Knee

According to their classic article, Kozinn and Scott¹² outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.^13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.^18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.^18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.²⁴ For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues²³ used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold²³. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues⁸ focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;⁸ however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues²⁵ investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues²⁶ reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues²⁷ reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues¹⁷ compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.²⁸

Continue to: Our data indicate...

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.²⁹ Bolognesi and colleagues²³ reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.^30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

According to their classic article, Kozinn and Scott¹² outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.^13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.^18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.^18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.²⁴ For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues²³ used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold²³. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues⁸ focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;⁸ however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues²⁵ investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues²⁶ reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues²⁷ reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues¹⁷ compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.²⁸

Continue to: Our data indicate...

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.²⁹ Bolognesi and colleagues²³ reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.^30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

According to their classic article, Kozinn and Scott¹² outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.^13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.^18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.^18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.²⁴ For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues²³ used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold²³. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues⁸ focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;⁸ however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues²⁵ investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues²⁶ reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues²⁷ reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues¹⁷ compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.²⁸

Continue to: Our data indicate...

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.²⁹ Bolognesi and colleagues²³ reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.^30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.³ Also, the mean life expectancy post-fragility fracture was only 527 days.³ Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.⁴ Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.⁵ A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.⁴ Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.⁶

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.⁷ The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.⁷ Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.⁸ In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.⁹ The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.¹⁰

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H₂ receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.¹¹ Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.¹² Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.¹³ Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.¹⁴ Proton pump inhibitors and H₂ receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.¹⁵ However, exposure lasting <7 years does not increase the risk of fracture.¹⁶ It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.¹⁷ Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.¹⁸

Continue to: DIAGNOSIS...

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.¹⁹ Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.²⁰

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.¹⁹ The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.¹⁹ Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.²⁰ Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.²¹ Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

Table 2. Z Score Criteria

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.²² Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.²³ As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.²⁴ The recommended daily total calcium intake is 1200 mg.²⁵ Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.²⁴Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.²⁴ Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.²⁶ Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.²⁷ Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.²⁸

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.²⁹ In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.²⁹ Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.²⁹ Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.²⁶

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.³⁰

Continue to: The recommended daily dose for abaloparatide...

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.³¹ Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.³⁰ The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.³¹ It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.³² It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.³³ Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.^34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.^34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

Anatomic factors that contribute to PFI include ligament laxity, trochlear dysplasia, patella alta, excessive femoral anteversion or tibial torsion, genu valgum, and increased tibial tubercle-to-trochlear groove distance.^1,3,8-11 When considering surgical treatment for PFI, all anatomic factors should be considered, with an emphasis on, and understanding of, the role of residual growth and development. One must also consider balancing static soft tissue, dynamic soft tissue, and osseous constraints of the patellofemoral joint to optimize the overall health and balance of the patella (Figure 1).

CHALLENGES IN TREATING PEDIATRIC PFI

A primary challenge in the treatment of PFI in pediatric patients is accounting for the impact of anatomic changes occurring secondary to growth and maturity. From birth to adulthood, the collagen composition of soft tissue changes from an elastic type III collagen to a stiffer type I collagen.¹² These physiologic changes may influence the rigidity of the soft tissue restraints around the patellofemoral joint during periods of rapid growth. Longitudinal growth and rotational changes can also occur at the distal femoral and proximal tibial physes. The position of the tibial tubercle and the magnitude of femoral anteversion may also change after growth in adolescents.

Developing effective technical analogs of surgical procedures performed in mature patients with PFI for use in skeletally immature patients has been a second challenge. For example, a varus-producing distal femoral osteotomy to address genu valgum and PFI¹³ is contraindicated in immature patients, when a hemiepiphysiodesis for guided growth should be considered.¹⁴ Similarly, a periosteal sleeve medialization of the insertion of the patellar tendon may be used instead of a tibial tubercle transfer.¹⁵

If a medial patellofemoral ligament (MPFL) reconstruction is considered in immature patients, careful consideration of the position of the MPFL in relation to the distal femoral physis is paramount. Shea and colleagues¹⁶ originally described the position of the MPFL, based on Schottle’s point¹⁷ on lateral radiographs, to be proximal to the distal femoral physis (Figure 2). However, due to the undulation of the physis, the lateral projection may falsely demonstrate Schottle’s point to be on or just proximal to the physis. Other researchers have evaluated the position of the distal femoral physis to be proximal to the origin of the MPFL by a range of 2.9 mm to 8.5 mm on AP radiograph and MRI, respectively.^18,19 More recent cadaveric studies have demonstrated the origin of the MPFL in pediatric specimens in relation to the physis to be variable.²⁰ Although we believe that a relative anatomic femoral position of the MPFL origin can be achieved without disrupting the physis using Schottle’s point, some have indicated concerns that this may produce a nonisometric position, which has not been our experience.²¹

Continue to: TREATMENT OPTIONS...

The evaluation of a skeletally immature patient may differ from that of an adult patient.  (Table 1) represents a standard evaluation of a skeletally immature patient with PFI. The injury, physical examination findings, activity level, presence of an osteochondral fracture, and severity of bony dysplasia may indicate surgical treatment and influence selection of the surgical technique. Indications for surgical treatment include recurrent patellar instability, symptomatic patellar instability, the presence of a chondral or an osteochondral fracture, and a primary patella dislocation in patients with a high risk for recurrent dislocations. Table 2 represents a list of the possible surgical treatment options for the skeletally immature patient with PFI.^21,22 Variable outcomes and recurrence rates are noted with each procedure.^21,22

MPFL REPAIR VS RECONSTRUCTION

Although there is increased consensus for restoring normal anatomy, continued controversy exists regarding the utility of an MPFL repair versus reconstruction. An MPFL repair to the patella has been reported in a large series and was noted to have a 72% success rate.²³ Although a perceived benefit of the procedure is the absence of risk to the physis, concerns exist regarding the unacceptable rate of continued patellar instability after a repair of native tissue.

Several studies have demonstrated that reconstruction of the MPFL yields lower rates of recurrent dislocation, improved knee function, and an ability to return to prior levels of activity with little to no functional impairment.^1,2,24-26 Studies have also shown that MPFL reconstruction can be performed safely in skeletally immature patients, with little risk of growth impairment, good to excellent results, and low re-rupture rates.^27,28

We propose that MPFL reconstruction for the skeletally immature patient with PFI should be the primary surgical treatment. Any patient with atypical or severe bony dysplasia may warrant additional intervention. Additional correction of valgus, in the form of guided growth, should be considered in conjunction with an MPFL reconstruction if the patient demonstrates a valgus of grade >2 or a lateral distal femoral angle of <84°.

GRAFT OPTIONS

When an MPFL reconstruction is indicated, graft options include autologous hamstring, quadriceps, adductor, or patellar tendon grafts. Allograft tendon may be an acceptable choice, and use of synthetic graft has also been described. A recent systematic review²⁹ concluded that there was no difference in recurrence rates or outcomes based on graft type. However, in this study, the overall complication rates were higher in patients who had autologous graft than in those who had allograft. Although the use of allograft has not been specifically reported in a pediatric cohort, allografts have been successfully used in this age group. Obviating graft harvest eliminates an additional or extended incision, limits postoperative weakness, and may speed early recovery.

Continue to: PREFERRED SURGICAL TECHNIQUE FOR MPFL RECONSTRUCTION WITH ALLOGRAFT...

Surgery should be scheduled and performed as an outpatient procedure. Preoperative instructions may include crutch training, when indicated, and postoperative education regarding expected early therapy and pain management strategy may be employed. Chlorhexidine wipes are provided to patients preoperatively with instruction to use daily starting 3 days prior to surgery. A home exercise program with a focus on quadriceps activation and range of motion is provided and requested to be performed postoperatively.

A standard operating room setup for knee arthroscopy is employed (preference list noted in Table 3; items bolded may be unique to an MPFL reconstruction). Regional, single-shot anesthesia is employed using a sensory-only adductor canal block. A universal surgical timeout is performed before beginning the surgery to include verification of prophylactic antibiotics (Ancef or clindamycin in penicillin-allergic patients) and consideration of the use of a sequential compression device in children aged >10 years when ≥1 venous thromboembolic risk factors are detected in preoperative screening.

Nonirradiated allografts (semitendinosus or tibialis anterior), preferably from a donor <30 years, are our preferred graft choice. The minimum length of the graft should be 240 mm and the doubled thickness should be 5 to 6 mm. After thawing, the graft is lavaged with a mixture of antibiotic saline consisting of 50,000 U of bacitracin in 1 l of normal saline. Tension is then placed on the graft using the graft preparation board, and a whip stitch is placed on each side of the graft using a #2 FiberWire (Arthrex). The graft is sized with care to ensure that it is not thicker than 6.5 mm with an optimal goal of 6 mm.

A standard knee arthroscopy is performed with an emphasis on evaluating the patellofemoral anatomy. Although insufflation can cause distortion and, often, lateralize the patella, the surgeon should consider an estimate of when the patella engages the trochlea during knee flexion. This position of knee flexion will determine the appropriate position of the knee during graft fixation. A bipolar device (90°Arthrocare wand) may be used to debride synovial folds (ie, plica) when affecting the patellar tracking. To maximize visualization of the patella within the knee, we recommend switching the arthroscope from the anterolateral portal to the anteromedial portal. This allows for improved visualization of the lateral femoral condyle and the inferomedial patellar facet, common locations for chondral and osteochondral damage, as well as optimal visualization of patellar engagement within the trochlea. During an arthroscopic dynamic exam of the patella tracking, a lateralized patella may be observed. If the patella tilts upon manual medial translation toward the trochlear groove during the dynamic exam, the lateral retinaculum may be tight or constraining the patella laterally. If this occurs, a partial or complete lateral release may be indicated with a bipolar wand. Visualization of the posteromedial and the posterolateral compartments is required as loose chondral bodies may be present in these locations.     

Any osteochondral or chondral injuries are addressed during the arthroscopy. Large osteochondral fractures of the lateral femoral condyle or the patella are repaired using headless compression screws (Acutrak Screws, Acumed) or headed low-profile screws (1.5-mm screws, DePuy Synthes). Headless screws can be buried 2 to 3 mm below the chondral surface when the fragment has an appropriate thickness, whereas thin fragments may necessitate headed screws for adequate fixation and subsequent implant removal in 8 to 10 weeks. Defects in the patella most often require an open arthrotomy to evert the patella 90° to allow adequate exposure for treatment. Chronic chondral fragmentation may be debrided using the motorized chondrotome or removed and indicated for microfracture (<2 cm² in surface area and <4 mm in depth) or other types of chondral replacement. Chondral lesions over the inferior medial facet are typically not symptomatic and often require minimal treatment.

Continue to: There are 3 methods to identify...

There are 3 methods to identify the insertion of the MPFL into the patella. During the diagnostic arthroscopy, an 18-gauge needle can be used to mark the insertion of the MPFL as visualization of the ligament arthroscopically is often possible (Figure 3). Another useful technique is to follow the inferior aspect of the distal insertion of the vastus medialis oblique (VMO) into the patella. The typical insertion point of the MPFL is immediately distal to the insertion of the inferior aspect of the VMO (Figure 4). It is also helpful to note that the center point of the insertion of the MPFL is at the junction of the proximal one-third and distal two-thirds of the palpable osseous patella. The MPFL origin has been noted to be at the exact midpoint of the chondral surface of the patella or 5 mm proximal (41% of the length of the patella) to the midpoint of the osseous patella.³⁰

Following arthroscopic examination and treatment, a linear incision is made at the superior two-thirds of the patella, 1-finger breadth medial to the patella (Figure 5). During the subcutaneous dissection, the goal is to visualize the fascia overlying the VMO. Once this is identified, the dissection, in this layer, is carried over to expose the anterior and central surface of the patella. Army/navy retractors are used to retract the skin, and the assistant will place manual pressure on the patella to stabilize it for preparation of the patellar surface.

A bovie cautery or a knife is used to mark the insertion of the MPFL, which is immediately distal to the inferior border of the VMO. An incision over the medial surface of the patella creates a T-incision with elevation of the subsequent flaps proximal and distal. This allows exposure of the superficial and medial surface of the patella. During medial exposure of the patella, care is taken to avoid an arthrotomy by leaving the synovial lining attachment. A rongeur is used to decorticate the medial patella and the superficial surface (Figure 6). If an MPFL avulsion is present, it is often embedded within the soft tissues adjacent to the medial patellar. The MPFL avulsion can be exposed and removed if small. During an MPFL reconstruction, a repair of the avulsion is typically not performed. A double-loaded suture anchor is inserted at the site identified as the insertion of the native MPFL (3.0 Biocomposite SutureTak, Arthrex). A single suture anchor is used instead of an interosseous tunnel or double tunnels to avoid creating a large defect that may increase the risk of fracture in a small, skeletally immature patella.³¹

A hemostat is used to identify the layer between the medial retinaculum and the synovium over the medial soft tissue of the knee. The MPFL is a well-defined thickening of the medial retinaculum, and the ideal placement of the reconstruction is immediately inferior to this layer. Once this layer has been identified, a blunt hemostat is inserted to mark the end of a blind pouch that is apparent in this layer. This blind pouch is marked on the surface of the skin as the origin of the MPFL.

