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Partial Flexor Tendon Laceration Assessment: Interobserver and Intraobserver Reliability

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Partial Flexor Tendon Laceration Assessment: Interobserver and Intraobserver Reliability

How to manage complete flexor tendon lacerations in the hand is well documented and a subject of relative agreement among authors. However, treatment of partial flexor tendon lacerations is controversial and lacking clear consensus in the literature. Managing these injuries can be challenging, as clinicians must weigh the diminished tensile strength in the injured tendon and the potential for later complications (eg, entrapment, triggering, rupture) against the negative effects of tenorrhaphy.1 Several studies have found impaired tendon gliding on the basis of bulk and inflammatory reaction secondary to suture material within the flexor sheath as well as decreased tendon strength after tenorrhaphy.2-6 This finding led the investigators to recommend nonsurgical management for partial lacerations up to as much as 95% of the cross-sectional area (CSA) of the tendon. According to a survey by McCarthy and colleagues,7 45% of 591 members of the American Society for Surgery of the Hand (ASSH) indicated they would perform tenorrhaphy for a laceration that involved more than 50% of the tendon.

However, accurate assessment of partial-thickness flexor tendon lacerations is difficult owing to the subjectivity of evaluation. In the survey just mentioned,7 the majority of surgeons used the naked eye to make assessments, and only 14% used other means, such as a ruler, a pair of calipers, or loupe magnification. In addition, flexor tendon injuries are often evaluated under less than ideal circumstances—a dirty or bloody field, poor lighting, an uncomfortable patient.

We conducted a study to determine the interobserver and intraobserver reliability of surgeons assessing the percentage of CSA injured in partially lacerated digital flexor tendons. We hypothesized that participants’ accuracy and agreement would be poor.

Materials and Methods

Eight 1-cm transverse, volar skin incisions were made over the midportions of the middle and proximal phalanges of the index, middle, ring, and small fingers of a fresh-frozen human cadaver hand (Figure 1). The tendon sheaths were incised, and the flexor digitorum profundus tendons to each digit were delivered through the wound. With use of a method described previously by Manning and colleagues,8 the tendon was then placed over a flat metal post to be used as a cutting board, and the proposed laceration site was marked with ink. Under loupe magnification, a No. 15 blade was used to create a partial transverse, volar-to-dorsal laceration in each tendon.8 The goal was to create lacerations of about 30%, 50%, and 70% of the total CSA of the tendon. The tendons were then returned to the wound, and visibility of the marked laceration within the wound was ensured. A similar exercise was performed at the level of the proximal palmar crease. Four flexor digitorum superficialis tendons were exposed through 1-cm transverse incisions, and partial lacerations were made in the volar substance of the tendons. The tendons were then returned to the wound, resulting in 12 partially lacerated tendons (8 flexor digitorum profundus, 4 flexor digitorum superficialis).

Six orthopedic surgery residents (2 postgraduate year 1 [PGY-1], 2 PGY-3, 2 PGY-5) and 4 fellowship-trained hand surgeons participated in our study. Each was asked to evaluate the tendons and determine the percentage of total CSA lacerated. Loupe magnification and measuring tools were not permitted, but participants were allowed to handle the tendons. In addition, they were asked if they would perform tenorrhaphy on the injured tendons, given only the amount of injury. The participants repeated this exercise 4 weeks later.

After all measurements were made, a longitudinal incision was made down each of the digits, and the flexor tendons were exposed within the flexor sheath. The transverse incisions in the palm were connected to expose the flexor digitorum superficialis tendons. Under an operating microscope, a pair of digital microcalipers (Kobalt 0.5-ft Metric and SAE Caliper; Figure 2) accurate to 0.01 mm was used to measure the external width (a) and height (b + bˈ) of the tendons just proximal to the lacerations. Measurements were made with the caliper blades just touching the edges of the lacerated tendon, thus minimizing deformation of the tendon. Other measurements made at the laceration site were width of the remaining tendon (c) and height of the remaining tendon (bˈ). CSA of the tendon was calculated assuming a regular ellipsoid shape and using the equation:

Area = 1/2π(b+b')

The area of the tendon injured was determined by calculating the area under a parabola and using the equation:

Area = 2/3c[(b+b')-b']

Last, the percentage of total CSA lacerated was calculated using the equation:

Area' (area of injured tendon)    ×100%
Area (total area)

Statistical analysis was performed to determine accuracy and interobserver and intraobserver reliability. Paired t tests were used in the assessment of accuracy to determine if there were differences between estimated and calibrated measurements.

 

 

Results

The 10 participants’ estimates differed significantly (P < .0006) from the calibrated measurements, as did residents’ estimates (P < .0025) and fellowship-trained hand surgeons’ estimates (P < .0002). Estimates were scored 1 to 5 on the basis of proximity to calibrated measurements (Table 1). Thus, more accurate estimates received lower scores. Individual estimates were then scored and stratified into groups for comparison. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. These results are listed in Table 2. Once overall and grouped accuracy was analyzed, κ statistics were calculated to compare interobserver and intraobserver reliability. Overall interobserver agreement was poor for both initial readings (κ = 0.16) and secondary readings (κ = 0.16), indicating poor strength of agreement between individuals both initially and secondarily. Table 3 presents the κ interpretations. There was moderate overall intraobserver agreement (45.83%), indicating participants’ secondary estimates agreed with their primary estimates 46% of the time. Fellowship-trained hand surgeons and first-year residents had the highest intraobserver agreement (50.0%). These results are listed in Table 4.

 
 
 

Discussion

Accurate assessment of partial flexor tendon lacerations is difficult and subjective. There is no standardized method for determining the extent of injury, regardless of whether the evaluation is performed in an emergency department or in the operating room. As McCarthy and colleagues7 noted in their survey of ASSH members, naked eye assessment was by far the most popular means of estimating percentage injured in partial lacerations, and only 10% of the survey respondents used intraoperative measuring devices. Our study showed that participants agreed with one another less than 50% of the time when evaluating injuries without the aid of measuring devices. In addition, interobserver agreement in this study was about 50%, high­lighting the difficulty in making an accurate and reproducible assessment.

In a study of canine flexor tendons, McCarthy and colleagues9 found calipers are inaccurate as well and do not provide a reliable means of assessing partial flexor tendon lacerations. They compared caliper measurements with laser micrometer measurements, and the differences averaged 29.3%. They suggested that methods for calculating loss of CSA and for creating precise lacerations must be developed in order to evaluate treatments. One such method is the “tenotome,” devised by Hitchcock and colleagues10: A device with standard scalpel blades is used to make uniform lacerations in tendons by leaving a constant area of the tendon intact, regardless of the size or shape of the original tendon. Measurements made with calipers or rulers assume the tendon has a regular ellipsoid shape, but in reality the shape is a double-ellipse, particularly within the flexor sheath.

Dobyns and colleagues11 observed that changes in CSA size can be related to changes in the size of the bundle pattern of the tendon. They found that, on average, the radial bundle comprised about 60% of the total CSA of the tendon. This finding was clarified by Grewal and colleagues.12 Using histologic sections of tendons plus photomicrographs, they determined that, in zone II of the index and small fingers, the ulnar bundle had an area consistently larger than 50% and the radial bundle less than 50% of the total tendon area. In the ring and middle fingers, the areas of both bundles were almost 50% of the total tendon area. The authors suggested that, using this bundle pattern theory of injury, surgeons could more accurately evaluate the extent of injury with the naked eye.

One of the questions that prompted our study is how reliable is the information a surgeon receives regarding a partial flexor tendon injury evaluated by someone else in another setting. What is done with this information is another question. The scenario can be considered in 2 settings: emergency department and operating room.

Given the poor accuracy and interobserver agreement found in our study, along with the inaccuracy of caliper and ruler measurements, it seems decisions to perform tenorrhaphy based on reported percentages lacerated are unreliable. Our results showed that the ability to accurately assess partial tendon injuries does not improve with surgeon experience, as fellowship-trained hand surgeons were not statistically more accurate or consistent than residents. To this effect, one institution treats all its partial flexor tendon lacerations with wound inspection and irrigation in the emergency department, under digital block and after neurovascular injury has been excluded.8 If the patient is able to actively flex and extend the digit without triggering, then the wound is closed without closing the tendon sheath, a dorsal blocking splint is applied, and motion is begun early, 48 hours later, regardless of laceration severity.

 

 

Once the decision has been made to go to the operating room and the injury is being evaluated, what should be done with the information from the measurement, whether made with loupe magnification, calipers, rulers, or the naked eye? Surgeons must weigh the risks for triggering, entrapment, and rupture of untreated partial tendon lacerations1 with the added bulk and potential for adhesions, along with the tensile strength reduction that accompanies tendon repair. Both Reynolds and colleagues13 and Ollinger and colleagues14 found tensile strength significantly diminished in sutured tendons. Ollinger and colleagues14 showed a decrease in tendon gliding after surgical exposure and tenorrhaphy for partial tendon lacerations. Reynolds and colleagues13 concluded that surgical repair leads to poorer results than nonsurgical treatment.

Clinical studies have demonstrated excellent results with nonintervention, and in vivo and in vitro studies have indicated that early motion can be initiated in partial lacerations of up to 95% of total CSA. Wray and Weeks6 treated 26 patients with partial lacerations varying from 25% to 95% of total CSA and noted 1 incidence of trigger finger (which resolved) and no late ruptures. They advocated treatment with early motion and excision or repair of beveled partial lacerations with simple sutures. Stahl and colleagues2 reported comparable outcomes in children with partial lacerations up to 75% of total CSA treated with and without surgery and noted no complications in either group. In a biomechanical study, Hariharan and colleagues4 found lacerations up to 75% can withstand forces associated with active unresisted mobilization.

Conversely, how many patients or surgeons want to return to the operating room to fix a late rupture when it could have been repaired in the primary setting? Schlenker and colleagues,1 reporting on a late flexor pollicus tendon rupture that required tendon grafting, recommended exploration and primary repair of all partial flexor tendon lacerations. Often, it is difficult to determine whether surgical repair is necessary to ensure the best outcome for the patient.

Our study results showed that, in the evaluation of flexor tendon lacerations, both accuracy and interobserver agreement were poor among residents and fellowship-trained hand surgeons, and intraobserver agreement was moderate. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. Our results highlight the difficulty in making accurate assessments of flexor tendon lacerations owing to the subjectivity of evaluation, which appear not to improve with surgeon experience.

References

1.    Schlenker JD, Lister GD, Kleinert HE. Three complications of untreated partial laceration of flexor tendon—entrapment, rupture, and triggering. J Hand Surg Am. 1981;6(4):392-398.

2.    Stahl S, Kaufman T, Bialik V. Partial lacerations of flexor tendons in children. Primary repair versus conservative treatment. J Hand Surg Br. 1997;22(3):377-380.

3.    Al-Qattan MM. Conservative management of zone II partial flexor tendon lacerations greater than half the width of the tendon. J Hand Surg Am. 2000;25(6):1118-1121.

4.    Hariharan JS, Diao E, Soejima O, Lotz JC. Partial lacerations of human digital flexor tendons: a biomechanical analysis. J Hand Surg Am. 1997;22(6):1011-1015.

5.    Bishop AT, Cooney WP 3rd, Wood MB. Treatment of partial flexor tendon lacerations: the effect of tenorrhaphy and early protected mobilization. J Trauma. 1986;26(4):301-312.

6.    Wray RC Jr, Weeks PM. Treatment of partial tendon lacerations. Hand. 1980;12(2):163-166.

7.    McCarthy DM, Boardman ND 3rd, Tramaglini DM, Sotereanos DG, Herndon JH. Clinical management of partially lacerated digital flexor tendons: a survey of hand surgeons. J Hand Surg Am. 1995;20(2):273-275.

8.    Manning DW, Spiguel AR, Mass DP. Biomechanical analysis of partial flexor tendon lacerations in zone II of human cadavers. J Hand Surg Am. 2010;35(1):11-18.

9.    McCarthy DM, Tramaglini DM, Chan SS, Schmidt CC, Sotereanos DG, Herndon JH. Effect of partial laceration on the structural properties of the canine FDP tendon: an in vitro study. J Hand Surg Am. 1995;20(5):795-800.

10.  Hitchcock TF, Candel AG, Light TR, Blevens AD. New technique for producing uniform partial lacerations of tendons. J Orthop Res. 1989;7(3):451-455.

11.  Dobyns RC, Cooney WC, Wood MB. Effect of partial lacerations on canine flexor tendons. Minn Med. 1982;65(1):27-32.

12.  Grewal R, Sotereanos DG, Rao U, Herndon JH, Woo SL. Bundle pattern of the flexor digitorum profundus tendon in zone II of the hand: a quantitative assessment of the size of a laceration. J Hand Surg Am. 1996;21(6):978-983.

13.  Reynolds B, Wray RC Jr, Weeks PM. Should an incompletely severed tendon be sutured? Plast Reconstr Surg. 1976;57(1):36-38.

14.  Ollinger H, Wray RC Jr, Weeks PM. Effects of suture on tensile strength gain of partially and completely severed tendons. Surg Forum. 1975;26:63-64.

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B. Justin Barker, MD, Gregory P. Kolovich, MD, and Ryan D. Klinefelter, MD

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

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The American Journal of Orthopedics - 45(3)
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tendon, laceration, flexor tendon, hand, thickness, original study, study, online exclusive, barker, kolovich, klinefelter
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B. Justin Barker, MD, Gregory P. Kolovich, MD, and Ryan D. Klinefelter, MD

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B. Justin Barker, MD, Gregory P. Kolovich, MD, and Ryan D. Klinefelter, MD

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How to manage complete flexor tendon lacerations in the hand is well documented and a subject of relative agreement among authors. However, treatment of partial flexor tendon lacerations is controversial and lacking clear consensus in the literature. Managing these injuries can be challenging, as clinicians must weigh the diminished tensile strength in the injured tendon and the potential for later complications (eg, entrapment, triggering, rupture) against the negative effects of tenorrhaphy.1 Several studies have found impaired tendon gliding on the basis of bulk and inflammatory reaction secondary to suture material within the flexor sheath as well as decreased tendon strength after tenorrhaphy.2-6 This finding led the investigators to recommend nonsurgical management for partial lacerations up to as much as 95% of the cross-sectional area (CSA) of the tendon. According to a survey by McCarthy and colleagues,7 45% of 591 members of the American Society for Surgery of the Hand (ASSH) indicated they would perform tenorrhaphy for a laceration that involved more than 50% of the tendon.

However, accurate assessment of partial-thickness flexor tendon lacerations is difficult owing to the subjectivity of evaluation. In the survey just mentioned,7 the majority of surgeons used the naked eye to make assessments, and only 14% used other means, such as a ruler, a pair of calipers, or loupe magnification. In addition, flexor tendon injuries are often evaluated under less than ideal circumstances—a dirty or bloody field, poor lighting, an uncomfortable patient.

We conducted a study to determine the interobserver and intraobserver reliability of surgeons assessing the percentage of CSA injured in partially lacerated digital flexor tendons. We hypothesized that participants’ accuracy and agreement would be poor.

Materials and Methods

Eight 1-cm transverse, volar skin incisions were made over the midportions of the middle and proximal phalanges of the index, middle, ring, and small fingers of a fresh-frozen human cadaver hand (Figure 1). The tendon sheaths were incised, and the flexor digitorum profundus tendons to each digit were delivered through the wound. With use of a method described previously by Manning and colleagues,8 the tendon was then placed over a flat metal post to be used as a cutting board, and the proposed laceration site was marked with ink. Under loupe magnification, a No. 15 blade was used to create a partial transverse, volar-to-dorsal laceration in each tendon.8 The goal was to create lacerations of about 30%, 50%, and 70% of the total CSA of the tendon. The tendons were then returned to the wound, and visibility of the marked laceration within the wound was ensured. A similar exercise was performed at the level of the proximal palmar crease. Four flexor digitorum superficialis tendons were exposed through 1-cm transverse incisions, and partial lacerations were made in the volar substance of the tendons. The tendons were then returned to the wound, resulting in 12 partially lacerated tendons (8 flexor digitorum profundus, 4 flexor digitorum superficialis).

Six orthopedic surgery residents (2 postgraduate year 1 [PGY-1], 2 PGY-3, 2 PGY-5) and 4 fellowship-trained hand surgeons participated in our study. Each was asked to evaluate the tendons and determine the percentage of total CSA lacerated. Loupe magnification and measuring tools were not permitted, but participants were allowed to handle the tendons. In addition, they were asked if they would perform tenorrhaphy on the injured tendons, given only the amount of injury. The participants repeated this exercise 4 weeks later.

After all measurements were made, a longitudinal incision was made down each of the digits, and the flexor tendons were exposed within the flexor sheath. The transverse incisions in the palm were connected to expose the flexor digitorum superficialis tendons. Under an operating microscope, a pair of digital microcalipers (Kobalt 0.5-ft Metric and SAE Caliper; Figure 2) accurate to 0.01 mm was used to measure the external width (a) and height (b + bˈ) of the tendons just proximal to the lacerations. Measurements were made with the caliper blades just touching the edges of the lacerated tendon, thus minimizing deformation of the tendon. Other measurements made at the laceration site were width of the remaining tendon (c) and height of the remaining tendon (bˈ). CSA of the tendon was calculated assuming a regular ellipsoid shape and using the equation:

Area = 1/2π(b+b')

The area of the tendon injured was determined by calculating the area under a parabola and using the equation:

Area = 2/3c[(b+b')-b']

Last, the percentage of total CSA lacerated was calculated using the equation:

Area' (area of injured tendon)    ×100%
Area (total area)

Statistical analysis was performed to determine accuracy and interobserver and intraobserver reliability. Paired t tests were used in the assessment of accuracy to determine if there were differences between estimated and calibrated measurements.

 

 

Results

The 10 participants’ estimates differed significantly (P < .0006) from the calibrated measurements, as did residents’ estimates (P < .0025) and fellowship-trained hand surgeons’ estimates (P < .0002). Estimates were scored 1 to 5 on the basis of proximity to calibrated measurements (Table 1). Thus, more accurate estimates received lower scores. Individual estimates were then scored and stratified into groups for comparison. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. These results are listed in Table 2. Once overall and grouped accuracy was analyzed, κ statistics were calculated to compare interobserver and intraobserver reliability. Overall interobserver agreement was poor for both initial readings (κ = 0.16) and secondary readings (κ = 0.16), indicating poor strength of agreement between individuals both initially and secondarily. Table 3 presents the κ interpretations. There was moderate overall intraobserver agreement (45.83%), indicating participants’ secondary estimates agreed with their primary estimates 46% of the time. Fellowship-trained hand surgeons and first-year residents had the highest intraobserver agreement (50.0%). These results are listed in Table 4.

 
 
 

Discussion

Accurate assessment of partial flexor tendon lacerations is difficult and subjective. There is no standardized method for determining the extent of injury, regardless of whether the evaluation is performed in an emergency department or in the operating room. As McCarthy and colleagues7 noted in their survey of ASSH members, naked eye assessment was by far the most popular means of estimating percentage injured in partial lacerations, and only 10% of the survey respondents used intraoperative measuring devices. Our study showed that participants agreed with one another less than 50% of the time when evaluating injuries without the aid of measuring devices. In addition, interobserver agreement in this study was about 50%, high­lighting the difficulty in making an accurate and reproducible assessment.

In a study of canine flexor tendons, McCarthy and colleagues9 found calipers are inaccurate as well and do not provide a reliable means of assessing partial flexor tendon lacerations. They compared caliper measurements with laser micrometer measurements, and the differences averaged 29.3%. They suggested that methods for calculating loss of CSA and for creating precise lacerations must be developed in order to evaluate treatments. One such method is the “tenotome,” devised by Hitchcock and colleagues10: A device with standard scalpel blades is used to make uniform lacerations in tendons by leaving a constant area of the tendon intact, regardless of the size or shape of the original tendon. Measurements made with calipers or rulers assume the tendon has a regular ellipsoid shape, but in reality the shape is a double-ellipse, particularly within the flexor sheath.

Dobyns and colleagues11 observed that changes in CSA size can be related to changes in the size of the bundle pattern of the tendon. They found that, on average, the radial bundle comprised about 60% of the total CSA of the tendon. This finding was clarified by Grewal and colleagues.12 Using histologic sections of tendons plus photomicrographs, they determined that, in zone II of the index and small fingers, the ulnar bundle had an area consistently larger than 50% and the radial bundle less than 50% of the total tendon area. In the ring and middle fingers, the areas of both bundles were almost 50% of the total tendon area. The authors suggested that, using this bundle pattern theory of injury, surgeons could more accurately evaluate the extent of injury with the naked eye.

One of the questions that prompted our study is how reliable is the information a surgeon receives regarding a partial flexor tendon injury evaluated by someone else in another setting. What is done with this information is another question. The scenario can be considered in 2 settings: emergency department and operating room.

Given the poor accuracy and interobserver agreement found in our study, along with the inaccuracy of caliper and ruler measurements, it seems decisions to perform tenorrhaphy based on reported percentages lacerated are unreliable. Our results showed that the ability to accurately assess partial tendon injuries does not improve with surgeon experience, as fellowship-trained hand surgeons were not statistically more accurate or consistent than residents. To this effect, one institution treats all its partial flexor tendon lacerations with wound inspection and irrigation in the emergency department, under digital block and after neurovascular injury has been excluded.8 If the patient is able to actively flex and extend the digit without triggering, then the wound is closed without closing the tendon sheath, a dorsal blocking splint is applied, and motion is begun early, 48 hours later, regardless of laceration severity.

 

 

Once the decision has been made to go to the operating room and the injury is being evaluated, what should be done with the information from the measurement, whether made with loupe magnification, calipers, rulers, or the naked eye? Surgeons must weigh the risks for triggering, entrapment, and rupture of untreated partial tendon lacerations1 with the added bulk and potential for adhesions, along with the tensile strength reduction that accompanies tendon repair. Both Reynolds and colleagues13 and Ollinger and colleagues14 found tensile strength significantly diminished in sutured tendons. Ollinger and colleagues14 showed a decrease in tendon gliding after surgical exposure and tenorrhaphy for partial tendon lacerations. Reynolds and colleagues13 concluded that surgical repair leads to poorer results than nonsurgical treatment.

Clinical studies have demonstrated excellent results with nonintervention, and in vivo and in vitro studies have indicated that early motion can be initiated in partial lacerations of up to 95% of total CSA. Wray and Weeks6 treated 26 patients with partial lacerations varying from 25% to 95% of total CSA and noted 1 incidence of trigger finger (which resolved) and no late ruptures. They advocated treatment with early motion and excision or repair of beveled partial lacerations with simple sutures. Stahl and colleagues2 reported comparable outcomes in children with partial lacerations up to 75% of total CSA treated with and without surgery and noted no complications in either group. In a biomechanical study, Hariharan and colleagues4 found lacerations up to 75% can withstand forces associated with active unresisted mobilization.

Conversely, how many patients or surgeons want to return to the operating room to fix a late rupture when it could have been repaired in the primary setting? Schlenker and colleagues,1 reporting on a late flexor pollicus tendon rupture that required tendon grafting, recommended exploration and primary repair of all partial flexor tendon lacerations. Often, it is difficult to determine whether surgical repair is necessary to ensure the best outcome for the patient.

Our study results showed that, in the evaluation of flexor tendon lacerations, both accuracy and interobserver agreement were poor among residents and fellowship-trained hand surgeons, and intraobserver agreement was moderate. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. Our results highlight the difficulty in making accurate assessments of flexor tendon lacerations owing to the subjectivity of evaluation, which appear not to improve with surgeon experience.

How to manage complete flexor tendon lacerations in the hand is well documented and a subject of relative agreement among authors. However, treatment of partial flexor tendon lacerations is controversial and lacking clear consensus in the literature. Managing these injuries can be challenging, as clinicians must weigh the diminished tensile strength in the injured tendon and the potential for later complications (eg, entrapment, triggering, rupture) against the negative effects of tenorrhaphy.1 Several studies have found impaired tendon gliding on the basis of bulk and inflammatory reaction secondary to suture material within the flexor sheath as well as decreased tendon strength after tenorrhaphy.2-6 This finding led the investigators to recommend nonsurgical management for partial lacerations up to as much as 95% of the cross-sectional area (CSA) of the tendon. According to a survey by McCarthy and colleagues,7 45% of 591 members of the American Society for Surgery of the Hand (ASSH) indicated they would perform tenorrhaphy for a laceration that involved more than 50% of the tendon.

However, accurate assessment of partial-thickness flexor tendon lacerations is difficult owing to the subjectivity of evaluation. In the survey just mentioned,7 the majority of surgeons used the naked eye to make assessments, and only 14% used other means, such as a ruler, a pair of calipers, or loupe magnification. In addition, flexor tendon injuries are often evaluated under less than ideal circumstances—a dirty or bloody field, poor lighting, an uncomfortable patient.

We conducted a study to determine the interobserver and intraobserver reliability of surgeons assessing the percentage of CSA injured in partially lacerated digital flexor tendons. We hypothesized that participants’ accuracy and agreement would be poor.

Materials and Methods

Eight 1-cm transverse, volar skin incisions were made over the midportions of the middle and proximal phalanges of the index, middle, ring, and small fingers of a fresh-frozen human cadaver hand (Figure 1). The tendon sheaths were incised, and the flexor digitorum profundus tendons to each digit were delivered through the wound. With use of a method described previously by Manning and colleagues,8 the tendon was then placed over a flat metal post to be used as a cutting board, and the proposed laceration site was marked with ink. Under loupe magnification, a No. 15 blade was used to create a partial transverse, volar-to-dorsal laceration in each tendon.8 The goal was to create lacerations of about 30%, 50%, and 70% of the total CSA of the tendon. The tendons were then returned to the wound, and visibility of the marked laceration within the wound was ensured. A similar exercise was performed at the level of the proximal palmar crease. Four flexor digitorum superficialis tendons were exposed through 1-cm transverse incisions, and partial lacerations were made in the volar substance of the tendons. The tendons were then returned to the wound, resulting in 12 partially lacerated tendons (8 flexor digitorum profundus, 4 flexor digitorum superficialis).

