help in addressing the needs of the patient judiciously. Some institutions have dedicated multidisciplinary teams to help providers deal with dangerous and difficult patients. The implementation of the teams has reduced confrontation and litigation.28 If the impasse remains despite intervention, the physician should step aside after the patient’s care is transitioned to a provider that satisfies the needs of the patient.

 In clinically emergent scenarios, ethics consultation or prolonged discussion may not be feasible. In such cases, the patient’s wishes should be honored and attempts should be made to receive permission for life-saving or limb-saving intervention. At large tertiary care centers, the wishes of the patient can be more easily granted than at an outlying facility or rural clinic. If the patient’s wishes cannot be respected in a life-or-death scenario and the patient continues to refuse care, the principle of patient autonomy dictates that no care can be provided. Much in the same way Jehovah’s Witnesses can refuse transfusion of blood products based upon their belief system, any patient can and should be allowed to freely refuse care from a provider.

Racism is a societal disease that is complex and multilayered, and it can be deeply entrenched in the minds of those afflicted and, thus, difficult to eradicate. The manifestations of bigotry in medical settings are only one example of a mindset that likely exists in multiple aspects of life. Hospitals and clinics can become a place to establish dialogue between racially intolerant patients and their providers, but they are not the venue where firmly held racist views can be expected to be wholly reversed. Having the objective to reverse prejudiced beliefs prior to providing care is discordant to the practice of medicine and can harm a patient if an unnecessary delay ensues. Although hospitals should try to avoid offending staff members, there should be an understanding that appropriate and timely patient care is the primary goal in medicine.29 As we move to a more multicultural society, it is the hope of the authors that these already infrequent racist encounters will continue to diminish, and that medical schools and residency programs will train physicians who are highly understanding and culturally competent.

References

1.    Dimick J, Ruhter J, Sarrazin MV, Birkmeyer JD. Black patients more likely than whites to undergo surgery at low-quality hospitals in segregated regions. Health Aff (Millwood). 2013;32(6):1046-1053.

2.    Kelaher MA, Ferdinand AS, Paradies Y. Experiencing racism in health care: the mental health impacts for Victorian Aboriginal communities. Med J Aust. 2014;201(1):44-47.

3.    Johnson RL, Roter D, Powe NR, Cooper LA. Patient race/ethnicity and quality of patient-physician communication during medical visits. Am J Public Health. 2004;94(12):2084-2090.

4.    US Public Health Service Syphilis Study at Tuskegee. Centers for Disease Control and Prevention website. http://www.cdc.gov/tuskegee. Updated December 30, 2013. Accessed October 27, 2015.

5.    Fact Sheet on the 1946-1948 US Public Health Service Sexually Transmitted Diseases (STD) Inoculation Study. US Department of Health and Human Services website. http://www.hhs.gov/1946inoculationstudy/factsheet.html. Accessed October 27, 2015.

6.    Inoue M, Tsukano K, Muraoka M, Kaneko F, Okamura H. Psychological impact of verbal abuse and violence by patients on nurses working in psychiatric departments. Psychiatry Clin Neurosci. 2006;60(1):29-36.

7.    Jain SH. The racist patient. Ann Intern Med. 2013;158(8):632.

8.    Chen PW. When the patient is racist. New York Times. July 25, 2013. http://well.blogs.nytimes.com/2013/07/25/when-the-patient-is-racist/?_php=true&_type=blogs&_php=true&_type=blogs&_r=1. Accessed October 27, 2015.

9.     Castillo-Page L. Diversity in Medical Education: Facts & Figures 2012. Washington, DC: Association of American Medical Colleges; 2012:26-32. https://members.aamc.org/eweb/upload/Diversity%20in%20Medical%20Education_Facts%20and%20Figures%202012.pdf. Accessed October 27, 2015.

10.  The patient-physician relationship. Opinion 10.015. Code of Medical Ethics. American Medical Association website. http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion10015.page?. Issued December 2001. Accessed October 27, 2015.

11.  Civil Rights Act of 1964, 42 US Code § 2000e (1964). US Government Printing Office website. http://www.gpo.gov/fdsys/pkg/USCODE-2011-title42/html/USCODE-2011-title42-chap21.htm. Accessed October 27, 2015.

12.  Some hospitals grant patients’ racist requests. Houston Chronicle. February 23, 2013. http://www.chron.com/life/healthzone/article/Some-hospitals-grant-patients-racist-requests-4302145.php. Accessed October 27, 2015.

13.  Prichard O. Three workers sue Abington Hospital over racist incident; supervisors obliged a 2003 demand for only white staff in a delivery. The suits follow a federal ruling. Philadelphia Inquirer. September 16, 2005. http://articles.philly.com/2005-09-16/news/25429798_1_nursing-racial-slur-obstetrical-resident. Accessed October 27, 2015.

14.  Nurses told not to touch white patient. WNEM website. http://www.wnem.com/story/22911660/nurses-told-not-to-touch-white-patient. Published July 23, 2013. Updated August 20, 2013. Accessed October 27, 2015.

15.  Kipnis K. Quality care and the wounds of diversity. In: Mappes T DD, ed. Biomedical Ethics. 6th ed. Boston, MA: McGraw-Hill; 2006.

16.  Moghal N. Allowing patients to choose the ethnicity of attending doctors is institutional racism. BMJ. 2014;348:g265.

17.  Saha S, Taggart SH, Komaromy M, Bindman AB. Do patients choose physicians of their own race? Health Aff (Millwood). 2000;19(4):76-83.

18.  Malat J, van Ryn M. African-American preference for same-race healthcare providers: the role of healthcare discrimination. Ethnicity Dis. 2005;15(4):740-747.

19.  LaVeist TA, Carroll T. Race of physician and satisfaction with care among African-American patients. J Natl Med Assoc. 2002;94(11):937-943.