Fluoroscopy is now used to identify the origin of the MPFL on the medial femoral condyle. A perfect lateral is obtained by lining up the posterior condyle. Often, existent trochlear dysplasia will modify the normal appearance of the anterior structures of the condyles. Schottle’s point¹⁷ is USED to locate the origin of the MPFL. This is defined by drawing a line from the posterior cortex distally through the condyles (Figure 7). Two perpendicular lines are drawn, one to the extension of the posterior cortex at the level of the posterior extent of Blumensaat’s line and a second at the metaphyseal flare. Schottle’s point is located just anterior to the posterior cortex and in between these perpendicular lines. In a skeletally immature patient, this point appears to be at the level of the physis, on the lateral projection.

Continue to: An anteroposterior and/or a notch view projection...

An anteroposterior and/or a notch view projection is then performed to confirm the location of Schottle’s point, distal to the physis. Because the origin of the MPFL is posterior to the condyle, the notch view should be used to visualize Schottle’s point in relation to the physis in the coronal plane. This location has been confirmed to approximate the origin of the MPFL by published anatomic studies. If the graft measures 6 mm, an ideal distance of 5 to 8 mm distal to the physis will ensure a tunnel location with a proximal margin 2 to 4 mm distal to the physis. In our experience, Schottle’s point is approximately 5 to 7 mm distal to the physis, and rarely do we adjust our position. The guide wire is placed on the medial femoral condyle at this point and then angled 30° proximal to distal to allow tunnel trajectory distal to the undulating physis (Figure 8).

A 6-mm reamer is used over the guide wire to a depth of 20 mm. The newly created tunnel is now exposed and visualized. The graft is folded over at the center aspect and marked 20 mm from the tip of a Bio-tenodesis screwdriver (Arthrex). A 6.25 × 15 mm Bio-tenodesis screw is used. The graft and the screw are inserted into the condyle, and the appropriate graft fixation is confirmed by longitudinal tension placed upon the graft.

The hemostat or the passing suture previously placed into the blind pouch below the native MPFL is used to pass the graft immediately superficial to the synovial lining, in an extra-articular location. The ends of the graft are now exposed through the incision adjacent to the patella. The knee is confirmed to be flexed to approximately 45° on the surgical positioning triangleor at the flexion position determined during diagnostic arthroscopy at which the patella engages the trochlea. The graft is set to length alongside the medial surface of the patella at the position of the suture anchor, and a single stitch is placed through both ends of the graft at this adjacent position using a free needle (Davis Tonsil ½ Circle Taper Point; Vessel Medical). A hemostat is placed on the single suture throw to provisionally secure the graft in this trial position. This allows the surgeon to trial and examine the MPFL graft in extension, 45° of flexion, and terminal flexion. The goal is to provide a check rein to lateral translation of the patella and provide a firm endpoint to avoid further dislocation without overtension of the graft that may lead to increased contact pressures in the patellofemoral joint.

Once appropriate graft position is confirmed, using the double-loaded suture, we prefer to secure each limb separately to the decorticated medial patella. One end of the suture is threaded through the graft once and will act as a post. The other end of the suture is threaded through the graft 3 times in a modified Mason-Allen stitch. With the knee in that same position of flexion, the knot is tied and the graft is secured to the medial side of the patella. For secondary fixation, the remaining ends of the graft are passed below the periosteum on the anterior surface of the patella. Using a 0 Vicryl (Ethicon US), the periosteal flaps are sutured on top of the graft, incorporating the residual graft. The ends are cut and a repeat dynamic examination is performed to confirm the position of the patella and the patellar tracking and to ensure that overtensioning did not occur. Following irrigation, a standard closure is performed. The patient is placed in a hinged knee brace and cryotherapy is applied (Polar Care, Breg Inc).

POSTOPERATIVE PROTOCOL

For the initial or the acute postoperative phases, an emphasis on edema control, early quadriceps activation, and range of motion is recommended. We recommend weight-bearing as tolerated with the leg locked in extension until adequate quadriceps control is achieved. The patient must be able to perform 10 straight leg raises without an extension loss to be cleared to weight-bear as tolerated without motion restriction in the brace. Full motion is allowed immediately.

OUTCOMES

In our experience using isolated MPFL reconstruction in the skeletally immature patient, we have had no evidence of physeal arrest, leg-length inequality, or angular deformity, and only11.4% of patients have had recurrent instability. The mean Kujala score in this cohort was 90.4, with a mean Tegner activity of 7, after the procedure. All failures in our cohort had had severe trochlear dysplasia.

Anatomic factors that contribute to PFI include ligament laxity, trochlear dysplasia, patella alta, excessive femoral anteversion or tibial torsion, genu valgum, and increased tibial tubercle-to-trochlear groove distance.^1,3,8-11 When considering surgical treatment for PFI, all anatomic factors should be considered, with an emphasis on, and understanding of, the role of residual growth and development. One must also consider balancing static soft tissue, dynamic soft tissue, and osseous constraints of the patellofemoral joint to optimize the overall health and balance of the patella (Figure 1).

CHALLENGES IN TREATING PEDIATRIC PFI

A primary challenge in the treatment of PFI in pediatric patients is accounting for the impact of anatomic changes occurring secondary to growth and maturity. From birth to adulthood, the collagen composition of soft tissue changes from an elastic type III collagen to a stiffer type I collagen.¹² These physiologic changes may influence the rigidity of the soft tissue restraints around the patellofemoral joint during periods of rapid growth. Longitudinal growth and rotational changes can also occur at the distal femoral and proximal tibial physes. The position of the tibial tubercle and the magnitude of femoral anteversion may also change after growth in adolescents.

Developing effective technical analogs of surgical procedures performed in mature patients with PFI for use in skeletally immature patients has been a second challenge. For example, a varus-producing distal femoral osteotomy to address genu valgum and PFI¹³ is contraindicated in immature patients, when a hemiepiphysiodesis for guided growth should be considered.¹⁴ Similarly, a periosteal sleeve medialization of the insertion of the patellar tendon may be used instead of a tibial tubercle transfer.¹⁵

If a medial patellofemoral ligament (MPFL) reconstruction is considered in immature patients, careful consideration of the position of the MPFL in relation to the distal femoral physis is paramount. Shea and colleagues¹⁶ originally described the position of the MPFL, based on Schottle’s point¹⁷ on lateral radiographs, to be proximal to the distal femoral physis (Figure 2). However, due to the undulation of the physis, the lateral projection may falsely demonstrate Schottle’s point to be on or just proximal to the physis. Other researchers have evaluated the position of the distal femoral physis to be proximal to the origin of the MPFL by a range of 2.9 mm to 8.5 mm on AP radiograph and MRI, respectively.^18,19 More recent cadaveric studies have demonstrated the origin of the MPFL in pediatric specimens in relation to the physis to be variable.²⁰ Although we believe that a relative anatomic femoral position of the MPFL origin can be achieved without disrupting the physis using Schottle’s point, some have indicated concerns that this may produce a nonisometric position, which has not been our experience.²¹

Continue to: TREATMENT OPTIONS...

The evaluation of a skeletally immature patient may differ from that of an adult patient.  (Table 1) represents a standard evaluation of a skeletally immature patient with PFI. The injury, physical examination findings, activity level, presence of an osteochondral fracture, and severity of bony dysplasia may indicate surgical treatment and influence selection of the surgical technique. Indications for surgical treatment include recurrent patellar instability, symptomatic patellar instability, the presence of a chondral or an osteochondral fracture, and a primary patella dislocation in patients with a high risk for recurrent dislocations. Table 2 represents a list of the possible surgical treatment options for the skeletally immature patient with PFI.^21,22 Variable outcomes and recurrence rates are noted with each procedure.^21,22

MPFL REPAIR VS RECONSTRUCTION

Although there is increased consensus for restoring normal anatomy, continued controversy exists regarding the utility of an MPFL repair versus reconstruction. An MPFL repair to the patella has been reported in a large series and was noted to have a 72% success rate.²³ Although a perceived benefit of the procedure is the absence of risk to the physis, concerns exist regarding the unacceptable rate of continued patellar instability after a repair of native tissue.

Several studies have demonstrated that reconstruction of the MPFL yields lower rates of recurrent dislocation, improved knee function, and an ability to return to prior levels of activity with little to no functional impairment.^1,2,24-26 Studies have also shown that MPFL reconstruction can be performed safely in skeletally immature patients, with little risk of growth impairment, good to excellent results, and low re-rupture rates.^27,28

We propose that MPFL reconstruction for the skeletally immature patient with PFI should be the primary surgical treatment. Any patient with atypical or severe bony dysplasia may warrant additional intervention. Additional correction of valgus, in the form of guided growth, should be considered in conjunction with an MPFL reconstruction if the patient demonstrates a valgus of grade >2 or a lateral distal femoral angle of <84°.

GRAFT OPTIONS

When an MPFL reconstruction is indicated, graft options include autologous hamstring, quadriceps, adductor, or patellar tendon grafts. Allograft tendon may be an acceptable choice, and use of synthetic graft has also been described. A recent systematic review²⁹ concluded that there was no difference in recurrence rates or outcomes based on graft type. However, in this study, the overall complication rates were higher in patients who had autologous graft than in those who had allograft. Although the use of allograft has not been specifically reported in a pediatric cohort, allografts have been successfully used in this age group. Obviating graft harvest eliminates an additional or extended incision, limits postoperative weakness, and may speed early recovery.

Continue to: PREFERRED SURGICAL TECHNIQUE FOR MPFL RECONSTRUCTION WITH ALLOGRAFT...

Surgery should be scheduled and performed as an outpatient procedure. Preoperative instructions may include crutch training, when indicated, and postoperative education regarding expected early therapy and pain management strategy may be employed. Chlorhexidine wipes are provided to patients preoperatively with instruction to use daily starting 3 days prior to surgery. A home exercise program with a focus on quadriceps activation and range of motion is provided and requested to be performed postoperatively.

A standard operating room setup for knee arthroscopy is employed (preference list noted in Table 3; items bolded may be unique to an MPFL reconstruction). Regional, single-shot anesthesia is employed using a sensory-only adductor canal block. A universal surgical timeout is performed before beginning the surgery to include verification of prophylactic antibiotics (Ancef or clindamycin in penicillin-allergic patients) and consideration of the use of a sequential compression device in children aged >10 years when ≥1 venous thromboembolic risk factors are detected in preoperative screening.

Nonirradiated allografts (semitendinosus or tibialis anterior), preferably from a donor <30 years, are our preferred graft choice. The minimum length of the graft should be 240 mm and the doubled thickness should be 5 to 6 mm. After thawing, the graft is lavaged with a mixture of antibiotic saline consisting of 50,000 U of bacitracin in 1 l of normal saline. Tension is then placed on the graft using the graft preparation board, and a whip stitch is placed on each side of the graft using a #2 FiberWire (Arthrex). The graft is sized with care to ensure that it is not thicker than 6.5 mm with an optimal goal of 6 mm.

A standard knee arthroscopy is performed with an emphasis on evaluating the patellofemoral anatomy. Although insufflation can cause distortion and, often, lateralize the patella, the surgeon should consider an estimate of when the patella engages the trochlea during knee flexion. This position of knee flexion will determine the appropriate position of the knee during graft fixation. A bipolar device (90°Arthrocare wand) may be used to debride synovial folds (ie, plica) when affecting the patellar tracking. To maximize visualization of the patella within the knee, we recommend switching the arthroscope from the anterolateral portal to the anteromedial portal. This allows for improved visualization of the lateral femoral condyle and the inferomedial patellar facet, common locations for chondral and osteochondral damage, as well as optimal visualization of patellar engagement within the trochlea. During an arthroscopic dynamic exam of the patella tracking, a lateralized patella may be observed. If the patella tilts upon manual medial translation toward the trochlear groove during the dynamic exam, the lateral retinaculum may be tight or constraining the patella laterally. If this occurs, a partial or complete lateral release may be indicated with a bipolar wand. Visualization of the posteromedial and the posterolateral compartments is required as loose chondral bodies may be present in these locations.     