Six orthopedic surgery residents (2 postgraduate year 1 [PGY-1], 2 PGY-3, 2 PGY-5) and 4 fellowship-trained hand surgeons participated in our study. Each was asked to evaluate the tendons and determine the percentage of total CSA lacerated. Loupe magnification and measuring tools were not permitted, but participants were allowed to handle the tendons. In addition, they were asked if they would perform tenorrhaphy on the injured tendons, given only the amount of injury. The participants repeated this exercise 4 weeks later.

After all measurements were made, a longitudinal incision was made down each of the digits, and the flexor tendons were exposed within the flexor sheath. The transverse incisions in the palm were connected to expose the flexor digitorum superficialis tendons. Under an operating microscope, a pair of digital microcalipers (Kobalt 0.5-ft Metric and SAE Caliper; Figure 2) accurate to 0.01 mm was used to measure the external width (a) and height (b + bˈ) of the tendons just proximal to the lacerations. Measurements were made with the caliper blades just touching the edges of the lacerated tendon, thus minimizing deformation of the tendon. Other measurements made at the laceration site were width of the remaining tendon (c) and height of the remaining tendon (bˈ). CSA of the tendon was calculated assuming a regular ellipsoid shape and using the equation:

Area = 1/2π(b+b')

The area of the tendon injured was determined by calculating the area under a parabola and using the equation:

Area = 2/3c[(b+b')-b']

Last, the percentage of total CSA lacerated was calculated using the equation:

Area' (area of injured tendon)    ×100%
Area (total area)

Statistical analysis was performed to determine accuracy and interobserver and intraobserver reliability. Paired t tests were used in the assessment of accuracy to determine if there were differences between estimated and calibrated measurements.

 

 

Results

The 10 participants’ estimates differed significantly (P < .0006) from the calibrated measurements, as did residents’ estimates (P < .0025) and fellowship-trained hand surgeons’ estimates (P < .0002). Estimates were scored 1 to 5 on the basis of proximity to calibrated measurements (Table 1). Thus, more accurate estimates received lower scores. Individual estimates were then scored and stratified into groups for comparison. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. These results are listed in Table 2. Once overall and grouped accuracy was analyzed, κ statistics were calculated to compare interobserver and intraobserver reliability. Overall interobserver agreement was poor for both initial readings (κ = 0.16) and secondary readings (κ = 0.16), indicating poor strength of agreement between individuals both initially and secondarily. Table 3 presents the κ interpretations. There was moderate overall intraobserver agreement (45.83%), indicating participants’ secondary estimates agreed with their primary estimates 46% of the time. Fellowship-trained hand surgeons and first-year residents had the highest intraobserver agreement (50.0%). These results are listed in Table 4.

 
 
 

Discussion

Accurate assessment of partial flexor tendon lacerations is difficult and subjective. There is no standardized method for determining the extent of injury, regardless of whether the evaluation is performed in an emergency department or in the operating room. As McCarthy and colleagues7 noted in their survey of ASSH members, naked eye assessment was by far the most popular means of estimating percentage injured in partial lacerations, and only 10% of the survey respondents used intraoperative measuring devices. Our study showed that participants agreed with one another less than 50% of the time when evaluating injuries without the aid of measuring devices. In addition, interobserver agreement in this study was about 50%, high­lighting the difficulty in making an accurate and reproducible assessment.

In a study of canine flexor tendons, McCarthy and colleagues9 found calipers are inaccurate as well and do not provide a reliable means of assessing partial flexor tendon lacerations. They compared caliper measurements with laser micrometer measurements, and the differences averaged 29.3%. They suggested that methods for calculating loss of CSA and for creating precise lacerations must be developed in order to evaluate treatments. One such method is the “tenotome,” devised by Hitchcock and colleagues10: A device with standard scalpel blades is used to make uniform lacerations in tendons by leaving a constant area of the tendon intact, regardless of the size or shape of the original tendon. Measurements made with calipers or rulers assume the tendon has a regular ellipsoid shape, but in reality the shape is a double-ellipse, particularly within the flexor sheath.

Dobyns and colleagues11 observed that changes in CSA size can be related to changes in the size of the bundle pattern of the tendon. They found that, on average, the radial bundle comprised about 60% of the total CSA of the tendon. This finding was clarified by Grewal and colleagues.12 Using histologic sections of tendons plus photomicrographs, they determined that, in zone II of the index and small fingers, the ulnar bundle had an area consistently larger than 50% and the radial bundle less than 50% of the total tendon area. In the ring and middle fingers, the areas of both bundles were almost 50% of the total tendon area. The authors suggested that, using this bundle pattern theory of injury, surgeons could more accurately evaluate the extent of injury with the naked eye.

One of the questions that prompted our study is how reliable is the information a surgeon receives regarding a partial flexor tendon injury evaluated by someone else in another setting. What is done with this information is another question. The scenario can be considered in 2 settings: emergency department and operating room.

Given the poor accuracy and interobserver agreement found in our study, along with the inaccuracy of caliper and ruler measurements, it seems decisions to perform tenorrhaphy based on reported percentages lacerated are unreliable. Our results showed that the ability to accurately assess partial tendon injuries does not improve with surgeon experience, as fellowship-trained hand surgeons were not statistically more accurate or consistent than residents. To this effect, one institution treats all its partial flexor tendon lacerations with wound inspection and irrigation in the emergency department, under digital block and after neurovascular injury has been excluded.8 If the patient is able to actively flex and extend the digit without triggering, then the wound is closed without closing the tendon sheath, a dorsal blocking splint is applied, and motion is begun early, 48 hours later, regardless of laceration severity.

 

 

Once the decision has been made to go to the operating room and the injury is being evaluated, what should be done with the information from the measurement, whether made with loupe magnification, calipers, rulers, or the naked eye? Surgeons must weigh the risks for triggering, entrapment, and rupture of untreated partial tendon lacerations1 with the added bulk and potential for adhesions, along with the tensile strength reduction that accompanies tendon repair. Both Reynolds and colleagues13 and Ollinger and colleagues14 found tensile strength significantly diminished in sutured tendons. Ollinger and colleagues14 showed a decrease in tendon gliding after surgical exposure and tenorrhaphy for partial tendon lacerations. Reynolds and colleagues13 concluded that surgical repair leads to poorer results than nonsurgical treatment.

Clinical studies have demonstrated excellent results with nonintervention, and in vivo and in vitro studies have indicated that early motion can be initiated in partial lacerations of up to 95% of total CSA. Wray and Weeks6 treated 26 patients with partial lacerations varying from 25% to 95% of total CSA and noted 1 incidence of trigger finger (which resolved) and no late ruptures. They advocated treatment with early motion and excision or repair of beveled partial lacerations with simple sutures. Stahl and colleagues2 reported comparable outcomes in children with partial lacerations up to 75% of total CSA treated with and without surgery and noted no complications in either group. In a biomechanical study, Hariharan and colleagues4 found lacerations up to 75% can withstand forces associated with active unresisted mobilization.

Conversely, how many patients or surgeons want to return to the operating room to fix a late rupture when it could have been repaired in the primary setting? Schlenker and colleagues,1 reporting on a late flexor pollicus tendon rupture that required tendon grafting, recommended exploration and primary repair of all partial flexor tendon lacerations. Often, it is difficult to determine whether surgical repair is necessary to ensure the best outcome for the patient.

Our study results showed that, in the evaluation of flexor tendon lacerations, both accuracy and interobserver agreement were poor among residents and fellowship-trained hand surgeons, and intraobserver agreement was moderate. Third-year residents were the most accurate residents, and there was no difference in accuracy between residents and fellowship-trained hand surgeons. Our results highlight the difficulty in making accurate assessments of flexor tendon lacerations owing to the subjectivity of evaluation, which appear not to improve with surgeon experience.

References

1.    Schlenker JD, Lister GD, Kleinert HE. Three complications of untreated partial laceration of flexor tendon—entrapment, rupture, and triggering. J Hand Surg Am. 1981;6(4):392-398.

2.    Stahl S, Kaufman T, Bialik V. Partial lacerations of flexor tendons in children. Primary repair versus conservative treatment. J Hand Surg Br. 1997;22(3):377-380.

3.    Al-Qattan MM. Conservative management of zone II partial flexor tendon lacerations greater than half the width of the tendon. J Hand Surg Am. 2000;25(6):1118-1121.

4.    Hariharan JS, Diao E, Soejima O, Lotz JC. Partial lacerations of human digital flexor tendons: a biomechanical analysis. J Hand Surg Am. 1997;22(6):1011-1015.

5.    Bishop AT, Cooney WP 3rd, Wood MB. Treatment of partial flexor tendon lacerations: the effect of tenorrhaphy and early protected mobilization. J Trauma. 1986;26(4):301-312.

6.    Wray RC Jr, Weeks PM. Treatment of partial tendon lacerations. Hand. 1980;12(2):163-166.

7.    McCarthy DM, Boardman ND 3rd, Tramaglini DM, Sotereanos DG, Herndon JH. Clinical management of partially lacerated digital flexor tendons: a survey of hand surgeons. J Hand Surg Am. 1995;20(2):273-275.

8.    Manning DW, Spiguel AR, Mass DP. Biomechanical analysis of partial flexor tendon lacerations in zone II of human cadavers. J Hand Surg Am. 2010;35(1):11-18.

9.    McCarthy DM, Tramaglini DM, Chan SS, Schmidt CC, Sotereanos DG, Herndon JH. Effect of partial laceration on the structural properties of the canine FDP tendon: an in vitro study. J Hand Surg Am. 1995;20(5):795-800.

10.  Hitchcock TF, Candel AG, Light TR, Blevens AD. New technique for producing uniform partial lacerations of tendons. J Orthop Res. 1989;7(3):451-455.

11.  Dobyns RC, Cooney WC, Wood MB. Effect of partial lacerations on canine flexor tendons. Minn Med. 1982;65(1):27-32.

12.  Grewal R, Sotereanos DG, Rao U, Herndon JH, Woo SL. Bundle pattern of the flexor digitorum profundus tendon in zone II of the hand: a quantitative assessment of the size of a laceration. J Hand Surg Am. 1996;21(6):978-983.

13.  Reynolds B, Wray RC Jr, Weeks PM. Should an incompletely severed tendon be sutured? Plast Reconstr Surg. 1976;57(1):36-38.

14.  Ollinger H, Wray RC Jr, Weeks PM. Effects of suture on tensile strength gain of partially and completely severed tendons. Surg Forum. 1975;26:63-64.

References

1.    Schlenker JD, Lister GD, Kleinert HE. Three complications of untreated partial laceration of flexor tendon—entrapment, rupture, and triggering. J Hand Surg Am. 1981;6(4):392-398.

2.    Stahl S, Kaufman T, Bialik V. Partial lacerations of flexor tendons in children. Primary repair versus conservative treatment. J Hand Surg Br. 1997;22(3):377-380.

3.    Al-Qattan MM. Conservative management of zone II partial flexor tendon lacerations greater than half the width of the tendon. J Hand Surg Am. 2000;25(6):1118-1121.

4.    Hariharan JS, Diao E, Soejima O, Lotz JC. Partial lacerations of human digital flexor tendons: a biomechanical analysis. J Hand Surg Am. 1997;22(6):1011-1015.

5.    Bishop AT, Cooney WP 3rd, Wood MB. Treatment of partial flexor tendon lacerations: the effect of tenorrhaphy and early protected mobilization. J Trauma. 1986;26(4):301-312.

6.    Wray RC Jr, Weeks PM. Treatment of partial tendon lacerations. Hand. 1980;12(2):163-166.

7.    McCarthy DM, Boardman ND 3rd, Tramaglini DM, Sotereanos DG, Herndon JH. Clinical management of partially lacerated digital flexor tendons: a survey of hand surgeons. J Hand Surg Am. 1995;20(2):273-275.

8.    Manning DW, Spiguel AR, Mass DP. Biomechanical analysis of partial flexor tendon lacerations in zone II of human cadavers. J Hand Surg Am. 2010;35(1):11-18.

9.    McCarthy DM, Tramaglini DM, Chan SS, Schmidt CC, Sotereanos DG, Herndon JH. Effect of partial laceration on the structural properties of the canine FDP tendon: an in vitro study. J Hand Surg Am. 1995;20(5):795-800.

10.  Hitchcock TF, Candel AG, Light TR, Blevens AD. New technique for producing uniform partial lacerations of tendons. J Orthop Res. 1989;7(3):451-455.

11.  Dobyns RC, Cooney WC, Wood MB. Effect of partial lacerations on canine flexor tendons. Minn Med. 1982;65(1):27-32.

12.  Grewal R, Sotereanos DG, Rao U, Herndon JH, Woo SL. Bundle pattern of the flexor digitorum profundus tendon in zone II of the hand: a quantitative assessment of the size of a laceration. J Hand Surg Am. 1996;21(6):978-983.

13.  Reynolds B, Wray RC Jr, Weeks PM. Should an incompletely severed tendon be sutured? Plast Reconstr Surg. 1976;57(1):36-38.

14.  Ollinger H, Wray RC Jr, Weeks PM. Effects of suture on tensile strength gain of partially and completely severed tendons. Surg Forum. 1975;26:63-64.

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Technical Errors May Affect Accuracy of Torque Limiter in Locking Plate Osteosynthesis

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Technical Errors May Affect Accuracy of Torque Limiter in Locking Plate Osteosynthesis

Proper surgical technique must be used to ensure that surgical fracture management is long-lasting. Plate implantation and screw implantation are among the most common orthopedic procedures performed. Plate and screw osteosynthesis can be done with nonlocking or locking plate and screw constructs or with hybrid fixation that incorporates both methods.

Nonlocking plate and screw osteosynthesis uses friction-fit for fixation. In osteoporotic bone, less torque is generated because of poor bone quality, and thus less friction force between plate and bone.1,2 Locked plating has dramatically changed fracture management, especially in frail and comminuted osteoporotic bone, with significant advantages over conventional plating.3-7

Development of locked plating systems, including the Less Invasive Stabilization System (LISS; DePuy Synthes) with its soft-tissue and fracture-fragment preservation, has changed treatment of distal femur and proximal tibia fractures. Cole and colleagues8 reported stable fixation and union in 97% of their patients. The LISS system proved to be stable, but there were cases of implant removal difficulty with this titanium construct. In 1 of the 10 cases in which the LISS plate was removed, 4 of the 11 locking screws were welded to the plate.8

Cold welding, in which similar metals are chemically bonded together under extreme pressure, is a complication associated with use of titanium-only plates and screws.9 This process, which is more likely to happen if cross-threading occurs within the screw–plate interface, can make screw removal extremely difficult. Screw removal difficulty strips screw heads, and often the surgeon must use either metal cutting instruments or trephines to remove screw remnants, which often results in retained implant or debris and damage or necrosis to surrounding bone.9,10

Locking screws are often inserted under power with a torque-limiting device attached to the drill mechanism to reduce the risk of lock screw overtightening and to try to prevent difficult implant removal. Although standard practice is to insert the screw and stop just before screw head engagement, with final tightening with a torque limiter and hand power, final tightening is often inadvertently done under power.3 Most technique guides instruct surgeons how to insert screws under power while using a torque limiter, but the exact technique is not emphasized.

We conducted a study to determine if rotational speed of screw insertion affects maximum torque on screw with use of a torque limiter. We describe proper use of a torque limiter as well as possible pitfalls. We hypothesized that improper use would result in substantially higher than expected insertion torque.

Materials and Methods

Torque-Limiting Attachments, Torque Wrench, and Drill

The Small Fragment Locking Compression Plate System (Synthes) includes a 1.5-Nm torque-limiting attachment and quick-coupling wooden handles and Star Drive attachments. All devices in this study were in active use at 6 urban institutions (3 level I trauma centers, 2 level II trauma centers, 1 level III hospital). Permission to obtain and test each device was granted by each institution.

A 0.25-inch dial torque wrench (751LDIN; CDI Torque Products) was purchased through an established distributor. The manufacturer includes a traceable certificate of accuracy to verify correct calibration. The torque wrench has a torque range of 0 to 9 Nm with visual increment demarcations of 0.2 Nm and a memory needle to retain maximum torque measurement. The same torque wrench was used in each experiment in order to maintain consistent measurements between devices. It was reset to zero after each use.

This study used a 0.5-inch, 19.2-V lithium drill (Craftsman C3) with 2 speed options: 0 to 440 rpm high torque and 0 to 1600 rpm high speed. This device provides variable torque output with a maximum output of 38.4 Nm. For this study, all measurements were done with the device on its high torque setting.

Maximum Torque Determination for Different Scenarios

Each torque limiter was evaluated for variations in maximum torque under 4 different scenarios. In each scenario, the torque limiter was coupled to the Star Drive attachment and then to that scenario’s rotating force. The completed system was then inserted into the torque wrench, which was secured to a flat working surface and rotated in accordance with each scenario; maximum torque was measured and recorded (Figures 1, 2). A torque-limiting event was defined as a single audible click on the torque limiter.

 

In scenario 1, each torque-limiting attachment system was attached to a quick-coupling wooden handle. The completed system was then rotated at controlled low velocity under hand power until 1 torque-limiting event occurred. This scenario was also used as an internal control to verify that the torque limiters were calibrated correctly.

In Scenario 2, the device was again attached to a quick-coupling wooden handle. The completed system was rotated at high velocity under hand power until multiple torque-limiting events occurred in a row. High velocity was defined as the operator freely rotating the wooden handle in a single action with full power resulting in multiple torque-limiting events.

 

 

In Scenario 3, the device was attached to a power drill braced to the flat working surface and rotated at low velocity under power until 1 torque-limiting event occurred.

In Scenario 4, the device was again attached to a power drill braced to the flat working surface. The completed system was rotated at high velocity under power until multiple torque-limiting events occurred.

After each trial, we recorded maximum torque achieved before each device’s torque-limiting event. Either an orthopedic surgery resident or a qualified medical student tested each torque-limiting device in each standardized testing scenario.

Statistical Analysis

Experiments for each torque limiter were repeated for 3 trials of each of the 4 different scenarios. For comparative statistics between experiments, maximum torque measurements were expressed as means and SDs; 95% confidence interval (95% CI) was calculated and reported to determine extent of variation within a single group. One-way analysis of variance (ANOVA) and Tukey post hoc tests were performed between groups for comparison of the normally distributed data. Significance was set at P ≤ .05.

Results

During simulation, we successfully measured maximum torque achieved with each torque limiter under the 4 different scenarios. All testing was done by 2 operators. ANOVA demonstrated significant (P ≤ .001) differences in torque among the scenarios.

In scenario 1, mean (SD) maximum torque under hand power at low velocity was 1.49 (0.15) Nm (95% CI, 1.43-1.55), near the advertised maximum torque of 1.5 Nm, with relatively minimal variation between devices. This scenario confirmed proper calibration of properly used torque limiters. Mean maximum torque ranged from 1.25 to 1.93 Nm.

In scenario 2, mean (SD) maximum torque under hand power at high velocity was 3.73 (0.79) Nm (95% CI, 3.33-4.13), a 2.5-fold increase compared with scenario 1 (P < .0001) (Figure 3). There also was an increase in variation of maximum torque between trials of individual devices and between different devices. Mean maximum torque ranged from 2.27 to 5.53 Nm.

In scenario 3, mean (SD) maximum torque under drill power at controlled low velocity was 1.47 (0.14) Nm (95% CI, 1.37-1.56), again near the advertised maximum torque of 1.5 Nm, with relatively minimal variation. Mean maximum torque ranged from 1.10 to 1.73 Nm.

In scenario 4, mean (SD) maximum torque under drill power at full power/high velocity was 5.37 (0.90) Nm (95% CI, 4.92-5.83), a 3.65-fold increase compared with scenario 3 (P < .0001) (Figure 3). Mean maximum torque measured in 3 tests ranged from 3.40 to 6.92 Nm.

There was no significant difference in mean maximum torque between the scenarios of hand power at low velocity and drill power at low velocities (P = .999) (Figure 4). Highest maximum torque from any device was 9.0 Nm (drill at full power). Results are summarized in the Table. There was no statistical significance in the test between the 2 test operators.

 

Discussion

Maximum torque was measured using a torque-limiting attachment under 4 different simulated scenarios. Our goals were to determine if varying practice and rotational velocity would affect maximum insertional torque and to measure consistency among torque limiters. We designed the scenarios to mimic practice patterns, including hand insertion and power insertion of locking screws. Results demonstrated that misuse of a torque-limiting device may inadvertently produce insertional torque substantially higher than recommended. Highest maximum torque was 9.0 Nm, which is 6.0-fold higher than expected for a locking screw using a 1.5-Nm torque limiter.

Our study results showed that insertion under controlled hand power (and low-velocity drill power) until 1 torque-limiting event occurred produced the most consistent and predictable results. Insertion under drill power or high-velocity hand power produced multiple sequential torque-limiting events, yielding inaccurate insertion torque. Low-velocity insertion under hand power, or carefully controlled drill power, consistently produced torque similar to advertised values.

Manufacturers’ technique guides are available for proximal humerus locking compression plate (LCP) systems, small-fragment LCP systems, the Proximal Humeral Interlocking System (PHILOS; DePuy Synthes), and the LISS. These technique guides clearly state that insertion can be performed under power. Only the PHILOS and LISS guides state that insertion should be performed under power until a single click is heard or that final tightening should be completed under hand power. The proximal humerus LCP guide states that surgeons should insert the locking screw under power until the torque-limiting device clicks. The small-fragment LCP guide states that insertion under power should always be completed with the torque-limiting attachment; there is no mention of reducing power or a single click (this may give the surgeon a false sense of security).

 

 

Screw overtightening and head/thread stripping can make screw removal challenging.10 Removal rates for LISS plates range from 8% to 26%, and removal is often reported as taking longer than the index procedure, with complication rates as high as 47%.11-13 Bae and colleagues3 reported significant difficulty in removing 24 of 279 self-tapping locking screws (3.5 mm).

It is important to note that these complications, most notably cold welding, are mostly associated with titanium locking plate and screw constructs. Although stainless steel constructs have gained favor, titanium constructs are still widely used around the world.14,15

In 10% of cases in a laboratory setting, insertion of a 3.5-mm locking screw at 4 to 6 Nm damaged the screw.9 Removal of 3.5-mm locking screws had a stripping rate of 8.6%, and use of the torque limiter did not make removal easy all the time.3 Torque limiters are set specific to each screw diameter to reduce the risk of damage/stripping or even overtightening. Even when a surgeon intends to stop a drill before locking, final tightening often inadvertently occurs under power.3

Cold welding is often described as a cause of difficult implant removal.3,12 According to a newer definition, this process is independent of temperature and can occur when 2 metallic surfaces are in direct contact.16 High contact pressures between 2 similar metals can lead to this solid state welding.17 Theoretically, improper use of torque limiters can increase the risk of welding; however, it appears to be associated only with titanium locking plate and screw constructs.

Locked plating osteosynthesis is a valuable tool for fracture management, but improper use can have significant consequences, including morbid implant removal procedures, which are more difficult and time-consuming than the index surgery. We determined that proper use of torque limiters involves insertion under hand or power control at slow velocity until 1 torque-limiting event occurs. Many orthopedic surgeons may assume that torque limiters are accurate no matter how screws are inserted into locking plates. In addition, they may be unaware guidelines exist, as these are often deeply embedded within text. Therefore, we must emphasize that torque limiters can be inaccurate when used improperly.

One limitation of this study is that it tested only the Synthes 1.5-Nm torque-limiting attachment, though we can speculate that torque limiters designed for larger screws and limiters manufactured by different companies will behave similarly. Another limitation is that we did not obtain the hospitals’ service records for the tested equipment and assumed the equipment was properly checked for accuracy by the providing company. However, we hypothesized that, if maintenance were an issue, then our results would not be similar across all sites tested.

These tests involved a torque limiter linked to a torque-measuring device and may not perfectly represent actual torque measured at the locked screw–thread interface. However, we think our construct accurately determines the torque produced at the level of the driver tip. Also, we can speculate that the torque produced with improper use will lead to the complications mentioned and demonstrated in previous studies. Welding of the screw–plate interface may simply be a result of improper trajectory and cross-threading. However, if we assume that torque limiters prevent excessive torque no matter how they are used, high insertion speeds may compound the effect of welding. Additional biomechanical studies with full locked plate osteosynthesis constructs on bone specimens are planned to further characterize the potential complications of this issue.

References

1.    Sommer C, Babst R, Müller M, Hanson B. Locking compression plate loosening and plate breakage: a report of four cases. J Orthop Trauma. 2004;18(8):571-577.

2.     Schütz M, Südkamp NP. Revolution in plate osteosynthesis: new internal fixator systems. J Orthop Sci. 2003;8(2):252-258.

3.    Bae JH, Oh JK, Oh CW, Hur CR. Technical difficulties of removal of locking screw after locking compression plating. Arch Orthop Trauma Surg. 2009;129(1):91-95.

4.    Frigg R. Locking compression plate (LCP). An osteosynthesis plate based on the dynamic compression plate and the point contact fixator (PC-Fix). Injury. 2001;32(suppl 2):63-66.

5.    Frigg R. Development of the locking compression plate. Injury. 2003;34(suppl 2):B6-B10.

6.    Korner J, Lill H, Müller LP, Rommens PM, Schneider E, Linke B. The LCP-concept in the operative treatment of distal humerus fractures—biological, biomechanical and surgical aspects. Injury. 2003;34(suppl 2):B20-B30.

7.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

8.    Cole PA, Zlowodzki M, Kregor PJ. Treatment of proximal tibia fractures using the Less Invasive Stabilization System: surgical experience and early clinical results in 77 fractures. J Orthop Trauma. 2004;18(8):528-535.

9.     Ehlinger M, Adam P, Simon P, Bonnomet F. Technical difficulties in hardware removal in titanium compression plates with locking screws. Orthop Traumatol Surg Res. 2009;95(5):373-376.

10.  Gopinathan NR, Dhillon MS, Kumar R. Surgical technique: simple technique for removing a locking recon plate with damaged screw heads. Clin Orthop Relat Res. 2013;471(5):1572-1575.