20.  Saha S, Komaromy M, Koepsell TD, Bindman AB. Patient-physician racial concordance and the perceived quality and use of health care. Arch Intern Med. 1999;159(9):997-1004.

21.  Cooper-Patrick L, Gallo JJ, Gonzales JJ, et al. Race, gender, and partnership in the patient-physician relationship. JAMA. 1999;282(6):583-589.

22.  Cooper LA, Roter DL, Johnson RL, Ford DE, Steinwachs DM, Powe NR. Patient-centered communication, ratings of care, and concordance of patient and physician race. Ann Intern Med. 2003;139(11):907-915.

23.  Garcia JA, Paterniti DA, Romano PS, Kravitz RL. Patient p for physician characteristics in university-based primary care clinics. Ethnicity Dis. 2003;13(2):259-267.

24.  Padela AI, Schneider SM, He H, Ali Z, Richardson TM. Patient choice of provider type in the emergency department: perceptions and factors relating to accommodation of requests for care providers. Emerg Med J. 2010;27(6):465-469.

25.  Paul-Emile K. Patients’ racial p and the medical culture of accommodation. UCLA Law Rev. 2012;60(2):462-504.

26.  Selby M. Ethical dilemma: dealing with racist patients. BMJ. 1999;318(7191):1129.

27.  Warshafsky RJ. Lack of support for staff to combat racism. BMJ. 2014;348:g1716.

28.  Carlson MJ, Baker LH. Difficult, dangerous, and drug seeking: the 3D way to better patient care. Am J Public Health. 1998;88(8):1250-1252.

29.   Lane-Fall M. A piece of my mind. Accommodating bigotry. JAMA. 2014;311(2):139-140

References

1.    Dimick J, Ruhter J, Sarrazin MV, Birkmeyer JD. Black patients more likely than whites to undergo surgery at low-quality hospitals in segregated regions. Health Aff (Millwood). 2013;32(6):1046-1053.

2.    Kelaher MA, Ferdinand AS, Paradies Y. Experiencing racism in health care: the mental health impacts for Victorian Aboriginal communities. Med J Aust. 2014;201(1):44-47.

3.    Johnson RL, Roter D, Powe NR, Cooper LA. Patient race/ethnicity and quality of patient-physician communication during medical visits. Am J Public Health. 2004;94(12):2084-2090.

4.    US Public Health Service Syphilis Study at Tuskegee. Centers for Disease Control and Prevention website. http://www.cdc.gov/tuskegee. Updated December 30, 2013. Accessed October 27, 2015.

5.    Fact Sheet on the 1946-1948 US Public Health Service Sexually Transmitted Diseases (STD) Inoculation Study. US Department of Health and Human Services website. http://www.hhs.gov/1946inoculationstudy/factsheet.html. Accessed October 27, 2015.

6.    Inoue M, Tsukano K, Muraoka M, Kaneko F, Okamura H. Psychological impact of verbal abuse and violence by patients on nurses working in psychiatric departments. Psychiatry Clin Neurosci. 2006;60(1):29-36.

7.    Jain SH. The racist patient. Ann Intern Med. 2013;158(8):632.

8.    Chen PW. When the patient is racist. New York Times. July 25, 2013. http://well.blogs.nytimes.com/2013/07/25/when-the-patient-is-racist/?_php=true&_type=blogs&_php=true&_type=blogs&_r=1. Accessed October 27, 2015.

9.     Castillo-Page L. Diversity in Medical Education: Facts & Figures 2012. Washington, DC: Association of American Medical Colleges; 2012:26-32. https://members.aamc.org/eweb/upload/Diversity%20in%20Medical%20Education_Facts%20and%20Figures%202012.pdf. Accessed October 27, 2015.

10.  The patient-physician relationship. Opinion 10.015. Code of Medical Ethics. American Medical Association website. http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion10015.page?. Issued December 2001. Accessed October 27, 2015.

11.  Civil Rights Act of 1964, 42 US Code § 2000e (1964). US Government Printing Office website. http://www.gpo.gov/fdsys/pkg/USCODE-2011-title42/html/USCODE-2011-title42-chap21.htm. Accessed October 27, 2015.

12.  Some hospitals grant patients’ racist requests. Houston Chronicle. February 23, 2013. http://www.chron.com/life/healthzone/article/Some-hospitals-grant-patients-racist-requests-4302145.php. Accessed October 27, 2015.

13.  Prichard O. Three workers sue Abington Hospital over racist incident; supervisors obliged a 2003 demand for only white staff in a delivery. The suits follow a federal ruling. Philadelphia Inquirer. September 16, 2005. http://articles.philly.com/2005-09-16/news/25429798_1_nursing-racial-slur-obstetrical-resident. Accessed October 27, 2015.

14.  Nurses told not to touch white patient. WNEM website. http://www.wnem.com/story/22911660/nurses-told-not-to-touch-white-patient. Published July 23, 2013. Updated August 20, 2013. Accessed October 27, 2015.

15.  Kipnis K. Quality care and the wounds of diversity. In: Mappes T DD, ed. Biomedical Ethics. 6th ed. Boston, MA: McGraw-Hill; 2006.

16.  Moghal N. Allowing patients to choose the ethnicity of attending doctors is institutional racism. BMJ. 2014;348:g265.

17.  Saha S, Taggart SH, Komaromy M, Bindman AB. Do patients choose physicians of their own race? Health Aff (Millwood). 2000;19(4):76-83.

18.  Malat J, van Ryn M. African-American preference for same-race healthcare providers: the role of healthcare discrimination. Ethnicity Dis. 2005;15(4):740-747.

19.  LaVeist TA, Carroll T. Race of physician and satisfaction with care among African-American patients. J Natl Med Assoc. 2002;94(11):937-943.