Any osteochondral or chondral injuries are addressed during the arthroscopy. Large osteochondral fractures of the lateral femoral condyle or the patella are repaired using headless compression screws (Acutrak Screws, Acumed) or headed low-profile screws (1.5-mm screws, DePuy Synthes). Headless screws can be buried 2 to 3 mm below the chondral surface when the fragment has an appropriate thickness, whereas thin fragments may necessitate headed screws for adequate fixation and subsequent implant removal in 8 to 10 weeks. Defects in the patella most often require an open arthrotomy to evert the patella 90° to allow adequate exposure for treatment. Chronic chondral fragmentation may be debrided using the motorized chondrotome or removed and indicated for microfracture (<2 cm² in surface area and <4 mm in depth) or other types of chondral replacement. Chondral lesions over the inferior medial facet are typically not symptomatic and often require minimal treatment.

Continue to: There are 3 methods to identify...

There are 3 methods to identify the insertion of the MPFL into the patella. During the diagnostic arthroscopy, an 18-gauge needle can be used to mark the insertion of the MPFL as visualization of the ligament arthroscopically is often possible (Figure 3). Another useful technique is to follow the inferior aspect of the distal insertion of the vastus medialis oblique (VMO) into the patella. The typical insertion point of the MPFL is immediately distal to the insertion of the inferior aspect of the VMO (Figure 4). It is also helpful to note that the center point of the insertion of the MPFL is at the junction of the proximal one-third and distal two-thirds of the palpable osseous patella. The MPFL origin has been noted to be at the exact midpoint of the chondral surface of the patella or 5 mm proximal (41% of the length of the patella) to the midpoint of the osseous patella.³⁰

Following arthroscopic examination and treatment, a linear incision is made at the superior two-thirds of the patella, 1-finger breadth medial to the patella (Figure 5). During the subcutaneous dissection, the goal is to visualize the fascia overlying the VMO. Once this is identified, the dissection, in this layer, is carried over to expose the anterior and central surface of the patella. Army/navy retractors are used to retract the skin, and the assistant will place manual pressure on the patella to stabilize it for preparation of the patellar surface.

A bovie cautery or a knife is used to mark the insertion of the MPFL, which is immediately distal to the inferior border of the VMO. An incision over the medial surface of the patella creates a T-incision with elevation of the subsequent flaps proximal and distal. This allows exposure of the superficial and medial surface of the patella. During medial exposure of the patella, care is taken to avoid an arthrotomy by leaving the synovial lining attachment. A rongeur is used to decorticate the medial patella and the superficial surface (Figure 6). If an MPFL avulsion is present, it is often embedded within the soft tissues adjacent to the medial patellar. The MPFL avulsion can be exposed and removed if small. During an MPFL reconstruction, a repair of the avulsion is typically not performed. A double-loaded suture anchor is inserted at the site identified as the insertion of the native MPFL (3.0 Biocomposite SutureTak, Arthrex). A single suture anchor is used instead of an interosseous tunnel or double tunnels to avoid creating a large defect that may increase the risk of fracture in a small, skeletally immature patella.³¹

A hemostat is used to identify the layer between the medial retinaculum and the synovium over the medial soft tissue of the knee. The MPFL is a well-defined thickening of the medial retinaculum, and the ideal placement of the reconstruction is immediately inferior to this layer. Once this layer has been identified, a blunt hemostat is inserted to mark the end of a blind pouch that is apparent in this layer. This blind pouch is marked on the surface of the skin as the origin of the MPFL.

Fluoroscopy is now used to identify the origin of the MPFL on the medial femoral condyle. A perfect lateral is obtained by lining up the posterior condyle. Often, existent trochlear dysplasia will modify the normal appearance of the anterior structures of the condyles. Schottle’s point¹⁷ is USED to locate the origin of the MPFL. This is defined by drawing a line from the posterior cortex distally through the condyles (Figure 7). Two perpendicular lines are drawn, one to the extension of the posterior cortex at the level of the posterior extent of Blumensaat’s line and a second at the metaphyseal flare. Schottle’s point is located just anterior to the posterior cortex and in between these perpendicular lines. In a skeletally immature patient, this point appears to be at the level of the physis, on the lateral projection.

Continue to: An anteroposterior and/or a notch view projection...

An anteroposterior and/or a notch view projection is then performed to confirm the location of Schottle’s point, distal to the physis. Because the origin of the MPFL is posterior to the condyle, the notch view should be used to visualize Schottle’s point in relation to the physis in the coronal plane. This location has been confirmed to approximate the origin of the MPFL by published anatomic studies. If the graft measures 6 mm, an ideal distance of 5 to 8 mm distal to the physis will ensure a tunnel location with a proximal margin 2 to 4 mm distal to the physis. In our experience, Schottle’s point is approximately 5 to 7 mm distal to the physis, and rarely do we adjust our position. The guide wire is placed on the medial femoral condyle at this point and then angled 30° proximal to distal to allow tunnel trajectory distal to the undulating physis (Figure 8).

A 6-mm reamer is used over the guide wire to a depth of 20 mm. The newly created tunnel is now exposed and visualized. The graft is folded over at the center aspect and marked 20 mm from the tip of a Bio-tenodesis screwdriver (Arthrex). A 6.25 × 15 mm Bio-tenodesis screw is used. The graft and the screw are inserted into the condyle, and the appropriate graft fixation is confirmed by longitudinal tension placed upon the graft.

The hemostat or the passing suture previously placed into the blind pouch below the native MPFL is used to pass the graft immediately superficial to the synovial lining, in an extra-articular location. The ends of the graft are now exposed through the incision adjacent to the patella. The knee is confirmed to be flexed to approximately 45° on the surgical positioning triangleor at the flexion position determined during diagnostic arthroscopy at which the patella engages the trochlea. The graft is set to length alongside the medial surface of the patella at the position of the suture anchor, and a single stitch is placed through both ends of the graft at this adjacent position using a free needle (Davis Tonsil ½ Circle Taper Point; Vessel Medical). A hemostat is placed on the single suture throw to provisionally secure the graft in this trial position. This allows the surgeon to trial and examine the MPFL graft in extension, 45° of flexion, and terminal flexion. The goal is to provide a check rein to lateral translation of the patella and provide a firm endpoint to avoid further dislocation without overtension of the graft that may lead to increased contact pressures in the patellofemoral joint.

Once appropriate graft position is confirmed, using the double-loaded suture, we prefer to secure each limb separately to the decorticated medial patella. One end of the suture is threaded through the graft once and will act as a post. The other end of the suture is threaded through the graft 3 times in a modified Mason-Allen stitch. With the knee in that same position of flexion, the knot is tied and the graft is secured to the medial side of the patella. For secondary fixation, the remaining ends of the graft are passed below the periosteum on the anterior surface of the patella. Using a 0 Vicryl (Ethicon US), the periosteal flaps are sutured on top of the graft, incorporating the residual graft. The ends are cut and a repeat dynamic examination is performed to confirm the position of the patella and the patellar tracking and to ensure that overtensioning did not occur. Following irrigation, a standard closure is performed. The patient is placed in a hinged knee brace and cryotherapy is applied (Polar Care, Breg Inc).

POSTOPERATIVE PROTOCOL

For the initial or the acute postoperative phases, an emphasis on edema control, early quadriceps activation, and range of motion is recommended. We recommend weight-bearing as tolerated with the leg locked in extension until adequate quadriceps control is achieved. The patient must be able to perform 10 straight leg raises without an extension loss to be cleared to weight-bear as tolerated without motion restriction in the brace. Full motion is allowed immediately.

OUTCOMES

In our experience using isolated MPFL reconstruction in the skeletally immature patient, we have had no evidence of physeal arrest, leg-length inequality, or angular deformity, and only11.4% of patients have had recurrent instability. The mean Kujala score in this cohort was 90.4, with a mean Tegner activity of 7, after the procedure. All failures in our cohort had had severe trochlear dysplasia.

Anatomic factors that contribute to PFI include ligament laxity, trochlear dysplasia, patella alta, excessive femoral anteversion or tibial torsion, genu valgum, and increased tibial tubercle-to-trochlear groove distance.^1,3,8-11 When considering surgical treatment for PFI, all anatomic factors should be considered, with an emphasis on, and understanding of, the role of residual growth and development. One must also consider balancing static soft tissue, dynamic soft tissue, and osseous constraints of the patellofemoral joint to optimize the overall health and balance of the patella (Figure 1).

CHALLENGES IN TREATING PEDIATRIC PFI

A primary challenge in the treatment of PFI in pediatric patients is accounting for the impact of anatomic changes occurring secondary to growth and maturity. From birth to adulthood, the collagen composition of soft tissue changes from an elastic type III collagen to a stiffer type I collagen.¹² These physiologic changes may influence the rigidity of the soft tissue restraints around the patellofemoral joint during periods of rapid growth. Longitudinal growth and rotational changes can also occur at the distal femoral and proximal tibial physes. The position of the tibial tubercle and the magnitude of femoral anteversion may also change after growth in adolescents.

Developing effective technical analogs of surgical procedures performed in mature patients with PFI for use in skeletally immature patients has been a second challenge. For example, a varus-producing distal femoral osteotomy to address genu valgum and PFI¹³ is contraindicated in immature patients, when a hemiepiphysiodesis for guided growth should be considered.¹⁴ Similarly, a periosteal sleeve medialization of the insertion of the patellar tendon may be used instead of a tibial tubercle transfer.¹⁵

If a medial patellofemoral ligament (MPFL) reconstruction is considered in immature patients, careful consideration of the position of the MPFL in relation to the distal femoral physis is paramount. Shea and colleagues¹⁶ originally described the position of the MPFL, based on Schottle’s point¹⁷ on lateral radiographs, to be proximal to the distal femoral physis (Figure 2). However, due to the undulation of the physis, the lateral projection may falsely demonstrate Schottle’s point to be on or just proximal to the physis. Other researchers have evaluated the position of the distal femoral physis to be proximal to the origin of the MPFL by a range of 2.9 mm to 8.5 mm on AP radiograph and MRI, respectively.^18,19 More recent cadaveric studies have demonstrated the origin of the MPFL in pediatric specimens in relation to the physis to be variable.²⁰ Although we believe that a relative anatomic femoral position of the MPFL origin can be achieved without disrupting the physis using Schottle’s point, some have indicated concerns that this may produce a nonisometric position, which has not been our experience.²¹

Continue to: TREATMENT OPTIONS...

The evaluation of a skeletally immature patient may differ from that of an adult patient.  (Table 1) represents a standard evaluation of a skeletally immature patient with PFI. The injury, physical examination findings, activity level, presence of an osteochondral fracture, and severity of bony dysplasia may indicate surgical treatment and influence selection of the surgical technique. Indications for surgical treatment include recurrent patellar instability, symptomatic patellar instability, the presence of a chondral or an osteochondral fracture, and a primary patella dislocation in patients with a high risk for recurrent dislocations. Table 2 represents a list of the possible surgical treatment options for the skeletally immature patient with PFI.^21,22 Variable outcomes and recurrence rates are noted with each procedure.^21,22

MPFL REPAIR VS RECONSTRUCTION

Although there is increased consensus for restoring normal anatomy, continued controversy exists regarding the utility of an MPFL repair versus reconstruction. An MPFL repair to the patella has been reported in a large series and was noted to have a 72% success rate.²³ Although a perceived benefit of the procedure is the absence of risk to the physis, concerns exist regarding the unacceptable rate of continued patellar instability after a repair of native tissue.

Several studies have demonstrated that reconstruction of the MPFL yields lower rates of recurrent dislocation, improved knee function, and an ability to return to prior levels of activity with little to no functional impairment.^1,2,24-26 Studies have also shown that MPFL reconstruction can be performed safely in skeletally immature patients, with little risk of growth impairment, good to excellent results, and low re-rupture rates.^27,28

We propose that MPFL reconstruction for the skeletally immature patient with PFI should be the primary surgical treatment. Any patient with atypical or severe bony dysplasia may warrant additional intervention. Additional correction of valgus, in the form of guided growth, should be considered in conjunction with an MPFL reconstruction if the patient demonstrates a valgus of grade >2 or a lateral distal femoral angle of <84°.

GRAFT OPTIONS

When an MPFL reconstruction is indicated, graft options include autologous hamstring, quadriceps, adductor, or patellar tendon grafts. Allograft tendon may be an acceptable choice, and use of synthetic graft has also been described. A recent systematic review²⁹ concluded that there was no difference in recurrence rates or outcomes based on graft type. However, in this study, the overall complication rates were higher in patients who had autologous graft than in those who had allograft. Although the use of allograft has not been specifically reported in a pediatric cohort, allografts have been successfully used in this age group. Obviating graft harvest eliminates an additional or extended incision, limits postoperative weakness, and may speed early recovery.