11.  Pattison G, Reynolds J, Hardy J. Salvaging a stripped drive connection when removing screws. Injury. 1999;30(1):74-75.

12.  Raja S, Imbuldeniya AM, Garg S, Groom G. Difficulties encountered removing locked plates. Ann R Coll Surg Engl. 2012;94(7):502-505.

13.  Kumar G, Dunlop C. Case report: a technique to remove a jammed locking screw from a locking plate. Clin Orthop Relat Res. 2011;469(2):613-616.

14.  Disegi JA. Titanium alloys for fracture fixation implants. Injury. 2000;31(suppl 4):14-17.

15.  El-Zayat BF, Ruchholtz S, Efe T, Paletta J, Kreslo D, Zettl R. Results of titanium locking plate and stainless steel cerclage wire combination in femoral fractures. Indian J Orthop. 2013;47(5):454-458.

16.  Van Nortwick SS, Yao J, Ladd AL. Titanium integration with bone, welding, and screw head destruction complicating hardware removal of the distal radius: report of 2 cases. J Hand Surg. 2012;37(7):1388-1392.

17.  Ferguson GS, Chaudhury MK, Sigal GB, Whitesides GM. Contact adhesion of thin gold films on elastomeric supports: cold welding under ambient conditions. Science. 1991;253(5021):776-778.

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David D. Savin, MD, Simon Lee, MD, MPH, Frank C. Bohnenkamp, MD, Andrew Pastor, MD, Rajeev Garapati, MD, and Benjamin A. Goldberg, MD

Authors’ Disclosure Statement: Dr. Garapati is a consultant for Arthrex and Stryker. Dr. Goldberg is a consultant for Acumed, Allen Medical, Aston Medical, and Stryker; owns stock in Mako; and is on the American Academy of Orthopaedic Surgeons (AAOS) Committee for Scientific Exhibits and Electronic Skills Pavilion. The other authors report no actual or potential conflict of interest in relation to this article.

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David D. Savin, MD, Simon Lee, MD, MPH, Frank C. Bohnenkamp, MD, Andrew Pastor, MD, Rajeev Garapati, MD, and Benjamin A. Goldberg, MD

Authors’ Disclosure Statement: Dr. Garapati is a consultant for Arthrex and Stryker. Dr. Goldberg is a consultant for Acumed, Allen Medical, Aston Medical, and Stryker; owns stock in Mako; and is on the American Academy of Orthopaedic Surgeons (AAOS) Committee for Scientific Exhibits and Electronic Skills Pavilion. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

David D. Savin, MD, Simon Lee, MD, MPH, Frank C. Bohnenkamp, MD, Andrew Pastor, MD, Rajeev Garapati, MD, and Benjamin A. Goldberg, MD

Authors’ Disclosure Statement: Dr. Garapati is a consultant for Arthrex and Stryker. Dr. Goldberg is a consultant for Acumed, Allen Medical, Aston Medical, and Stryker; owns stock in Mako; and is on the American Academy of Orthopaedic Surgeons (AAOS) Committee for Scientific Exhibits and Electronic Skills Pavilion. The other authors report no actual or potential conflict of interest in relation to this article.

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Proper surgical technique must be used to ensure that surgical fracture management is long-lasting. Plate implantation and screw implantation are among the most common orthopedic procedures performed. Plate and screw osteosynthesis can be done with nonlocking or locking plate and screw constructs or with hybrid fixation that incorporates both methods.

Nonlocking plate and screw osteosynthesis uses friction-fit for fixation. In osteoporotic bone, less torque is generated because of poor bone quality, and thus less friction force between plate and bone.1,2 Locked plating has dramatically changed fracture management, especially in frail and comminuted osteoporotic bone, with significant advantages over conventional plating.3-7

Development of locked plating systems, including the Less Invasive Stabilization System (LISS; DePuy Synthes) with its soft-tissue and fracture-fragment preservation, has changed treatment of distal femur and proximal tibia fractures. Cole and colleagues8 reported stable fixation and union in 97% of their patients. The LISS system proved to be stable, but there were cases of implant removal difficulty with this titanium construct. In 1 of the 10 cases in which the LISS plate was removed, 4 of the 11 locking screws were welded to the plate.8

Cold welding, in which similar metals are chemically bonded together under extreme pressure, is a complication associated with use of titanium-only plates and screws.9 This process, which is more likely to happen if cross-threading occurs within the screw–plate interface, can make screw removal extremely difficult. Screw removal difficulty strips screw heads, and often the surgeon must use either metal cutting instruments or trephines to remove screw remnants, which often results in retained implant or debris and damage or necrosis to surrounding bone.9,10

Locking screws are often inserted under power with a torque-limiting device attached to the drill mechanism to reduce the risk of lock screw overtightening and to try to prevent difficult implant removal. Although standard practice is to insert the screw and stop just before screw head engagement, with final tightening with a torque limiter and hand power, final tightening is often inadvertently done under power.3 Most technique guides instruct surgeons how to insert screws under power while using a torque limiter, but the exact technique is not emphasized.

We conducted a study to determine if rotational speed of screw insertion affects maximum torque on screw with use of a torque limiter. We describe proper use of a torque limiter as well as possible pitfalls. We hypothesized that improper use would result in substantially higher than expected insertion torque.

Materials and Methods

Torque-Limiting Attachments, Torque Wrench, and Drill

The Small Fragment Locking Compression Plate System (Synthes) includes a 1.5-Nm torque-limiting attachment and quick-coupling wooden handles and Star Drive attachments. All devices in this study were in active use at 6 urban institutions (3 level I trauma centers, 2 level II trauma centers, 1 level III hospital). Permission to obtain and test each device was granted by each institution.

A 0.25-inch dial torque wrench (751LDIN; CDI Torque Products) was purchased through an established distributor. The manufacturer includes a traceable certificate of accuracy to verify correct calibration. The torque wrench has a torque range of 0 to 9 Nm with visual increment demarcations of 0.2 Nm and a memory needle to retain maximum torque measurement. The same torque wrench was used in each experiment in order to maintain consistent measurements between devices. It was reset to zero after each use.

This study used a 0.5-inch, 19.2-V lithium drill (Craftsman C3) with 2 speed options: 0 to 440 rpm high torque and 0 to 1600 rpm high speed. This device provides variable torque output with a maximum output of 38.4 Nm. For this study, all measurements were done with the device on its high torque setting.

Maximum Torque Determination for Different Scenarios

Each torque limiter was evaluated for variations in maximum torque under 4 different scenarios. In each scenario, the torque limiter was coupled to the Star Drive attachment and then to that scenario’s rotating force. The completed system was then inserted into the torque wrench, which was secured to a flat working surface and rotated in accordance with each scenario; maximum torque was measured and recorded (Figures 1, 2). A torque-limiting event was defined as a single audible click on the torque limiter.

 

In scenario 1, each torque-limiting attachment system was attached to a quick-coupling wooden handle. The completed system was then rotated at controlled low velocity under hand power until 1 torque-limiting event occurred. This scenario was also used as an internal control to verify that the torque limiters were calibrated correctly.

In Scenario 2, the device was again attached to a quick-coupling wooden handle. The completed system was rotated at high velocity under hand power until multiple torque-limiting events occurred in a row. High velocity was defined as the operator freely rotating the wooden handle in a single action with full power resulting in multiple torque-limiting events.

 

 

In Scenario 3, the device was attached to a power drill braced to the flat working surface and rotated at low velocity under power until 1 torque-limiting event occurred.

In Scenario 4, the device was again attached to a power drill braced to the flat working surface. The completed system was rotated at high velocity under power until multiple torque-limiting events occurred.

After each trial, we recorded maximum torque achieved before each device’s torque-limiting event. Either an orthopedic surgery resident or a qualified medical student tested each torque-limiting device in each standardized testing scenario.

Statistical Analysis

Experiments for each torque limiter were repeated for 3 trials of each of the 4 different scenarios. For comparative statistics between experiments, maximum torque measurements were expressed as means and SDs; 95% confidence interval (95% CI) was calculated and reported to determine extent of variation within a single group. One-way analysis of variance (ANOVA) and Tukey post hoc tests were performed between groups for comparison of the normally distributed data. Significance was set at P ≤ .05.

Results

During simulation, we successfully measured maximum torque achieved with each torque limiter under the 4 different scenarios. All testing was done by 2 operators. ANOVA demonstrated significant (P ≤ .001) differences in torque among the scenarios.

In scenario 1, mean (SD) maximum torque under hand power at low velocity was 1.49 (0.15) Nm (95% CI, 1.43-1.55), near the advertised maximum torque of 1.5 Nm, with relatively minimal variation between devices. This scenario confirmed proper calibration of properly used torque limiters. Mean maximum torque ranged from 1.25 to 1.93 Nm.

In scenario 2, mean (SD) maximum torque under hand power at high velocity was 3.73 (0.79) Nm (95% CI, 3.33-4.13), a 2.5-fold increase compared with scenario 1 (P < .0001) (Figure 3). There also was an increase in variation of maximum torque between trials of individual devices and between different devices. Mean maximum torque ranged from 2.27 to 5.53 Nm.

In scenario 3, mean (SD) maximum torque under drill power at controlled low velocity was 1.47 (0.14) Nm (95% CI, 1.37-1.56), again near the advertised maximum torque of 1.5 Nm, with relatively minimal variation. Mean maximum torque ranged from 1.10 to 1.73 Nm.

In scenario 4, mean (SD) maximum torque under drill power at full power/high velocity was 5.37 (0.90) Nm (95% CI, 4.92-5.83), a 3.65-fold increase compared with scenario 3 (P < .0001) (Figure 3). Mean maximum torque measured in 3 tests ranged from 3.40 to 6.92 Nm.

There was no significant difference in mean maximum torque between the scenarios of hand power at low velocity and drill power at low velocities (P = .999) (Figure 4). Highest maximum torque from any device was 9.0 Nm (drill at full power). Results are summarized in the Table. There was no statistical significance in the test between the 2 test operators.

 

Discussion

Maximum torque was measured using a torque-limiting attachment under 4 different simulated scenarios. Our goals were to determine if varying practice and rotational velocity would affect maximum insertional torque and to measure consistency among torque limiters. We designed the scenarios to mimic practice patterns, including hand insertion and power insertion of locking screws. Results demonstrated that misuse of a torque-limiting device may inadvertently produce insertional torque substantially higher than recommended. Highest maximum torque was 9.0 Nm, which is 6.0-fold higher than expected for a locking screw using a 1.5-Nm torque limiter.

Our study results showed that insertion under controlled hand power (and low-velocity drill power) until 1 torque-limiting event occurred produced the most consistent and predictable results. Insertion under drill power or high-velocity hand power produced multiple sequential torque-limiting events, yielding inaccurate insertion torque. Low-velocity insertion under hand power, or carefully controlled drill power, consistently produced torque similar to advertised values.

Manufacturers’ technique guides are available for proximal humerus locking compression plate (LCP) systems, small-fragment LCP systems, the Proximal Humeral Interlocking System (PHILOS; DePuy Synthes), and the LISS. These technique guides clearly state that insertion can be performed under power. Only the PHILOS and LISS guides state that insertion should be performed under power until a single click is heard or that final tightening should be completed under hand power. The proximal humerus LCP guide states that surgeons should insert the locking screw under power until the torque-limiting device clicks. The small-fragment LCP guide states that insertion under power should always be completed with the torque-limiting attachment; there is no mention of reducing power or a single click (this may give the surgeon a false sense of security).

 

 

Screw overtightening and head/thread stripping can make screw removal challenging.10 Removal rates for LISS plates range from 8% to 26%, and removal is often reported as taking longer than the index procedure, with complication rates as high as 47%.11-13 Bae and colleagues3 reported significant difficulty in removing 24 of 279 self-tapping locking screws (3.5 mm).

It is important to note that these complications, most notably cold welding, are mostly associated with titanium locking plate and screw constructs. Although stainless steel constructs have gained favor, titanium constructs are still widely used around the world.14,15

In 10% of cases in a laboratory setting, insertion of a 3.5-mm locking screw at 4 to 6 Nm damaged the screw.9 Removal of 3.5-mm locking screws had a stripping rate of 8.6%, and use of the torque limiter did not make removal easy all the time.3 Torque limiters are set specific to each screw diameter to reduce the risk of damage/stripping or even overtightening. Even when a surgeon intends to stop a drill before locking, final tightening often inadvertently occurs under power.3

Cold welding is often described as a cause of difficult implant removal.3,12 According to a newer definition, this process is independent of temperature and can occur when 2 metallic surfaces are in direct contact.16 High contact pressures between 2 similar metals can lead to this solid state welding.17 Theoretically, improper use of torque limiters can increase the risk of welding; however, it appears to be associated only with titanium locking plate and screw constructs.

Locked plating osteosynthesis is a valuable tool for fracture management, but improper use can have significant consequences, including morbid implant removal procedures, which are more difficult and time-consuming than the index surgery. We determined that proper use of torque limiters involves insertion under hand or power control at slow velocity until 1 torque-limiting event occurs. Many orthopedic surgeons may assume that torque limiters are accurate no matter how screws are inserted into locking plates. In addition, they may be unaware guidelines exist, as these are often deeply embedded within text. Therefore, we must emphasize that torque limiters can be inaccurate when used improperly.

One limitation of this study is that it tested only the Synthes 1.5-Nm torque-limiting attachment, though we can speculate that torque limiters designed for larger screws and limiters manufactured by different companies will behave similarly. Another limitation is that we did not obtain the hospitals’ service records for the tested equipment and assumed the equipment was properly checked for accuracy by the providing company. However, we hypothesized that, if maintenance were an issue, then our results would not be similar across all sites tested.

These tests involved a torque limiter linked to a torque-measuring device and may not perfectly represent actual torque measured at the locked screw–thread interface. However, we think our construct accurately determines the torque produced at the level of the driver tip. Also, we can speculate that the torque produced with improper use will lead to the complications mentioned and demonstrated in previous studies. Welding of the screw–plate interface may simply be a result of improper trajectory and cross-threading. However, if we assume that torque limiters prevent excessive torque no matter how they are used, high insertion speeds may compound the effect of welding. Additional biomechanical studies with full locked plate osteosynthesis constructs on bone specimens are planned to further characterize the potential complications of this issue.

Proper surgical technique must be used to ensure that surgical fracture management is long-lasting. Plate implantation and screw implantation are among the most common orthopedic procedures performed. Plate and screw osteosynthesis can be done with nonlocking or locking plate and screw constructs or with hybrid fixation that incorporates both methods.

Nonlocking plate and screw osteosynthesis uses friction-fit for fixation. In osteoporotic bone, less torque is generated because of poor bone quality, and thus less friction force between plate and bone.1,2 Locked plating has dramatically changed fracture management, especially in frail and comminuted osteoporotic bone, with significant advantages over conventional plating.3-7

Development of locked plating systems, including the Less Invasive Stabilization System (LISS; DePuy Synthes) with its soft-tissue and fracture-fragment preservation, has changed treatment of distal femur and proximal tibia fractures. Cole and colleagues8 reported stable fixation and union in 97% of their patients. The LISS system proved to be stable, but there were cases of implant removal difficulty with this titanium construct. In 1 of the 10 cases in which the LISS plate was removed, 4 of the 11 locking screws were welded to the plate.8

Cold welding, in which similar metals are chemically bonded together under extreme pressure, is a complication associated with use of titanium-only plates and screws.9 This process, which is more likely to happen if cross-threading occurs within the screw–plate interface, can make screw removal extremely difficult. Screw removal difficulty strips screw heads, and often the surgeon must use either metal cutting instruments or trephines to remove screw remnants, which often results in retained implant or debris and damage or necrosis to surrounding bone.9,10

Locking screws are often inserted under power with a torque-limiting device attached to the drill mechanism to reduce the risk of lock screw overtightening and to try to prevent difficult implant removal. Although standard practice is to insert the screw and stop just before screw head engagement, with final tightening with a torque limiter and hand power, final tightening is often inadvertently done under power.3 Most technique guides instruct surgeons how to insert screws under power while using a torque limiter, but the exact technique is not emphasized.

We conducted a study to determine if rotational speed of screw insertion affects maximum torque on screw with use of a torque limiter. We describe proper use of a torque limiter as well as possible pitfalls. We hypothesized that improper use would result in substantially higher than expected insertion torque.

Materials and Methods

Torque-Limiting Attachments, Torque Wrench, and Drill

The Small Fragment Locking Compression Plate System (Synthes) includes a 1.5-Nm torque-limiting attachment and quick-coupling wooden handles and Star Drive attachments. All devices in this study were in active use at 6 urban institutions (3 level I trauma centers, 2 level II trauma centers, 1 level III hospital). Permission to obtain and test each device was granted by each institution.

A 0.25-inch dial torque wrench (751LDIN; CDI Torque Products) was purchased through an established distributor. The manufacturer includes a traceable certificate of accuracy to verify correct calibration. The torque wrench has a torque range of 0 to 9 Nm with visual increment demarcations of 0.2 Nm and a memory needle to retain maximum torque measurement. The same torque wrench was used in each experiment in order to maintain consistent measurements between devices. It was reset to zero after each use.

This study used a 0.5-inch, 19.2-V lithium drill (Craftsman C3) with 2 speed options: 0 to 440 rpm high torque and 0 to 1600 rpm high speed. This device provides variable torque output with a maximum output of 38.4 Nm. For this study, all measurements were done with the device on its high torque setting.

Maximum Torque Determination for Different Scenarios

Each torque limiter was evaluated for variations in maximum torque under 4 different scenarios. In each scenario, the torque limiter was coupled to the Star Drive attachment and then to that scenario’s rotating force. The completed system was then inserted into the torque wrench, which was secured to a flat working surface and rotated in accordance with each scenario; maximum torque was measured and recorded (Figures 1, 2). A torque-limiting event was defined as a single audible click on the torque limiter.

 

In scenario 1, each torque-limiting attachment system was attached to a quick-coupling wooden handle. The completed system was then rotated at controlled low velocity under hand power until 1 torque-limiting event occurred. This scenario was also used as an internal control to verify that the torque limiters were calibrated correctly.

In Scenario 2, the device was again attached to a quick-coupling wooden handle. The completed system was rotated at high velocity under hand power until multiple torque-limiting events occurred in a row. High velocity was defined as the operator freely rotating the wooden handle in a single action with full power resulting in multiple torque-limiting events.

 

 

In Scenario 3, the device was attached to a power drill braced to the flat working surface and rotated at low velocity under power until 1 torque-limiting event occurred.

In Scenario 4, the device was again attached to a power drill braced to the flat working surface. The completed system was rotated at high velocity under power until multiple torque-limiting events occurred.

After each trial, we recorded maximum torque achieved before each device’s torque-limiting event. Either an orthopedic surgery resident or a qualified medical student tested each torque-limiting device in each standardized testing scenario.

Statistical Analysis

Experiments for each torque limiter were repeated for 3 trials of each of the 4 different scenarios. For comparative statistics between experiments, maximum torque measurements were expressed as means and SDs; 95% confidence interval (95% CI) was calculated and reported to determine extent of variation within a single group. One-way analysis of variance (ANOVA) and Tukey post hoc tests were performed between groups for comparison of the normally distributed data. Significance was set at P ≤ .05.

Results

During simulation, we successfully measured maximum torque achieved with each torque limiter under the 4 different scenarios. All testing was done by 2 operators. ANOVA demonstrated significant (P ≤ .001) differences in torque among the scenarios.

In scenario 1, mean (SD) maximum torque under hand power at low velocity was 1.49 (0.15) Nm (95% CI, 1.43-1.55), near the advertised maximum torque of 1.5 Nm, with relatively minimal variation between devices. This scenario confirmed proper calibration of properly used torque limiters. Mean maximum torque ranged from 1.25 to 1.93 Nm.

In scenario 2, mean (SD) maximum torque under hand power at high velocity was 3.73 (0.79) Nm (95% CI, 3.33-4.13), a 2.5-fold increase compared with scenario 1 (P < .0001) (Figure 3). There also was an increase in variation of maximum torque between trials of individual devices and between different devices. Mean maximum torque ranged from 2.27 to 5.53 Nm.

In scenario 3, mean (SD) maximum torque under drill power at controlled low velocity was 1.47 (0.14) Nm (95% CI, 1.37-1.56), again near the advertised maximum torque of 1.5 Nm, with relatively minimal variation. Mean maximum torque ranged from 1.10 to 1.73 Nm.

In scenario 4, mean (SD) maximum torque under drill power at full power/high velocity was 5.37 (0.90) Nm (95% CI, 4.92-5.83), a 3.65-fold increase compared with scenario 3 (P < .0001) (Figure 3). Mean maximum torque measured in 3 tests ranged from 3.40 to 6.92 Nm.

There was no significant difference in mean maximum torque between the scenarios of hand power at low velocity and drill power at low velocities (P = .999) (Figure 4). Highest maximum torque from any device was 9.0 Nm (drill at full power). Results are summarized in the Table. There was no statistical significance in the test between the 2 test operators.

 

Discussion

Maximum torque was measured using a torque-limiting attachment under 4 different simulated scenarios. Our goals were to determine if varying practice and rotational velocity would affect maximum insertional torque and to measure consistency among torque limiters. We designed the scenarios to mimic practice patterns, including hand insertion and power insertion of locking screws. Results demonstrated that misuse of a torque-limiting device may inadvertently produce insertional torque substantially higher than recommended. Highest maximum torque was 9.0 Nm, which is 6.0-fold higher than expected for a locking screw using a 1.5-Nm torque limiter.

Our study results showed that insertion under controlled hand power (and low-velocity drill power) until 1 torque-limiting event occurred produced the most consistent and predictable results. Insertion under drill power or high-velocity hand power produced multiple sequential torque-limiting events, yielding inaccurate insertion torque. Low-velocity insertion under hand power, or carefully controlled drill power, consistently produced torque similar to advertised values.

Manufacturers’ technique guides are available for proximal humerus locking compression plate (LCP) systems, small-fragment LCP systems, the Proximal Humeral Interlocking System (PHILOS; DePuy Synthes), and the LISS. These technique guides clearly state that insertion can be performed under power. Only the PHILOS and LISS guides state that insertion should be performed under power until a single click is heard or that final tightening should be completed under hand power. The proximal humerus LCP guide states that surgeons should insert the locking screw under power until the torque-limiting device clicks. The small-fragment LCP guide states that insertion under power should always be completed with the torque-limiting attachment; there is no mention of reducing power or a single click (this may give the surgeon a false sense of security).

 

 

Screw overtightening and head/thread stripping can make screw removal challenging.10 Removal rates for LISS plates range from 8% to 26%, and removal is often reported as taking longer than the index procedure, with complication rates as high as 47%.11-13 Bae and colleagues3 reported significant difficulty in removing 24 of 279 self-tapping locking screws (3.5 mm).

It is important to note that these complications, most notably cold welding, are mostly associated with titanium locking plate and screw constructs. Although stainless steel constructs have gained favor, titanium constructs are still widely used around the world.14,15

In 10% of cases in a laboratory setting, insertion of a 3.5-mm locking screw at 4 to 6 Nm damaged the screw.9 Removal of 3.5-mm locking screws had a stripping rate of 8.6%, and use of the torque limiter did not make removal easy all the time.3 Torque limiters are set specific to each screw diameter to reduce the risk of damage/stripping or even overtightening. Even when a surgeon intends to stop a drill before locking, final tightening often inadvertently occurs under power.3

Cold welding is often described as a cause of difficult implant removal.3,12 According to a newer definition, this process is independent of temperature and can occur when 2 metallic surfaces are in direct contact.16 High contact pressures between 2 similar metals can lead to this solid state welding.17 Theoretically, improper use of torque limiters can increase the risk of welding; however, it appears to be associated only with titanium locking plate and screw constructs.

Locked plating osteosynthesis is a valuable tool for fracture management, but improper use can have significant consequences, including morbid implant removal procedures, which are more difficult and time-consuming than the index surgery. We determined that proper use of torque limiters involves insertion under hand or power control at slow velocity until 1 torque-limiting event occurs. Many orthopedic surgeons may assume that torque limiters are accurate no matter how screws are inserted into locking plates. In addition, they may be unaware guidelines exist, as these are often deeply embedded within text. Therefore, we must emphasize that torque limiters can be inaccurate when used improperly.

One limitation of this study is that it tested only the Synthes 1.5-Nm torque-limiting attachment, though we can speculate that torque limiters designed for larger screws and limiters manufactured by different companies will behave similarly. Another limitation is that we did not obtain the hospitals’ service records for the tested equipment and assumed the equipment was properly checked for accuracy by the providing company. However, we hypothesized that, if maintenance were an issue, then our results would not be similar across all sites tested.

These tests involved a torque limiter linked to a torque-measuring device and may not perfectly represent actual torque measured at the locked screw–thread interface. However, we think our construct accurately determines the torque produced at the level of the driver tip. Also, we can speculate that the torque produced with improper use will lead to the complications mentioned and demonstrated in previous studies. Welding of the screw–plate interface may simply be a result of improper trajectory and cross-threading. However, if we assume that torque limiters prevent excessive torque no matter how they are used, high insertion speeds may compound the effect of welding. Additional biomechanical studies with full locked plate osteosynthesis constructs on bone specimens are planned to further characterize the potential complications of this issue.

References

1.    Sommer C, Babst R, Müller M, Hanson B. Locking compression plate loosening and plate breakage: a report of four cases. J Orthop Trauma. 2004;18(8):571-577.

2.     Schütz M, Südkamp NP. Revolution in plate osteosynthesis: new internal fixator systems. J Orthop Sci. 2003;8(2):252-258.

3.    Bae JH, Oh JK, Oh CW, Hur CR. Technical difficulties of removal of locking screw after locking compression plating. Arch Orthop Trauma Surg. 2009;129(1):91-95.

4.    Frigg R. Locking compression plate (LCP). An osteosynthesis plate based on the dynamic compression plate and the point contact fixator (PC-Fix). Injury. 2001;32(suppl 2):63-66.