20.  Saha S, Komaromy M, Koepsell TD, Bindman AB. Patient-physician racial concordance and the perceived quality and use of health care. Arch Intern Med. 1999;159(9):997-1004.

21.  Cooper-Patrick L, Gallo JJ, Gonzales JJ, et al. Race, gender, and partnership in the patient-physician relationship. JAMA. 1999;282(6):583-589.

22.  Cooper LA, Roter DL, Johnson RL, Ford DE, Steinwachs DM, Powe NR. Patient-centered communication, ratings of care, and concordance of patient and physician race. Ann Intern Med. 2003;139(11):907-915.

23.  Garcia JA, Paterniti DA, Romano PS, Kravitz RL. Patient p for physician characteristics in university-based primary care clinics. Ethnicity Dis. 2003;13(2):259-267.

24.  Padela AI, Schneider SM, He H, Ali Z, Richardson TM. Patient choice of provider type in the emergency department: perceptions and factors relating to accommodation of requests for care providers. Emerg Med J. 2010;27(6):465-469.

25.  Paul-Emile K. Patients’ racial p and the medical culture of accommodation. UCLA Law Rev. 2012;60(2):462-504.

26.  Selby M. Ethical dilemma: dealing with racist patients. BMJ. 1999;318(7191):1129.

27.  Warshafsky RJ. Lack of support for staff to combat racism. BMJ. 2014;348:g1716.

28.  Carlson MJ, Baker LH. Difficult, dangerous, and drug seeking: the 3D way to better patient care. Am J Public Health. 1998;88(8):1250-1252.

29.   Lane-Fall M. A piece of my mind. Accommodating bigotry. JAMA. 2014;311(2):139-140

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Intra-articular Olecranon Fracture Fixed with an Iso-Elastic Tension Band

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Intra-articular Olecranon Fracture Fixed with an Iso-Elastic Tension Band

Surgical technique using isoelastic tension band for treatment of olecranon fractures.

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Surgical technique using isoelastic tension band for treatment of olecranon fractures.

To read the authors' full article click here.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Surgical technique using isoelastic tension band for treatment of olecranon fractures.

To read the authors' full article click here.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
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Practice Transition Planning: When Is the Right Time?

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If you are a solo orthopedic surgeon or practice in a small group and are 55 years or older, this article is for you. The answer to the question “When is the right time to begin planning for the transition out of practice?” is now. And planning is the most important word in that sentence.

Joining your peers who’ve quit, often rather quickly, because of Obamacare, electronic health records (EHRs), or the implementation of ICD-10 (International Classification of Diseases, Tenth Revision) may prove unsatisfying. As the saying goes, “act in haste, repent at leisure.” And as a gerontologist friend of mine liked to say, “Retiring from medicine without retiring to something is risky.” He often quipped that golf didn’t count.

Recent survey results help support his point. In the 2014 Medscape Orthopedist Compensation Report,1 respondents were asked:

What is the most rewarding part of your job?

  • Gratitude/relationships with patients            43%
  • Being very good at what I do/Finding answers, diagnoses          31%
  • Making good money at a job that I like        10%
  • Knowing that I’m making the world a better place      7%
  • Being proud of being a doctor        4%
  • Nothing 1%
  • Let’s hope you are not part of the 1%!

In the often-quoted Deloitte 2013 Survey of U.S. Physicians,2 6 in 10 respondents predicted that many physicians will retire earlier than planned in the next 1 to 3 years. Yet even in that survey, 41% of surgical specialists said that patient relationships were the most satisfying factor about practicing medicine. Protecting and promoting individual health was second (33%), and intellectual stimulation was third (16%).2   

As Steve Marsh, managing partner at The Medicus Firm, Dallas, was quoted as saying about this data, “For older doctors, being a physician is much more of a lifestyle than a job.”3 In my 40 years of working with physicians, I agree. And that’s why you, dear readers, must begin the transition planning process now, if you are 55 years or older, or soon, if you are approaching this age. Unraveling yourself from the patient relationships and the profession you have enjoyed for so long will feel like a big loss for the majority of you. There will be a grieving process. You’re not just leaving a “job,” you’re leaving your “life’s work,” and the sooner you begin planning for this shift, the less uncomfortable it will be.

Transition Planning Timeline

As the Chinese saying goes, “the longest journey begins with a single step.” The first, most challenging step in transition planning is deciding to address the issue head on—whether you see yourself practicing well into your late 60s or stepping aside 3 years from now.

Here are 7 questions to get you started. Discuss them with your spouse and a trusted advisor or mentor.

1.  Have you done everything that you wanted to accomplish professionally? What’s left on your “to-do” list?  

2.  Are you satisfied with the legacy you are leaving to your community, partners, or employees?

3.  What does your spouse think? His or her age and stage may dictate some choices. One wife said she believed in Henny Youngman’s advice: “Promise to take your wife for better or worse, but not for lunch.” Younger spouses in satisfying careers may not be ready to quit or slow down.

4.  What could fill the void of, as the Medscape survey indicated, the “gratitude/patient relationships” and “being good at what you do” that you would be leaving behind? Could going on medical missions satisfy your need to keep your hands in? Or volunteering for the community clinic?

5. If you were to retire within the next 6 months, what would your routine look like? Because the first year is often filled with travel and long-postponed fun, think beyond that and describe year 3. (Assume good health and adequate finances.) 

6.  Are there options for part-time practice? Could you ease out instead of going basically full throttle until your retirement date?

7.  Are challenges such as stress, fatigue, cognitive decline, or a feeling of burnout a reality for you? Be honest with yourself. These are real issues that not only impact your decision about when to transition, but also patient safety and care.

If you’ve reached 60 years of age and haven’t thought about questions like these, you aren’t alone. Many orthopedic surgeons delay this planning exercise for the same reasons other business owners do:

You are too busy spending all of your time putting out fires. Who has time to plan? Learning the new ICD-10 codes for local coverage determinations (LCDs), hiring a new physician assistant, firing the receptionist, and, oh by the way, taking care of a full schedule of patients, takes time and reduces the time to plan.