Continue to: PREFERRED SURGICAL TECHNIQUE FOR MPFL RECONSTRUCTION WITH ALLOGRAFT...

Surgery should be scheduled and performed as an outpatient procedure. Preoperative instructions may include crutch training, when indicated, and postoperative education regarding expected early therapy and pain management strategy may be employed. Chlorhexidine wipes are provided to patients preoperatively with instruction to use daily starting 3 days prior to surgery. A home exercise program with a focus on quadriceps activation and range of motion is provided and requested to be performed postoperatively.

A standard operating room setup for knee arthroscopy is employed (preference list noted in Table 3; items bolded may be unique to an MPFL reconstruction). Regional, single-shot anesthesia is employed using a sensory-only adductor canal block. A universal surgical timeout is performed before beginning the surgery to include verification of prophylactic antibiotics (Ancef or clindamycin in penicillin-allergic patients) and consideration of the use of a sequential compression device in children aged >10 years when ≥1 venous thromboembolic risk factors are detected in preoperative screening.

Nonirradiated allografts (semitendinosus or tibialis anterior), preferably from a donor <30 years, are our preferred graft choice. The minimum length of the graft should be 240 mm and the doubled thickness should be 5 to 6 mm. After thawing, the graft is lavaged with a mixture of antibiotic saline consisting of 50,000 U of bacitracin in 1 l of normal saline. Tension is then placed on the graft using the graft preparation board, and a whip stitch is placed on each side of the graft using a #2 FiberWire (Arthrex). The graft is sized with care to ensure that it is not thicker than 6.5 mm with an optimal goal of 6 mm.

A standard knee arthroscopy is performed with an emphasis on evaluating the patellofemoral anatomy. Although insufflation can cause distortion and, often, lateralize the patella, the surgeon should consider an estimate of when the patella engages the trochlea during knee flexion. This position of knee flexion will determine the appropriate position of the knee during graft fixation. A bipolar device (90°Arthrocare wand) may be used to debride synovial folds (ie, plica) when affecting the patellar tracking. To maximize visualization of the patella within the knee, we recommend switching the arthroscope from the anterolateral portal to the anteromedial portal. This allows for improved visualization of the lateral femoral condyle and the inferomedial patellar facet, common locations for chondral and osteochondral damage, as well as optimal visualization of patellar engagement within the trochlea. During an arthroscopic dynamic exam of the patella tracking, a lateralized patella may be observed. If the patella tilts upon manual medial translation toward the trochlear groove during the dynamic exam, the lateral retinaculum may be tight or constraining the patella laterally. If this occurs, a partial or complete lateral release may be indicated with a bipolar wand. Visualization of the posteromedial and the posterolateral compartments is required as loose chondral bodies may be present in these locations.     

Any osteochondral or chondral injuries are addressed during the arthroscopy. Large osteochondral fractures of the lateral femoral condyle or the patella are repaired using headless compression screws (Acutrak Screws, Acumed) or headed low-profile screws (1.5-mm screws, DePuy Synthes). Headless screws can be buried 2 to 3 mm below the chondral surface when the fragment has an appropriate thickness, whereas thin fragments may necessitate headed screws for adequate fixation and subsequent implant removal in 8 to 10 weeks. Defects in the patella most often require an open arthrotomy to evert the patella 90° to allow adequate exposure for treatment. Chronic chondral fragmentation may be debrided using the motorized chondrotome or removed and indicated for microfracture (<2 cm² in surface area and <4 mm in depth) or other types of chondral replacement. Chondral lesions over the inferior medial facet are typically not symptomatic and often require minimal treatment.

Continue to: There are 3 methods to identify...

There are 3 methods to identify the insertion of the MPFL into the patella. During the diagnostic arthroscopy, an 18-gauge needle can be used to mark the insertion of the MPFL as visualization of the ligament arthroscopically is often possible (Figure 3). Another useful technique is to follow the inferior aspect of the distal insertion of the vastus medialis oblique (VMO) into the patella. The typical insertion point of the MPFL is immediately distal to the insertion of the inferior aspect of the VMO (Figure 4). It is also helpful to note that the center point of the insertion of the MPFL is at the junction of the proximal one-third and distal two-thirds of the palpable osseous patella. The MPFL origin has been noted to be at the exact midpoint of the chondral surface of the patella or 5 mm proximal (41% of the length of the patella) to the midpoint of the osseous patella.³⁰

Following arthroscopic examination and treatment, a linear incision is made at the superior two-thirds of the patella, 1-finger breadth medial to the patella (Figure 5). During the subcutaneous dissection, the goal is to visualize the fascia overlying the VMO. Once this is identified, the dissection, in this layer, is carried over to expose the anterior and central surface of the patella. Army/navy retractors are used to retract the skin, and the assistant will place manual pressure on the patella to stabilize it for preparation of the patellar surface.

A bovie cautery or a knife is used to mark the insertion of the MPFL, which is immediately distal to the inferior border of the VMO. An incision over the medial surface of the patella creates a T-incision with elevation of the subsequent flaps proximal and distal. This allows exposure of the superficial and medial surface of the patella. During medial exposure of the patella, care is taken to avoid an arthrotomy by leaving the synovial lining attachment. A rongeur is used to decorticate the medial patella and the superficial surface (Figure 6). If an MPFL avulsion is present, it is often embedded within the soft tissues adjacent to the medial patellar. The MPFL avulsion can be exposed and removed if small. During an MPFL reconstruction, a repair of the avulsion is typically not performed. A double-loaded suture anchor is inserted at the site identified as the insertion of the native MPFL (3.0 Biocomposite SutureTak, Arthrex). A single suture anchor is used instead of an interosseous tunnel or double tunnels to avoid creating a large defect that may increase the risk of fracture in a small, skeletally immature patella.³¹

A hemostat is used to identify the layer between the medial retinaculum and the synovium over the medial soft tissue of the knee. The MPFL is a well-defined thickening of the medial retinaculum, and the ideal placement of the reconstruction is immediately inferior to this layer. Once this layer has been identified, a blunt hemostat is inserted to mark the end of a blind pouch that is apparent in this layer. This blind pouch is marked on the surface of the skin as the origin of the MPFL.

Fluoroscopy is now used to identify the origin of the MPFL on the medial femoral condyle. A perfect lateral is obtained by lining up the posterior condyle. Often, existent trochlear dysplasia will modify the normal appearance of the anterior structures of the condyles. Schottle’s point¹⁷ is USED to locate the origin of the MPFL. This is defined by drawing a line from the posterior cortex distally through the condyles (Figure 7). Two perpendicular lines are drawn, one to the extension of the posterior cortex at the level of the posterior extent of Blumensaat’s line and a second at the metaphyseal flare. Schottle’s point is located just anterior to the posterior cortex and in between these perpendicular lines. In a skeletally immature patient, this point appears to be at the level of the physis, on the lateral projection.

Continue to: An anteroposterior and/or a notch view projection...

An anteroposterior and/or a notch view projection is then performed to confirm the location of Schottle’s point, distal to the physis. Because the origin of the MPFL is posterior to the condyle, the notch view should be used to visualize Schottle’s point in relation to the physis in the coronal plane. This location has been confirmed to approximate the origin of the MPFL by published anatomic studies. If the graft measures 6 mm, an ideal distance of 5 to 8 mm distal to the physis will ensure a tunnel location with a proximal margin 2 to 4 mm distal to the physis. In our experience, Schottle’s point is approximately 5 to 7 mm distal to the physis, and rarely do we adjust our position. The guide wire is placed on the medial femoral condyle at this point and then angled 30° proximal to distal to allow tunnel trajectory distal to the undulating physis (Figure 8).

A 6-mm reamer is used over the guide wire to a depth of 20 mm. The newly created tunnel is now exposed and visualized. The graft is folded over at the center aspect and marked 20 mm from the tip of a Bio-tenodesis screwdriver (Arthrex). A 6.25 × 15 mm Bio-tenodesis screw is used. The graft and the screw are inserted into the condyle, and the appropriate graft fixation is confirmed by longitudinal tension placed upon the graft.

The hemostat or the passing suture previously placed into the blind pouch below the native MPFL is used to pass the graft immediately superficial to the synovial lining, in an extra-articular location. The ends of the graft are now exposed through the incision adjacent to the patella. The knee is confirmed to be flexed to approximately 45° on the surgical positioning triangleor at the flexion position determined during diagnostic arthroscopy at which the patella engages the trochlea. The graft is set to length alongside the medial surface of the patella at the position of the suture anchor, and a single stitch is placed through both ends of the graft at this adjacent position using a free needle (Davis Tonsil ½ Circle Taper Point; Vessel Medical). A hemostat is placed on the single suture throw to provisionally secure the graft in this trial position. This allows the surgeon to trial and examine the MPFL graft in extension, 45° of flexion, and terminal flexion. The goal is to provide a check rein to lateral translation of the patella and provide a firm endpoint to avoid further dislocation without overtension of the graft that may lead to increased contact pressures in the patellofemoral joint.

Once appropriate graft position is confirmed, using the double-loaded suture, we prefer to secure each limb separately to the decorticated medial patella. One end of the suture is threaded through the graft once and will act as a post. The other end of the suture is threaded through the graft 3 times in a modified Mason-Allen stitch. With the knee in that same position of flexion, the knot is tied and the graft is secured to the medial side of the patella. For secondary fixation, the remaining ends of the graft are passed below the periosteum on the anterior surface of the patella. Using a 0 Vicryl (Ethicon US), the periosteal flaps are sutured on top of the graft, incorporating the residual graft. The ends are cut and a repeat dynamic examination is performed to confirm the position of the patella and the patellar tracking and to ensure that overtensioning did not occur. Following irrigation, a standard closure is performed. The patient is placed in a hinged knee brace and cryotherapy is applied (Polar Care, Breg Inc).

POSTOPERATIVE PROTOCOL

For the initial or the acute postoperative phases, an emphasis on edema control, early quadriceps activation, and range of motion is recommended. We recommend weight-bearing as tolerated with the leg locked in extension until adequate quadriceps control is achieved. The patient must be able to perform 10 straight leg raises without an extension loss to be cleared to weight-bear as tolerated without motion restriction in the brace. Full motion is allowed immediately.

OUTCOMES

In our experience using isolated MPFL reconstruction in the skeletally immature patient, we have had no evidence of physeal arrest, leg-length inequality, or angular deformity, and only11.4% of patients have had recurrent instability. The mean Kujala score in this cohort was 90.4, with a mean Tegner activity of 7, after the procedure. All failures in our cohort had had severe trochlear dysplasia.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

It is interesting to note that the typical ACL injury pattern occurs during a normal sport-specific movement, yet most rehabilitation protocols fail to recognize the potential causes of the aberrant movement pattern and how to best modify it so that the risk of repeated stress to the ACL can be minimized. It should be understood that movement occurs through the interaction of 3 discrete factors: the individual, the task being performed, and the environment in which it is performed.¹ All of these factors will play a role in how the final movement pattern is produced. For example, a soccer player (individual) may backpedal and pivot to the left 60° and accelerate to sprint after a player moving towards the touchline (task) while receiving instructions from teammates and monitoring the movements of opposing players (environment). A small variance in any 1 of these factors could significantly impact the movement pattern as the player completes the task.

In most rehabilitation programs, each of these factors may be treated in a singular, non-specific manner, but if these factors are not coordinated effectively throughout the program to produce the desired sport-specific movement, a faulty pattern may persist, leaving the player at risk for injury. Current rehabilitation programs seem to have a strong focus on creating stability, mobility, and strength, but these are trained in silos, with an internal focus of control, which only solves the biomechanical equation. Often, it is difficult for the player to coordinate good biomechanics into an efficient, protective movement pattern that is specific to the tasks performed on the field during the normal course of play. The missing link here is the central nervous system (CNS).

Limitations to the current ACL protocols may be that they rely heavily on musculoskeletal rehabilitation and that they have limited emphasis on neurological rehabilitation. As will be discussed later, the CNS has a large impact on the final movement selected by the player. In fact, cognition, perception, and action are the three factors that comprise the individual’s part of the movement paradigm,¹ yet rarely are these factors addressed in most ACL rehabilitation programs. These elements are a large part of the movement equation, so it is easy to understand how failing to address these features can lead to poor movement quality and subsequent ACL re-injury.