5.    Frigg R. Development of the locking compression plate. Injury. 2003;34(suppl 2):B6-B10.

6.    Korner J, Lill H, Müller LP, Rommens PM, Schneider E, Linke B. The LCP-concept in the operative treatment of distal humerus fractures—biological, biomechanical and surgical aspects. Injury. 2003;34(suppl 2):B20-B30.

7.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

8.    Cole PA, Zlowodzki M, Kregor PJ. Treatment of proximal tibia fractures using the Less Invasive Stabilization System: surgical experience and early clinical results in 77 fractures. J Orthop Trauma. 2004;18(8):528-535.

9.     Ehlinger M, Adam P, Simon P, Bonnomet F. Technical difficulties in hardware removal in titanium compression plates with locking screws. Orthop Traumatol Surg Res. 2009;95(5):373-376.

10.  Gopinathan NR, Dhillon MS, Kumar R. Surgical technique: simple technique for removing a locking recon plate with damaged screw heads. Clin Orthop Relat Res. 2013;471(5):1572-1575.

11.  Pattison G, Reynolds J, Hardy J. Salvaging a stripped drive connection when removing screws. Injury. 1999;30(1):74-75.

12.  Raja S, Imbuldeniya AM, Garg S, Groom G. Difficulties encountered removing locked plates. Ann R Coll Surg Engl. 2012;94(7):502-505.

13.  Kumar G, Dunlop C. Case report: a technique to remove a jammed locking screw from a locking plate. Clin Orthop Relat Res. 2011;469(2):613-616.

14.  Disegi JA. Titanium alloys for fracture fixation implants. Injury. 2000;31(suppl 4):14-17.

15.  El-Zayat BF, Ruchholtz S, Efe T, Paletta J, Kreslo D, Zettl R. Results of titanium locking plate and stainless steel cerclage wire combination in femoral fractures. Indian J Orthop. 2013;47(5):454-458.

16.  Van Nortwick SS, Yao J, Ladd AL. Titanium integration with bone, welding, and screw head destruction complicating hardware removal of the distal radius: report of 2 cases. J Hand Surg. 2012;37(7):1388-1392.

17.  Ferguson GS, Chaudhury MK, Sigal GB, Whitesides GM. Contact adhesion of thin gold films on elastomeric supports: cold welding under ambient conditions. Science. 1991;253(5021):776-778.

References

1.    Sommer C, Babst R, Müller M, Hanson B. Locking compression plate loosening and plate breakage: a report of four cases. J Orthop Trauma. 2004;18(8):571-577.

2.     Schütz M, Südkamp NP. Revolution in plate osteosynthesis: new internal fixator systems. J Orthop Sci. 2003;8(2):252-258.

3.    Bae JH, Oh JK, Oh CW, Hur CR. Technical difficulties of removal of locking screw after locking compression plating. Arch Orthop Trauma Surg. 2009;129(1):91-95.

4.    Frigg R. Locking compression plate (LCP). An osteosynthesis plate based on the dynamic compression plate and the point contact fixator (PC-Fix). Injury. 2001;32(suppl 2):63-66.

5.    Frigg R. Development of the locking compression plate. Injury. 2003;34(suppl 2):B6-B10.

6.    Korner J, Lill H, Müller LP, Rommens PM, Schneider E, Linke B. The LCP-concept in the operative treatment of distal humerus fractures—biological, biomechanical and surgical aspects. Injury. 2003;34(suppl 2):B20-B30.

7.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

8.    Cole PA, Zlowodzki M, Kregor PJ. Treatment of proximal tibia fractures using the Less Invasive Stabilization System: surgical experience and early clinical results in 77 fractures. J Orthop Trauma. 2004;18(8):528-535.

9.     Ehlinger M, Adam P, Simon P, Bonnomet F. Technical difficulties in hardware removal in titanium compression plates with locking screws. Orthop Traumatol Surg Res. 2009;95(5):373-376.

10.  Gopinathan NR, Dhillon MS, Kumar R. Surgical technique: simple technique for removing a locking recon plate with damaged screw heads. Clin Orthop Relat Res. 2013;471(5):1572-1575.

11.  Pattison G, Reynolds J, Hardy J. Salvaging a stripped drive connection when removing screws. Injury. 1999;30(1):74-75.

12.  Raja S, Imbuldeniya AM, Garg S, Groom G. Difficulties encountered removing locked plates. Ann R Coll Surg Engl. 2012;94(7):502-505.

13.  Kumar G, Dunlop C. Case report: a technique to remove a jammed locking screw from a locking plate. Clin Orthop Relat Res. 2011;469(2):613-616.

14.  Disegi JA. Titanium alloys for fracture fixation implants. Injury. 2000;31(suppl 4):14-17.

15.  El-Zayat BF, Ruchholtz S, Efe T, Paletta J, Kreslo D, Zettl R. Results of titanium locking plate and stainless steel cerclage wire combination in femoral fractures. Indian J Orthop. 2013;47(5):454-458.

16.  Van Nortwick SS, Yao J, Ladd AL. Titanium integration with bone, welding, and screw head destruction complicating hardware removal of the distal radius: report of 2 cases. J Hand Surg. 2012;37(7):1388-1392.

17.  Ferguson GS, Chaudhury MK, Sigal GB, Whitesides GM. Contact adhesion of thin gold films on elastomeric supports: cold welding under ambient conditions. Science. 1991;253(5021):776-778.

Issue
The American Journal of Orthopedics - 45(3)
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The American Journal of Orthopedics - 45(3)
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Technical Errors May Affect Accuracy of Torque Limiter in Locking Plate Osteosynthesis
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14-Year-Old Boy With Mild Antecedent Neck Pain in Setting of Acute Trauma: A Rare Case of Benign Fibrous Histiocytoma of the Spine

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14-Year-Old Boy With Mild Antecedent Neck Pain in Setting of Acute Trauma: A Rare Case of Benign Fibrous Histiocytoma of the Spine

Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.1 In addition, spinal BFH appears to have no predilection for sex.

 

 

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.7 Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.6

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.4 GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.13

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.17 OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.13 In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern6 which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.1 In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.2,5,9,19 Clarke and colleagues9 reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.2,9 The only case of lung metastasis, reported by Unni and Dahlin6 in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

References

1.    Demiralp B, Kose O, Oguz E, Sanal T, Ozcan A, Sehirlioglu A. Benign fibrous histiocytoma of the lumbar vertebrae. Skeletal Radiol. 2009;38(2):187-191.

2.     Kuruvath S, O’Donovan DG, Aspoas AR, David KM. Benign fibrous histiocytoma of the thoracic spine: case report and review of the literature. J Neurosurg Spine. 2006;4(3):260-264.

3.    Ceroni D, Dayer R, De Coulon G, Kaelin A. Benign fibrous histiocytoma of bone in a paediatric population: a report of 6 cases. Musculoskelet Surg. 2011;95(2):107-114.

4.    Dorfman HD, Czerniak B. Bone Tumors. St. Louis, MO: Mosby; 1998.

5.     Grohs JG, Nicolakis M, Kainberger F, Lang S, Kotz R. Benign fibrous histiocytoma of bone: a report of ten cases and review of literature. Wien Klin Wochenschr. 2002;114(1-2):56-63.

6.    Unni KK, Dahlin DC. Dahlin’s Bone Tumors. 5th ed. Philadelphia, PA: Lippincott-Raven; 1996.

7.    Balasubramanian C, Rajaraman G, Singh CS, Baliga DK. Benign fibrous histiocytoma of the sacrum—diagnostic difficulties facing this rare bone tumor. Pediatr Neurosurg. 2005;41(5):253-257.

8.    van Giffen NH, van Rhijn LW, van Ooij A, et al. Benign fibrous histiocytoma of the posterior arch of C1 in a 6-year old boy: a case report. Spine. 2003;28(18):E359-E363.

9.    Clarke BE, Xipell JM, Thomas DP. Benign fibrous histiocytoma of bone. Am J Surg Pathol. 1985;9(11):806-815.

10.  Peicha G, Siebert FJ, Bratschitsch G, Fankhauser F, Grechenig W. Pathologic odontoid fracture and benign fibrous histiocytoma of bone. Eur Spine J. 1999;8(2):161-163.

11.  Unni KK, Inwards CY, Bridge JA, Kindblom LG, Wold LE. Tumors of the Bones and Joints (AFIP Atlas of Tumor Pathology Series IV). Annapolis Junction, MD: American Registry of Pathology Press; 2005.

12.  Dee R. Principles of Orthopaedic Practice. 2nd ed. New York, NY: McGraw-Hill; 1997.

13.    Murphey M, Andrews C, Flemming D, Temple HT, Smith WS, Smirniotopoulos JG. Primary tumors of the spine: radiologic–pathologic correlation. Radiographics. 1996;16(5):1131-1158.

14.  Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.

15.  Mirra JM, Picci P, Gold RH. Bone Tumors: Clinical, Radiologic, and Pathologic Correlations. Vol 1. Philadelphia, PA: Lea & Febiger; 1989.

16.  Theodorou DJ, Theodorou SJ, Sartoris DJ. An imaging overview of primary tumors of the spine: part 1. Benign tumors. Clin Imaging. 2008;32(3):196-203.

17.  Li X, Meng Z, Li D, Tan J, Song X. Benign fibrous histiocytoma of a rib. Clin Nucl Med. 2014;39(9): 837-841.

18.  Roessner A, Immenkamp M, Weidner A, Hobik HP, Grundmann E. Benign fibrous histiocytoma of bone. Light- and electron-microscopic observations. J Cancer Res Clin Oncol. 1981;101(2):191-202.

19.  Destouet JM, Kyriakos M, Gilula LA. Fibrous histiocytoma (fibroxanthoma) of a cervical vertebra. A report with a review of the literature. Skeletal Radiol. 1980;5(4):241-246.

20.  Hoeffel JC, Bomand-Ferrand F, Tachet F, Lascombes P, Czorny A, Bernard C. So-called benign fibrous histiocytoma: report of a case. J Pediatr Surg. 1992;27(5):672-674.

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Raymond Skunda, MD, Timothy Puckett, MD, Michael Martin, MD, Jose Sanclement, MD, and Jo Elle Peterson, MD

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neck, neck pain, pain, pain management, trauma, spine, boy, case report, online exclusive, football, benign fibrous histiocytoma, BFH, pediatrics, bone, tumor, imaging, skunda, puckett, martin, sanclement, peterson
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Raymond Skunda, MD, Timothy Puckett, MD, Michael Martin, MD, Jose Sanclement, MD, and Jo Elle Peterson, MD

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Raymond Skunda, MD, Timothy Puckett, MD, Michael Martin, MD, Jose Sanclement, MD, and Jo Elle Peterson, MD

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Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.1 In addition, spinal BFH appears to have no predilection for sex.

 

 

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.7 Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.6

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.4 GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.13

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.17 OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.13 In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern6 which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.1 In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.2,5,9,19 Clarke and colleagues9 reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.2,9 The only case of lung metastasis, reported by Unni and Dahlin6 in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.1 In addition, spinal BFH appears to have no predilection for sex.

 

 

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.7 Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.6

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.4 GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.13

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.17 OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.13 In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern6 which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.1 In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.2,5,9,19 Clarke and colleagues9 reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.2,9 The only case of lung metastasis, reported by Unni and Dahlin6 in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

References

1.    Demiralp B, Kose O, Oguz E, Sanal T, Ozcan A, Sehirlioglu A. Benign fibrous histiocytoma of the lumbar vertebrae. Skeletal Radiol. 2009;38(2):187-191.

2.     Kuruvath S, O’Donovan DG, Aspoas AR, David KM. Benign fibrous histiocytoma of the thoracic spine: case report and review of the literature. J Neurosurg Spine. 2006;4(3):260-264.

3.    Ceroni D, Dayer R, De Coulon G, Kaelin A. Benign fibrous histiocytoma of bone in a paediatric population: a report of 6 cases. Musculoskelet Surg. 2011;95(2):107-114.

4.    Dorfman HD, Czerniak B. Bone Tumors. St. Louis, MO: Mosby; 1998.

5.     Grohs JG, Nicolakis M, Kainberger F, Lang S, Kotz R. Benign fibrous histiocytoma of bone: a report of ten cases and review of literature. Wien Klin Wochenschr. 2002;114(1-2):56-63.

6.    Unni KK, Dahlin DC. Dahlin’s Bone Tumors. 5th ed. Philadelphia, PA: Lippincott-Raven; 1996.

7.    Balasubramanian C, Rajaraman G, Singh CS, Baliga DK. Benign fibrous histiocytoma of the sacrum—diagnostic difficulties facing this rare bone tumor. Pediatr Neurosurg. 2005;41(5):253-257.

8.    van Giffen NH, van Rhijn LW, van Ooij A, et al. Benign fibrous histiocytoma of the posterior arch of C1 in a 6-year old boy: a case report. Spine. 2003;28(18):E359-E363.

9.    Clarke BE, Xipell JM, Thomas DP. Benign fibrous histiocytoma of bone. Am J Surg Pathol. 1985;9(11):806-815.

10.  Peicha G, Siebert FJ, Bratschitsch G, Fankhauser F, Grechenig W. Pathologic odontoid fracture and benign fibrous histiocytoma of bone. Eur Spine J. 1999;8(2):161-163.

11.  Unni KK, Inwards CY, Bridge JA, Kindblom LG, Wold LE. Tumors of the Bones and Joints (AFIP Atlas of Tumor Pathology Series IV). Annapolis Junction, MD: American Registry of Pathology Press; 2005.

12.  Dee R. Principles of Orthopaedic Practice. 2nd ed. New York, NY: McGraw-Hill; 1997.

13.    Murphey M, Andrews C, Flemming D, Temple HT, Smith WS, Smirniotopoulos JG. Primary tumors of the spine: radiologic–pathologic correlation. Radiographics. 1996;16(5):1131-1158.

14.  Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.

15.  Mirra JM, Picci P, Gold RH. Bone Tumors: Clinical, Radiologic, and Pathologic Correlations. Vol 1. Philadelphia, PA: Lea & Febiger; 1989.

16.  Theodorou DJ, Theodorou SJ, Sartoris DJ. An imaging overview of primary tumors of the spine: part 1. Benign tumors. Clin Imaging. 2008;32(3):196-203.

17.  Li X, Meng Z, Li D, Tan J, Song X. Benign fibrous histiocytoma of a rib. Clin Nucl Med. 2014;39(9): 837-841.

18.  Roessner A, Immenkamp M, Weidner A, Hobik HP, Grundmann E. Benign fibrous histiocytoma of bone. Light- and electron-microscopic observations. J Cancer Res Clin Oncol. 1981;101(2):191-202.

19.  Destouet JM, Kyriakos M, Gilula LA. Fibrous histiocytoma (fibroxanthoma) of a cervical vertebra. A report with a review of the literature. Skeletal Radiol. 1980;5(4):241-246.

20.  Hoeffel JC, Bomand-Ferrand F, Tachet F, Lascombes P, Czorny A, Bernard C. So-called benign fibrous histiocytoma: report of a case. J Pediatr Surg. 1992;27(5):672-674.

References

1.    Demiralp B, Kose O, Oguz E, Sanal T, Ozcan A, Sehirlioglu A. Benign fibrous histiocytoma of the lumbar vertebrae. Skeletal Radiol. 2009;38(2):187-191.

2.     Kuruvath S, O’Donovan DG, Aspoas AR, David KM. Benign fibrous histiocytoma of the thoracic spine: case report and review of the literature. J Neurosurg Spine. 2006;4(3):260-264.

3.    Ceroni D, Dayer R, De Coulon G, Kaelin A. Benign fibrous histiocytoma of bone in a paediatric population: a report of 6 cases. Musculoskelet Surg. 2011;95(2):107-114.

4.    Dorfman HD, Czerniak B. Bone Tumors. St. Louis, MO: Mosby; 1998.

5.     Grohs JG, Nicolakis M, Kainberger F, Lang S, Kotz R. Benign fibrous histiocytoma of bone: a report of ten cases and review of literature. Wien Klin Wochenschr. 2002;114(1-2):56-63.

6.    Unni KK, Dahlin DC. Dahlin’s Bone Tumors. 5th ed. Philadelphia, PA: Lippincott-Raven; 1996.

7.    Balasubramanian C, Rajaraman G, Singh CS, Baliga DK. Benign fibrous histiocytoma of the sacrum—diagnostic difficulties facing this rare bone tumor. Pediatr Neurosurg. 2005;41(5):253-257.

8.    van Giffen NH, van Rhijn LW, van Ooij A, et al. Benign fibrous histiocytoma of the posterior arch of C1 in a 6-year old boy: a case report. Spine. 2003;28(18):E359-E363.

9.    Clarke BE, Xipell JM, Thomas DP. Benign fibrous histiocytoma of bone. Am J Surg Pathol. 1985;9(11):806-815.

10.  Peicha G, Siebert FJ, Bratschitsch G, Fankhauser F, Grechenig W. Pathologic odontoid fracture and benign fibrous histiocytoma of bone. Eur Spine J. 1999;8(2):161-163.

11.  Unni KK, Inwards CY, Bridge JA, Kindblom LG, Wold LE. Tumors of the Bones and Joints (AFIP Atlas of Tumor Pathology Series IV). Annapolis Junction, MD: American Registry of Pathology Press; 2005.

12.  Dee R. Principles of Orthopaedic Practice. 2nd ed. New York, NY: McGraw-Hill; 1997.

13.    Murphey M, Andrews C, Flemming D, Temple HT, Smith WS, Smirniotopoulos JG. Primary tumors of the spine: radiologic–pathologic correlation. Radiographics. 1996;16(5):1131-1158.

14.  Hamada T, Ito H, Araki Y, Fujii K, Inoue M, Ishida O. Benign fibrous histiocytoma of the femur: review of three cases. Skeletal Radiol. 1996;25(1):25-29.

15.  Mirra JM, Picci P, Gold RH. Bone Tumors: Clinical, Radiologic, and Pathologic Correlations. Vol 1. Philadelphia, PA: Lea & Febiger; 1989.

16.  Theodorou DJ, Theodorou SJ, Sartoris DJ. An imaging overview of primary tumors of the spine: part 1. Benign tumors. Clin Imaging. 2008;32(3):196-203.

17.  Li X, Meng Z, Li D, Tan J, Song X. Benign fibrous histiocytoma of a rib. Clin Nucl Med. 2014;39(9): 837-841.

18.  Roessner A, Immenkamp M, Weidner A, Hobik HP, Grundmann E. Benign fibrous histiocytoma of bone. Light- and electron-microscopic observations. J Cancer Res Clin Oncol. 1981;101(2):191-202.

19.  Destouet JM, Kyriakos M, Gilula LA. Fibrous histiocytoma (fibroxanthoma) of a cervical vertebra. A report with a review of the literature. Skeletal Radiol. 1980;5(4):241-246.

20.  Hoeffel JC, Bomand-Ferrand F, Tachet F, Lascombes P, Czorny A, Bernard C. So-called benign fibrous histiocytoma: report of a case. J Pediatr Surg. 1992;27(5):672-674.

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14-Year-Old Boy With Mild Antecedent Neck Pain in Setting of Acute Trauma: A Rare Case of Benign Fibrous Histiocytoma of the Spine
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Treating Tibia Fractures With Far Cortical Locking Implants

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Treating Tibia Fractures With Far Cortical Locking Implants

Fracture healing can be categorized as primary or secondary. Primary healing requires precise reapproximation of bone fragments and compression of cortices. Osteons are formed across the fracture line, allowing blood supply and endothelial cells to gain access, leading to osteoblast infiltration and subsequent bone formation.1 This type of bone healing can be accomplished only with absolute stability—specifically, only with less than 2% strain at the fracture site, necessitating operative intervention with compression plating (Figure 1).2 This type of construct generates friction between the bone fragments against a metal plate, created by tightening screws that purchase both far and near cortices of bone.3 Although this type of fixation works well with many fractures, there are several instances in which compression plating is not ideal.4 Osteoporotic bone, for example, limits the amount of compression that can be developed, as screws strip the bone more readily, leading to weakened constructs prone to failure. Metaphyseal fractures in which there is minimal cortex for screw thread purchase are a similar challenge.5 Highly comminuted fractures do not allow for sufficient fragment compression and stability. In addition, compression plating requires periosteal stripping at the fracture, and often substantial soft-tissue disruption, which is especially a problem in areas of tenuous blood supply (eg, the tibia).

Locked plating therefore has become a valuable technique in managing osteoporotic fractures.2 Locking plates may be used to achieve secondary bone healing through a small amount of interfragmentary motion, 0.2 to 10 mm, as seen with bridge plating for example, whereby the locking plates act as internal fixators. Much as with external fixators, as the distance from the fixator bar (or plate) to bone decreases, construct stiffness increases. Thus, locking plates function as extremely stiff fixators when the plate is very near bone. It has therefore been speculated that such stiffness is insufficient to provide optimal secondary healing conditions.6,7 Titanium (vs stainless steel) plates have been used, and screws have been omitted just adjacent to either side of the fracture site, in attempts to increase plate flexibility and thus interfragmentary motion.8,9 In addition, biomechanical and animal model studies have demonstrated that, with use of locking plates, motion at the fracture site is asymmetric and leads to unequal callus formation at the near and far cortices, thus weakening the fracture site.10,11

The locking plate design was recently modified to address these concerns. Far cortical locking (FCL) uses locking screws threaded only distally (Figure 2), which allows for purchase into the far cortex but not the near cortex, which increases pin length from plate to bone. The near cortex is no longer anchored to the plate and thus increases construct flexibility. Pilot holes in the near cortex allow for movement of the nonthreaded screw shaft in a controlled, biphasic manner.12 This design decreases stiffness while sacrificing very little construct strength.10 In addition, motion at the far and near cortices is nearly parallel. It has been shown in an ovine tibial osteotomy model that, compared with the traditional locking plate design, FCL generates symmetric callus formation and improved fracture healing.11 Although these results are promising, there are only limited clinical data on use of the FCL technique in fracture repair. Our null hypothesis was that, despite the theoretical advantages of FCL constructs over conventional locking plates, there would be no clinically observed differences between the constructs.

Patients and Methods

After obtaining Institutional Review Board approval from the 2 level I trauma centers and 1 level II trauma center involved in this study, we retrospectively reviewed the cases of all adults who presented with a tibia fracture and were treated with FCL technology (MotionLoc, Zimmer) by a fellowship-trained trauma surgeon at these hospitals (Figures 3A–3C). Any primary tibia fracture treated with FCL was considered. Only patients with follow-up of at least 20 weeks were included in the analysis. Exclusion criteria were tibial malunions or nonunions treated with FCL and fractures treated with a combination of intramedullary fixation and plating.

We reviewed the patient charts for demographic data, mechanism of injury, fracture type, and comorbidities. Risk factors for poor healing—such as diabetes and tobacco use, either current or prior—were recorded. We also reviewed the radiographs of the initial injuries for analysis of the tibia fracture types (Table 1) as well as the follow-up radiographs for evaluation of fracture healing. Using the Orthopaedic Trauma Association classification system, we identified a variety of fracture patterns. Fracture healing rates were recorded and used to calculate the overall healing rates for each group. Union was defined as either radiographic evidence of a completely healed fracture (≥3 cortices) or radiographic evidence of osseous bridging at the fracture site in addition to full weight-bearing without pain. Infection was defined as positive intraoperative cultures or grossly infected wounds with purulence and erythema.

 

 

For statistical analysis, we used Welch 2-sample t test to compare categorical data, including rates of fracture union, infection, and revision surgery. We chose this test because it was unclear whether variance in the groups would be similar. FCL and control data were compared for significant differences by calculating P values. Similarly, for continuous data, Fisher exact test was used to calculate P values for mean time to union and mean time to full weight-bearing in order to compare FCL and control outcomes.

Results

Twelve patients treated at 2 level I and 1 level II trauma centers between November 2010 and May 2012 met the inclusion and exclusion criteria for this study. Another 10 patients were treated with standard plating techniques (control group). Mean age was 52 years (range, 25-72 years) for the FCL group and 46 years (range, 28-67 years) for the control group. The FCL group included 2 open fractures (control, 0) and 2 patients with diabetes (control, 1) (Table 1).

Eleven of the 12 FCL patients and all 10 control patients achieved fracture union by most recent follow-up (Table 2). The difference was not statistically significant (P = .363). The FCL-treated fracture that did not heal received an interfragmentary screw in addition to the standard FCL technology construct. The interfragmentary screw inhibited motion at the fracture site and could potentially have led to nonunion. For this patient, revision surgery to an intramedullary nail was required. Removal of the interfragmentary screw was uneventful. Each of the 2 open fractures in the FCL group required bone grafting because of large segmental bone loss. One of these fractures, a type 3B, became infected after bone grafting, and complete healing required plate removal. The patient was eventually treated with a brace. An infection that occurred after union in a closed tibia fracture in the FCL group required hardware removal. No patient in either group experienced loss or failure of fixation.

Discussion

Far cortical locking is a relatively new technology designed to increase fracture fixation flexibility by functionally lengthening the distance between the locking plate and the screw cortical purchase, which occurs at the far cortex rather than the near cortex. This construct thereby functions as an internal fixator and is functionally similar to an external fixator. Rather than there being bars external to the skin, a plate is placed internally, adjacent to but without compressing fracture fragments or the plate to the bone. This theoretically leads to a desirable amount of interfragmentary motion, promoting callus formation and secondary healing. However, too much motion at the fracture site disrupts healing by shearing proliferating cells attempting to bridge the fracture gap. Therefore, there is a narrow target zone of desirable motion between fracture fragments required to promote secondary bone healing—defined as 2% to 10% gap strain.2 FCL constructs are thought to fall in this range of gap strain and thus better promote secondary healing over standard locked plates. Although biomechanical studies have been used as proof of concept, there are no published clinical data on the effectiveness of FCL implants. The present article describes early data on clinical outcomes of this new type of implant.

The main limitation of this study is its small cohort size, which is largely a result of the short time these implants have been available and our attempt to compare only similar fractures in this analysis. In addition, follow-up was on average less than 1 year. We consider such follow-up acceptable, though, as all fractures essentially reached final healing status within that period. Another limitation is that we combined compression plating and locked plating in the control group. Considering the mechanism of the theoretical advantage of FCL implants, with larger cohorts it would be useful to perform a subanalysis in which compression and standard locking plates are separately compared with FCL implants.