 

 

You think “it’s not time yet.” We often hear surgeons say, “Gosh, I don’t feel __ years old!” or “I plan to work until I’m 70.” Sound familiar?

You’re afraid to think about what life would be like without your profession. So you do nothing. Imagining a life without being needed on a daily basis can be daunting. Reread the survey results above. If you don’t have interesting and emotionally rewarding activities that will fill the void, that can cause anxiety. And the fact is, the demands on physicians, especially those in solo practice, haven’t left much time for outside interests.   

Discussing personal goals and financial matters with others is messy or taboo. Transitioning out of practice is an awkward and uncomfortable topic. Plus, whom do you call for help with planning the next stage of your life? 

These and others on a long list of excuses and anxieties result in fewer than 70% of all surgical specialists we talk with having a viable transition plan. Many, of course, have done a superb job of funding their retirement plans and have the assets set aside to fund a comfortable lifestyle. A lot has been written on the financial aspects of retirement. Your financial advisor, broker, or banker has formulas, tools, and advice that you’ve probably been following for decades. The 2014 Medscape Orthopedist Compensation Report shows the average salary is $413,000, with private practice doctors earning even more, $439,000 on average.1 Although such salaries should ensure the funding of retirement savings plans, undeniably, the financial crisis and stock market collapse of 2008 delayed many surgeons’ retirement. Even today, some surgeons who are considering their practice finish line are looking over their shoulder at market returns with a sense of insecurity.

Recruitment Is More Likely Than Cash Out

Thinking you can sell your practice for big bucks is a false hope. In the 1970s and early 1980s, before the onslaught of managed care, it was possible to sell your practice. A young surgeon would welcome having space, staff, and patients at the ready. This is no longer the case, since patient loyalty is now impacted by health insurance plan membership.

Pocketing a hefty sum from selling the office building may not be much of a windfall either. It depends on that all-important real estate formula: location, location, location. In addition, dividends from and investment in a surgery center rarely continue once you are no longer operating.

To maximize the profit potential that remains in this last phase of practice—which in turn can attract surgical talent as you transition—you’ve got to sharpen the sword and pay attention. One surgeon attributed a revenue decline of about 30% over the last 5 years to a combination of lesser insurance reimbursements, his taking more time off, and failing to pay attention to his staff’s write-off habits. Revenue cycle, management, coding, and practice operations must be finely tuned to optimize profitability, and failing to manage your practice effectively will make it less attractive when recruiting a younger surgeon to take your place or assume the patient base. Consider a practice evaluation regardless of where you are in your planning, which will help the practice prioritize improvements that deliver the best benefit and value within the context of your transition plan.

And if recruitment is part of that plan, be prepared to spend significant time on the search. Solo and small groups are finding it challenging to recruit just-out-of-training associates. This generation of new physicians values work-life balance and is more likely to prefer employment to entrepreneurship. Additionally, established physicians who have not invested in or adopted new technologies, such as EHR, will have a tough time attracting top talent. Having been trained using EHRs, few, if any, young doctors will find a reversion to paper records acceptable—and, in fact, most find it a turnoff. Thus, depending on your transition plan and your age and stage, updating technology may be a necessary investment. 

Stepping Down But Not Out

If you’re thinking about slowing down but not ceasing practice completely just yet, 2 options are worth considering: practicing part-time and/or becoming a nonoperative orthopedist. 

The 2014 Orthopaedic Practice in the United States (OPUS) report issued by the American Academy of Orthopaedic Surgeons shows that the average age of part-time surgeons is 69.14 years and that 48.6% are generalists.5 Part-time surgeons surveyed reported working an average of 23 hours per week and performing 5 procedures per month, compared with full-time surgeons who clock in at 56 hours per week and perform 31 procedures per month.5

 

 

Senior surgeons who want to pull back their hours or become nonoperative orthopedists may be quite marketable to group practices. There are several reasons for this. First, population growth will not be supported by the number of physicians graduating from Medicare-sponsored residency slots—which have not increased since 1997. Second, the physician workforce is growing older, and younger surgeons are harder to recruit. They tend to emphasize work-life balance over working the countless hours their senior counterparts did, and, thus, don’t treat as many patients as older colleagues did. And, third, a nonoperative or part-time physician may be more appealing to patients than nonphysician providers, yet accomplish the same purpose of keeping operating surgeons out of the office and in the operating room. So, that former competitor down the street may become a potential employer. You won’t be a voting partner, but that may be a low priority as you step into part-time practice.

We imagine an opportunity for nonoperative orthopedists similar to concierge internists, who go out of network and charge reasonable fees for longer appointments and less paperwork hassle. And this opportunity isn’t only for those practicing in groups. Solo orthopedists may see this change in practice attractive, as it offers reduced professional liability premiums, holds some clear attraction for patients not eager to go under the knife, and makes it easier to arrange time off for the doctor.  

As I often tell clients about their business: “Plan your work, and work your plan.” This same maxim holds true of planning for retirement. The intangible aspects of leaving your livelihood require thought and contemplation. My hope is that you’ll put pen to paper and document the answers to the questions posed in this article, so they begin to become as important as the financial aspects of your retirement planning. Of course, the plan may be waylaid midstream owing to reimbursement challenges, an offer you can’t refuse from the hospital, or a change in your health or that of your spouse. However, taking that single step and starting your plan will give you the foundation necessary to move forward or pivot in the journey ahead.

References

1.    Peckham C. Medscape Orthopedist Compensation Report 2014. Medscape website. http://www.medscape.com/features/slideshow/compensation/2014/orthopedics#1. Published April 15, 2014. Accessed October 29, 2015.