In addition to central neurological factors, cognitive issues may play a role in the player’s ability to return to sport. Determining optimal readiness for return to play is a difficult task for the medical community, with many variables to consider. Previous research studies have assessed the variability in return to play for various sports, including football, rugby, soccer, skiing, running, and tennis, with return-to-play rates ranging from 18% to 100%.^2,3,4-10 The risk of secondary injury may cast doubt and fear on athletes as they contemplate their successful return to play.^8,11 Although robust functional testing has become commonplace for determining athlete readiness after injury,^12-20 the assessment of psychological readiness, persistent fear, and loss of confidence are often neglected and not as commonly integrated into the return-to-play algorithm.^21-24 The purpose of this paper is to assess the various cognitive and central neural factors affecting a soccer player’s ability to recover from an ACL injury and offer suggestions for integrating treatments into the protocols to address these issues.

Continue to: CENTRAL NERVOUS SYSTEM NEUROPLASTICITY... 

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

Continue to: The reorganization that results in movement planning...

The reorganization that results in movement planning, transitioning from subcortical levels to cortical levels, is a phenomenon that researchers believe can lead to deficiencies even as the athlete has returned to sport. Grooms et al⁷²revealed in a case report that a subject with an ACLR showed higher levels of activity in the crus region of the cerebellum. This area contains corticobulbar and corticospinal tracts that transmit neural input to maintain balance and coordination.⁷³ These changes in the cerebellum, combined with increased motor cortex activity, are thought to be indicative of a global neural strategy that uses higher levels of the CNS, as opposed to subcortical processing.⁷²

The current research makes a clear and compelling argument for the importance of CNS reorganization after an ACL injury, placing increased reliance on higher cortical levels of control, as well as the visual system to coordinate balance and movement. It is thought that this reorganized method of neural transmission can then become imprinted within the CNS, if not corrected.^35,74 If this is the case, then traditional strength programs may not be sufficient to restore these connections to their pre-injury level. If the CNS has the ability to reorganize based on the aberrant input that it receives from the periphery, then it also certainly has the potential to adapt to more specific structured input via the ascending afferent pathways.^41,45 The rehabilitation program, however, needs to be structured specifically to target the reorganized regions of the brain. There needs to be an emphasis on rehabilitating not only the peripheral neuromotor structures but also the CNS.⁷⁵

CENTRAL NERVOUS SYSTEM REHABILITATION PRINCIPLES

For a neurological rehabilitation to be successful, the interventions need to be repetitive and task-specific, involve learning, employ whole and part practice, and transition from using an internal to an external focus of control.⁷⁶Movements that are repetitive, but which lack structured learning and skill, have been shown to have no effect on inducing neuroplastic changes in the primary motor cortex.^77,78 However, using neurological rehabilitation techniques that facilitate the acquisition of new motor skills by the CNS have been shown to cause neuroplastic adaptation in the motor cortex.^79-85 This occurs because neuroplasticity is determined by experience and practice.⁷⁸ The CNS operates on cues received in the ascending tracts by mechanoreceptors in the joint. If a new movement pattern is being learned by the athlete, then this new afferent input received from the periphery will start to initiate reorganization in the higher learning centers. If this occurs with optimal repetition and precision, then a positive reorganization can take place within the CNS that results in a higher percentage of motor planning and control being filtered down to a subcortical level. Essentially, the movements become instinctive, which is crucial in athletics, where attention in higher cortical areas is frequently diverted to external aspects of the competition and not solely used to focus on movement.

This is why shifting neurological rehabilitation from an internal focus of control to an external focus of control is paramount. While using an internal focus of control is required early in rehabilitation to enable the athlete to understand the specific tasks required in a composite movement, a gradual transition to an external focus of control is necessary as the athlete begins to perform tasks that are more soccer-specific. This autonomous stage of motor learning is crucial because it transfers the burden of motor planning from higher to lower levels of the CNS and frees up the pre-SMA and primary motor cortex to handle more complex patterns.^58,86-88

Continue to: ANTERIOR CRUCIATE LIGAMENT RISK POTENTIAL IN SOCCER PLAYERS...

If a comprehensive neuromotor rehabilitation program is to be used effectively with soccer athletes, then the first priority is to define how the players should move, so that they can demonstrate protective kinematics with all soccer-specific tasks and minimize stress to the ACL. As the ideal movement pattern becomes autonomous, then it should be trained within the context of a dynamic environment; remembering that environmental changes have a large impact on the final movement pattern selected by the individual. Brophy et al⁸⁹ evaluated videos of non-contact ACL injuries in male and female soccer players and determined that 45% occurred while cutting, 25% while landing, and 16% during deceleration. These 3 patterns represent 86% of the ACL injuries observed and offer an opportunity for evaluation and treatment with specific central neuromotor rehabilitation techniques.

The foundational movement patterns for the soccer player should focus on producing leverage that minimizes stress to the ACL during the 3 primary tasks outlined above. To achieve this, it is necessary to reduce posterior ground reaction forces at the hip and knee joint during these movements. There is a high correlation between the magnitude of the posterior ground reaction force, and anterior tibial shear, and subsequent displacement.^90,91 This stress can be reduced by increasing the hip and knee flexion angles during soccer-specific movements that involve pivoting, decelerating, and landing from a jump in a unipedal stance.⁹²

This phenomenon can be explained by observing changes in the ACL elevation angle, hamstring insertion angle, and patella tendon-tibial tuberosity insertion angle. As the knee moves into flexion, the ACL takes on a more parallel orientation to the tibia, and its fibers are better able to resist elastic deformation accompanied by a posterior ground reaction force.^93,94 The quadriceps will produce less anterior translation on the tibia because the patella tendon insertion angle is reduced relative to the longitudinal axis of the tibia, and the mechanical advantage of the quadriceps is decreased.⁹⁵ Lastly, the hamstrings will be able to provide better leverage posteriorly because the resultant force trends toward a more parallel orientation to the tibial plateau, which enables the player to counter, more effectively, the posterior ground reaction force and the anterior pull directed by the quadriceps.⁹⁵

This theory is supported by the work of Li and colleagues,⁹⁶ who showed that there is an inverse relationship between knee flexion angle and ACL loading. In their study, they applied a constant quadriceps force of 200 N at 15°, 30°, and 60° angles. The anterior shear force was obviously the highest at 15° and reduced by 20% at 30° and 60% at 60°. When hamstrings co-contraction was added, there was an additional 30% reduction in anterior shear at 15° and 50% at 30° and 60°. From a more flexed position, the hamstrings can increase joint compression and reduce the anterior translation by allowing the concave medial tibial plateau to limit the anterior drawer effect and absorb the forces that occur with excessive anterior shear, internal rotation, and valgus loads.⁹⁷ As the knee flexion angle approximates 60°, the hamstring leverage is increased, and the quadriceps leverage is diminished to the point where its ability to produce anterior tibial translation is neutralized.⁹⁸ Daniel and colleagues98 referred to this as the quadriceps neutral angle.

For soccer-specific movements that are potentially injurious to the ACL, it may then be beneficial to create a default movement pattern at the knee that approximates this value. In keeping with the information presented in this paper, it will be important to have the player reproduce this angle consistently during activities that involve pivoting, decelerating, and landing from a jump within the context of match play. This will certainly require that segments located both proximal and distal to the knee are able to function within specific parameters so that a cohesive protective synergy is produced throughout the lower quarter which minimizes posterior ground reaction forces and is protective of the ACL. This is where structured neuromotor training that is able to modulate networks within the CNS may be beneficial.

Continue to: CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER...

CENTRAL NERVOUS SYSTEM TREATMENT TECHNIQUES FOR THE SOCCER PLAYER

The ultimate goal is to create a foundational movement pattern that optimizes leverage and is protective of the ACL during decelerating, pivoting, and landing in a unipedal stance from a jump. The composite segments that are necessary to achieve this include local core stability to create lumbopelvic stiffness, and global core activation to enhance posterior chain stability. This should enable the player to feel more balanced when placing the pelvis in a more posterior and inferior position while still maintaining the trunk in a position that is parallel with the tibia, as the knee is flexed to an approximate 60° angle (Figure 1). From a frontal plane perspective, the acetabulum should bisect the malleoli of the stance leg, with a neutral tibiofemoral joint alignment (Figure 1).

The neuromotor training for the composite segments of this movement can begin in the “acute postoperative phase” (Table 1).   Because the surgical repair will limit the player’s capabilities in this stage, this is a good time to break down the foundational movement pattern into its component parts and ensure that the CNS receives a high number of quality repetitions of parts. In this phase, the player may begin an isolated training for the transversus abdominis, multifidus, and pubococcygeus. This can start in a supine position using biofeedback with an isometric contraction, progress to a standing position, and incorporate deep core activation with stance-phase gait training, mini squats, and lunge variations. This phase will require an abundance of visual and verbal feedback with an internal focus of control as the player gets used to activating the deep core and quad/hip synergy during functional lower extremity movements. Even in this early phase, the player should look to minimize anterior and/or posterior pelvic tilting and maintain a stiff thoracolumbar segment that remains parallel with the tibia during all functional movements.

Table 1. Adjunct CNS Treatment Principles for ACL Reconstruction in Soccer Athletes

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

As the player moves into the “subacute postoperative phase” (Table 1).   He or she will continue to use an internal focus of control to activate the local/global core synergy with functional movements progressing from double-leg, to single-leg positions. Partial practice, instead of whole practice, is still the predominant theme of the neural training process. In this phase, the knee and hip flexion angles can increase, and the player’s trunk and pelvic position should be critiqued in a single-leg position so that the trunk remains parallel with the tibia in the sagittal plane with a slight forward hip hinge. The pelvis should remain level throughout single-leg stance to ensure adequate activation of the lateral hip stabilizers. This is the stage where the player can learn to isolate closed kinetic chain hip rotation for pivoting, and so, single-leg hip internal and external rotation drills are useful, both with and without resistance. Skill acquisition is crucial in this phase because the patterns that the CNS adopts will form the foundation for more dynamic patterns that will occur in the later soccer-specific stages. Higher levels of cortical planning are still needed in this phase. For this reason, it is important that poor quality repetitions are recognized by the player and clinician so that he or she can learn to perform them correctly, albeit still with an internal focus of control. This is also a good time to begin to employ constraint-induced movement therapy as the player is able to replicate the desired pattern with more precision. For example, by eliminating the use of the upper extremities as a source of balance, the CNS is forced to program alternate synergies such as the lumbopelvic, and foot and ankle segments to maintain the desired alignment.

The “lower quarter static stability phase” (Table 1) marks a point where it may be useful to use direct strategies that have the capability to change CNS efferent owutput from a primary reliance on the visual processing areas in the posterior-inferior temporal gyrus back to the somatosensory area. It is critical that the player is able to make this transition in cortical reorganization and control, because ACL-injured subjects have been shown to have balance scores similar to healthy controls when they are able to use their vision, but this is reduced when vision is taken away.^99-105  Their balance will diminish even further if vision is modulated during more complex landing and pivoting maneuvers.^99-105 This may certainly explain why defending is a riskier task for ACL-injured players⁸⁹ as their visual system is focused more on tracking a player than attending to precision with movement planning.

To enhance this cortical reorganization within the context of soccer-specific movements, it is useful to start from a foundational single-leg position, with the knee approximating 60° of flexion and the trunk parallel to the tibia. In the frontal plane, the pelvis should be level, the trunk vertical, and the acetabulum bisecting the malleoli of the stance leg (Figure 1).   The player may initially work on getting into this foundational position with vision either partially obstructed using stroboscopic eyewear or completely obstructed if this equipment is unavailable.^106-108 The pattern can be progressed by constraining the upper extremities to force reliance on the lumbopelvic and foot/ankle strategies for balance. Head and/or trunk turns can be added to simulate the external focus of control that is required with movement in soccer. These should progress from slow to fast and anticipated to unanticipated as the player demonstrates competence in maintaining stability at each segment within the foundational stance position. Once this is in play, a ball should be introduced into the drills. As the player maintains the foundational position with vision diminished and upper extremities constrained, they should attempt to reach for or trap a ball from this position. If vision is completely obstructed, then the player can be instructed to open his/her eyes just as the ball arrives to induce a reactive response. Again, quality repetitions are essential for learning to occur, and subsequent skill acquisition to take place in the CNS; thus, close scrutiny should be paid to the qualitative essence of the movement patterns to ensure pristine biomechanics during this phase.