This study found no statistically significant difference between FCL and standard plating, suggesting FCL likely is not inferior to standard plating. Although the FCL group included a nonunion, it is important to note that, in this case, there was a technical discrepancy in the ideal technique whereby another interfragmentary screw was placed, eliminating the interfragmentary motion that establishes the premise of FCL technology. This case thereby demonstrated that a breach in the FCL technique, as with standard locking techniques, may lead to fracture-healing complications. In the FCL group, 2 open fractures with significant segmental bone loss requiring bone graft subsequently healed. In addition, compared with the control group, the FCL group included more patients with diabetes and more tobacco users (both diabetes and tobacco use are associated with poor bone and wound healing). The FCL group was also, on average, 6 years older than the control group. None of these group differences, however, reached statistical significance. Indeed, part of the impetus to use FCL implants in this population was that these patients likely were at higher risk for poor healing and nonunion. This factor therefore represents a selection bias—the FCL group was more predisposed to nonunion—and a study limitation.

 

 

Together, our data show neither superiority nor inferiority of the FCL technique. This study is an important step in furthering investigations into FCL constructs. The finding of similar efficacy with FCL and conventional plating may assuage safety concerns and pave the way for more definitive studies of FCL technology and fuller evaluations of its effectiveness. These studies will be essential in determining whether the theoretical advantage of FCL translates into better clinical outcomes. Larger, prospective randomized studies with longer follow-ups will be needed to better compare FCL technology with current implants and techniques. At this early stage, however, FCL technology appears to be a viable option for complex fractures of the tibia.

References

1.    Bernstein J, ed. Musculoskeletal Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2003.

2.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

3.    Bagby GW. Compression bone-plating: historical considerations. J Bone Joint Surg Am. 1977;59(5):625-631.

4.    Kubiak EN, Fulkerson E, Strauss E, Egol KA. The evolution of locked plates. J Bone Joint Surg Am. 2006;88(suppl 4):189-200.

5.    Fitzpatrick DC, Doornink J, Madey SM, Bottlang M. Relative stability of conventional and locked plating fixation in a model of the osteoporotic femoral diaphysis. Clin Biomech. 2009;24(2):203-209.

6.    Henderson CE, Bottlang M, Marsh JL, Fitzpatrick DC, Madey SM. Does locked plating of periprosthetic supracondylar femur fractures promote bone healing by callus formation? Two cases with opposite outcomes. Iowa Orthop J. 2008;28:73-76.

7.    Lujan TJ, Henderson CE, Madey SM, Fitzpatrick DC, Marsh JL, Bottlang M. Locked plating of distal femur fractures leads to inconsistent and asymmetric callus formation. J Orthop Trauma. 2010;24(3):156-162.

8.    Stoffel K, Dieter U, Stachowiak G, Gächter A, Kuster MS. Biomechanical testing of the LCP—how can stability in locked internal fixators be controlled? Injury. 2003;34(suppl 2):B11-B19.

9.    Schmal H, Strohm PC, Jaeger M, Südkamp NP. Flexible fixation and fracture healing: do locked plating ‘internal fixators’ resemble external fixators? J Orthop Trauma. 2011;25(suppl 1):S15-S20.

10.  Bottlang M, Doornink J, Fitzpatrick DC, Madey SM. Far cortical locking can reduce stiffness of locked plating constructs while retaining construct strength. J Bone Joint Surg Am. 2009;91(8):1985-1994.

11.  Bottlang M, Lesser M, Koerber J, et al. Far cortical locking can improve healing of fractures stabilized with locking plates. J Bone Joint Surg Am. 2010;92(7):1652-1660.

12.  Bottlang M, Feist F. Biomechanics of far cortical locking. J Orthop Trauma. 2011;25(suppl 1):S21-S28.

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Christopher Rice, MD, Thomas Christensen, MD, Michael Bottlang, PhD, Dan Fitzpatrick, MS, MD, and Erik Kubiak, MD

Authors’ Disclosure Statement: This research was supported by the University of Utah Study Design and Biostatistics Center, with funding in part from the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health (grant 8UL1TR000105, formerly UL1RR025764). Dr. Bottlang, Dr. Fitzpatrick, and Dr. Kubiak report that they are consultants for Zimmer. The other authors report no actual or potential conflict of interest in relation to this article.

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Christopher Rice, MD, Thomas Christensen, MD, Michael Bottlang, PhD, Dan Fitzpatrick, MS, MD, and Erik Kubiak, MD

Authors’ Disclosure Statement: This research was supported by the University of Utah Study Design and Biostatistics Center, with funding in part from the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health (grant 8UL1TR000105, formerly UL1RR025764). Dr. Bottlang, Dr. Fitzpatrick, and Dr. Kubiak report that they are consultants for Zimmer. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Christopher Rice, MD, Thomas Christensen, MD, Michael Bottlang, PhD, Dan Fitzpatrick, MS, MD, and Erik Kubiak, MD

Authors’ Disclosure Statement: This research was supported by the University of Utah Study Design and Biostatistics Center, with funding in part from the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health (grant 8UL1TR000105, formerly UL1RR025764). Dr. Bottlang, Dr. Fitzpatrick, and Dr. Kubiak report that they are consultants for Zimmer. The other authors report no actual or potential conflict of interest in relation to this article.

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Fracture healing can be categorized as primary or secondary. Primary healing requires precise reapproximation of bone fragments and compression of cortices. Osteons are formed across the fracture line, allowing blood supply and endothelial cells to gain access, leading to osteoblast infiltration and subsequent bone formation.1 This type of bone healing can be accomplished only with absolute stability—specifically, only with less than 2% strain at the fracture site, necessitating operative intervention with compression plating (Figure 1).2 This type of construct generates friction between the bone fragments against a metal plate, created by tightening screws that purchase both far and near cortices of bone.3 Although this type of fixation works well with many fractures, there are several instances in which compression plating is not ideal.4 Osteoporotic bone, for example, limits the amount of compression that can be developed, as screws strip the bone more readily, leading to weakened constructs prone to failure. Metaphyseal fractures in which there is minimal cortex for screw thread purchase are a similar challenge.5 Highly comminuted fractures do not allow for sufficient fragment compression and stability. In addition, compression plating requires periosteal stripping at the fracture, and often substantial soft-tissue disruption, which is especially a problem in areas of tenuous blood supply (eg, the tibia).

Locked plating therefore has become a valuable technique in managing osteoporotic fractures.2 Locking plates may be used to achieve secondary bone healing through a small amount of interfragmentary motion, 0.2 to 10 mm, as seen with bridge plating for example, whereby the locking plates act as internal fixators. Much as with external fixators, as the distance from the fixator bar (or plate) to bone decreases, construct stiffness increases. Thus, locking plates function as extremely stiff fixators when the plate is very near bone. It has therefore been speculated that such stiffness is insufficient to provide optimal secondary healing conditions.6,7 Titanium (vs stainless steel) plates have been used, and screws have been omitted just adjacent to either side of the fracture site, in attempts to increase plate flexibility and thus interfragmentary motion.8,9 In addition, biomechanical and animal model studies have demonstrated that, with use of locking plates, motion at the fracture site is asymmetric and leads to unequal callus formation at the near and far cortices, thus weakening the fracture site.10,11

The locking plate design was recently modified to address these concerns. Far cortical locking (FCL) uses locking screws threaded only distally (Figure 2), which allows for purchase into the far cortex but not the near cortex, which increases pin length from plate to bone. The near cortex is no longer anchored to the plate and thus increases construct flexibility. Pilot holes in the near cortex allow for movement of the nonthreaded screw shaft in a controlled, biphasic manner.12 This design decreases stiffness while sacrificing very little construct strength.10 In addition, motion at the far and near cortices is nearly parallel. It has been shown in an ovine tibial osteotomy model that, compared with the traditional locking plate design, FCL generates symmetric callus formation and improved fracture healing.11 Although these results are promising, there are only limited clinical data on use of the FCL technique in fracture repair. Our null hypothesis was that, despite the theoretical advantages of FCL constructs over conventional locking plates, there would be no clinically observed differences between the constructs.

Patients and Methods

After obtaining Institutional Review Board approval from the 2 level I trauma centers and 1 level II trauma center involved in this study, we retrospectively reviewed the cases of all adults who presented with a tibia fracture and were treated with FCL technology (MotionLoc, Zimmer) by a fellowship-trained trauma surgeon at these hospitals (Figures 3A–3C). Any primary tibia fracture treated with FCL was considered. Only patients with follow-up of at least 20 weeks were included in the analysis. Exclusion criteria were tibial malunions or nonunions treated with FCL and fractures treated with a combination of intramedullary fixation and plating.

We reviewed the patient charts for demographic data, mechanism of injury, fracture type, and comorbidities. Risk factors for poor healing—such as diabetes and tobacco use, either current or prior—were recorded. We also reviewed the radiographs of the initial injuries for analysis of the tibia fracture types (Table 1) as well as the follow-up radiographs for evaluation of fracture healing. Using the Orthopaedic Trauma Association classification system, we identified a variety of fracture patterns. Fracture healing rates were recorded and used to calculate the overall healing rates for each group. Union was defined as either radiographic evidence of a completely healed fracture (≥3 cortices) or radiographic evidence of osseous bridging at the fracture site in addition to full weight-bearing without pain. Infection was defined as positive intraoperative cultures or grossly infected wounds with purulence and erythema.

 

 

For statistical analysis, we used Welch 2-sample t test to compare categorical data, including rates of fracture union, infection, and revision surgery. We chose this test because it was unclear whether variance in the groups would be similar. FCL and control data were compared for significant differences by calculating P values. Similarly, for continuous data, Fisher exact test was used to calculate P values for mean time to union and mean time to full weight-bearing in order to compare FCL and control outcomes.

Results

Twelve patients treated at 2 level I and 1 level II trauma centers between November 2010 and May 2012 met the inclusion and exclusion criteria for this study. Another 10 patients were treated with standard plating techniques (control group). Mean age was 52 years (range, 25-72 years) for the FCL group and 46 years (range, 28-67 years) for the control group. The FCL group included 2 open fractures (control, 0) and 2 patients with diabetes (control, 1) (Table 1).

Eleven of the 12 FCL patients and all 10 control patients achieved fracture union by most recent follow-up (Table 2). The difference was not statistically significant (P = .363). The FCL-treated fracture that did not heal received an interfragmentary screw in addition to the standard FCL technology construct. The interfragmentary screw inhibited motion at the fracture site and could potentially have led to nonunion. For this patient, revision surgery to an intramedullary nail was required. Removal of the interfragmentary screw was uneventful. Each of the 2 open fractures in the FCL group required bone grafting because of large segmental bone loss. One of these fractures, a type 3B, became infected after bone grafting, and complete healing required plate removal. The patient was eventually treated with a brace. An infection that occurred after union in a closed tibia fracture in the FCL group required hardware removal. No patient in either group experienced loss or failure of fixation.

Discussion

Far cortical locking is a relatively new technology designed to increase fracture fixation flexibility by functionally lengthening the distance between the locking plate and the screw cortical purchase, which occurs at the far cortex rather than the near cortex. This construct thereby functions as an internal fixator and is functionally similar to an external fixator. Rather than there being bars external to the skin, a plate is placed internally, adjacent to but without compressing fracture fragments or the plate to the bone. This theoretically leads to a desirable amount of interfragmentary motion, promoting callus formation and secondary healing. However, too much motion at the fracture site disrupts healing by shearing proliferating cells attempting to bridge the fracture gap. Therefore, there is a narrow target zone of desirable motion between fracture fragments required to promote secondary bone healing—defined as 2% to 10% gap strain.2 FCL constructs are thought to fall in this range of gap strain and thus better promote secondary healing over standard locked plates. Although biomechanical studies have been used as proof of concept, there are no published clinical data on the effectiveness of FCL implants. The present article describes early data on clinical outcomes of this new type of implant.

The main limitation of this study is its small cohort size, which is largely a result of the short time these implants have been available and our attempt to compare only similar fractures in this analysis. In addition, follow-up was on average less than 1 year. We consider such follow-up acceptable, though, as all fractures essentially reached final healing status within that period. Another limitation is that we combined compression plating and locked plating in the control group. Considering the mechanism of the theoretical advantage of FCL implants, with larger cohorts it would be useful to perform a subanalysis in which compression and standard locking plates are separately compared with FCL implants.

This study found no statistically significant difference between FCL and standard plating, suggesting FCL likely is not inferior to standard plating. Although the FCL group included a nonunion, it is important to note that, in this case, there was a technical discrepancy in the ideal technique whereby another interfragmentary screw was placed, eliminating the interfragmentary motion that establishes the premise of FCL technology. This case thereby demonstrated that a breach in the FCL technique, as with standard locking techniques, may lead to fracture-healing complications. In the FCL group, 2 open fractures with significant segmental bone loss requiring bone graft subsequently healed. In addition, compared with the control group, the FCL group included more patients with diabetes and more tobacco users (both diabetes and tobacco use are associated with poor bone and wound healing). The FCL group was also, on average, 6 years older than the control group. None of these group differences, however, reached statistical significance. Indeed, part of the impetus to use FCL implants in this population was that these patients likely were at higher risk for poor healing and nonunion. This factor therefore represents a selection bias—the FCL group was more predisposed to nonunion—and a study limitation.

 

 

Together, our data show neither superiority nor inferiority of the FCL technique. This study is an important step in furthering investigations into FCL constructs. The finding of similar efficacy with FCL and conventional plating may assuage safety concerns and pave the way for more definitive studies of FCL technology and fuller evaluations of its effectiveness. These studies will be essential in determining whether the theoretical advantage of FCL translates into better clinical outcomes. Larger, prospective randomized studies with longer follow-ups will be needed to better compare FCL technology with current implants and techniques. At this early stage, however, FCL technology appears to be a viable option for complex fractures of the tibia.

Fracture healing can be categorized as primary or secondary. Primary healing requires precise reapproximation of bone fragments and compression of cortices. Osteons are formed across the fracture line, allowing blood supply and endothelial cells to gain access, leading to osteoblast infiltration and subsequent bone formation.1 This type of bone healing can be accomplished only with absolute stability—specifically, only with less than 2% strain at the fracture site, necessitating operative intervention with compression plating (Figure 1).2 This type of construct generates friction between the bone fragments against a metal plate, created by tightening screws that purchase both far and near cortices of bone.3 Although this type of fixation works well with many fractures, there are several instances in which compression plating is not ideal.4 Osteoporotic bone, for example, limits the amount of compression that can be developed, as screws strip the bone more readily, leading to weakened constructs prone to failure. Metaphyseal fractures in which there is minimal cortex for screw thread purchase are a similar challenge.5 Highly comminuted fractures do not allow for sufficient fragment compression and stability. In addition, compression plating requires periosteal stripping at the fracture, and often substantial soft-tissue disruption, which is especially a problem in areas of tenuous blood supply (eg, the tibia).

Locked plating therefore has become a valuable technique in managing osteoporotic fractures.2 Locking plates may be used to achieve secondary bone healing through a small amount of interfragmentary motion, 0.2 to 10 mm, as seen with bridge plating for example, whereby the locking plates act as internal fixators. Much as with external fixators, as the distance from the fixator bar (or plate) to bone decreases, construct stiffness increases. Thus, locking plates function as extremely stiff fixators when the plate is very near bone. It has therefore been speculated that such stiffness is insufficient to provide optimal secondary healing conditions.6,7 Titanium (vs stainless steel) plates have been used, and screws have been omitted just adjacent to either side of the fracture site, in attempts to increase plate flexibility and thus interfragmentary motion.8,9 In addition, biomechanical and animal model studies have demonstrated that, with use of locking plates, motion at the fracture site is asymmetric and leads to unequal callus formation at the near and far cortices, thus weakening the fracture site.10,11

The locking plate design was recently modified to address these concerns. Far cortical locking (FCL) uses locking screws threaded only distally (Figure 2), which allows for purchase into the far cortex but not the near cortex, which increases pin length from plate to bone. The near cortex is no longer anchored to the plate and thus increases construct flexibility. Pilot holes in the near cortex allow for movement of the nonthreaded screw shaft in a controlled, biphasic manner.12 This design decreases stiffness while sacrificing very little construct strength.10 In addition, motion at the far and near cortices is nearly parallel. It has been shown in an ovine tibial osteotomy model that, compared with the traditional locking plate design, FCL generates symmetric callus formation and improved fracture healing.11 Although these results are promising, there are only limited clinical data on use of the FCL technique in fracture repair. Our null hypothesis was that, despite the theoretical advantages of FCL constructs over conventional locking plates, there would be no clinically observed differences between the constructs.

Patients and Methods

After obtaining Institutional Review Board approval from the 2 level I trauma centers and 1 level II trauma center involved in this study, we retrospectively reviewed the cases of all adults who presented with a tibia fracture and were treated with FCL technology (MotionLoc, Zimmer) by a fellowship-trained trauma surgeon at these hospitals (Figures 3A–3C). Any primary tibia fracture treated with FCL was considered. Only patients with follow-up of at least 20 weeks were included in the analysis. Exclusion criteria were tibial malunions or nonunions treated with FCL and fractures treated with a combination of intramedullary fixation and plating.

We reviewed the patient charts for demographic data, mechanism of injury, fracture type, and comorbidities. Risk factors for poor healing—such as diabetes and tobacco use, either current or prior—were recorded. We also reviewed the radiographs of the initial injuries for analysis of the tibia fracture types (Table 1) as well as the follow-up radiographs for evaluation of fracture healing. Using the Orthopaedic Trauma Association classification system, we identified a variety of fracture patterns. Fracture healing rates were recorded and used to calculate the overall healing rates for each group. Union was defined as either radiographic evidence of a completely healed fracture (≥3 cortices) or radiographic evidence of osseous bridging at the fracture site in addition to full weight-bearing without pain. Infection was defined as positive intraoperative cultures or grossly infected wounds with purulence and erythema.

 

 

For statistical analysis, we used Welch 2-sample t test to compare categorical data, including rates of fracture union, infection, and revision surgery. We chose this test because it was unclear whether variance in the groups would be similar. FCL and control data were compared for significant differences by calculating P values. Similarly, for continuous data, Fisher exact test was used to calculate P values for mean time to union and mean time to full weight-bearing in order to compare FCL and control outcomes.

Results

Twelve patients treated at 2 level I and 1 level II trauma centers between November 2010 and May 2012 met the inclusion and exclusion criteria for this study. Another 10 patients were treated with standard plating techniques (control group). Mean age was 52 years (range, 25-72 years) for the FCL group and 46 years (range, 28-67 years) for the control group. The FCL group included 2 open fractures (control, 0) and 2 patients with diabetes (control, 1) (Table 1).

Eleven of the 12 FCL patients and all 10 control patients achieved fracture union by most recent follow-up (Table 2). The difference was not statistically significant (P = .363). The FCL-treated fracture that did not heal received an interfragmentary screw in addition to the standard FCL technology construct. The interfragmentary screw inhibited motion at the fracture site and could potentially have led to nonunion. For this patient, revision surgery to an intramedullary nail was required. Removal of the interfragmentary screw was uneventful. Each of the 2 open fractures in the FCL group required bone grafting because of large segmental bone loss. One of these fractures, a type 3B, became infected after bone grafting, and complete healing required plate removal. The patient was eventually treated with a brace. An infection that occurred after union in a closed tibia fracture in the FCL group required hardware removal. No patient in either group experienced loss or failure of fixation.

Discussion

Far cortical locking is a relatively new technology designed to increase fracture fixation flexibility by functionally lengthening the distance between the locking plate and the screw cortical purchase, which occurs at the far cortex rather than the near cortex. This construct thereby functions as an internal fixator and is functionally similar to an external fixator. Rather than there being bars external to the skin, a plate is placed internally, adjacent to but without compressing fracture fragments or the plate to the bone. This theoretically leads to a desirable amount of interfragmentary motion, promoting callus formation and secondary healing. However, too much motion at the fracture site disrupts healing by shearing proliferating cells attempting to bridge the fracture gap. Therefore, there is a narrow target zone of desirable motion between fracture fragments required to promote secondary bone healing—defined as 2% to 10% gap strain.2 FCL constructs are thought to fall in this range of gap strain and thus better promote secondary healing over standard locked plates. Although biomechanical studies have been used as proof of concept, there are no published clinical data on the effectiveness of FCL implants. The present article describes early data on clinical outcomes of this new type of implant.

The main limitation of this study is its small cohort size, which is largely a result of the short time these implants have been available and our attempt to compare only similar fractures in this analysis. In addition, follow-up was on average less than 1 year. We consider such follow-up acceptable, though, as all fractures essentially reached final healing status within that period. Another limitation is that we combined compression plating and locked plating in the control group. Considering the mechanism of the theoretical advantage of FCL implants, with larger cohorts it would be useful to perform a subanalysis in which compression and standard locking plates are separately compared with FCL implants.

This study found no statistically significant difference between FCL and standard plating, suggesting FCL likely is not inferior to standard plating. Although the FCL group included a nonunion, it is important to note that, in this case, there was a technical discrepancy in the ideal technique whereby another interfragmentary screw was placed, eliminating the interfragmentary motion that establishes the premise of FCL technology. This case thereby demonstrated that a breach in the FCL technique, as with standard locking techniques, may lead to fracture-healing complications. In the FCL group, 2 open fractures with significant segmental bone loss requiring bone graft subsequently healed. In addition, compared with the control group, the FCL group included more patients with diabetes and more tobacco users (both diabetes and tobacco use are associated with poor bone and wound healing). The FCL group was also, on average, 6 years older than the control group. None of these group differences, however, reached statistical significance. Indeed, part of the impetus to use FCL implants in this population was that these patients likely were at higher risk for poor healing and nonunion. This factor therefore represents a selection bias—the FCL group was more predisposed to nonunion—and a study limitation.

 

 

Together, our data show neither superiority nor inferiority of the FCL technique. This study is an important step in furthering investigations into FCL constructs. The finding of similar efficacy with FCL and conventional plating may assuage safety concerns and pave the way for more definitive studies of FCL technology and fuller evaluations of its effectiveness. These studies will be essential in determining whether the theoretical advantage of FCL translates into better clinical outcomes. Larger, prospective randomized studies with longer follow-ups will be needed to better compare FCL technology with current implants and techniques. At this early stage, however, FCL technology appears to be a viable option for complex fractures of the tibia.

References

1.    Bernstein J, ed. Musculoskeletal Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2003.

2.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

3.    Bagby GW. Compression bone-plating: historical considerations. J Bone Joint Surg Am. 1977;59(5):625-631.

4.    Kubiak EN, Fulkerson E, Strauss E, Egol KA. The evolution of locked plates. J Bone Joint Surg Am. 2006;88(suppl 4):189-200.

5.    Fitzpatrick DC, Doornink J, Madey SM, Bottlang M. Relative stability of conventional and locked plating fixation in a model of the osteoporotic femoral diaphysis. Clin Biomech. 2009;24(2):203-209.

6.    Henderson CE, Bottlang M, Marsh JL, Fitzpatrick DC, Madey SM. Does locked plating of periprosthetic supracondylar femur fractures promote bone healing by callus formation? Two cases with opposite outcomes. Iowa Orthop J. 2008;28:73-76.

7.    Lujan TJ, Henderson CE, Madey SM, Fitzpatrick DC, Marsh JL, Bottlang M. Locked plating of distal femur fractures leads to inconsistent and asymmetric callus formation. J Orthop Trauma. 2010;24(3):156-162.

8.    Stoffel K, Dieter U, Stachowiak G, Gächter A, Kuster MS. Biomechanical testing of the LCP—how can stability in locked internal fixators be controlled? Injury. 2003;34(suppl 2):B11-B19.

9.    Schmal H, Strohm PC, Jaeger M, Südkamp NP. Flexible fixation and fracture healing: do locked plating ‘internal fixators’ resemble external fixators? J Orthop Trauma. 2011;25(suppl 1):S15-S20.

10.  Bottlang M, Doornink J, Fitzpatrick DC, Madey SM. Far cortical locking can reduce stiffness of locked plating constructs while retaining construct strength. J Bone Joint Surg Am. 2009;91(8):1985-1994.

11.  Bottlang M, Lesser M, Koerber J, et al. Far cortical locking can improve healing of fractures stabilized with locking plates. J Bone Joint Surg Am. 2010;92(7):1652-1660.

12.  Bottlang M, Feist F. Biomechanics of far cortical locking. J Orthop Trauma. 2011;25(suppl 1):S21-S28.

References

1.    Bernstein J, ed. Musculoskeletal Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2003.

2.    Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma. 2004;18(8):488-493.

3.    Bagby GW. Compression bone-plating: historical considerations. J Bone Joint Surg Am. 1977;59(5):625-631.

4.    Kubiak EN, Fulkerson E, Strauss E, Egol KA. The evolution of locked plates. J Bone Joint Surg Am. 2006;88(suppl 4):189-200.

5.    Fitzpatrick DC, Doornink J, Madey SM, Bottlang M. Relative stability of conventional and locked plating fixation in a model of the osteoporotic femoral diaphysis. Clin Biomech. 2009;24(2):203-209.

6.    Henderson CE, Bottlang M, Marsh JL, Fitzpatrick DC, Madey SM. Does locked plating of periprosthetic supracondylar femur fractures promote bone healing by callus formation? Two cases with opposite outcomes. Iowa Orthop J. 2008;28:73-76.

7.    Lujan TJ, Henderson CE, Madey SM, Fitzpatrick DC, Marsh JL, Bottlang M. Locked plating of distal femur fractures leads to inconsistent and asymmetric callus formation. J Orthop Trauma. 2010;24(3):156-162.

8.    Stoffel K, Dieter U, Stachowiak G, Gächter A, Kuster MS. Biomechanical testing of the LCP—how can stability in locked internal fixators be controlled? Injury. 2003;34(suppl 2):B11-B19.

9.    Schmal H, Strohm PC, Jaeger M, Südkamp NP. Flexible fixation and fracture healing: do locked plating ‘internal fixators’ resemble external fixators? J Orthop Trauma. 2011;25(suppl 1):S15-S20.