2.    Deloitte 2013 Survey of U.S. Physicians: Physician Perspectives About Health Care Reform and the Future of the Medical Profession. Deloitte Center for Health Solutions website. http://www2.deloitte.com/content/dam/Deloitte/us/Documents/life-sciences-health-care/us-lshc-deloitte-2013-physician-survey-10012014.pdf. Accessed October 29, 2015.

3.    Hyden M. Are physicians retiring early? MGMA Connection Plus. Medical Group Management Association website. http://www.mgma.com/practice-resources/mgma-connection-plus/online-only/2015/august-(1)/are-physicians-retiring-early. Published July 28, 2015. Accessed November 10, 2015.

4.    The Doctor is Out: A Physician’s Guide to Closing a Practice. North Carolina Medical Board website. http://www.ncmedboard.org/images/uploads/article_images/Physicians_Guide_to_Closing_a_Practice_05_12_2014.pdf. Published May 12, 2014. Accessed October 29, 2015.

5.    Oreluk H, Cherf J. Practice settings and productivity. AAOS Now. 2015;9(10). http://www.aaos.org/news/aaosnow/oct15/managing1.asp. Accessed October 29, 2015.

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Karen Zupko, BSJ

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If you are a solo orthopedic surgeon or practice in a small group and are 55 years or older, this article is for you. The answer to the question “When is the right time to begin planning for the transition out of practice?” is now. And planning is the most important word in that sentence.

Joining your peers who’ve quit, often rather quickly, because of Obamacare, electronic health records (EHRs), or the implementation of ICD-10 (International Classification of Diseases, Tenth Revision) may prove unsatisfying. As the saying goes, “act in haste, repent at leisure.” And as a gerontologist friend of mine liked to say, “Retiring from medicine without retiring to something is risky.” He often quipped that golf didn’t count.

Recent survey results help support his point. In the 2014 Medscape Orthopedist Compensation Report,1 respondents were asked:

What is the most rewarding part of your job?

  • Gratitude/relationships with patients            43%
  • Being very good at what I do/Finding answers, diagnoses          31%
  • Making good money at a job that I like        10%
  • Knowing that I’m making the world a better place      7%
  • Being proud of being a doctor        4%
  • Nothing 1%
  • Let’s hope you are not part of the 1%!

In the often-quoted Deloitte 2013 Survey of U.S. Physicians,2 6 in 10 respondents predicted that many physicians will retire earlier than planned in the next 1 to 3 years. Yet even in that survey, 41% of surgical specialists said that patient relationships were the most satisfying factor about practicing medicine. Protecting and promoting individual health was second (33%), and intellectual stimulation was third (16%).2   

As Steve Marsh, managing partner at The Medicus Firm, Dallas, was quoted as saying about this data, “For older doctors, being a physician is much more of a lifestyle than a job.”3 In my 40 years of working with physicians, I agree. And that’s why you, dear readers, must begin the transition planning process now, if you are 55 years or older, or soon, if you are approaching this age. Unraveling yourself from the patient relationships and the profession you have enjoyed for so long will feel like a big loss for the majority of you. There will be a grieving process. You’re not just leaving a “job,” you’re leaving your “life’s work,” and the sooner you begin planning for this shift, the less uncomfortable it will be.

Transition Planning Timeline

As the Chinese saying goes, “the longest journey begins with a single step.” The first, most challenging step in transition planning is deciding to address the issue head on—whether you see yourself practicing well into your late 60s or stepping aside 3 years from now.

Here are 7 questions to get you started. Discuss them with your spouse and a trusted advisor or mentor.

1.  Have you done everything that you wanted to accomplish professionally? What’s left on your “to-do” list?  

2.  Are you satisfied with the legacy you are leaving to your community, partners, or employees?

3.  What does your spouse think? His or her age and stage may dictate some choices. One wife said she believed in Henny Youngman’s advice: “Promise to take your wife for better or worse, but not for lunch.” Younger spouses in satisfying careers may not be ready to quit or slow down.

4.  What could fill the void of, as the Medscape survey indicated, the “gratitude/patient relationships” and “being good at what you do” that you would be leaving behind? Could going on medical missions satisfy your need to keep your hands in? Or volunteering for the community clinic?

5. If you were to retire within the next 6 months, what would your routine look like? Because the first year is often filled with travel and long-postponed fun, think beyond that and describe year 3. (Assume good health and adequate finances.) 

6.  Are there options for part-time practice? Could you ease out instead of going basically full throttle until your retirement date?

7.  Are challenges such as stress, fatigue, cognitive decline, or a feeling of burnout a reality for you? Be honest with yourself. These are real issues that not only impact your decision about when to transition, but also patient safety and care.

If you’ve reached 60 years of age and haven’t thought about questions like these, you aren’t alone. Many orthopedic surgeons delay this planning exercise for the same reasons other business owners do:

You are too busy spending all of your time putting out fires. Who has time to plan? Learning the new ICD-10 codes for local coverage determinations (LCDs), hiring a new physician assistant, firing the receptionist, and, oh by the way, taking care of a full schedule of patients, takes time and reduces the time to plan.

 

 

You think “it’s not time yet.” We often hear surgeons say, “Gosh, I don’t feel __ years old!” or “I plan to work until I’m 70.” Sound familiar?

You’re afraid to think about what life would be like without your profession. So you do nothing. Imagining a life without being needed on a daily basis can be daunting. Reread the survey results above. If you don’t have interesting and emotionally rewarding activities that will fill the void, that can cause anxiety. And the fact is, the demands on physicians, especially those in solo practice, haven’t left much time for outside interests.   

Discussing personal goals and financial matters with others is messy or taboo. Transitioning out of practice is an awkward and uncomfortable topic. Plus, whom do you call for help with planning the next stage of your life? 