The “lower quarter dynamic stability phase” (Table 1) should continue with the same neuromotor training principles employed in the previous phase, except that the drills will now involve plyometrics. The player should ultimately progress from double-leg, to single-leg jumps and then linear to diagonal. Vision should still be obstructed and upper extremities constrained to channel the lumbopelvic region for force production and balance. Movement quality in the foundational position remains paramount with these drills to ensure that skill acquisition is occurring and injury risk is being mitigated. An external focus of control can be introduced by applying an unanticipated perturbation during a jump. Additional learning opportunities should include unanticipated head and trunk turns while landing in a unipedal stance from a jump. The task can be made more specific by having the player trap a pass while doing linear or diagonal single-leg hop progressions. In this manner, the player’s CNS can become reorganized to program the requisite synergies to maintain a protective foundational position on the stance leg, as the contralateral limb is required to perform work that is far outside the player’s base of support.

Continue to: The final segment of the CNS neuromotor rehabilitation program...

The final segment of the CNS neuromotor rehabilitation program is the “lower quarter dynamic agility phase” (Table 1), when the player will learn to perform an unanticipated directional change in a foundational position for the pivot leg. The player can begin this phase by initiating sprint-deceleration-pivot efforts, progressing at 45°, 90°, 120°, and 180° turns. This should be trained in both a forward and backpedal position. Close attention should be paid to the deceleration phase of the sprint-pivot effort, as this will set the player up to demonstrate protective kinematics during the pivot phase of the task. In this phase, the center of mass should become lower and move posteriorly, so that a deeper knee and hip flexion angle, supported by posterior chain synergies, can occur at the pivot point. This is an important skill for the player to acquire, as Cortes and colleagues⁹² have reported that female collegiate soccer players tend to perform a pivoting task with a more erect trunk position. In the same cohort, they also measured the mean knee flexion angle at initial contact during pivoting to be 24°.⁹² Movement patterns that reflect an elevated center of mass, with arms abducted away from the trunk, should be discouraged here. The drills can be progressed to have the player react to a command and perform unanticipated pivots within a 5 × 5-meter box to simulate defending. This should be progressed from eyes open and arms unconstrained, to vision disrupted and arms constrained. From here, an external focus of control can be added by playing a ball to the athlete. Vision should be withheld until the instant that the ball arrives at the player, when he/she is required to play the ball to an unanticipated spot. As is the case in all other phases of the neuromotor training, the quality of movement is the most important parameter to critique with each drill. From a qualitative standpoint, the player should demonstrate stiffness throughout the thoracolumbar region and power and control through the pelvis with each directional change. In addition, he or she should maintain a low and posteriorly oriented center of mass to optimize leverage in the hamstrings/gluteals compared with the quadriceps and reduce posterior ground reaction forces.

PSYCHOLOGICAL READINESS FOR RETURN TO PLAY

After an injury is sustained, an athlete is often subjected to a range of psychological responses in addition to the functional impairment, including stress, hesitancy, alterations in self-esteem, depression, fear of re-injury, and anxiety.^43,109-111 The aforementioned responses are often at their height in the time immediately following an injury and generally subside over time during the rehabilitation process.¹¹⁰ The rates at which athletes experience psychological distress following an injury range between 5% and 19%; the levels are comparable with patients receiving treatment for mental health illness.⁴³ However, these elements may persist, or even increase, in the later stages of the rehabilitation process as the topic of return to play is deliberated.^112,113 If these fears are left unresolved, then a significant delay can be incurred during the rehabilitation process, which might ultimately jeopardize the successful return to play.^114,115

When athletes have been cleared to return to sport, fear tends to be the most common reason for their decision to not return to play.^21,116 The persistence of fear has clinical implications and warrants close monitoring to ensure that the athlete feels adequately supported in the decision to return to sport.^117,118 Building the athlete’s confidence by addressing hesitation, lack of confidence, heightened awareness of risk or re-injury, and safe reintegration into athletic participation are important themes identified to encourage a safe return to play.⁴³ A variety of validated tools  can be integrated into an existing return-to-play decision-making algorithm (Table 2).^118-120 

Abbreviations: ACL, anterior cruciate ligament; CNS, central nervous system; CIMT, constraint-induced movement therapy.

Table 2. Self-Report Measurement Tools to Integrate into Return-to-Play Decision-Making Algorithm

By integrating the necessary screening of patients for kinesiophobia and assessing patient expectations after enduring an ACL injury, clinicians may be able to identify patients who are at risk for poorer functional outcomes. A consideration of psychosocial elements such as activity avoidance, fear of movement and re-injury, loss of confidence and expectations/assumptions during the continuum of the rehabilitation process, and the decision to return to play may favorably impact the individual’s ability to safely return to sport. It is critical to address both the physical and psychosocial factors during the rehabilitation process to more optimally transition individuals back to their prior level of athleticism.

CONCLUSION

Psychosocial factors may play a role in determining a player’s readiness to return to sport, as well as a potential for re-injury. A number of tests are available for use with this patient population to identify mental deficits that may impact player performance upon return. Additionally, the CNS should be considered as a source of impairment in players with ACL injuries. Current protocols may not fully appreciate the CNS’ impact on the player’s functional outcome. Therefore, an approach that includes CNS neuromotor training with traditional musculoskeletal rehabilitation, which also incorporates cognitive and psychosocial factors, may define an improved paradigm for treating soccer athletes following an ACL injury and assessing return-to-play capability.

The intervastus approach (Figure 1A) described by Jojima⁴ and others utilizes the interval between the quadriceps tendon and vastus medialis. Although it is a simple approach to perform that is extensile, it is not considered tendon-sparing since the vastus medialis inserts onto the medial aspect of the quadriceps tendon (Figure 2).⁵  Therefore, dissecting through this interval, without elevation of the vastus medialis (Figure 3A), damages the quadriceps tendon, and strangulation of the muscle occurs with repair of the arthrotomy site (Figure 3B).  This situation is even more likely in patients with a low-lying vastus medialis.⁶

The modified intervastus (MIV) approach described previously,⁷ may be used in the majority of patients undergoing TKA. The advantages of this approach include its extensile nature, similarities to an MP approach, and preservation of both the extensor mechanism and the vastus medialis, leading to a more rapid return to active knee extension than is traditionally observed.^2,7 The approach is simple to perform, easy to close, and is compatible with more extensile approaches such as a quadriceps snip if required in revision scenarios.⁷ However, functional outcomes of the MIV approach have not been quantified. It is unknown whether these outcomes will offer any advantages compared with the SV approach. Therefore, the objective of this study was to measure functional outcomes of the MIV approach and to compare the results with those previously published for the SV approach. We hypothesized that using the MIV approach for TKA surgery would lead to early straight-leg raise and increase in knee range of motion (ROM) postoperatively.

SURGICAL TECHNIQUE

The MIV approach preserves the quadriceps tendon and vastus medialis.⁷ After exposure of the vastus medialis muscle, the interval between the quadriceps tendon and vastus medialis is identified (Figure 4).  The fascia overlying the lateral edge of the vastus medialis is incised where it meets the quadriceps tendon (Figure 5).  The muscle is then bluntly elevated off the underlying capsule just enough to allow for a capsular repair later (Figure 6).  An arthrotomy is then performed from cephalad to caudal (Figure 7).  This interval may be extended proximally between the vastus intermedius and vastus medialis to expose the distal femur if needed. The closure is performed by repairing the capsule with absorbable suture (Figure 8A), and the vastus medialis fascia is repaired back to the medial edge of the quadriceps tendon, restoring the anatomy (Figure 8B).

Continue to: PATIENTS AND METHODS...

PATIENTS AND METHODS

A retrospective review of functional outcomes after TKA using the MIV approach was conducted; the study was approved by the University of Illinois Institutional Review Board. A total of 127 patients of mean age 66.75 years (range, 48–86 years) with primary osteoarthritis of the knee who were indicated for a total knee replacement with 1-year follow-up were included. The patient demographics are shown in Table 1.  All patients underwent TKA using the MIV approach described above by 2 experienced orthopedic surgeons at the same institution. Patients received spinal anesthesia and a periarticular pain block intraoperatively. A measured resection technique was used by 1 surgeon, and a gap-balancing technique by the other. Surgeon 1 used the Persona PS cemented knee system (Zimmer Biomet, and Surgeon 2 used the Sigma PS cemented knee system (Depuy). Patellar resurfacing was done in all cases. Patellar tracking was checked intraoperatively using the ‘no-touch’ technique, and the need for a lateral release was noted. Drains were removed on postoperative day 1. Oral opioids were given as needed. Intravenous antibiotics were continued for 24 hours. Oral anticoagulants were used for thromboembolism prophylaxis for 3 weeks. Patients were mobilized on the day of surgery with full weight-bearing under the supervision of an experienced physical therapist. Static and dynamic quadriceps exercises were started on the same day of surgery along with active knee ROM exercises. Pain score, extensor lag, ROM, walking ability, and complications were recorded in all patients.

Table 1. Patient Demographics

The visual analog score (VAS) was obtained preoperatively and recorded on postoperative day 1. Patient walking distance with assistance was measured on the day of surgery, after surgery, and on the day of hospital discharge. Patients were assessed preoperatively and postoperatively at 1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year for knee ROM. A one-way ANOVA was conducted to compare the preoperative and postoperative day 1 VAS with significance set at P < .05 (OriginPro 2015, OriginLab Corporation). Differences in knee ROM between preoperative and postoperative follow-up periods (1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year) were identified using a 1-way ANOVA with a post hoc Tukey test. Significance was set at P < .05.

RESULTS

All patients were able to fully straight-leg raise and demonstrate functional knee ROM by postoperative day 1. The patella tracked centrally in all patients, and none required a lateral retinacular release. The majority of patients were discharged in the first 48 hours after surgery on oral narcotics. None required IV narcotics during their hospital stay or a blood transfusion. Two cases were complicated by severe knee skin blistering postoperatively due to a reaction to an adhesive dressing; one was complicated by skin necrosis leading to a flap reconstruction that became infected, requiring a 2-stage revision. A separate case had an acute postoperative infection that required irrigation and debridement with polyethylene exchange. After a 12-week course of antibiotics, the infection was eradicated. All patients reported a high satisfaction rate during their acute postoperative phase.

Postoperatively, all patients were able to walk on the day of surgery either independently or with some assistance. On the day of surgery, 10% of patients were able to walk >200 feet, and this increased to 65% of patients able to walk >200 feet on the day of discharge (compare Figure 9A and Figure 9B).  Within 2 weeks of surgery, 30% of patients could walk independently (without assistive devices), and this number increased to 78% by 8 weeks after surgery (Figure 10).

Pain assessed using the VAS was lower on postoperative day 1 (3.17 ± 1.97) than the preoperative score (3.69 ± 2.22, P< .05). Overall, knee ROM significantly increased during the follow-up after surgery. Initially, the ROM decreased 1 week after surgery (90.82 ± 10.28) compared with preoperative ROM (101.04 ± 19.48, P < .001) (Figure 10).  At 2 weeks after surgery, knee ROM returned to the preoperative value (100.70 ± 13.36). By 6 weeks after surgery, knee ROM was 17° greater than the preoperative ROM (118.45 ± 11.89, P < .001). Knee ROM remained stable at 3- and 6-month assessments, and showed further improvement by 1 year (126.62 ± 9.81, P < .001) compared with the preoperative state (Figure 10). The net improvement in knee ROM was 25° of increased knee flexion by 1 year.

Continue to: DISCUSSION...

DISCUSSION

TKA is a successful procedure that restores knee function with pain relief in osteoarthritis patients. The SV approach for TKA has better outcomes in terms of the VAS, ROM, straight-leg raise with faster rehabilitation compared with the standard MP approach;^8–12 however, it can be challenging and time-consuming when used in morbidly obese and muscular patients.³ The SV approach can also increase the risk of complications such as patellar tendon avulsion or medial collateral injury because of the difficulty in exposure specifically for knees with limited ROM.¹³ Here we introduce the MIV approach as an alternative to the SV approach, overcoming most of these difficulties.

With the prevalence of morbid obesity and the market demand for minimally invasive techniques, we believe the MIV approach represents a good approach for surgeons since it is easy to perform, does not require specialized instrumentation, and is a reproducible approach even on the most complex deformities. The minimal time added to ensure blunt elevation of the vastus medialis muscle and an anatomic repair of the underlying knee capsule and vastus medialis fascia to the medial edge of the quadriceps tendon allows restoration of the anatomy and a robust double-layered watertight seal closure with no strangulation of soft tissues. We believe this reproducible muscle- and tendon-sparing approach that allows gentle, soft tissue handling even in the most complex primary total knee cases may lead to less soft tissue swelling, and therefore, less postoperative pain resulting in an accelerated recovery.