10.  Bottlang M, Doornink J, Fitzpatrick DC, Madey SM. Far cortical locking can reduce stiffness of locked plating constructs while retaining construct strength. J Bone Joint Surg Am. 2009;91(8):1985-1994.

11.  Bottlang M, Lesser M, Koerber J, et al. Far cortical locking can improve healing of fractures stabilized with locking plates. J Bone Joint Surg Am. 2010;92(7):1652-1660.

12.  Bottlang M, Feist F. Biomechanics of far cortical locking. J Orthop Trauma. 2011;25(suppl 1):S21-S28.

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Sports Medicine Fellowship: What Should I Be Looking For?

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The Orthopaedic Sports Medicine Fellowship Match was first established in 2008 as a joint-sponsored venture between the American Orthopaedic Society for Sports Medicine and the Arthroscopy Association of North America to pair applicants with participating training programs.1 Operated under the San Francisco Match,2 the current fellowship match process was adopted to systematically coordinate training appointments and eliminate the role of “exploding offers,” which are pressured early decisions predicated on immediate acceptance. Other advantages of this system include its operation through a central application service to avoid redundancy of submitted paperwork, as well as to create greater awareness and to publicize training options and standardization of the match timeline.1

In its current state, the orthopedic sports medicine match represents 96 programs with 230 positions, accounting for approximately 97% of training programs and fellowship positions.1 While unaccredited options remain available through the Match, many programs have migrated towards American Council for Graduate Medical Education (ACGME) accreditation because of an increased focus on objective learning metrics during fellowship and the requirement for Subspecialty Certification in Orthopaedic Sports Medicine through the American Board of Orthopaedic Surgery.3 However, other programs have also eschewed the increasing constraints and administrative resources associated with ACGME accreditation, particularly among fellowships based at community-based hospitals or private practices that lack formal affiliation with academic institutions or residency training programs.

Along with a greater understanding of the historical background of the match process, fellowship applicants must also appreciate the relative merits of fellowship training. More than 90% of orthopedic surgery residents now pursue further subspecialty fellowship training, with some individuals opting for 2 additional fellowship opportunities.4 As a so-called “nontraditional applicant,” I represent a different demographic, returning to fellowship after years of clinical practice while serving in the military. Individual preferences notwithstanding, I wanted to take the opportunity to emphasize some important considerations in deliberating between different fellowship programs.

  • Geography. Your eventual desired practice location may play a role in determining fellowship location or, at least, region of the country. Additionally, this can be an important factor in family happiness. In competitive markets, such as the Northeast or the West Coast, you may make inroads and establish professional connections that result in potential job opportunities. Conversely, other programs may adopt anticompetitive measures to limit local practice options.
  • Training setting. Despite the trending consolidation of fellowship training programs in affiliated university and hospital-based teaching systems, many community-based programs and private-practice models thrive, providing an alternative to traditional academic training centers. The latter may provide more in-depth exposure to practice management, billing/coding, and ancillary services. The former typically offer a more structured, academically oriented environment with formal teaching conferences and a broader department hierarchy.
  • Program size. Some applicants may prefer a larger, more diverse array of teaching staff or fellows, while others gravitate toward fewer, more personal mentoring relationships that allow more intimate familiarity with practice habits or surgical techniques.
  • Associated training programs. Affiliations with a residency or physician-extender training program can offer benefits and drawbacks, including offloading clerical work, shared hands-on experience in the clinic and operating room, and midlevel supervisory responsibilities. This can offer useful opportunities to formulate an individual teaching style and valuable mentoring relationships. However, it can also impose greater time requirements or detract from one-on-one teaching with staff.
  • Reputation. Applicants may attach distinction to a well-established regional or national reputation associated with a given training program. Often, certain programs may carry prestige as a result of their academic name, hospital affiliation, or accomplishments. This can offer certain marketing advantages for patient recruitment. However, less renowned programs may provide better training opportunities and confer higher esteem among your professional colleagues. Program reputation can change dramatically with time, so this should be balanced with other potential strengths and overall training experience.
  • Practice “niches”/areas of interest. With increasing adoption of arthroscopic techniques among practicing surgeons and a relative excess of sports medicine–trained orthopedists, it is paramount to develop a novel skill set during fellowship to differentiate you from other graduates. I sought a sports medicine fellowship that would offer me a broad-based exposure to arthroscopic and open knee and shoulder reconstruction, chondral restoration techniques, hip arthroscopy and preservation, and shoulder arthroplasty. Opportunities in elbow reconstruction, foot and ankle arthroscopy, and pediatric sports medicine may also be valuable as a distinguishing factor in searching for jobs after training.
  • Marketability. Closely intertwined with reputation and scope of practice, an institution’s marketability is another intangible attribute to consider. Professional or collegiate team coverage offers significant market value for patient advertising, and it is frequently publicized by orthopedic practices and hospital systems. Additionally, the importance of ACGME accreditation should also be considered.
  • Nonmedical training. This is increasingly important in subsequent subspecialty training. Further education on the business aspects of orthopedic surgery should be emphasized. Additionally, dedicated curricula on professional or leadership development are important for career progression.
  • Mentorship. Throughout the interview process, one of my foremost priorities was a strong and enduring pattern of mentorship. Fellowship offers the opportunity to establish 1 or multiple mentors in your subspecialty. These individuals will be instrumental in the development of your early professional career and your approach to clinical practice. From discussions about complicated patients to advice on contract negotiations, your ideal mentor should champion your early successes and work generously on your behalf, even long after fellowship has ended. 

  • Research opportunities. Given my academic career goals, I actively pursued a program with rich clinical and laboratory resources, and an established infrastructure for accomplishing high-quality, relevant research. Interested individuals should gauge the availability of research support staff, biomechanical or bench-level laboratory collaboration, grant or institutional research funding, cadaveric specimens, or clinical outcomes data for research conducted by fellows. However, not all fellowship applicants have a vested interest in research during fellowship, so I would encourage inquiries regarding core research requirements and expectations.
  • Clinical exposure. This encompasses several different and equally important variables, including diversity of clinical or surgical caseloads, case complexity, operative exposure, athletic team coverage, and office or clinical experience. Interestingly, this latter aspect of training is often neglected but cannot be overemphasized. Outpatient clinical evaluation is key to honing important physical examination techniques and critically evaluating patients’ outcomes postoperatively.
  • Surgical autonomy. Hands-on operative experience and surgical autonomy vary widely among fellowship programs. Most fellowships advocate for a graduated level of surgical responsibility dependent on individual abilities and staff comfort, while others offer greater potential for independence. Conversely, some programs espouse more of an “observership” model, and arthroscopic simulators and/or cadaveric skills laboratories are designed to complement operative experience. While most fellowship applicants desire maximal case participation, we must also recognize the value in watching talented surgeons performing technically demanding procedures.
  • Family. You cannot put a premium on your personal contentment and family’s well-being. Proximity to a support network can be important with the work demands and time constraints of fellowship.
 

 

Despite financial obligations and significant time commitments, the fellowship match process offers an incredible range of programs and practice environments. Inevitably, no program can completely fulfill all your criteria, but you should be able to tailor your learning style, professional ambitions, and personal preferences with an excellent training program. For many, fellowship represents the last, and perhaps most integral, stage of formal surgical training. Considering all factors of your chosen fellowship program will ensure a rich and fulfilling educational experience.

References

1.    Sports medicine/arthroscopy fellowship match. American Orthopaedic Society for Sports Medicine website. https://www.sportsmed.org/AOSSMIMIS/Members/Members/Education/Sports_Medicine_Arthroscopy_Fellowship_Match.aspx. Accessed December 21, 2015.

2.    Orthopaedic sports medicine fellowship. SF Match website. https://www.sfmatch.org/SpecialtyInsideAll.aspx?id=11&typ=1&name=Orthopaedic%20Sports%20Medicine. Accessed December 21, 2015.

3.    Orthopaedic sports medicine. American Board of Orthopaedic Surgery website. https://www.abos.org/certification/sports-subspecialty.aspx. Accessed December 21, 2015.

4.    Hariri S, York SC, O’Connor MI, Parsley BS, McCarthy JC. Career plans of current orthopaedic residents with a focus on sex-based and generational differences. J Bone Joint Surg Am. 2011;93(5):e16.

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Brian R. Waterman, MD

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The Orthopaedic Sports Medicine Fellowship Match was first established in 2008 as a joint-sponsored venture between the American Orthopaedic Society for Sports Medicine and the Arthroscopy Association of North America to pair applicants with participating training programs.1 Operated under the San Francisco Match,2 the current fellowship match process was adopted to systematically coordinate training appointments and eliminate the role of “exploding offers,” which are pressured early decisions predicated on immediate acceptance. Other advantages of this system include its operation through a central application service to avoid redundancy of submitted paperwork, as well as to create greater awareness and to publicize training options and standardization of the match timeline.1

In its current state, the orthopedic sports medicine match represents 96 programs with 230 positions, accounting for approximately 97% of training programs and fellowship positions.1 While unaccredited options remain available through the Match, many programs have migrated towards American Council for Graduate Medical Education (ACGME) accreditation because of an increased focus on objective learning metrics during fellowship and the requirement for Subspecialty Certification in Orthopaedic Sports Medicine through the American Board of Orthopaedic Surgery.3 However, other programs have also eschewed the increasing constraints and administrative resources associated with ACGME accreditation, particularly among fellowships based at community-based hospitals or private practices that lack formal affiliation with academic institutions or residency training programs.

Along with a greater understanding of the historical background of the match process, fellowship applicants must also appreciate the relative merits of fellowship training. More than 90% of orthopedic surgery residents now pursue further subspecialty fellowship training, with some individuals opting for 2 additional fellowship opportunities.4 As a so-called “nontraditional applicant,” I represent a different demographic, returning to fellowship after years of clinical practice while serving in the military. Individual preferences notwithstanding, I wanted to take the opportunity to emphasize some important considerations in deliberating between different fellowship programs.

  • Geography. Your eventual desired practice location may play a role in determining fellowship location or, at least, region of the country. Additionally, this can be an important factor in family happiness. In competitive markets, such as the Northeast or the West Coast, you may make inroads and establish professional connections that result in potential job opportunities. Conversely, other programs may adopt anticompetitive measures to limit local practice options.
  • Training setting. Despite the trending consolidation of fellowship training programs in affiliated university and hospital-based teaching systems, many community-based programs and private-practice models thrive, providing an alternative to traditional academic training centers. The latter may provide more in-depth exposure to practice management, billing/coding, and ancillary services. The former typically offer a more structured, academically oriented environment with formal teaching conferences and a broader department hierarchy.
  • Program size. Some applicants may prefer a larger, more diverse array of teaching staff or fellows, while others gravitate toward fewer, more personal mentoring relationships that allow more intimate familiarity with practice habits or surgical techniques.
  • Associated training programs. Affiliations with a residency or physician-extender training program can offer benefits and drawbacks, including offloading clerical work, shared hands-on experience in the clinic and operating room, and midlevel supervisory responsibilities. This can offer useful opportunities to formulate an individual teaching style and valuable mentoring relationships. However, it can also impose greater time requirements or detract from one-on-one teaching with staff.
  • Reputation. Applicants may attach distinction to a well-established regional or national reputation associated with a given training program. Often, certain programs may carry prestige as a result of their academic name, hospital affiliation, or accomplishments. This can offer certain marketing advantages for patient recruitment. However, less renowned programs may provide better training opportunities and confer higher esteem among your professional colleagues. Program reputation can change dramatically with time, so this should be balanced with other potential strengths and overall training experience.
  • Practice “niches”/areas of interest. With increasing adoption of arthroscopic techniques among practicing surgeons and a relative excess of sports medicine–trained orthopedists, it is paramount to develop a novel skill set during fellowship to differentiate you from other graduates. I sought a sports medicine fellowship that would offer me a broad-based exposure to arthroscopic and open knee and shoulder reconstruction, chondral restoration techniques, hip arthroscopy and preservation, and shoulder arthroplasty. Opportunities in elbow reconstruction, foot and ankle arthroscopy, and pediatric sports medicine may also be valuable as a distinguishing factor in searching for jobs after training.
  • Marketability. Closely intertwined with reputation and scope of practice, an institution’s marketability is another intangible attribute to consider. Professional or collegiate team coverage offers significant market value for patient advertising, and it is frequently publicized by orthopedic practices and hospital systems. Additionally, the importance of ACGME accreditation should also be considered.
  • Nonmedical training. This is increasingly important in subsequent subspecialty training. Further education on the business aspects of orthopedic surgery should be emphasized. Additionally, dedicated curricula on professional or leadership development are important for career progression.
  • Mentorship. Throughout the interview process, one of my foremost priorities was a strong and enduring pattern of mentorship. Fellowship offers the opportunity to establish 1 or multiple mentors in your subspecialty. These individuals will be instrumental in the development of your early professional career and your approach to clinical practice. From discussions about complicated patients to advice on contract negotiations, your ideal mentor should champion your early successes and work generously on your behalf, even long after fellowship has ended. 

  • Research opportunities. Given my academic career goals, I actively pursued a program with rich clinical and laboratory resources, and an established infrastructure for accomplishing high-quality, relevant research. Interested individuals should gauge the availability of research support staff, biomechanical or bench-level laboratory collaboration, grant or institutional research funding, cadaveric specimens, or clinical outcomes data for research conducted by fellows. However, not all fellowship applicants have a vested interest in research during fellowship, so I would encourage inquiries regarding core research requirements and expectations.
  • Clinical exposure. This encompasses several different and equally important variables, including diversity of clinical or surgical caseloads, case complexity, operative exposure, athletic team coverage, and office or clinical experience. Interestingly, this latter aspect of training is often neglected but cannot be overemphasized. Outpatient clinical evaluation is key to honing important physical examination techniques and critically evaluating patients’ outcomes postoperatively.
  • Surgical autonomy. Hands-on operative experience and surgical autonomy vary widely among fellowship programs. Most fellowships advocate for a graduated level of surgical responsibility dependent on individual abilities and staff comfort, while others offer greater potential for independence. Conversely, some programs espouse more of an “observership” model, and arthroscopic simulators and/or cadaveric skills laboratories are designed to complement operative experience. While most fellowship applicants desire maximal case participation, we must also recognize the value in watching talented surgeons performing technically demanding procedures.
  • Family. You cannot put a premium on your personal contentment and family’s well-being. Proximity to a support network can be important with the work demands and time constraints of fellowship.
 

 

Despite financial obligations and significant time commitments, the fellowship match process offers an incredible range of programs and practice environments. Inevitably, no program can completely fulfill all your criteria, but you should be able to tailor your learning style, professional ambitions, and personal preferences with an excellent training program. For many, fellowship represents the last, and perhaps most integral, stage of formal surgical training. Considering all factors of your chosen fellowship program will ensure a rich and fulfilling educational experience.

The Orthopaedic Sports Medicine Fellowship Match was first established in 2008 as a joint-sponsored venture between the American Orthopaedic Society for Sports Medicine and the Arthroscopy Association of North America to pair applicants with participating training programs.1 Operated under the San Francisco Match,2 the current fellowship match process was adopted to systematically coordinate training appointments and eliminate the role of “exploding offers,” which are pressured early decisions predicated on immediate acceptance. Other advantages of this system include its operation through a central application service to avoid redundancy of submitted paperwork, as well as to create greater awareness and to publicize training options and standardization of the match timeline.1

In its current state, the orthopedic sports medicine match represents 96 programs with 230 positions, accounting for approximately 97% of training programs and fellowship positions.1 While unaccredited options remain available through the Match, many programs have migrated towards American Council for Graduate Medical Education (ACGME) accreditation because of an increased focus on objective learning metrics during fellowship and the requirement for Subspecialty Certification in Orthopaedic Sports Medicine through the American Board of Orthopaedic Surgery.3 However, other programs have also eschewed the increasing constraints and administrative resources associated with ACGME accreditation, particularly among fellowships based at community-based hospitals or private practices that lack formal affiliation with academic institutions or residency training programs.

Along with a greater understanding of the historical background of the match process, fellowship applicants must also appreciate the relative merits of fellowship training. More than 90% of orthopedic surgery residents now pursue further subspecialty fellowship training, with some individuals opting for 2 additional fellowship opportunities.4 As a so-called “nontraditional applicant,” I represent a different demographic, returning to fellowship after years of clinical practice while serving in the military. Individual preferences notwithstanding, I wanted to take the opportunity to emphasize some important considerations in deliberating between different fellowship programs.

  • Geography. Your eventual desired practice location may play a role in determining fellowship location or, at least, region of the country. Additionally, this can be an important factor in family happiness. In competitive markets, such as the Northeast or the West Coast, you may make inroads and establish professional connections that result in potential job opportunities. Conversely, other programs may adopt anticompetitive measures to limit local practice options.
  • Training setting. Despite the trending consolidation of fellowship training programs in affiliated university and hospital-based teaching systems, many community-based programs and private-practice models thrive, providing an alternative to traditional academic training centers. The latter may provide more in-depth exposure to practice management, billing/coding, and ancillary services. The former typically offer a more structured, academically oriented environment with formal teaching conferences and a broader department hierarchy.
  • Program size. Some applicants may prefer a larger, more diverse array of teaching staff or fellows, while others gravitate toward fewer, more personal mentoring relationships that allow more intimate familiarity with practice habits or surgical techniques.
  • Associated training programs. Affiliations with a residency or physician-extender training program can offer benefits and drawbacks, including offloading clerical work, shared hands-on experience in the clinic and operating room, and midlevel supervisory responsibilities. This can offer useful opportunities to formulate an individual teaching style and valuable mentoring relationships. However, it can also impose greater time requirements or detract from one-on-one teaching with staff.
  • Reputation. Applicants may attach distinction to a well-established regional or national reputation associated with a given training program. Often, certain programs may carry prestige as a result of their academic name, hospital affiliation, or accomplishments. This can offer certain marketing advantages for patient recruitment. However, less renowned programs may provide better training opportunities and confer higher esteem among your professional colleagues. Program reputation can change dramatically with time, so this should be balanced with other potential strengths and overall training experience.
  • Practice “niches”/areas of interest. With increasing adoption of arthroscopic techniques among practicing surgeons and a relative excess of sports medicine–trained orthopedists, it is paramount to develop a novel skill set during fellowship to differentiate you from other graduates. I sought a sports medicine fellowship that would offer me a broad-based exposure to arthroscopic and open knee and shoulder reconstruction, chondral restoration techniques, hip arthroscopy and preservation, and shoulder arthroplasty. Opportunities in elbow reconstruction, foot and ankle arthroscopy, and pediatric sports medicine may also be valuable as a distinguishing factor in searching for jobs after training.
  • Marketability. Closely intertwined with reputation and scope of practice, an institution’s marketability is another intangible attribute to consider. Professional or collegiate team coverage offers significant market value for patient advertising, and it is frequently publicized by orthopedic practices and hospital systems. Additionally, the importance of ACGME accreditation should also be considered.
  • Nonmedical training. This is increasingly important in subsequent subspecialty training. Further education on the business aspects of orthopedic surgery should be emphasized. Additionally, dedicated curricula on professional or leadership development are important for career progression.
  • Mentorship. Throughout the interview process, one of my foremost priorities was a strong and enduring pattern of mentorship. Fellowship offers the opportunity to establish 1 or multiple mentors in your subspecialty. These individuals will be instrumental in the development of your early professional career and your approach to clinical practice. From discussions about complicated patients to advice on contract negotiations, your ideal mentor should champion your early successes and work generously on your behalf, even long after fellowship has ended. 

  • Research opportunities. Given my academic career goals, I actively pursued a program with rich clinical and laboratory resources, and an established infrastructure for accomplishing high-quality, relevant research. Interested individuals should gauge the availability of research support staff, biomechanical or bench-level laboratory collaboration, grant or institutional research funding, cadaveric specimens, or clinical outcomes data for research conducted by fellows. However, not all fellowship applicants have a vested interest in research during fellowship, so I would encourage inquiries regarding core research requirements and expectations.
  • Clinical exposure. This encompasses several different and equally important variables, including diversity of clinical or surgical caseloads, case complexity, operative exposure, athletic team coverage, and office or clinical experience. Interestingly, this latter aspect of training is often neglected but cannot be overemphasized. Outpatient clinical evaluation is key to honing important physical examination techniques and critically evaluating patients’ outcomes postoperatively.
  • Surgical autonomy. Hands-on operative experience and surgical autonomy vary widely among fellowship programs. Most fellowships advocate for a graduated level of surgical responsibility dependent on individual abilities and staff comfort, while others offer greater potential for independence. Conversely, some programs espouse more of an “observership” model, and arthroscopic simulators and/or cadaveric skills laboratories are designed to complement operative experience. While most fellowship applicants desire maximal case participation, we must also recognize the value in watching talented surgeons performing technically demanding procedures.
  • Family. You cannot put a premium on your personal contentment and family’s well-being. Proximity to a support network can be important with the work demands and time constraints of fellowship.
 

 

Despite financial obligations and significant time commitments, the fellowship match process offers an incredible range of programs and practice environments. Inevitably, no program can completely fulfill all your criteria, but you should be able to tailor your learning style, professional ambitions, and personal preferences with an excellent training program. For many, fellowship represents the last, and perhaps most integral, stage of formal surgical training. Considering all factors of your chosen fellowship program will ensure a rich and fulfilling educational experience.

References

1.    Sports medicine/arthroscopy fellowship match. American Orthopaedic Society for Sports Medicine website. https://www.sportsmed.org/AOSSMIMIS/Members/Members/Education/Sports_Medicine_Arthroscopy_Fellowship_Match.aspx. Accessed December 21, 2015.

2.    Orthopaedic sports medicine fellowship. SF Match website. https://www.sfmatch.org/SpecialtyInsideAll.aspx?id=11&typ=1&name=Orthopaedic%20Sports%20Medicine. Accessed December 21, 2015.

3.    Orthopaedic sports medicine. American Board of Orthopaedic Surgery website. https://www.abos.org/certification/sports-subspecialty.aspx. Accessed December 21, 2015.

4.    Hariri S, York SC, O’Connor MI, Parsley BS, McCarthy JC. Career plans of current orthopaedic residents with a focus on sex-based and generational differences. J Bone Joint Surg Am. 2011;93(5):e16.

References

1.    Sports medicine/arthroscopy fellowship match. American Orthopaedic Society for Sports Medicine website. https://www.sportsmed.org/AOSSMIMIS/Members/Members/Education/Sports_Medicine_Arthroscopy_Fellowship_Match.aspx. Accessed December 21, 2015.

2.    Orthopaedic sports medicine fellowship. SF Match website. https://www.sfmatch.org/SpecialtyInsideAll.aspx?id=11&typ=1&name=Orthopaedic%20Sports%20Medicine. Accessed December 21, 2015.

3.    Orthopaedic sports medicine. American Board of Orthopaedic Surgery website. https://www.abos.org/certification/sports-subspecialty.aspx. Accessed December 21, 2015.

4.    Hariri S, York SC, O’Connor MI, Parsley BS, McCarthy JC. Career plans of current orthopaedic residents with a focus on sex-based and generational differences. J Bone Joint Surg Am. 2011;93(5):e16.

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On Track to Professorship? A Bibliometric Analysis of Early Scholarly Output

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On Track to Professorship? A Bibliometric Analysis of Early Scholarly Output

Professors of orthopedic surgery, by dint of their elevation to the highest academic rank, are men and women of achievement. Some of these surgeons have made their professional contribution primarily as clinicians; some have excelled as teachers. The common attribute of all medical school professors, though, is academic productivity, manifest in the form of scholarly publications.

The question of how much scholarly productivity is enough is of practical concern to junior faculty members contemplating their own chances for being promoted to the rank of professor. Specifically, a junior faculty member may wonder if his or her current performance augurs well for promotion. For these young faculty members (and the mentors advising them), there are not much objective data to offer guidance.

Research within other surgical subspecialties has revealed that the Hirsch index (h-index) is correlated with promotion to full professorship status.1,2 (An author earns an h-index of h if h of his or her papers has at least h citations.3 For example, an author of 10 papers each cited once and an author of 1 paper cited 10 times both have an h-index of 1, whereas an author of 5 papers each cited 5 times has an h-index of 5, as does an author of 10 papers, 5 of which were cited 5 times or more, and 5 of which were cited 4 or fewer times.) To our knowledge, within orthopedic surgery there has been only 1 study of the relationship between early-career academic output and ultimate academic rank—a single-institution study of 130 residents showing that those pursuing academic careers published more articles during residency.4

To help address the relationship between early-career academic output and the attainment of professorship, we performed a bibliometric benchmarking analysis of current orthopedic surgery professors’ productivity at a point likely before they were promoted to that rank. In measuring the early scholarly output of these now senior surgeons, we aim to give younger faculty members a basis of comparison for their own output and thus a sense of where they stand. Although a purely bibliometric analysis must be understood as a crude measure—one that fails to capture any of a professor’s attributes in a domain other than scholarly output—it may nevertheless serve as a basis for meaningful advice.

Therefore, we performed a bibliometric analysis to determine the number of scholarly papers published by current professors of orthopedic surgery within 5 years after their having acquired American Board of Orthopaedic Surgery (ABOS) certification (termed early scholarly output). We tried to determine not only quantity (how many papers were published) but quality (how often papers were cited). Last, by comparing professors across periods, we tried to address the relevant question of whether professor-worthy early output is increasing over time.

Methods

A cohort of orthopedic surgery professors at nominally elite medical schools was constructed as follows. The U.S. News & World Report ranking list was consulted to identify the top 10 US medical schools, and in February 2014 the website of each school was accessed to identify the orthopedic surgery faculty. Names of orthopedic surgery professors were noted. The website for Duke University did not list academic ranks, so data for this school were obtained by personal communication. Whether a professor’s title included the clinical descriptor was documented.

The ABOS website was then consulted to determine which of the faculty members were board-certified. Only certified faculty members were retained.