These and others on a long list of excuses and anxieties result in fewer than 70% of all surgical specialists we talk with having a viable transition plan. Many, of course, have done a superb job of funding their retirement plans and have the assets set aside to fund a comfortable lifestyle. A lot has been written on the financial aspects of retirement. Your financial advisor, broker, or banker has formulas, tools, and advice that you’ve probably been following for decades. The 2014 Medscape Orthopedist Compensation Report shows the average salary is $413,000, with private practice doctors earning even more, $439,000 on average.1 Although such salaries should ensure the funding of retirement savings plans, undeniably, the financial crisis and stock market collapse of 2008 delayed many surgeons’ retirement. Even today, some surgeons who are considering their practice finish line are looking over their shoulder at market returns with a sense of insecurity.

Recruitment Is More Likely Than Cash Out

Thinking you can sell your practice for big bucks is a false hope. In the 1970s and early 1980s, before the onslaught of managed care, it was possible to sell your practice. A young surgeon would welcome having space, staff, and patients at the ready. This is no longer the case, since patient loyalty is now impacted by health insurance plan membership.

Pocketing a hefty sum from selling the office building may not be much of a windfall either. It depends on that all-important real estate formula: location, location, location. In addition, dividends from and investment in a surgery center rarely continue once you are no longer operating.

To maximize the profit potential that remains in this last phase of practice—which in turn can attract surgical talent as you transition—you’ve got to sharpen the sword and pay attention. One surgeon attributed a revenue decline of about 30% over the last 5 years to a combination of lesser insurance reimbursements, his taking more time off, and failing to pay attention to his staff’s write-off habits. Revenue cycle, management, coding, and practice operations must be finely tuned to optimize profitability, and failing to manage your practice effectively will make it less attractive when recruiting a younger surgeon to take your place or assume the patient base. Consider a practice evaluation regardless of where you are in your planning, which will help the practice prioritize improvements that deliver the best benefit and value within the context of your transition plan.

And if recruitment is part of that plan, be prepared to spend significant time on the search. Solo and small groups are finding it challenging to recruit just-out-of-training associates. This generation of new physicians values work-life balance and is more likely to prefer employment to entrepreneurship. Additionally, established physicians who have not invested in or adopted new technologies, such as EHR, will have a tough time attracting top talent. Having been trained using EHRs, few, if any, young doctors will find a reversion to paper records acceptable—and, in fact, most find it a turnoff. Thus, depending on your transition plan and your age and stage, updating technology may be a necessary investment. 

Stepping Down But Not Out

If you’re thinking about slowing down but not ceasing practice completely just yet, 2 options are worth considering: practicing part-time and/or becoming a nonoperative orthopedist. 

The 2014 Orthopaedic Practice in the United States (OPUS) report issued by the American Academy of Orthopaedic Surgeons shows that the average age of part-time surgeons is 69.14 years and that 48.6% are generalists.5 Part-time surgeons surveyed reported working an average of 23 hours per week and performing 5 procedures per month, compared with full-time surgeons who clock in at 56 hours per week and perform 31 procedures per month.5

 

 

Senior surgeons who want to pull back their hours or become nonoperative orthopedists may be quite marketable to group practices. There are several reasons for this. First, population growth will not be supported by the number of physicians graduating from Medicare-sponsored residency slots—which have not increased since 1997. Second, the physician workforce is growing older, and younger surgeons are harder to recruit. They tend to emphasize work-life balance over working the countless hours their senior counterparts did, and, thus, don’t treat as many patients as older colleagues did. And, third, a nonoperative or part-time physician may be more appealing to patients than nonphysician providers, yet accomplish the same purpose of keeping operating surgeons out of the office and in the operating room. So, that former competitor down the street may become a potential employer. You won’t be a voting partner, but that may be a low priority as you step into part-time practice.

We imagine an opportunity for nonoperative orthopedists similar to concierge internists, who go out of network and charge reasonable fees for longer appointments and less paperwork hassle. And this opportunity isn’t only for those practicing in groups. Solo orthopedists may see this change in practice attractive, as it offers reduced professional liability premiums, holds some clear attraction for patients not eager to go under the knife, and makes it easier to arrange time off for the doctor.  

As I often tell clients about their business: “Plan your work, and work your plan.” This same maxim holds true of planning for retirement. The intangible aspects of leaving your livelihood require thought and contemplation. My hope is that you’ll put pen to paper and document the answers to the questions posed in this article, so they begin to become as important as the financial aspects of your retirement planning. Of course, the plan may be waylaid midstream owing to reimbursement challenges, an offer you can’t refuse from the hospital, or a change in your health or that of your spouse. However, taking that single step and starting your plan will give you the foundation necessary to move forward or pivot in the journey ahead.

If you are a solo orthopedic surgeon or practice in a small group and are 55 years or older, this article is for you. The answer to the question “When is the right time to begin planning for the transition out of practice?” is now. And planning is the most important word in that sentence.

Joining your peers who’ve quit, often rather quickly, because of Obamacare, electronic health records (EHRs), or the implementation of ICD-10 (International Classification of Diseases, Tenth Revision) may prove unsatisfying. As the saying goes, “act in haste, repent at leisure.” And as a gerontologist friend of mine liked to say, “Retiring from medicine without retiring to something is risky.” He often quipped that golf didn’t count.

Recent survey results help support his point. In the 2014 Medscape Orthopedist Compensation Report,1 respondents were asked:

What is the most rewarding part of your job?

  • Gratitude/relationships with patients            43%
  • Being very good at what I do/Finding answers, diagnoses          31%
  • Making good money at a job that I like        10%
  • Knowing that I’m making the world a better place      7%
  • Being proud of being a doctor        4%
  • Nothing 1%
  • Let’s hope you are not part of the 1%!