The pain level in this group of patients was reduced after the MIV approach as indicated by the VAS. The VAS was significantly decreased on postoperative day 1 compared with the VAS recorded preoperatively (P < .05), indicating patients felt less pain on the day after surgery. The average VAS on postoperative day 1 from other studies for SV approach ranged from 2.1 to 5,^9,12,14–19 whereas our MIV approach value was 3.17. Periarticular blocks were available for this study group, and no peripheral nerve blocks were used. Some studies of the SV approach mention the use of peripheral nerve blocks, while others did not describe the method used for treatment or control of postoperative pain. The decreased reported pain levels and the observed increased knee ROM seen in the MIV and SV approach study groups might be attributable to the treatment of postoperative pain.

Patient ambulation also increased from the day of surgery to the day of discharge for the MIV approach. Only 10% of patients were able to walk with assistance >200 feet on the day of surgery; however, this percentage increased to 65% on the discharge day showing an excellent recovery of walking ability within 2 days of surgery. Mehta and colleagues²⁰reported that 95% of patients undergoing subvastus/midvastus approaches could walk >10 blocks at 6 months follow-up. For the MIV approach, 78% of patients were able to walk independently within 8 weeks of surgery.

Continue to: The MIV approach shows improvement...

The MIV approach shows improvement in functional outcomes in terms of knee ROM from preoperative to postoperative. Although knee ROM decreased significantly at postoperative week 1, which is most likely because of a peak in postoperative pain and swelling; the ROM started to increase significantly at postoperative week 6. After 1 year, the knee ROM increased by 25% compared with preoperative ROM for the MIV approach. We found the average knee ROM at postoperative 3 months using the MIV approach to be 120.4°. Knee ROM at postoperative 3 months using the SV approach reported by other studies ranged from 87.1° to 120°.^19,21–23 Similarly, after 1 year, the average ROM by MIV approach was 126.62°, whereas average knee ROM from other studies using the SV approach was 114.1°.^2,10,19,21 Achieving a knee ROM of 120° allows patients to return to their baseline function and perform activities of daily living without limitation. With the prevalence of knee osteoarthritis in the younger population, the need for increased knee ROM post-TKA becomes more important so patients can return to work and function at their baseline.

In addition to being both a muscle- and tendon-sparing approach, other advantages of the MIV approach are that it is simple to perform and gives similar exposure to the MP approach even in difficult primary cases. It is also as extensile as the medial parapatellar approach, and it can be converted to a quadriceps snip if required. There is also minimal, if any, muscle retraction preventing muscle injury that may be seen with some other muscle-sparing approaches to the knee, especially in more difficult primary total knee cases. Another advantage to this approach, as opposed to the other approaches to the knee described here, is that it allows a double-layered closure, decreasing the possibility of arthrotomy dehiscence. Because of this double-layered closure, there is no muscle strangulation with repair of the arthrotomy site as seen in some other approaches to the knee, and both vascularity and innervation to the vastus medialis are preserved.

One limitation of this study is that it is a retrospective analysis. Future studies of the consequences of using this approach need to include quantitative assessment of muscle function using electromyography or dynamometer measurements, utilization of any number of validated knee score systems to measure functional outcomes, and incorporation of a randomized controlled trial.

In summary, the new MIV approach is easy to perform and is compatible with more extensile approaches such as a quadriceps snip, if required in revision scenarios. The MIV approach preserves the extensor mechanism, vascularity, and innervation to the vastus medialis. Our study documents both safety and good clinical outcomes using the MIV approach in TKA. Therefore, the MIV approach may be used in the majority of patients undergoing TKA.

The intervastus approach (Figure 1A) described by Jojima⁴ and others utilizes the interval between the quadriceps tendon and vastus medialis. Although it is a simple approach to perform that is extensile, it is not considered tendon-sparing since the vastus medialis inserts onto the medial aspect of the quadriceps tendon (Figure 2).⁵  Therefore, dissecting through this interval, without elevation of the vastus medialis (Figure 3A), damages the quadriceps tendon, and strangulation of the muscle occurs with repair of the arthrotomy site (Figure 3B).  This situation is even more likely in patients with a low-lying vastus medialis.⁶

The modified intervastus (MIV) approach described previously,⁷ may be used in the majority of patients undergoing TKA. The advantages of this approach include its extensile nature, similarities to an MP approach, and preservation of both the extensor mechanism and the vastus medialis, leading to a more rapid return to active knee extension than is traditionally observed.^2,7 The approach is simple to perform, easy to close, and is compatible with more extensile approaches such as a quadriceps snip if required in revision scenarios.⁷ However, functional outcomes of the MIV approach have not been quantified. It is unknown whether these outcomes will offer any advantages compared with the SV approach. Therefore, the objective of this study was to measure functional outcomes of the MIV approach and to compare the results with those previously published for the SV approach. We hypothesized that using the MIV approach for TKA surgery would lead to early straight-leg raise and increase in knee range of motion (ROM) postoperatively.

SURGICAL TECHNIQUE

The MIV approach preserves the quadriceps tendon and vastus medialis.⁷ After exposure of the vastus medialis muscle, the interval between the quadriceps tendon and vastus medialis is identified (Figure 4).  The fascia overlying the lateral edge of the vastus medialis is incised where it meets the quadriceps tendon (Figure 5).  The muscle is then bluntly elevated off the underlying capsule just enough to allow for a capsular repair later (Figure 6).  An arthrotomy is then performed from cephalad to caudal (Figure 7).  This interval may be extended proximally between the vastus intermedius and vastus medialis to expose the distal femur if needed. The closure is performed by repairing the capsule with absorbable suture (Figure 8A), and the vastus medialis fascia is repaired back to the medial edge of the quadriceps tendon, restoring the anatomy (Figure 8B).

Continue to: PATIENTS AND METHODS...

PATIENTS AND METHODS

A retrospective review of functional outcomes after TKA using the MIV approach was conducted; the study was approved by the University of Illinois Institutional Review Board. A total of 127 patients of mean age 66.75 years (range, 48–86 years) with primary osteoarthritis of the knee who were indicated for a total knee replacement with 1-year follow-up were included. The patient demographics are shown in Table 1.  All patients underwent TKA using the MIV approach described above by 2 experienced orthopedic surgeons at the same institution. Patients received spinal anesthesia and a periarticular pain block intraoperatively. A measured resection technique was used by 1 surgeon, and a gap-balancing technique by the other. Surgeon 1 used the Persona PS cemented knee system (Zimmer Biomet, and Surgeon 2 used the Sigma PS cemented knee system (Depuy). Patellar resurfacing was done in all cases. Patellar tracking was checked intraoperatively using the ‘no-touch’ technique, and the need for a lateral release was noted. Drains were removed on postoperative day 1. Oral opioids were given as needed. Intravenous antibiotics were continued for 24 hours. Oral anticoagulants were used for thromboembolism prophylaxis for 3 weeks. Patients were mobilized on the day of surgery with full weight-bearing under the supervision of an experienced physical therapist. Static and dynamic quadriceps exercises were started on the same day of surgery along with active knee ROM exercises. Pain score, extensor lag, ROM, walking ability, and complications were recorded in all patients.

Table 1. Patient Demographics

The visual analog score (VAS) was obtained preoperatively and recorded on postoperative day 1. Patient walking distance with assistance was measured on the day of surgery, after surgery, and on the day of hospital discharge. Patients were assessed preoperatively and postoperatively at 1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year for knee ROM. A one-way ANOVA was conducted to compare the preoperative and postoperative day 1 VAS with significance set at P < .05 (OriginPro 2015, OriginLab Corporation). Differences in knee ROM between preoperative and postoperative follow-up periods (1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year) were identified using a 1-way ANOVA with a post hoc Tukey test. Significance was set at P < .05.

RESULTS

All patients were able to fully straight-leg raise and demonstrate functional knee ROM by postoperative day 1. The patella tracked centrally in all patients, and none required a lateral retinacular release. The majority of patients were discharged in the first 48 hours after surgery on oral narcotics. None required IV narcotics during their hospital stay or a blood transfusion. Two cases were complicated by severe knee skin blistering postoperatively due to a reaction to an adhesive dressing; one was complicated by skin necrosis leading to a flap reconstruction that became infected, requiring a 2-stage revision. A separate case had an acute postoperative infection that required irrigation and debridement with polyethylene exchange. After a 12-week course of antibiotics, the infection was eradicated. All patients reported a high satisfaction rate during their acute postoperative phase.

Postoperatively, all patients were able to walk on the day of surgery either independently or with some assistance. On the day of surgery, 10% of patients were able to walk >200 feet, and this increased to 65% of patients able to walk >200 feet on the day of discharge (compare Figure 9A and Figure 9B).  Within 2 weeks of surgery, 30% of patients could walk independently (without assistive devices), and this number increased to 78% by 8 weeks after surgery (Figure 10).

Pain assessed using the VAS was lower on postoperative day 1 (3.17 ± 1.97) than the preoperative score (3.69 ± 2.22, P< .05). Overall, knee ROM significantly increased during the follow-up after surgery. Initially, the ROM decreased 1 week after surgery (90.82 ± 10.28) compared with preoperative ROM (101.04 ± 19.48, P < .001) (Figure 10).  At 2 weeks after surgery, knee ROM returned to the preoperative value (100.70 ± 13.36). By 6 weeks after surgery, knee ROM was 17° greater than the preoperative ROM (118.45 ± 11.89, P < .001). Knee ROM remained stable at 3- and 6-month assessments, and showed further improvement by 1 year (126.62 ± 9.81, P < .001) compared with the preoperative state (Figure 10). The net improvement in knee ROM was 25° of increased knee flexion by 1 year.

Continue to: DISCUSSION...

DISCUSSION

TKA is a successful procedure that restores knee function with pain relief in osteoarthritis patients. The SV approach for TKA has better outcomes in terms of the VAS, ROM, straight-leg raise with faster rehabilitation compared with the standard MP approach;^8–12 however, it can be challenging and time-consuming when used in morbidly obese and muscular patients.³ The SV approach can also increase the risk of complications such as patellar tendon avulsion or medial collateral injury because of the difficulty in exposure specifically for knees with limited ROM.¹³ Here we introduce the MIV approach as an alternative to the SV approach, overcoming most of these difficulties.

With the prevalence of morbid obesity and the market demand for minimally invasive techniques, we believe the MIV approach represents a good approach for surgeons since it is easy to perform, does not require specialized instrumentation, and is a reproducible approach even on the most complex deformities. The minimal time added to ensure blunt elevation of the vastus medialis muscle and an anatomic repair of the underlying knee capsule and vastus medialis fascia to the medial edge of the quadriceps tendon allows restoration of the anatomy and a robust double-layered watertight seal closure with no strangulation of soft tissues. We believe this reproducible muscle- and tendon-sparing approach that allows gentle, soft tissue handling even in the most complex primary total knee cases may lead to less soft tissue swelling, and therefore, less postoperative pain resulting in an accelerated recovery.

The pain level in this group of patients was reduced after the MIV approach as indicated by the VAS. The VAS was significantly decreased on postoperative day 1 compared with the VAS recorded preoperatively (P < .05), indicating patients felt less pain on the day after surgery. The average VAS on postoperative day 1 from other studies for SV approach ranged from 2.1 to 5,^9,12,14–19 whereas our MIV approach value was 3.17. Periarticular blocks were available for this study group, and no peripheral nerve blocks were used. Some studies of the SV approach mention the use of peripheral nerve blocks, while others did not describe the method used for treatment or control of postoperative pain. The decreased reported pain levels and the observed increased knee ROM seen in the MIV and SV approach study groups might be attributable to the treatment of postoperative pain.

Patient ambulation also increased from the day of surgery to the day of discharge for the MIV approach. Only 10% of patients were able to walk with assistance >200 feet on the day of surgery; however, this percentage increased to 65% on the discharge day showing an excellent recovery of walking ability within 2 days of surgery. Mehta and colleagues²⁰reported that 95% of patients undergoing subvastus/midvastus approaches could walk >10 blocks at 6 months follow-up. For the MIV approach, 78% of patients were able to walk independently within 8 weeks of surgery.

Continue to: The MIV approach shows improvement...

The MIV approach shows improvement in functional outcomes in terms of knee ROM from preoperative to postoperative. Although knee ROM decreased significantly at postoperative week 1, which is most likely because of a peak in postoperative pain and swelling; the ROM started to increase significantly at postoperative week 6. After 1 year, the knee ROM increased by 25% compared with preoperative ROM for the MIV approach. We found the average knee ROM at postoperative 3 months using the MIV approach to be 120.4°. Knee ROM at postoperative 3 months using the SV approach reported by other studies ranged from 87.1° to 120°.^19,21–23 Similarly, after 1 year, the average ROM by MIV approach was 126.62°, whereas average knee ROM from other studies using the SV approach was 114.1°.^2,10,19,21 Achieving a knee ROM of 120° allows patients to return to their baseline function and perform activities of daily living without limitation. With the prevalence of knee osteoarthritis in the younger population, the need for increased knee ROM post-TKA becomes more important so patients can return to work and function at their baseline.

