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In Vitro and In Situ Characterization of Arthroscopic Loop Security and Knot Security of Braided Polyblend Sutures: A Biomechanical Study
Open-surgery knot tying is easily learned and performed, but knot tying during arthroscopic procedures can be both challenging and frustrating. According to Burkhart and colleagues,1,2 knot security is defined as the effectiveness of the knot in resisting slippage when load is applied, whereas loop security is the effectiveness in maintaining a tight suture loop while a knot is being tied. Arthroscopic knots commonly begin with an initial slipknot locked in place with a series of half-hitches. During arthroscopic surgery, the surgeon usually must tie an arthroscopic knot to obtain secure tissue fixation, an essential component of soft-tissue repair. A secure knot provides optimal tissue apposition for healing, which will ultimately improve functional outcome. For a knot to be effective, it must have both knot security and loop security. Knot security depends on knot configuration, the coefficient of friction, ductility, handling properties, solubility and diameter of suture material, internal interference, slack between throws, and surgeon experience. Tissue fluid and tissue reaction to suture material may affect knot and loop security.
The ideal knot would be easy to tie and reproducible and would not slip or stretch before tissue is healed. The ideal suture material should provide adequate strength to hold soft tissue in an anatomically correct position until healing can occur. It should also be easily and efficiently manipulated by arthroscopic means when tissues are being secured with knots and secure suture loops. Studies have been conducted to evaluate the security of knots tied with arthroscopic techniques, knot configurations, and suture materials, and these investigations have often evaluated knot performance under single load-to-failure (LTF) test scenarios and cyclic loading in vitro (dry environment) in a room-temperature environment.2-10 To our knowledge, few if any attempts have been made to simulate in situ conditions at body temperature when testing knot security. The fluid environment and the temperature could potentially affect the effectiveness of knots, as knot security depends on friction, internal interference, and slack between throws.1
We conducted a study to evaluate biomechanical performance (knot security, loop security) during destructive testing of several different suture materials with various arthroscopic knot configurations. The study was performed under in vitro (dry environment) and in situ (wet environment) conditions by surgeons with different levels of experience.
Materials and Methods
This investigation was conducted at the Orthopaedic Research Institute at Via Christi Health in Wichita, Kansas. The study compared 4 different suture materials tied with 3 different commonly used arthroscopic knots by 3 surgeons with different levels of experience. The 4 types of braided polyblend polyethylene sutures were Fiberwire (Arthrex, Naples, Florida), ForceFiber (Stryker, San Jose, California), Orthocord (DePuy-Mitek, Warsaw, Indiana), and Ultrabraid (Smith & Nephew, Memphis, Tennessee). Each suture material was tied with 3 arthroscopic knots—static surgeon’s knot, Weston knot,11 Tennessee slider12—and a series of 3 reversing half-hitches on alternating posts (RHAPs) (Figure 1). These knots were chosen based on studies showing they have a higher maximum force to failure when combined with 3 RHAPs.1,2,5,9,13-17
We evaluated performer variability with the help of 3 investigator-surgeons who differed in their level of experience tying arthroscopic knots. This experience was defined on the basis of total number of arthroscopies performed—one of the most important factors predicting basic arthroscopic skills. Our surgeon A was a sports medicine fellowship–trained surgeon with 10 years of experience and a significant number of arthroscopies performed annually (350); surgeon B was a sports medicine fellowship–trained surgeon with 3 years of experience and an annual arthroscopy volume of more than 250 procedures; and surgeon C was a third-year orthopedic resident with about 100 arthroscopies performed.
All knots were tied on a standardized post 30 mm in circumference, which provided a consistent starting circumference for each knot and replicated the suture loop created during arthroscopic rotator cuff repair. All knots were tied using standard arthroscopic techniques, with a standard knot pusher and a modified arthroscopic cannula, in a dry environment (Figure 2). Servohydraulic materials testing system instruments (model 810; MTS Systems, Eden Prairie, Minnesota) were used to test the knot security and loop security of each combination of knots and suture types. Two round hooks (diameter, 3.9 mm) were attached to the actuator and the load cell (Figure 3). Loops were preloaded to 6 N to avoid potential errors caused by slack in the loops or by stretching of suture materials and to provide a well-defined starting point for data recording.