In the often-quoted Deloitte 2013 Survey of U.S. Physicians,2 6 in 10 respondents predicted that many physicians will retire earlier than planned in the next 1 to 3 years. Yet even in that survey, 41% of surgical specialists said that patient relationships were the most satisfying factor about practicing medicine. Protecting and promoting individual health was second (33%), and intellectual stimulation was third (16%).2   

As Steve Marsh, managing partner at The Medicus Firm, Dallas, was quoted as saying about this data, “For older doctors, being a physician is much more of a lifestyle than a job.”3 In my 40 years of working with physicians, I agree. And that’s why you, dear readers, must begin the transition planning process now, if you are 55 years or older, or soon, if you are approaching this age. Unraveling yourself from the patient relationships and the profession you have enjoyed for so long will feel like a big loss for the majority of you. There will be a grieving process. You’re not just leaving a “job,” you’re leaving your “life’s work,” and the sooner you begin planning for this shift, the less uncomfortable it will be.

Transition Planning Timeline

As the Chinese saying goes, “the longest journey begins with a single step.” The first, most challenging step in transition planning is deciding to address the issue head on—whether you see yourself practicing well into your late 60s or stepping aside 3 years from now.

Here are 7 questions to get you started. Discuss them with your spouse and a trusted advisor or mentor.

1.  Have you done everything that you wanted to accomplish professionally? What’s left on your “to-do” list?  

2.  Are you satisfied with the legacy you are leaving to your community, partners, or employees?

3.  What does your spouse think? His or her age and stage may dictate some choices. One wife said she believed in Henny Youngman’s advice: “Promise to take your wife for better or worse, but not for lunch.” Younger spouses in satisfying careers may not be ready to quit or slow down.

4.  What could fill the void of, as the Medscape survey indicated, the “gratitude/patient relationships” and “being good at what you do” that you would be leaving behind? Could going on medical missions satisfy your need to keep your hands in? Or volunteering for the community clinic?

5. If you were to retire within the next 6 months, what would your routine look like? Because the first year is often filled with travel and long-postponed fun, think beyond that and describe year 3. (Assume good health and adequate finances.) 

6.  Are there options for part-time practice? Could you ease out instead of going basically full throttle until your retirement date?

7.  Are challenges such as stress, fatigue, cognitive decline, or a feeling of burnout a reality for you? Be honest with yourself. These are real issues that not only impact your decision about when to transition, but also patient safety and care.

If you’ve reached 60 years of age and haven’t thought about questions like these, you aren’t alone. Many orthopedic surgeons delay this planning exercise for the same reasons other business owners do:

You are too busy spending all of your time putting out fires. Who has time to plan? Learning the new ICD-10 codes for local coverage determinations (LCDs), hiring a new physician assistant, firing the receptionist, and, oh by the way, taking care of a full schedule of patients, takes time and reduces the time to plan.

 

 

You think “it’s not time yet.” We often hear surgeons say, “Gosh, I don’t feel __ years old!” or “I plan to work until I’m 70.” Sound familiar?

You’re afraid to think about what life would be like without your profession. So you do nothing. Imagining a life without being needed on a daily basis can be daunting. Reread the survey results above. If you don’t have interesting and emotionally rewarding activities that will fill the void, that can cause anxiety. And the fact is, the demands on physicians, especially those in solo practice, haven’t left much time for outside interests.   

Discussing personal goals and financial matters with others is messy or taboo. Transitioning out of practice is an awkward and uncomfortable topic. Plus, whom do you call for help with planning the next stage of your life? 

These and others on a long list of excuses and anxieties result in fewer than 70% of all surgical specialists we talk with having a viable transition plan. Many, of course, have done a superb job of funding their retirement plans and have the assets set aside to fund a comfortable lifestyle. A lot has been written on the financial aspects of retirement. Your financial advisor, broker, or banker has formulas, tools, and advice that you’ve probably been following for decades. The 2014 Medscape Orthopedist Compensation Report shows the average salary is $413,000, with private practice doctors earning even more, $439,000 on average.1 Although such salaries should ensure the funding of retirement savings plans, undeniably, the financial crisis and stock market collapse of 2008 delayed many surgeons’ retirement. Even today, some surgeons who are considering their practice finish line are looking over their shoulder at market returns with a sense of insecurity.

Recruitment Is More Likely Than Cash Out

Thinking you can sell your practice for big bucks is a false hope. In the 1970s and early 1980s, before the onslaught of managed care, it was possible to sell your practice. A young surgeon would welcome having space, staff, and patients at the ready. This is no longer the case, since patient loyalty is now impacted by health insurance plan membership.

Pocketing a hefty sum from selling the office building may not be much of a windfall either. It depends on that all-important real estate formula: location, location, location. In addition, dividends from and investment in a surgery center rarely continue once you are no longer operating.

To maximize the profit potential that remains in this last phase of practice—which in turn can attract surgical talent as you transition—you’ve got to sharpen the sword and pay attention. One surgeon attributed a revenue decline of about 30% over the last 5 years to a combination of lesser insurance reimbursements, his taking more time off, and failing to pay attention to his staff’s write-off habits. Revenue cycle, management, coding, and practice operations must be finely tuned to optimize profitability, and failing to manage your practice effectively will make it less attractive when recruiting a younger surgeon to take your place or assume the patient base. Consider a practice evaluation regardless of where you are in your planning, which will help the practice prioritize improvements that deliver the best benefit and value within the context of your transition plan.

And if recruitment is part of that plan, be prepared to spend significant time on the search. Solo and small groups are finding it challenging to recruit just-out-of-training associates. This generation of new physicians values work-life balance and is more likely to prefer employment to entrepreneurship. Additionally, established physicians who have not invested in or adopted new technologies, such as EHR, will have a tough time attracting top talent. Having been trained using EHRs, few, if any, young doctors will find a reversion to paper records acceptable—and, in fact, most find it a turnoff. Thus, depending on your transition plan and your age and stage, updating technology may be a necessary investment. 