The Web of Science research platform (wokinfo.com) was used to identify each faculty member’s early scholarly output in the field of orthopedics. After limiting the period under consideration to 5 years after the author was ABOS-certified, we performed an author search using all combinations of first and middle initials. Results were then refined by category orthopedics and document type article. To reinforce the search specificity, we manually reviewed the generated bibliography and retained only correctly identified papers.

A Web of Science citation report was then generated for the author. All bibliometric data were recorded. The quantity of early output was logged as number of papers in 1 of 3 bins: first author, last author, and middle author (any author except first or last). Quality was approximated by total number of times the author was cited across total output. In addition, number of publications in Clinical Orthopaedics and Related Research (CORR) and Journal of Bone and Joint Surgery (JBJS) was recorded.

To further make an inference about the importance of papers published in this early career window, we calculated an h-index for this “5 years post ABOS certification” bibliography. As noted, an author earns an h-index of h if h of his or her papers has at least h citations.

 

 

The faculty member was assessed for publication of any “blockbuster” research, defined as a paper that had been cited at least 50 times between publication date and present day.

Last, to assess trends, we compared our output metrics for nonclinical professors ABOS-certified before 1990 versus after 1995. Significance was set at P < .006 using a conservative Bonferroni correction. Scatter plots were generated for total publications, citations, and h-index versus time since ABOS certification. Stata Statistical Software Release 11 (StataCorp) was used to analyze the data.

Results

Of the 108 professors identified, 88 did not have a clinical designation. Within this nonclinical group, median number of total publications and total citations 5 years after ABOS certification were 11.5 (mean, 15.4; SD, 12.3) and 33.5 (mean, 87.5; SD, 130.4), respectively. This group had a median h-index of 3 (mean, 3.9; SD, 3.1). Median number of papers published in CORR and JBJS was 4 (mean, 6.2; SD, 6.2). Median number of papers cited at least 50 times was 2 (mean, 3.2; SD, 4.0). A complete bibliometric summary is detailed in Tables 1 and 2.

 

Mean certification year was 1989 (range, 1968-2005; SD, 9.1 years). T tests revealed that total publications, first-author publications, last-author publications, middle-author publications, total citations, and h­-indexes were higher (Ps < .001-.004) for those certified after 1995 (n = 30) than for those certified before 1990 (n = 39) (Table 3). Scatter plots suggested that early total publications, citations, and h-indexes were increasing over time (Figure).

 

Discussion

Publication in the medical literature is an indication of academic productivity. However, there are no data establishing early-career productivity milestones. These data would interest young faculty members aspiring to attain professor status. We conducted the present study to describe the early academic productivity of current professors of orthopedic surgery at elite medical schools.

This study had several limitations. First, using bibliometric analysis to measure merit is admittedly crude, as it fails to capture contributions in nonacademic domains. For some faculty members, achievement in nonclinical areas may be substantial, and indeed the reason for their promotion. Second, the method used here tends to emphasize quantity over quality. Although we attempted to compensate for this bias—by reporting total citations, h-indexes, and numbers of CORR, JBJS, and blockbuster publications—we could not remove it completely. Third, choice of schools was arbitrary. Fourth, the sample included only those who attained professor rank; no data are available for orthopedic surgeons who were once assistant or associate professors and were not promoted further. Thus, even if number of publications was the sole criterion for promotion, no statement can be made about the likelihood of promotion given a certain number. Meaningful inferences about a candidate’s chance for promotion (assuming that the standards have not changed) can be made only with complete data, including “failures.”

Despite its limitations, this study provided novel information that can be useful to junior faculty members. Our cohort of orthopedic surgery professors at a select group of schools published 11 papers by year 5 after ABOS certification. A faculty member was the first or last author of 7 of these papers, and 3 papers were published in CORR or JBJS. Each of the 11 papers was cited almost 30 times, and 2 of the 11 eventually received at least 50 citations each. Faculty members had an h-index of about 3 at the 5-year mark. As expected, those who were clinical professors were less academically productive (nevertheless, some had formidable achievements). As schools may have different criteria for various academic titles, it is not possible to generalize across all schools. Of particular importance is the wide range for all data categories, particularly at the low end—buttressing the idea that, at some schools, clinical or teaching work may be sufficient for promotion.

Younger professors demonstrated higher early output than their senior counterparts did, as evidenced by increases in publications of any authorship, citations, and h-indexes. However, number of publications in CORR and JBJS was stagnant, as was number of publications cited more than 50 times. These findings may parallel the proliferation of journals, publications, and citations since the digitization of scientific media. For example, number of orthopedic Medline articles nearly doubled over the period 2000–2010, from 29,471 to 55,074 per year; in addition, number of authors per JBJS article increased from 1.6 in 1949 to 5.1 in 2009.5 This inflationary landscape may impose higher expectations on young faculty members, and, though this report suggests that professor-worthy output is increasing, it makes no effort to predict future milestones.To be sure, the information presented here does not represent a complete assessment of a faculty member’s contribution. In addition, standards for promotion will be different in the future than they were in the past. Nevertheless, our study results provide the best available (though imperfect) benchmarks for professor-worthy early productivity.

References

1.    Tomei KL, Nahass MM, Husain Q, et al. A gender-based comparison of academic rank and scholarly productivity in academic neurological surgery. J Clin Neurosci. 2014;21(7):1102-1105.

2.    Svider PF, Choudhry ZA, Choudhry OJ, Baredes S, Liu JK, Eloy JA. The use of the h-index in academic otolaryngology. Laryngoscope. 2013;123(1):103-106.

3.    Sharma B, Boet S, Grantcharov T, Shin E, Barrowman NJ, Bould MD. The h-index outperforms other bibliometrics in the assessment of research performance in general surgery: a province-wide study. Surgery. 2013;153(4):493-501.

4.    Namdari S, Jani S, Baldwin K, Mehta S. What is the relationship between number of publications during orthopaedic residency and selection of an academic career? J Bone Joint Surg Am. 2013;95(7):e45.

5.    Camp M, Escott BG. Authorship proliferation in the orthopaedic literature. J Bone Joint Surg Am. 2013;95(7):e44.

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Professors of orthopedic surgery, by dint of their elevation to the highest academic rank, are men and women of achievement. Some of these surgeons have made their professional contribution primarily as clinicians; some have excelled as teachers. The common attribute of all medical school professors, though, is academic productivity, manifest in the form of scholarly publications.

The question of how much scholarly productivity is enough is of practical concern to junior faculty members contemplating their own chances for being promoted to the rank of professor. Specifically, a junior faculty member may wonder if his or her current performance augurs well for promotion. For these young faculty members (and the mentors advising them), there are not much objective data to offer guidance.

Research within other surgical subspecialties has revealed that the Hirsch index (h-index) is correlated with promotion to full professorship status.1,2 (An author earns an h-index of h if h of his or her papers has at least h citations.3 For example, an author of 10 papers each cited once and an author of 1 paper cited 10 times both have an h-index of 1, whereas an author of 5 papers each cited 5 times has an h-index of 5, as does an author of 10 papers, 5 of which were cited 5 times or more, and 5 of which were cited 4 or fewer times.) To our knowledge, within orthopedic surgery there has been only 1 study of the relationship between early-career academic output and ultimate academic rank—a single-institution study of 130 residents showing that those pursuing academic careers published more articles during residency.4

To help address the relationship between early-career academic output and the attainment of professorship, we performed a bibliometric benchmarking analysis of current orthopedic surgery professors’ productivity at a point likely before they were promoted to that rank. In measuring the early scholarly output of these now senior surgeons, we aim to give younger faculty members a basis of comparison for their own output and thus a sense of where they stand. Although a purely bibliometric analysis must be understood as a crude measure—one that fails to capture any of a professor’s attributes in a domain other than scholarly output—it may nevertheless serve as a basis for meaningful advice.

Therefore, we performed a bibliometric analysis to determine the number of scholarly papers published by current professors of orthopedic surgery within 5 years after their having acquired American Board of Orthopaedic Surgery (ABOS) certification (termed early scholarly output). We tried to determine not only quantity (how many papers were published) but quality (how often papers were cited). Last, by comparing professors across periods, we tried to address the relevant question of whether professor-worthy early output is increasing over time.

Methods

A cohort of orthopedic surgery professors at nominally elite medical schools was constructed as follows. The U.S. News & World Report ranking list was consulted to identify the top 10 US medical schools, and in February 2014 the website of each school was accessed to identify the orthopedic surgery faculty. Names of orthopedic surgery professors were noted. The website for Duke University did not list academic ranks, so data for this school were obtained by personal communication. Whether a professor’s title included the clinical descriptor was documented.

The ABOS website was then consulted to determine which of the faculty members were board-certified. Only certified faculty members were retained.

The Web of Science research platform (wokinfo.com) was used to identify each faculty member’s early scholarly output in the field of orthopedics. After limiting the period under consideration to 5 years after the author was ABOS-certified, we performed an author search using all combinations of first and middle initials. Results were then refined by category orthopedics and document type article. To reinforce the search specificity, we manually reviewed the generated bibliography and retained only correctly identified papers.

A Web of Science citation report was then generated for the author. All bibliometric data were recorded. The quantity of early output was logged as number of papers in 1 of 3 bins: first author, last author, and middle author (any author except first or last). Quality was approximated by total number of times the author was cited across total output. In addition, number of publications in Clinical Orthopaedics and Related Research (CORR) and Journal of Bone and Joint Surgery (JBJS) was recorded.

To further make an inference about the importance of papers published in this early career window, we calculated an h-index for this “5 years post ABOS certification” bibliography. As noted, an author earns an h-index of h if h of his or her papers has at least h citations.

 

 

The faculty member was assessed for publication of any “blockbuster” research, defined as a paper that had been cited at least 50 times between publication date and present day.

Last, to assess trends, we compared our output metrics for nonclinical professors ABOS-certified before 1990 versus after 1995. Significance was set at P < .006 using a conservative Bonferroni correction. Scatter plots were generated for total publications, citations, and h-index versus time since ABOS certification. Stata Statistical Software Release 11 (StataCorp) was used to analyze the data.

Results

Of the 108 professors identified, 88 did not have a clinical designation. Within this nonclinical group, median number of total publications and total citations 5 years after ABOS certification were 11.5 (mean, 15.4; SD, 12.3) and 33.5 (mean, 87.5; SD, 130.4), respectively. This group had a median h-index of 3 (mean, 3.9; SD, 3.1). Median number of papers published in CORR and JBJS was 4 (mean, 6.2; SD, 6.2). Median number of papers cited at least 50 times was 2 (mean, 3.2; SD, 4.0). A complete bibliometric summary is detailed in Tables 1 and 2.

 

Mean certification year was 1989 (range, 1968-2005; SD, 9.1 years). T tests revealed that total publications, first-author publications, last-author publications, middle-author publications, total citations, and h­-indexes were higher (Ps < .001-.004) for those certified after 1995 (n = 30) than for those certified before 1990 (n = 39) (Table 3). Scatter plots suggested that early total publications, citations, and h-indexes were increasing over time (Figure).

 

Discussion

Publication in the medical literature is an indication of academic productivity. However, there are no data establishing early-career productivity milestones. These data would interest young faculty members aspiring to attain professor status. We conducted the present study to describe the early academic productivity of current professors of orthopedic surgery at elite medical schools.

This study had several limitations. First, using bibliometric analysis to measure merit is admittedly crude, as it fails to capture contributions in nonacademic domains. For some faculty members, achievement in nonclinical areas may be substantial, and indeed the reason for their promotion. Second, the method used here tends to emphasize quantity over quality. Although we attempted to compensate for this bias—by reporting total citations, h-indexes, and numbers of CORR, JBJS, and blockbuster publications—we could not remove it completely. Third, choice of schools was arbitrary. Fourth, the sample included only those who attained professor rank; no data are available for orthopedic surgeons who were once assistant or associate professors and were not promoted further. Thus, even if number of publications was the sole criterion for promotion, no statement can be made about the likelihood of promotion given a certain number. Meaningful inferences about a candidate’s chance for promotion (assuming that the standards have not changed) can be made only with complete data, including “failures.”

Despite its limitations, this study provided novel information that can be useful to junior faculty members. Our cohort of orthopedic surgery professors at a select group of schools published 11 papers by year 5 after ABOS certification. A faculty member was the first or last author of 7 of these papers, and 3 papers were published in CORR or JBJS. Each of the 11 papers was cited almost 30 times, and 2 of the 11 eventually received at least 50 citations each. Faculty members had an h-index of about 3 at the 5-year mark. As expected, those who were clinical professors were less academically productive (nevertheless, some had formidable achievements). As schools may have different criteria for various academic titles, it is not possible to generalize across all schools. Of particular importance is the wide range for all data categories, particularly at the low end—buttressing the idea that, at some schools, clinical or teaching work may be sufficient for promotion.

Younger professors demonstrated higher early output than their senior counterparts did, as evidenced by increases in publications of any authorship, citations, and h-indexes. However, number of publications in CORR and JBJS was stagnant, as was number of publications cited more than 50 times. These findings may parallel the proliferation of journals, publications, and citations since the digitization of scientific media. For example, number of orthopedic Medline articles nearly doubled over the period 2000–2010, from 29,471 to 55,074 per year; in addition, number of authors per JBJS article increased from 1.6 in 1949 to 5.1 in 2009.5 This inflationary landscape may impose higher expectations on young faculty members, and, though this report suggests that professor-worthy output is increasing, it makes no effort to predict future milestones.To be sure, the information presented here does not represent a complete assessment of a faculty member’s contribution. In addition, standards for promotion will be different in the future than they were in the past. Nevertheless, our study results provide the best available (though imperfect) benchmarks for professor-worthy early productivity.

Professors of orthopedic surgery, by dint of their elevation to the highest academic rank, are men and women of achievement. Some of these surgeons have made their professional contribution primarily as clinicians; some have excelled as teachers. The common attribute of all medical school professors, though, is academic productivity, manifest in the form of scholarly publications.

The question of how much scholarly productivity is enough is of practical concern to junior faculty members contemplating their own chances for being promoted to the rank of professor. Specifically, a junior faculty member may wonder if his or her current performance augurs well for promotion. For these young faculty members (and the mentors advising them), there are not much objective data to offer guidance.

Research within other surgical subspecialties has revealed that the Hirsch index (h-index) is correlated with promotion to full professorship status.1,2 (An author earns an h-index of h if h of his or her papers has at least h citations.3 For example, an author of 10 papers each cited once and an author of 1 paper cited 10 times both have an h-index of 1, whereas an author of 5 papers each cited 5 times has an h-index of 5, as does an author of 10 papers, 5 of which were cited 5 times or more, and 5 of which were cited 4 or fewer times.) To our knowledge, within orthopedic surgery there has been only 1 study of the relationship between early-career academic output and ultimate academic rank—a single-institution study of 130 residents showing that those pursuing academic careers published more articles during residency.4

To help address the relationship between early-career academic output and the attainment of professorship, we performed a bibliometric benchmarking analysis of current orthopedic surgery professors’ productivity at a point likely before they were promoted to that rank. In measuring the early scholarly output of these now senior surgeons, we aim to give younger faculty members a basis of comparison for their own output and thus a sense of where they stand. Although a purely bibliometric analysis must be understood as a crude measure—one that fails to capture any of a professor’s attributes in a domain other than scholarly output—it may nevertheless serve as a basis for meaningful advice.

Therefore, we performed a bibliometric analysis to determine the number of scholarly papers published by current professors of orthopedic surgery within 5 years after their having acquired American Board of Orthopaedic Surgery (ABOS) certification (termed early scholarly output). We tried to determine not only quantity (how many papers were published) but quality (how often papers were cited). Last, by comparing professors across periods, we tried to address the relevant question of whether professor-worthy early output is increasing over time.

Methods

A cohort of orthopedic surgery professors at nominally elite medical schools was constructed as follows. The U.S. News & World Report ranking list was consulted to identify the top 10 US medical schools, and in February 2014 the website of each school was accessed to identify the orthopedic surgery faculty. Names of orthopedic surgery professors were noted. The website for Duke University did not list academic ranks, so data for this school were obtained by personal communication. Whether a professor’s title included the clinical descriptor was documented.

The ABOS website was then consulted to determine which of the faculty members were board-certified. Only certified faculty members were retained.

The Web of Science research platform (wokinfo.com) was used to identify each faculty member’s early scholarly output in the field of orthopedics. After limiting the period under consideration to 5 years after the author was ABOS-certified, we performed an author search using all combinations of first and middle initials. Results were then refined by category orthopedics and document type article. To reinforce the search specificity, we manually reviewed the generated bibliography and retained only correctly identified papers.

A Web of Science citation report was then generated for the author. All bibliometric data were recorded. The quantity of early output was logged as number of papers in 1 of 3 bins: first author, last author, and middle author (any author except first or last). Quality was approximated by total number of times the author was cited across total output. In addition, number of publications in Clinical Orthopaedics and Related Research (CORR) and Journal of Bone and Joint Surgery (JBJS) was recorded.

To further make an inference about the importance of papers published in this early career window, we calculated an h-index for this “5 years post ABOS certification” bibliography. As noted, an author earns an h-index of h if h of his or her papers has at least h citations.

 

 

The faculty member was assessed for publication of any “blockbuster” research, defined as a paper that had been cited at least 50 times between publication date and present day.

Last, to assess trends, we compared our output metrics for nonclinical professors ABOS-certified before 1990 versus after 1995. Significance was set at P < .006 using a conservative Bonferroni correction. Scatter plots were generated for total publications, citations, and h-index versus time since ABOS certification. Stata Statistical Software Release 11 (StataCorp) was used to analyze the data.

Results

Of the 108 professors identified, 88 did not have a clinical designation. Within this nonclinical group, median number of total publications and total citations 5 years after ABOS certification were 11.5 (mean, 15.4; SD, 12.3) and 33.5 (mean, 87.5; SD, 130.4), respectively. This group had a median h-index of 3 (mean, 3.9; SD, 3.1). Median number of papers published in CORR and JBJS was 4 (mean, 6.2; SD, 6.2). Median number of papers cited at least 50 times was 2 (mean, 3.2; SD, 4.0). A complete bibliometric summary is detailed in Tables 1 and 2.

 

Mean certification year was 1989 (range, 1968-2005; SD, 9.1 years). T tests revealed that total publications, first-author publications, last-author publications, middle-author publications, total citations, and h­-indexes were higher (Ps < .001-.004) for those certified after 1995 (n = 30) than for those certified before 1990 (n = 39) (Table 3). Scatter plots suggested that early total publications, citations, and h-indexes were increasing over time (Figure).

 

Discussion

Publication in the medical literature is an indication of academic productivity. However, there are no data establishing early-career productivity milestones. These data would interest young faculty members aspiring to attain professor status. We conducted the present study to describe the early academic productivity of current professors of orthopedic surgery at elite medical schools.

This study had several limitations. First, using bibliometric analysis to measure merit is admittedly crude, as it fails to capture contributions in nonacademic domains. For some faculty members, achievement in nonclinical areas may be substantial, and indeed the reason for their promotion. Second, the method used here tends to emphasize quantity over quality. Although we attempted to compensate for this bias—by reporting total citations, h-indexes, and numbers of CORR, JBJS, and blockbuster publications—we could not remove it completely. Third, choice of schools was arbitrary. Fourth, the sample included only those who attained professor rank; no data are available for orthopedic surgeons who were once assistant or associate professors and were not promoted further. Thus, even if number of publications was the sole criterion for promotion, no statement can be made about the likelihood of promotion given a certain number. Meaningful inferences about a candidate’s chance for promotion (assuming that the standards have not changed) can be made only with complete data, including “failures.”

Despite its limitations, this study provided novel information that can be useful to junior faculty members. Our cohort of orthopedic surgery professors at a select group of schools published 11 papers by year 5 after ABOS certification. A faculty member was the first or last author of 7 of these papers, and 3 papers were published in CORR or JBJS. Each of the 11 papers was cited almost 30 times, and 2 of the 11 eventually received at least 50 citations each. Faculty members had an h-index of about 3 at the 5-year mark. As expected, those who were clinical professors were less academically productive (nevertheless, some had formidable achievements). As schools may have different criteria for various academic titles, it is not possible to generalize across all schools. Of particular importance is the wide range for all data categories, particularly at the low end—buttressing the idea that, at some schools, clinical or teaching work may be sufficient for promotion.

Younger professors demonstrated higher early output than their senior counterparts did, as evidenced by increases in publications of any authorship, citations, and h-indexes. However, number of publications in CORR and JBJS was stagnant, as was number of publications cited more than 50 times. These findings may parallel the proliferation of journals, publications, and citations since the digitization of scientific media. For example, number of orthopedic Medline articles nearly doubled over the period 2000–2010, from 29,471 to 55,074 per year; in addition, number of authors per JBJS article increased from 1.6 in 1949 to 5.1 in 2009.5 This inflationary landscape may impose higher expectations on young faculty members, and, though this report suggests that professor-worthy output is increasing, it makes no effort to predict future milestones.To be sure, the information presented here does not represent a complete assessment of a faculty member’s contribution. In addition, standards for promotion will be different in the future than they were in the past. Nevertheless, our study results provide the best available (though imperfect) benchmarks for professor-worthy early productivity.

References

1.    Tomei KL, Nahass MM, Husain Q, et al. A gender-based comparison of academic rank and scholarly productivity in academic neurological surgery. J Clin Neurosci. 2014;21(7):1102-1105.

2.    Svider PF, Choudhry ZA, Choudhry OJ, Baredes S, Liu JK, Eloy JA. The use of the h-index in academic otolaryngology. Laryngoscope. 2013;123(1):103-106.

3.    Sharma B, Boet S, Grantcharov T, Shin E, Barrowman NJ, Bould MD. The h-index outperforms other bibliometrics in the assessment of research performance in general surgery: a province-wide study. Surgery. 2013;153(4):493-501.

4.    Namdari S, Jani S, Baldwin K, Mehta S. What is the relationship between number of publications during orthopaedic residency and selection of an academic career? J Bone Joint Surg Am. 2013;95(7):e45.

5.    Camp M, Escott BG. Authorship proliferation in the orthopaedic literature. J Bone Joint Surg Am. 2013;95(7):e44.

References

1.    Tomei KL, Nahass MM, Husain Q, et al. A gender-based comparison of academic rank and scholarly productivity in academic neurological surgery. J Clin Neurosci. 2014;21(7):1102-1105.

2.    Svider PF, Choudhry ZA, Choudhry OJ, Baredes S, Liu JK, Eloy JA. The use of the h-index in academic otolaryngology. Laryngoscope. 2013;123(1):103-106.

3.    Sharma B, Boet S, Grantcharov T, Shin E, Barrowman NJ, Bould MD. The h-index outperforms other bibliometrics in the assessment of research performance in general surgery: a province-wide study. Surgery. 2013;153(4):493-501.

4.    Namdari S, Jani S, Baldwin K, Mehta S. What is the relationship between number of publications during orthopaedic residency and selection of an academic career? J Bone Joint Surg Am. 2013;95(7):e45.

5.    Camp M, Escott BG. Authorship proliferation in the orthopaedic literature. J Bone Joint Surg Am. 2013;95(7):e44.

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Q) Recently, I have seen four or five Asian-American patients with really bad kidney function. All of them were thin but had diabetes, hypertension, and a serum creatinine > 2 mg/dL. The kidney disease was a shock to them (and me). Am I missing something here?

Diabetes and hypertension are the most common causes of chronic kidney disease (CKD), with diabetes slightly edging out hypertension for the number 1 slot.1 Although Asian Americans have a tendency toward a lower body mass index (BMI) than the general population, this does not exclude them from developing diabetes or hypertension.

About 20% (1 in 5) of Asian-American adults have both diabetes and hypertension. In fact, Asian Americans with a BMI ≤ 25 often develop type 2 diabetes (T2DM), which is a direct contrast to other racial and ethnic groups in whom T2DM is more prevalent at higher BMIs. The current thinking is that Asian Americans have a higher percentage of body fat at lower BMIs.2 Among racial and ethnic subgroups, Asian Americans have the highest prevalence of undiagnosed diabetes (close to 50%).2

In 2004, after adjusting for lower BMI, McNeely and Boyko found that the incidence of diabetes in Asian Americans was 60% higher than in the Hispanic population.3 In 2015, this influenced the American Diabetes Association (ADA) to change its recommendation for diabetes screening in Asian Americans, lowering the threshold to a BMI of 23.4

Since abdominal or visceral fat is a risk factor for heart disease, hypertension, and diabetes, and it appears that the Asian-American population carries excess fat centrally, this population is also at risk for cardiac disease.5 For that reason, in this population, the American Heart Association recommends measuring waist circumference to screen for hidden abdominal adiposity.6

Thus, the trend you are seeing in your patient population is really only the tip of the iceberg. The Asian-American population is the fastest-growing ethnic group in the United States.3 It’s time to update your diabetes screening protocols. —SWM

Shushanne Wynter-Minott, DNP, FNP-BC
Memorial Healthcare System, Hollywood, Florida

References
1. CDC. National Chronic Kidney Disease Fact Sheet, 2014. www.cdc.gov/diabetes/pubs/pdf/kidney_Factsheet.pdf. Accessed February 3, 2016.
2. Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-1029.
3. McNeely MJ, Boyko EJ. Type 2 diabetes prevalence in Asian Americans: results of a national health survey. Diabetes Care. 2004;27(1):66-69.
4. American Diabetes Association. Standards of medical care in diabetes­­—2015: summary of revisions. Diabetes Care. 2015;38(suppl):S4.
5. Park YW, Allison DB, Heymsfield SB, Gallagher D. Larger amounts of visceral adipose tissue in Asian Americans. Obes Res. 2001;9(7):381-387.
6. Rao G, Powell-Wiley TM, Ancheta I, et al; American Heart Association Obesity Committee of the Council on Lifestyle and Cardiometabolic Health. Identification of obesity and cardiovascular risk in ethnically and racially diverse populations: a scientific statement from the American Heart Association. Circulation. 2015;132(5):457-472.

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Q) Recently, I have seen four or five Asian-American patients with really bad kidney function. All of them were thin but had diabetes, hypertension, and a serum creatinine > 2 mg/dL. The kidney disease was a shock to them (and me). Am I missing something here?