LTF testing was performed for both in vitro and in situ conditions using 10 samples of each suture–knot configuration for each mechanical testing. Each type of testing was conducted for a total of 240 suture–knot combinations per investigator. For the in vitro condition, each suture loop was initiated with 5 preconditioning loading cycles, from 6 N to 30 N at 1 Hz. The load was then applied continuously at a crosshead speed of 1 mm/s until “clinical failure” (3 mm crosshead displacement). We used this criterion for clinical failure, as studies have indicated that 3 mm is the point at which tissue apposition is lost.15,18-21 After the crosshead reached the 3-mm displacement, the loads (under load control) were held for 5 minutes at maximum load, and then load was applied continuously at a crosshead speed of 1 mm/s until complete structure failure. Load and displacement data were collected at a frequency of 20 Hz.
For the in situ condition, the same test parameters were used, except that each combination of the suture loop was preloaded to 6 N and soaked in physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing in an effort to simulate the aqueous medium in vivo after surgery. The in situ tests were performed under physiologic solution maintained at 37°C to approximate postoperative physical conditions.
Statistical Analysis
Means and standard deviations of the knot security and loop security achieved by the surgeons (different experience levels) were calculated for each test configuration and each test condition. These values were used to determine the statistical relevance of the difference in arthroscopic loop security and knot security in each configuration. One-way analysis of variance (ANOVA) performed with SPSS Version 19.0 software (SPSS, Chicago, Illinois) with the least significant difference (LSD) multiple comparisons post hoc analysis was used to determine if any observed differences between the types of braided polyblend sutures, the types of sliding knots, the test conditions (in vitro, in situ), and the levels of surgeon experience were significant for each knot configuration. The level of significance of differences was set at P < .001.
Results
Figure 4 shows the mean maximum clinical failure load (3 mm of displacement) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. In the comparison of biomechanical performance (knot and loop security) under in vitro and in situ conditions, no significant difference was detected when Ultrabraid suture material was used, regardless of surgeon experience, for all knot configurations. For surgeon B, there was no significant difference between in vitro and in situ conditions for any knot configurations or suture materials. When Orthocord suture material was used, Weston knots tied by surgeon A, and static surgeon’s knots by surgeons A and C, resulted in a significant difference between the in vitro and in situ conditions. When ForceFiber suture material was used, only Weston knots and Tennessee slider knots by surgeon A had a significant difference between in vitro and in situ conditions. Weston knots by surgeon A exhibited a significant difference between in vitro and in situ conditions, except when Ultrabraid suture material was used.
Surgeon C’s Tennessee slider knots with all polyblend sutures showed significantly lower loads at clinical failure compared with all the other knot configurations and with knots tied by the other 2 surgeons under both in vitro and in situ conditions. Overall, knots tied by surgeon B had higher clinical failure load than knots tied by the other 2 surgeons.
Figure 5 shows the mean ultimate failure load (complete structural failure) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. Knots tied with Orthocord suture material had the overall lower ultimate failure load compared with other suture materials, whereas knots tied with Ultrabraid suture material had the overall highest ultimate failure load. However, the ultimate failure loads for all the knots tied using any suture material, regardless of surgeon experience, were more than 61 N, which is the estimated minimum required ultimate load per suture during a maximum muscle contraction.1
Figure 6 shows the percentage of knot slipping at constant clinical failure load. Orthocord and Fiberwire suture materials had the lowest incidence of knot slippage. Surgeon C had complete knot slippage at constant clinical failure load using ForceFiber with the Weston knot and Ultrabraid with the Tennessee slider knot. When using Ultrabraid or ForceFiber, surgeons A and C had at least 2 knots slip for all knot configurations.
Discussion
Optimization of knot security for any given knot configuration, suture material, and surgeon experience level during arthroscopic knot tying is crucial.1-10 Our study results showed that, under single LTF test scenarios, there was a significant difference between in vitro and in situ conditions with respect to both knot configuration and surgeon experience level, except when Ultrabraid suture material was used. Arthroscopic sliding knots are lockable or nonlockable.7,12 With lockable sliding knots, slippage may be prevented by tensioning the wrapping limb, which distorts the post in the distal part of the knot, resulting in a kink in the post, thereby increasing the internal interference that increases the resistance of the knot from backing off. With nonlockable sliding knots, slippage may be prevented by the tight grip of the wrappings around the initial post.7 The static surgeon’s knot and the Tennessee slider knot are nonlockable, whereas the Weston knot is a distal lockable sliding knot. Compared with nonlockable sliding knots, lockable sliding knots cause less suture loop enlargement. In 1976, Tera and Aberg22 studied the strength of knotted thread for 12 different types of suture knots combined with 11 types of suture material. They conducted their study 1 week after suture material was inserted into the subcutaneous tissue of rabbits. Their results show a greater propensity for certain suture materials to slip when tested in an aqueous environment. In 1998, Babetty and colleagues23 used Wistar rats to compare the in vivo strength, knot efficiency, and knot security of 4 types of sliding knots and to assess tissue reaction as a result of knot configuration, knot volume, and suture size. They found that 4/0 knots lost more strength than 2/0 knots did, and they concluded that the tissue response to all the knots, except 2/0 nylon, was similar. They indicated that the inflammatory sheath volume varied with knot volume, suture size, and knot configuration. Our results agree with observations that exposure to an aqueous environment alters the force to clinical failure of comparable suture and knot configurations.