Stepping Down But Not Out

If you’re thinking about slowing down but not ceasing practice completely just yet, 2 options are worth considering: practicing part-time and/or becoming a nonoperative orthopedist. 

The 2014 Orthopaedic Practice in the United States (OPUS) report issued by the American Academy of Orthopaedic Surgeons shows that the average age of part-time surgeons is 69.14 years and that 48.6% are generalists.5 Part-time surgeons surveyed reported working an average of 23 hours per week and performing 5 procedures per month, compared with full-time surgeons who clock in at 56 hours per week and perform 31 procedures per month.5

 

 

Senior surgeons who want to pull back their hours or become nonoperative orthopedists may be quite marketable to group practices. There are several reasons for this. First, population growth will not be supported by the number of physicians graduating from Medicare-sponsored residency slots—which have not increased since 1997. Second, the physician workforce is growing older, and younger surgeons are harder to recruit. They tend to emphasize work-life balance over working the countless hours their senior counterparts did, and, thus, don’t treat as many patients as older colleagues did. And, third, a nonoperative or part-time physician may be more appealing to patients than nonphysician providers, yet accomplish the same purpose of keeping operating surgeons out of the office and in the operating room. So, that former competitor down the street may become a potential employer. You won’t be a voting partner, but that may be a low priority as you step into part-time practice.

We imagine an opportunity for nonoperative orthopedists similar to concierge internists, who go out of network and charge reasonable fees for longer appointments and less paperwork hassle. And this opportunity isn’t only for those practicing in groups. Solo orthopedists may see this change in practice attractive, as it offers reduced professional liability premiums, holds some clear attraction for patients not eager to go under the knife, and makes it easier to arrange time off for the doctor.  

As I often tell clients about their business: “Plan your work, and work your plan.” This same maxim holds true of planning for retirement. The intangible aspects of leaving your livelihood require thought and contemplation. My hope is that you’ll put pen to paper and document the answers to the questions posed in this article, so they begin to become as important as the financial aspects of your retirement planning. Of course, the plan may be waylaid midstream owing to reimbursement challenges, an offer you can’t refuse from the hospital, or a change in your health or that of your spouse. However, taking that single step and starting your plan will give you the foundation necessary to move forward or pivot in the journey ahead.

References

1.    Peckham C. Medscape Orthopedist Compensation Report 2014. Medscape website. http://www.medscape.com/features/slideshow/compensation/2014/orthopedics#1. Published April 15, 2014. Accessed October 29, 2015.

2.    Deloitte 2013 Survey of U.S. Physicians: Physician Perspectives About Health Care Reform and the Future of the Medical Profession. Deloitte Center for Health Solutions website. http://www2.deloitte.com/content/dam/Deloitte/us/Documents/life-sciences-health-care/us-lshc-deloitte-2013-physician-survey-10012014.pdf. Accessed October 29, 2015.

3.    Hyden M. Are physicians retiring early? MGMA Connection Plus. Medical Group Management Association website. http://www.mgma.com/practice-resources/mgma-connection-plus/online-only/2015/august-(1)/are-physicians-retiring-early. Published July 28, 2015. Accessed November 10, 2015.

4.    The Doctor is Out: A Physician’s Guide to Closing a Practice. North Carolina Medical Board website. http://www.ncmedboard.org/images/uploads/article_images/Physicians_Guide_to_Closing_a_Practice_05_12_2014.pdf. Published May 12, 2014. Accessed October 29, 2015.

5.    Oreluk H, Cherf J. Practice settings and productivity. AAOS Now. 2015;9(10). http://www.aaos.org/news/aaosnow/oct15/managing1.asp. Accessed October 29, 2015.

References

1.    Peckham C. Medscape Orthopedist Compensation Report 2014. Medscape website. http://www.medscape.com/features/slideshow/compensation/2014/orthopedics#1. Published April 15, 2014. Accessed October 29, 2015.

2.    Deloitte 2013 Survey of U.S. Physicians: Physician Perspectives About Health Care Reform and the Future of the Medical Profession. Deloitte Center for Health Solutions website. http://www2.deloitte.com/content/dam/Deloitte/us/Documents/life-sciences-health-care/us-lshc-deloitte-2013-physician-survey-10012014.pdf. Accessed October 29, 2015.

3.    Hyden M. Are physicians retiring early? MGMA Connection Plus. Medical Group Management Association website. http://www.mgma.com/practice-resources/mgma-connection-plus/online-only/2015/august-(1)/are-physicians-retiring-early. Published July 28, 2015. Accessed November 10, 2015.

4.    The Doctor is Out: A Physician’s Guide to Closing a Practice. North Carolina Medical Board website. http://www.ncmedboard.org/images/uploads/article_images/Physicians_Guide_to_Closing_a_Practice_05_12_2014.pdf. Published May 12, 2014. Accessed October 29, 2015.

5.    Oreluk H, Cherf J. Practice settings and productivity. AAOS Now. 2015;9(10). http://www.aaos.org/news/aaosnow/oct15/managing1.asp. Accessed October 29, 2015.

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Magnetic Resonance Imaging of Complications of Anterior Cruciate Ligament Reconstruction

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Magnetic Resonance Imaging of Complications of Anterior Cruciate Ligament Reconstruction

Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1

Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).

MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4

Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).

 

Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7

Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.

MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.

References

1.    Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.

2.    Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.

3.    Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.

4.    Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.

5.    Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.

6.    Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.

7.    Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.

8.    Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.

9.    Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.

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Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1

Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).

MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4

Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).

 

Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7

Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.

MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.

Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1

Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).

MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4

Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).

 

Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7

Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.

MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.

References

1.    Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.

2.    Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.

3.    Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.

4.    Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.

5.    Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.

6.    Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.

7.    Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.

8.    Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.

9.    Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.

References

1.    Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.

2.    Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.

3.    Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.

4.    Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.

5.    Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.

6.    Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.

7.    Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.

8.    Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.

9.    Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.

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