In addition to being both a muscle- and tendon-sparing approach, other advantages of the MIV approach are that it is simple to perform and gives similar exposure to the MP approach even in difficult primary cases. It is also as extensile as the medial parapatellar approach, and it can be converted to a quadriceps snip if required. There is also minimal, if any, muscle retraction preventing muscle injury that may be seen with some other muscle-sparing approaches to the knee, especially in more difficult primary total knee cases. Another advantage to this approach, as opposed to the other approaches to the knee described here, is that it allows a double-layered closure, decreasing the possibility of arthrotomy dehiscence. Because of this double-layered closure, there is no muscle strangulation with repair of the arthrotomy site as seen in some other approaches to the knee, and both vascularity and innervation to the vastus medialis are preserved.

One limitation of this study is that it is a retrospective analysis. Future studies of the consequences of using this approach need to include quantitative assessment of muscle function using electromyography or dynamometer measurements, utilization of any number of validated knee score systems to measure functional outcomes, and incorporation of a randomized controlled trial.

In summary, the new MIV approach is easy to perform and is compatible with more extensile approaches such as a quadriceps snip, if required in revision scenarios. The MIV approach preserves the extensor mechanism, vascularity, and innervation to the vastus medialis. Our study documents both safety and good clinical outcomes using the MIV approach in TKA. Therefore, the MIV approach may be used in the majority of patients undergoing TKA.

The intervastus approach (Figure 1A) described by Jojima⁴ and others utilizes the interval between the quadriceps tendon and vastus medialis. Although it is a simple approach to perform that is extensile, it is not considered tendon-sparing since the vastus medialis inserts onto the medial aspect of the quadriceps tendon (Figure 2).⁵  Therefore, dissecting through this interval, without elevation of the vastus medialis (Figure 3A), damages the quadriceps tendon, and strangulation of the muscle occurs with repair of the arthrotomy site (Figure 3B).  This situation is even more likely in patients with a low-lying vastus medialis.⁶

The modified intervastus (MIV) approach described previously,⁷ may be used in the majority of patients undergoing TKA. The advantages of this approach include its extensile nature, similarities to an MP approach, and preservation of both the extensor mechanism and the vastus medialis, leading to a more rapid return to active knee extension than is traditionally observed.^2,7 The approach is simple to perform, easy to close, and is compatible with more extensile approaches such as a quadriceps snip if required in revision scenarios.⁷ However, functional outcomes of the MIV approach have not been quantified. It is unknown whether these outcomes will offer any advantages compared with the SV approach. Therefore, the objective of this study was to measure functional outcomes of the MIV approach and to compare the results with those previously published for the SV approach. We hypothesized that using the MIV approach for TKA surgery would lead to early straight-leg raise and increase in knee range of motion (ROM) postoperatively.

SURGICAL TECHNIQUE

The MIV approach preserves the quadriceps tendon and vastus medialis.⁷ After exposure of the vastus medialis muscle, the interval between the quadriceps tendon and vastus medialis is identified (Figure 4).  The fascia overlying the lateral edge of the vastus medialis is incised where it meets the quadriceps tendon (Figure 5).  The muscle is then bluntly elevated off the underlying capsule just enough to allow for a capsular repair later (Figure 6).  An arthrotomy is then performed from cephalad to caudal (Figure 7).  This interval may be extended proximally between the vastus intermedius and vastus medialis to expose the distal femur if needed. The closure is performed by repairing the capsule with absorbable suture (Figure 8A), and the vastus medialis fascia is repaired back to the medial edge of the quadriceps tendon, restoring the anatomy (Figure 8B).

Continue to: PATIENTS AND METHODS...

PATIENTS AND METHODS

A retrospective review of functional outcomes after TKA using the MIV approach was conducted; the study was approved by the University of Illinois Institutional Review Board. A total of 127 patients of mean age 66.75 years (range, 48–86 years) with primary osteoarthritis of the knee who were indicated for a total knee replacement with 1-year follow-up were included. The patient demographics are shown in Table 1.  All patients underwent TKA using the MIV approach described above by 2 experienced orthopedic surgeons at the same institution. Patients received spinal anesthesia and a periarticular pain block intraoperatively. A measured resection technique was used by 1 surgeon, and a gap-balancing technique by the other. Surgeon 1 used the Persona PS cemented knee system (Zimmer Biomet, and Surgeon 2 used the Sigma PS cemented knee system (Depuy). Patellar resurfacing was done in all cases. Patellar tracking was checked intraoperatively using the ‘no-touch’ technique, and the need for a lateral release was noted. Drains were removed on postoperative day 1. Oral opioids were given as needed. Intravenous antibiotics were continued for 24 hours. Oral anticoagulants were used for thromboembolism prophylaxis for 3 weeks. Patients were mobilized on the day of surgery with full weight-bearing under the supervision of an experienced physical therapist. Static and dynamic quadriceps exercises were started on the same day of surgery along with active knee ROM exercises. Pain score, extensor lag, ROM, walking ability, and complications were recorded in all patients.

Table 1. Patient Demographics

The visual analog score (VAS) was obtained preoperatively and recorded on postoperative day 1. Patient walking distance with assistance was measured on the day of surgery, after surgery, and on the day of hospital discharge. Patients were assessed preoperatively and postoperatively at 1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year for knee ROM. A one-way ANOVA was conducted to compare the preoperative and postoperative day 1 VAS with significance set at P < .05 (OriginPro 2015, OriginLab Corporation). Differences in knee ROM between preoperative and postoperative follow-up periods (1 week, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year) were identified using a 1-way ANOVA with a post hoc Tukey test. Significance was set at P < .05.

RESULTS

All patients were able to fully straight-leg raise and demonstrate functional knee ROM by postoperative day 1. The patella tracked centrally in all patients, and none required a lateral retinacular release. The majority of patients were discharged in the first 48 hours after surgery on oral narcotics. None required IV narcotics during their hospital stay or a blood transfusion. Two cases were complicated by severe knee skin blistering postoperatively due to a reaction to an adhesive dressing; one was complicated by skin necrosis leading to a flap reconstruction that became infected, requiring a 2-stage revision. A separate case had an acute postoperative infection that required irrigation and debridement with polyethylene exchange. After a 12-week course of antibiotics, the infection was eradicated. All patients reported a high satisfaction rate during their acute postoperative phase.

Postoperatively, all patients were able to walk on the day of surgery either independently or with some assistance. On the day of surgery, 10% of patients were able to walk >200 feet, and this increased to 65% of patients able to walk >200 feet on the day of discharge (compare Figure 9A and Figure 9B).  Within 2 weeks of surgery, 30% of patients could walk independently (without assistive devices), and this number increased to 78% by 8 weeks after surgery (Figure 10).

Pain assessed using the VAS was lower on postoperative day 1 (3.17 ± 1.97) than the preoperative score (3.69 ± 2.22, P< .05). Overall, knee ROM significantly increased during the follow-up after surgery. Initially, the ROM decreased 1 week after surgery (90.82 ± 10.28) compared with preoperative ROM (101.04 ± 19.48, P < .001) (Figure 10).  At 2 weeks after surgery, knee ROM returned to the preoperative value (100.70 ± 13.36). By 6 weeks after surgery, knee ROM was 17° greater than the preoperative ROM (118.45 ± 11.89, P < .001). Knee ROM remained stable at 3- and 6-month assessments, and showed further improvement by 1 year (126.62 ± 9.81, P < .001) compared with the preoperative state (Figure 10). The net improvement in knee ROM was 25° of increased knee flexion by 1 year.

Continue to: DISCUSSION...

DISCUSSION

TKA is a successful procedure that restores knee function with pain relief in osteoarthritis patients. The SV approach for TKA has better outcomes in terms of the VAS, ROM, straight-leg raise with faster rehabilitation compared with the standard MP approach;^8–12 however, it can be challenging and time-consuming when used in morbidly obese and muscular patients.³ The SV approach can also increase the risk of complications such as patellar tendon avulsion or medial collateral injury because of the difficulty in exposure specifically for knees with limited ROM.¹³ Here we introduce the MIV approach as an alternative to the SV approach, overcoming most of these difficulties.

With the prevalence of morbid obesity and the market demand for minimally invasive techniques, we believe the MIV approach represents a good approach for surgeons since it is easy to perform, does not require specialized instrumentation, and is a reproducible approach even on the most complex deformities. The minimal time added to ensure blunt elevation of the vastus medialis muscle and an anatomic repair of the underlying knee capsule and vastus medialis fascia to the medial edge of the quadriceps tendon allows restoration of the anatomy and a robust double-layered watertight seal closure with no strangulation of soft tissues. We believe this reproducible muscle- and tendon-sparing approach that allows gentle, soft tissue handling even in the most complex primary total knee cases may lead to less soft tissue swelling, and therefore, less postoperative pain resulting in an accelerated recovery.

The pain level in this group of patients was reduced after the MIV approach as indicated by the VAS. The VAS was significantly decreased on postoperative day 1 compared with the VAS recorded preoperatively (P < .05), indicating patients felt less pain on the day after surgery. The average VAS on postoperative day 1 from other studies for SV approach ranged from 2.1 to 5,^9,12,14–19 whereas our MIV approach value was 3.17. Periarticular blocks were available for this study group, and no peripheral nerve blocks were used. Some studies of the SV approach mention the use of peripheral nerve blocks, while others did not describe the method used for treatment or control of postoperative pain. The decreased reported pain levels and the observed increased knee ROM seen in the MIV and SV approach study groups might be attributable to the treatment of postoperative pain.

Patient ambulation also increased from the day of surgery to the day of discharge for the MIV approach. Only 10% of patients were able to walk with assistance >200 feet on the day of surgery; however, this percentage increased to 65% on the discharge day showing an excellent recovery of walking ability within 2 days of surgery. Mehta and colleagues²⁰reported that 95% of patients undergoing subvastus/midvastus approaches could walk >10 blocks at 6 months follow-up. For the MIV approach, 78% of patients were able to walk independently within 8 weeks of surgery.

Continue to: The MIV approach shows improvement...

The MIV approach shows improvement in functional outcomes in terms of knee ROM from preoperative to postoperative. Although knee ROM decreased significantly at postoperative week 1, which is most likely because of a peak in postoperative pain and swelling; the ROM started to increase significantly at postoperative week 6. After 1 year, the knee ROM increased by 25% compared with preoperative ROM for the MIV approach. We found the average knee ROM at postoperative 3 months using the MIV approach to be 120.4°. Knee ROM at postoperative 3 months using the SV approach reported by other studies ranged from 87.1° to 120°.^19,21–23 Similarly, after 1 year, the average ROM by MIV approach was 126.62°, whereas average knee ROM from other studies using the SV approach was 114.1°.^2,10,19,21 Achieving a knee ROM of 120° allows patients to return to their baseline function and perform activities of daily living without limitation. With the prevalence of knee osteoarthritis in the younger population, the need for increased knee ROM post-TKA becomes more important so patients can return to work and function at their baseline.

In addition to being both a muscle- and tendon-sparing approach, other advantages of the MIV approach are that it is simple to perform and gives similar exposure to the MP approach even in difficult primary cases. It is also as extensile as the medial parapatellar approach, and it can be converted to a quadriceps snip if required. There is also minimal, if any, muscle retraction preventing muscle injury that may be seen with some other muscle-sparing approaches to the knee, especially in more difficult primary total knee cases. Another advantage to this approach, as opposed to the other approaches to the knee described here, is that it allows a double-layered closure, decreasing the possibility of arthrotomy dehiscence. Because of this double-layered closure, there is no muscle strangulation with repair of the arthrotomy site as seen in some other approaches to the knee, and both vascularity and innervation to the vastus medialis are preserved.

One limitation of this study is that it is a retrospective analysis. Future studies of the consequences of using this approach need to include quantitative assessment of muscle function using electromyography or dynamometer measurements, utilization of any number of validated knee score systems to measure functional outcomes, and incorporation of a randomized controlled trial.

In summary, the new MIV approach is easy to perform and is compatible with more extensile approaches such as a quadriceps snip, if required in revision scenarios. The MIV approach preserves the extensor mechanism, vascularity, and innervation to the vastus medialis. Our study documents both safety and good clinical outcomes using the MIV approach in TKA. Therefore, the MIV approach may be used in the majority of patients undergoing TKA.