Diabetes and hypertension are the most common causes of chronic kidney disease (CKD), with diabetes slightly edging out hypertension for the number 1 slot.1 Although Asian Americans have a tendency toward a lower body mass index (BMI) than the general population, this does not exclude them from developing diabetes or hypertension.

About 20% (1 in 5) of Asian-American adults have both diabetes and hypertension. In fact, Asian Americans with a BMI ≤ 25 often develop type 2 diabetes (T2DM), which is a direct contrast to other racial and ethnic groups in whom T2DM is more prevalent at higher BMIs. The current thinking is that Asian Americans have a higher percentage of body fat at lower BMIs.2 Among racial and ethnic subgroups, Asian Americans have the highest prevalence of undiagnosed diabetes (close to 50%).2

In 2004, after adjusting for lower BMI, McNeely and Boyko found that the incidence of diabetes in Asian Americans was 60% higher than in the Hispanic population.3 In 2015, this influenced the American Diabetes Association (ADA) to change its recommendation for diabetes screening in Asian Americans, lowering the threshold to a BMI of 23.4

Since abdominal or visceral fat is a risk factor for heart disease, hypertension, and diabetes, and it appears that the Asian-American population carries excess fat centrally, this population is also at risk for cardiac disease.5 For that reason, in this population, the American Heart Association recommends measuring waist circumference to screen for hidden abdominal adiposity.6

Thus, the trend you are seeing in your patient population is really only the tip of the iceberg. The Asian-American population is the fastest-growing ethnic group in the United States.3 It’s time to update your diabetes screening protocols. —SWM

Shushanne Wynter-Minott, DNP, FNP-BC
Memorial Healthcare System, Hollywood, Florida

References
1. CDC. National Chronic Kidney Disease Fact Sheet, 2014. www.cdc.gov/diabetes/pubs/pdf/kidney_Factsheet.pdf. Accessed February 3, 2016.
2. Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-1029.
3. McNeely MJ, Boyko EJ. Type 2 diabetes prevalence in Asian Americans: results of a national health survey. Diabetes Care. 2004;27(1):66-69.
4. American Diabetes Association. Standards of medical care in diabetes­­—2015: summary of revisions. Diabetes Care. 2015;38(suppl):S4.
5. Park YW, Allison DB, Heymsfield SB, Gallagher D. Larger amounts of visceral adipose tissue in Asian Americans. Obes Res. 2001;9(7):381-387.
6. Rao G, Powell-Wiley TM, Ancheta I, et al; American Heart Association Obesity Committee of the Council on Lifestyle and Cardiometabolic Health. Identification of obesity and cardiovascular risk in ethnically and racially diverse populations: a scientific statement from the American Heart Association. Circulation. 2015;132(5):457-472.

Q) Recently, I have seen four or five Asian-American patients with really bad kidney function. All of them were thin but had diabetes, hypertension, and a serum creatinine > 2 mg/dL. The kidney disease was a shock to them (and me). Am I missing something here?

Diabetes and hypertension are the most common causes of chronic kidney disease (CKD), with diabetes slightly edging out hypertension for the number 1 slot.1 Although Asian Americans have a tendency toward a lower body mass index (BMI) than the general population, this does not exclude them from developing diabetes or hypertension.

About 20% (1 in 5) of Asian-American adults have both diabetes and hypertension. In fact, Asian Americans with a BMI ≤ 25 often develop type 2 diabetes (T2DM), which is a direct contrast to other racial and ethnic groups in whom T2DM is more prevalent at higher BMIs. The current thinking is that Asian Americans have a higher percentage of body fat at lower BMIs.2 Among racial and ethnic subgroups, Asian Americans have the highest prevalence of undiagnosed diabetes (close to 50%).2

In 2004, after adjusting for lower BMI, McNeely and Boyko found that the incidence of diabetes in Asian Americans was 60% higher than in the Hispanic population.3 In 2015, this influenced the American Diabetes Association (ADA) to change its recommendation for diabetes screening in Asian Americans, lowering the threshold to a BMI of 23.4

Since abdominal or visceral fat is a risk factor for heart disease, hypertension, and diabetes, and it appears that the Asian-American population carries excess fat centrally, this population is also at risk for cardiac disease.5 For that reason, in this population, the American Heart Association recommends measuring waist circumference to screen for hidden abdominal adiposity.6

Thus, the trend you are seeing in your patient population is really only the tip of the iceberg. The Asian-American population is the fastest-growing ethnic group in the United States.3 It’s time to update your diabetes screening protocols. —SWM

Shushanne Wynter-Minott, DNP, FNP-BC
Memorial Healthcare System, Hollywood, Florida

References
1. CDC. National Chronic Kidney Disease Fact Sheet, 2014. www.cdc.gov/diabetes/pubs/pdf/kidney_Factsheet.pdf. Accessed February 3, 2016.
2. Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-1029.
3. McNeely MJ, Boyko EJ. Type 2 diabetes prevalence in Asian Americans: results of a national health survey. Diabetes Care. 2004;27(1):66-69.
4. American Diabetes Association. Standards of medical care in diabetes­­—2015: summary of revisions. Diabetes Care. 2015;38(suppl):S4.
5. Park YW, Allison DB, Heymsfield SB, Gallagher D. Larger amounts of visceral adipose tissue in Asian Americans. Obes Res. 2001;9(7):381-387.
6. Rao G, Powell-Wiley TM, Ancheta I, et al; American Heart Association Obesity Committee of the Council on Lifestyle and Cardiometabolic Health. Identification of obesity and cardiovascular risk in ethnically and racially diverse populations: a scientific statement from the American Heart Association. Circulation. 2015;132(5):457-472.

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Q) We were operating on a 58-year-old woman for a subcapital fracture of her right hip. The orthopedist mentioned that the patient had kidney disease and that it probably caused her hip fracture. I didn’t know kidney disease causes hip fractures. Is this true?

Evolving evidence suggests an association between diminishing renal function and increased risk for fracture. Here’s a look at the available data:

Atherosclerosis Risk in Communities (ARIC) Study. During a median 13 years’ follow-up of 10,955 community-based older adults, investigators identified higher albuminuria level and decreased creatinine-based estimated glomerular filtration rate (eGFR) as significant risk factors for fracture. Other risk factors included older age, race (Caucasians had the highest incidence), and sex (women were more likely than men to sustain a fracture). A nonlinear relationship was observed between eGFR and fracture diagnosis, with a graded association between fracture and albuminuria level.7

Cardiovascular Health Study. In this study of 4,699 older community-based adults, kidney function was assessed by measurement of serum cystatin C. During a mean follow-up of 7.1 years, higher cystatin C levels correlated to a higher risk for hip fracture in both sexes. In women, there was a significant association between diminishing renal function and hip fracture status: Those with lower eGFRs had a higher incidence of fractures. There was a similar magnitude of association among men, but it was not ­significant.8

Health, Aging and Body Composite Study. In 2,754 older adults, an association was noted between decreased femoral neck bone mineral density (BMD) and increased risk for fracture in those with and without CKD stage 3 to 5. With a concurrent diagnosis of osteoporosis, there was a 110% increased risk for nonspinal fracture in those with CKD and a 63% increased risk for those without CKD.9 In a study of 485 adult hemodialysis patients, decreased total hip and femoral neck BMD was associated with an increased risk for fractures in women with parathyroid hormone levels on the lower range of acceptable in this population (intact parathyroid hormone level [IPTH] < 204 pg/mL) and for spinal fractures in both genders.10

Bone changes associated with deterioration of renal function are complex and multifactorial. Human bone is a composite of protein fused to mineral crystals, primarily calcium and phosphate. Bone is dynamic, being broken down and rebuilt throughout adulthood, with the skeleton almost completely rebuilt every 10 years.11

CKD–mineral and bone disorder (CKD–MBD) is a systemic disorder seen in those with kidney disease that affects bone and mineral metabolism. Its manifestations include abnormalities in the bone, calcifications of vascular and/or soft tissues, abnormal vitamin D metabolism, and disruptions in the phosphorus, calcium, and parathyroid hormone levels. These components, and the severity of the condition, vary by stage of CKD. One component of CKD–MBD, renal osteodystrophy, is associated with changes in bone morphology and is definitively diagnosed by bone biopsy.12

Care of these patients is complex and can be compounded by osteoporosis and/or loss of bone strength. Osteoporosis, like CKD, increases in incidence with age and is associated with fracture risk.11

While useful for diagnosing osteoporosis and predicting fracture risk in the general population, dual-energy X-ray densitometry (DXA) has not been recommended in those with CKD due to the type of bone changes that occur with diminished renal function.12 However, evolving evidence regarding use of DXA in these patients prompted a Kidney Disease: Improving Global Outcomes (KDIGO) “controversies” conference to recommend reexamination of the evidence regarding this recommendation.13 KDIGO’s 2009 clinical practice guideline on CKD–MBD (http://kdigo.org/home/mineral-bone-disorder/) can be of benefit in the assessment and care of affected patients. —CS

Cindy Smith, DNP, APRN, CNN-NP, FNP-BC
Renal Consultants, PLLC, South Charleston, West Virgina

References
7. Daya NR, Voskertchian A, Schneider ALC, et al. Kidney function and fracture risk: the Atherosclerosis Risk in Communities (ARIC) study. Am J Kidney Dis. 2016;67(2):218-226.
8. Fried LF, Biggs ML, Shlipak MG, et al. Association of kidney function with incident hip fracture in older adults. J Am Soc Nephrol. 2007;18:282-286.
9. Yenchek RH, Ix JH, Shlipak MG, et al. Bone mineral density and fracture risk in older individuals with CKD. Clin J Am Soc Nephrol. 2012;7(7):1130-1136.
10. Iimori S, Mori Y, Akita W, et al. Diagnostic usefulness of bone mineral density and biochemical markers of bone turnover in predicting fracture in CKD stage 5D patients­­—a single-center cohort study. Nephrol Dial Transplant. 2012;27:345-351.
11. Office of the Surgeon General (US). Bone Health and Osteoporosis: a Report of the Surgeon General. Rockville, MD: Office of the Surgeon General; 2004.
12. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl. 2009;113:S1-S130.
13. Ketteler M, Elder GJ, Evenepoel P, et al. Revisiting KDIGO clinical practice guideline on chronic kidney disease-mineral and bone disorder: a commentary from a Kidney Disease: Improving Global Outcomes controversies conference. Kidney Int. 2015;87(3):502-528.

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Q) We were operating on a 58-year-old woman for a subcapital fracture of her right hip. The orthopedist mentioned that the patient had kidney disease and that it probably caused her hip fracture. I didn’t know kidney disease causes hip fractures. Is this true?

Evolving evidence suggests an association between diminishing renal function and increased risk for fracture. Here’s a look at the available data:

Atherosclerosis Risk in Communities (ARIC) Study. During a median 13 years’ follow-up of 10,955 community-based older adults, investigators identified higher albuminuria level and decreased creatinine-based estimated glomerular filtration rate (eGFR) as significant risk factors for fracture. Other risk factors included older age, race (Caucasians had the highest incidence), and sex (women were more likely than men to sustain a fracture). A nonlinear relationship was observed between eGFR and fracture diagnosis, with a graded association between fracture and albuminuria level.7

Cardiovascular Health Study. In this study of 4,699 older community-based adults, kidney function was assessed by measurement of serum cystatin C. During a mean follow-up of 7.1 years, higher cystatin C levels correlated to a higher risk for hip fracture in both sexes. In women, there was a significant association between diminishing renal function and hip fracture status: Those with lower eGFRs had a higher incidence of fractures. There was a similar magnitude of association among men, but it was not ­significant.8

Health, Aging and Body Composite Study. In 2,754 older adults, an association was noted between decreased femoral neck bone mineral density (BMD) and increased risk for fracture in those with and without CKD stage 3 to 5. With a concurrent diagnosis of osteoporosis, there was a 110% increased risk for nonspinal fracture in those with CKD and a 63% increased risk for those without CKD.9 In a study of 485 adult hemodialysis patients, decreased total hip and femoral neck BMD was associated with an increased risk for fractures in women with parathyroid hormone levels on the lower range of acceptable in this population (intact parathyroid hormone level [IPTH] < 204 pg/mL) and for spinal fractures in both genders.10

Bone changes associated with deterioration of renal function are complex and multifactorial. Human bone is a composite of protein fused to mineral crystals, primarily calcium and phosphate. Bone is dynamic, being broken down and rebuilt throughout adulthood, with the skeleton almost completely rebuilt every 10 years.11

CKD–mineral and bone disorder (CKD–MBD) is a systemic disorder seen in those with kidney disease that affects bone and mineral metabolism. Its manifestations include abnormalities in the bone, calcifications of vascular and/or soft tissues, abnormal vitamin D metabolism, and disruptions in the phosphorus, calcium, and parathyroid hormone levels. These components, and the severity of the condition, vary by stage of CKD. One component of CKD–MBD, renal osteodystrophy, is associated with changes in bone morphology and is definitively diagnosed by bone biopsy.12

Care of these patients is complex and can be compounded by osteoporosis and/or loss of bone strength. Osteoporosis, like CKD, increases in incidence with age and is associated with fracture risk.11

While useful for diagnosing osteoporosis and predicting fracture risk in the general population, dual-energy X-ray densitometry (DXA) has not been recommended in those with CKD due to the type of bone changes that occur with diminished renal function.12 However, evolving evidence regarding use of DXA in these patients prompted a Kidney Disease: Improving Global Outcomes (KDIGO) “controversies” conference to recommend reexamination of the evidence regarding this recommendation.13 KDIGO’s 2009 clinical practice guideline on CKD–MBD (http://kdigo.org/home/mineral-bone-disorder/) can be of benefit in the assessment and care of affected patients. —CS

Cindy Smith, DNP, APRN, CNN-NP, FNP-BC
Renal Consultants, PLLC, South Charleston, West Virgina

References
7. Daya NR, Voskertchian A, Schneider ALC, et al. Kidney function and fracture risk: the Atherosclerosis Risk in Communities (ARIC) study. Am J Kidney Dis. 2016;67(2):218-226.
8. Fried LF, Biggs ML, Shlipak MG, et al. Association of kidney function with incident hip fracture in older adults. J Am Soc Nephrol. 2007;18:282-286.
9. Yenchek RH, Ix JH, Shlipak MG, et al. Bone mineral density and fracture risk in older individuals with CKD. Clin J Am Soc Nephrol. 2012;7(7):1130-1136.
10. Iimori S, Mori Y, Akita W, et al. Diagnostic usefulness of bone mineral density and biochemical markers of bone turnover in predicting fracture in CKD stage 5D patients­­—a single-center cohort study. Nephrol Dial Transplant. 2012;27:345-351.
11. Office of the Surgeon General (US). Bone Health and Osteoporosis: a Report of the Surgeon General. Rockville, MD: Office of the Surgeon General; 2004.
12. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl. 2009;113:S1-S130.
13. Ketteler M, Elder GJ, Evenepoel P, et al. Revisiting KDIGO clinical practice guideline on chronic kidney disease-mineral and bone disorder: a commentary from a Kidney Disease: Improving Global Outcomes controversies conference. Kidney Int. 2015;87(3):502-528.

Q) We were operating on a 58-year-old woman for a subcapital fracture of her right hip. The orthopedist mentioned that the patient had kidney disease and that it probably caused her hip fracture. I didn’t know kidney disease causes hip fractures. Is this true?

Evolving evidence suggests an association between diminishing renal function and increased risk for fracture. Here’s a look at the available data:

Atherosclerosis Risk in Communities (ARIC) Study. During a median 13 years’ follow-up of 10,955 community-based older adults, investigators identified higher albuminuria level and decreased creatinine-based estimated glomerular filtration rate (eGFR) as significant risk factors for fracture. Other risk factors included older age, race (Caucasians had the highest incidence), and sex (women were more likely than men to sustain a fracture). A nonlinear relationship was observed between eGFR and fracture diagnosis, with a graded association between fracture and albuminuria level.7

Cardiovascular Health Study. In this study of 4,699 older community-based adults, kidney function was assessed by measurement of serum cystatin C. During a mean follow-up of 7.1 years, higher cystatin C levels correlated to a higher risk for hip fracture in both sexes. In women, there was a significant association between diminishing renal function and hip fracture status: Those with lower eGFRs had a higher incidence of fractures. There was a similar magnitude of association among men, but it was not ­significant.8

Health, Aging and Body Composite Study. In 2,754 older adults, an association was noted between decreased femoral neck bone mineral density (BMD) and increased risk for fracture in those with and without CKD stage 3 to 5. With a concurrent diagnosis of osteoporosis, there was a 110% increased risk for nonspinal fracture in those with CKD and a 63% increased risk for those without CKD.9 In a study of 485 adult hemodialysis patients, decreased total hip and femoral neck BMD was associated with an increased risk for fractures in women with parathyroid hormone levels on the lower range of acceptable in this population (intact parathyroid hormone level [IPTH] < 204 pg/mL) and for spinal fractures in both genders.10

Bone changes associated with deterioration of renal function are complex and multifactorial. Human bone is a composite of protein fused to mineral crystals, primarily calcium and phosphate. Bone is dynamic, being broken down and rebuilt throughout adulthood, with the skeleton almost completely rebuilt every 10 years.11

CKD–mineral and bone disorder (CKD–MBD) is a systemic disorder seen in those with kidney disease that affects bone and mineral metabolism. Its manifestations include abnormalities in the bone, calcifications of vascular and/or soft tissues, abnormal vitamin D metabolism, and disruptions in the phosphorus, calcium, and parathyroid hormone levels. These components, and the severity of the condition, vary by stage of CKD. One component of CKD–MBD, renal osteodystrophy, is associated with changes in bone morphology and is definitively diagnosed by bone biopsy.12

Care of these patients is complex and can be compounded by osteoporosis and/or loss of bone strength. Osteoporosis, like CKD, increases in incidence with age and is associated with fracture risk.11

While useful for diagnosing osteoporosis and predicting fracture risk in the general population, dual-energy X-ray densitometry (DXA) has not been recommended in those with CKD due to the type of bone changes that occur with diminished renal function.12 However, evolving evidence regarding use of DXA in these patients prompted a Kidney Disease: Improving Global Outcomes (KDIGO) “controversies” conference to recommend reexamination of the evidence regarding this recommendation.13 KDIGO’s 2009 clinical practice guideline on CKD–MBD (http://kdigo.org/home/mineral-bone-disorder/) can be of benefit in the assessment and care of affected patients. —CS

Cindy Smith, DNP, APRN, CNN-NP, FNP-BC
Renal Consultants, PLLC, South Charleston, West Virgina

References
7. Daya NR, Voskertchian A, Schneider ALC, et al. Kidney function and fracture risk: the Atherosclerosis Risk in Communities (ARIC) study. Am J Kidney Dis. 2016;67(2):218-226.
8. Fried LF, Biggs ML, Shlipak MG, et al. Association of kidney function with incident hip fracture in older adults. J Am Soc Nephrol. 2007;18:282-286.
9. Yenchek RH, Ix JH, Shlipak MG, et al. Bone mineral density and fracture risk in older individuals with CKD. Clin J Am Soc Nephrol. 2012;7(7):1130-1136.
10. Iimori S, Mori Y, Akita W, et al. Diagnostic usefulness of bone mineral density and biochemical markers of bone turnover in predicting fracture in CKD stage 5D patients­­—a single-center cohort study. Nephrol Dial Transplant. 2012;27:345-351.
11. Office of the Surgeon General (US). Bone Health and Osteoporosis: a Report of the Surgeon General. Rockville, MD: Office of the Surgeon General; 2004.
12. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl. 2009;113:S1-S130.
13. Ketteler M, Elder GJ, Evenepoel P, et al. Revisiting KDIGO clinical practice guideline on chronic kidney disease-mineral and bone disorder: a commentary from a Kidney Disease: Improving Global Outcomes controversies conference. Kidney Int. 2015;87(3):502-528.

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Botulinum Injections Might Help Relieve Anterolateral Knee Pain

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A single injection of botulinum toxin type A into the tensor fasciae latae can improve symptoms of lateral patellaofemoral overload syndrome (LPOS), which is characterized by pain in the anterior and lateral parts of the knee during exercise, according to a study published online ahead of print in American Journal of Sports Medicine.

Researchers gave a botulinum injection to 45 patients who’d had LPOS for at least 3 months and hadn’t improved after a course of physical therapy. Patients reported on their symptoms before the injection; at 1, 4, and 12 weeks after the injection; and at a mean of 5 years post-injection.

There was significant improvement in pain scores from before the injection to 1, 4, and 12 weeks after treatment, and in 87% of patients, this improvement was maintained at the 5-year follow-up.

References

Suggested Reading
Stephen JM, Urquhart DW, van Arkel RJ, et al. The use of sonographically guided botulinum toxin type a (Dysport) injections into the tensor fasciae latae for the treatment of lateral patellofemoral overload syndrome. Am J Sports Med. 2016 Feb 22 [Epub ahead of print].

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A single injection of botulinum toxin type A into the tensor fasciae latae can improve symptoms of lateral patellaofemoral overload syndrome (LPOS), which is characterized by pain in the anterior and lateral parts of the knee during exercise, according to a study published online ahead of print in American Journal of Sports Medicine.

Researchers gave a botulinum injection to 45 patients who’d had LPOS for at least 3 months and hadn’t improved after a course of physical therapy. Patients reported on their symptoms before the injection; at 1, 4, and 12 weeks after the injection; and at a mean of 5 years post-injection.

There was significant improvement in pain scores from before the injection to 1, 4, and 12 weeks after treatment, and in 87% of patients, this improvement was maintained at the 5-year follow-up.

A single injection of botulinum toxin type A into the tensor fasciae latae can improve symptoms of lateral patellaofemoral overload syndrome (LPOS), which is characterized by pain in the anterior and lateral parts of the knee during exercise, according to a study published online ahead of print in American Journal of Sports Medicine.

Researchers gave a botulinum injection to 45 patients who’d had LPOS for at least 3 months and hadn’t improved after a course of physical therapy. Patients reported on their symptoms before the injection; at 1, 4, and 12 weeks after the injection; and at a mean of 5 years post-injection.

There was significant improvement in pain scores from before the injection to 1, 4, and 12 weeks after treatment, and in 87% of patients, this improvement was maintained at the 5-year follow-up.

References

Suggested Reading
Stephen JM, Urquhart DW, van Arkel RJ, et al. The use of sonographically guided botulinum toxin type a (Dysport) injections into the tensor fasciae latae for the treatment of lateral patellofemoral overload syndrome. Am J Sports Med. 2016 Feb 22 [Epub ahead of print].

References

Suggested Reading
Stephen JM, Urquhart DW, van Arkel RJ, et al. The use of sonographically guided botulinum toxin type a (Dysport) injections into the tensor fasciae latae for the treatment of lateral patellofemoral overload syndrome. Am J Sports Med. 2016 Feb 22 [Epub ahead of print].

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Do Genetics Influence Knee Osteoarthritis Patients’ Sensitivity to Pain?

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Preliminary evidence suggests that patients with knee osteoarthritis (OA) who have certain alleles of the catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genes experience more variability in their day-to-day pain and exacerbation of pain after daily physical activity, compared with patients with other genotypes, according to a study published in Scandinavian Journal of Pain.

Researchers looked at variability in day-to-day knee OA pain among patients with different variants of the COMT and OPRM1 genes. They assigned 120 patients with knee OA to a 22-day assessment protocol in which they wore an accelerometer to measure daily physical activity and completed a pain questionnaire 3 times a day. Multilevel modeling was used to examine the magnitude of within-person variability in pain by genetic group.

Patients with two copies of the Asn40 allele of OPRM1 rs 1799971 showed the greatest variability in day-to-day pain. Patients with the Val/Val genotype of COMT rs4680 showed the greatest pain variability and also experienced the greatest increase in pain as a result of physical activity.

References

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Martire LM, Wilson SJ, Small BJ, et al. COMT and OPRM1 genotype associations with daily knee pain variability and activity induced pain. Scand J Pain. 2016 Jan 1;10:6-12.

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Preliminary evidence suggests that patients with knee osteoarthritis (OA) who have certain alleles of the catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genes experience more variability in their day-to-day pain and exacerbation of pain after daily physical activity, compared with patients with other genotypes, according to a study published in Scandinavian Journal of Pain.

Researchers looked at variability in day-to-day knee OA pain among patients with different variants of the COMT and OPRM1 genes. They assigned 120 patients with knee OA to a 22-day assessment protocol in which they wore an accelerometer to measure daily physical activity and completed a pain questionnaire 3 times a day. Multilevel modeling was used to examine the magnitude of within-person variability in pain by genetic group.

Patients with two copies of the Asn40 allele of OPRM1 rs 1799971 showed the greatest variability in day-to-day pain. Patients with the Val/Val genotype of COMT rs4680 showed the greatest pain variability and also experienced the greatest increase in pain as a result of physical activity.

Preliminary evidence suggests that patients with knee osteoarthritis (OA) who have certain alleles of the catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genes experience more variability in their day-to-day pain and exacerbation of pain after daily physical activity, compared with patients with other genotypes, according to a study published in Scandinavian Journal of Pain.

Researchers looked at variability in day-to-day knee OA pain among patients with different variants of the COMT and OPRM1 genes. They assigned 120 patients with knee OA to a 22-day assessment protocol in which they wore an accelerometer to measure daily physical activity and completed a pain questionnaire 3 times a day. Multilevel modeling was used to examine the magnitude of within-person variability in pain by genetic group.

Patients with two copies of the Asn40 allele of OPRM1 rs 1799971 showed the greatest variability in day-to-day pain. Patients with the Val/Val genotype of COMT rs4680 showed the greatest pain variability and also experienced the greatest increase in pain as a result of physical activity.

References

Suggested Reading
Martire LM, Wilson SJ, Small BJ, et al. COMT and OPRM1 genotype associations with daily knee pain variability and activity induced pain. Scand J Pain. 2016 Jan 1;10:6-12.

References

Suggested Reading
Martire LM, Wilson SJ, Small BJ, et al. COMT and OPRM1 genotype associations with daily knee pain variability and activity induced pain. Scand J Pain. 2016 Jan 1;10:6-12.

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