In addition, our findings indicate that surgeon familiarity with certain knots has a major effect on knot security. The difference in our 3 surgeons’ levels of familiarity with certain knots was somewhat minimized by the knot tying they practiced before submitting knots for testing. The findings contrast with those of Milia and colleagues,24 who conducted a biomechanical study to determine the effect of experience level on knot security. They compared an experienced arthroscopic shoulder surgeon with a junior-level orthopedic resident surgeon and concluded that experience did not affect knot security. However, the knots in their study were tied by hand, not through an arthroscopic cannula with instruments. Our findings suggest that both experienced and less experienced orthopedic residents should be encouraged to practice arthroscopic knot tying in a nonsurgical environment in order to become comfortable tying arthroscopic knots.
Braided nonabsorbable polyester suture traditionally has been found to be stronger than monofilament absorbable polydioxanone (PDS) and to have less slippage potential.8,9,25 Several studies have determined that the braided polyblend sutures now commonly used for arthroscopic knots have better strength profiles over more traditional materials.12,26,27 Orthocord has a dyed absorbable core (PDS, 68%), an undyed nonabsorbable ultrahigh-molecular-weight polyethylene (UHMWPE, 32%) sleeve, and a polyglactin coating.9,10 Both Ultrabraid and ForceFiber are made with braided UHMWPE and have just a few variations in weave patterns. Fiberwire has a multifiber UHMWPE core covered with braided polyester suture material. Several biomechanical studies25,26,28 have evaluated different arthroscopic sliding knot configurations with different suture materials, and all concluded that a surgeon who is choosing an arthroscopic repair technique should know the differences in suture materials and the knot strengths afforded by different knot configurations, as suture material is an important aspect of loop security. Our findings agree with their findings, that suture materials have a major effect on knot security, even with a series of 3 RHAPs, as in theory the RHAPs should minimize suture friction, internal interference, and slack between knot loops—emphasizing the effect of material selection. Furthermore, our findings also indicated that suture materials with a core in their design (Fiberwire, Orthocord) tend to have the lowest incidence of knot slippage. We had suspected that suture surface characteristics and suture construction could be important factors in knot slippage.
Our experimental design had its limitations. First, although we simulated factors such as temperature, plasma environment, and surgeon experience, tying a knot on a standardized post (30 mm in circumference) differed from what is typically done clinically. Second, the metal hooks used in this study were not compressible and did not interpose in the substance of the knot as soft tissue does in the clinical setting. Third, knots were tied with no tension against the sutures, whereas clinically knots are tied under tension as tissues are pulled together in reconstructions. Fourth, it was assumed that soaking in a physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing was sufficient to simulate the aqueous medium in vivo after surgery, but these parameters may not represent conditions in a patient who has just undergone an arthroscopic shoulder repair and adheres to a passive motion protocol. Fifth, there was no blinding of knot type, and there was no randomization of tying order or testing order. Sixth, only a single LTF test was performed, and incremental cyclic loading can be more useful, as it has long been recognized as a leading source of failure in orthopedic repairs.
Conclusion
These study results advance our overall understanding of the biomechanics of the different knot configurations and loop security levels of the different braided polyblend sutures used in arthroscopic procedures through LTF in both in vitro and in situ conditions. Overall, no suture material was superior to any other in a fluid environment, as the combination of aqueous environment and surgeon level of experience with arthroscopic knot tying has a major effect on knot security under single LTF test scenarios. However, our data showed that Ultrabraid suture material had no effect on knot effectiveness over the fluid environment and the temperature. Furthermore, the study showed that the Tennessee slider knot had the steepest learning curve. This study may provide an alternative arthroscopic knots option for soft-tissue repair in which use of certain suture materials is limited.
1. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Knot security in simple sliding knots and its relationship to rotator cuff repair: how secure must the knot be? Arthroscopy. 2000;16(2):202-207.
2. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Loop security as a determinant of tissue fixation security. Arthroscopy. 1998;14(7):773-776.
3. Elkousy H, Hammerman SM, Edwards TB, et al. The arthroscopic square knot: a biomechanical comparison with open and arthroscopic knots. Arthroscopy. 2006;22(7):736-741.
4. Elkousy HA, Sekiya JK, Stabile KJ, McMahon PJ. A biomechanical comparison of arthroscopic sliding and sliding-locking knots. Arthroscopy. 2005;21(2):204-210.
5. Ilahi OA, Younas SA, Alexander J, Noble PC. Cyclic testing of arthroscopic knot security. Arthroscopy. 2004;20(1):62-68.
6. Loutzenheiser TD, Harryman DT 2nd, Ziegler DW, Yung SW. Optimizing arthroscopic knots using braided or monofilament suture. Arthroscopy. 1998;14(1):57-65.
7. Chan KC, Burkhart SS, Thiagarajan P, Goh JC. Optimization of stacked half-hitch knots for arthroscopic surgery. Arthroscopy. 2001;17(7):752-759.
8. Lee TQ, Matsuura PA, Fogolin RP, Lin AC, Kim D, McMahon PJ. Arthroscopic suture tying: a comparison of knot types and suture materials. Arthroscopy. 2001;17(4):348-352.
9. Mishra DK, Cannon WD Jr, Lucas DJ, Belzer JP. Elongation of arthroscopically tied knots. Am J Sports Med. 1997;25(1):113-117.
10. Kim SH, Ha KI, Kim SH, Kim JS. Significance of the internal locking mechanism for loop security enhancement in the arthroscopic knot. Arthroscopy. 2001;17(8):850-855.
11. Weston PV. A new clinch knot. Obstet Gynecol. 1991;78(1):144-147.
12. Lo IK, Burkhart SS, Chan KC, Athanasiou K. Arthroscopic knots: determining the optimal balance of loop security and knot security. Arthroscopy. 2004;20(5):489-502.
13. Lo IK, Burkhart SS, Athanasiou K. Abrasion resistance of two types of nonabsorbable braided suture. Arthroscopy. 2004;20(4):407-413.
14. De Beer JF, van Rooyen K, Boezaart AP. Nicky’s knot—a new slip knot for arthroscopic surgery. Arthroscopy. 1998;14(1):109-110.
15. Loutzenheiser TD, Harryman DT 2nd, Yung SW, France MP, Sidles JA. Optimizing arthroscopic knots. Arthroscopy. 1995;11(2):199-206.
16. Wetzler MJ, Bartolozzi AR, Gillespie MJ, et al. Fatigue properties of suture anchors in anterior shoulder reconstructions: Mitek GII. Arthroscopy. 1996;12(6):687-693.
17. Barber FA, Herbert MA, Beavis RC. Cyclic load and failure behavior of arthroscopic knots and high strength sutures. Arthroscopy. 2009;25(2):192-199.
18. Richmond JC. A comparison of ultrasonic suture welding and traditional knot tying. Am J Sports Med. 200;29(3):297-299.
19. James JD, Wu MM, Batra EK, Rodeheaver GT, Edlich RF. Technical considerations in manual and instrument tying techniques. J Emerg Med. 1992;10(4):469-480.
20. Batra EK, Franz DA, Towler MA, et al. Influence of emergency physician’s tying technique on knot security. J Emerg Med. 1992;10(3):309-316.
21. Livermore RW, Chong AC, Prohaska DJ, Cooke FW, Jones TL. Knot security, loop security and elongation of braided polyblend sutures used for arthroscopic knots. Am J Orthop. 2010;39(12):569-576.
22. Tera H, Aberg C. The strength of suture knots after one week in vivo. Acta Chir Scand. 1976;142(4):301-307.
23. Babetty Z, Sümer A, Altintaş S, Ergüney S, Göksel S. Changes in knot-holding capacity of sliding knots in vivo and tissue reaction. Arch Surg. 1998;133(7):727-734.
24. Milia MJ, Peindl RD, Connor PM. Arthroscopic knot tying: the role of instrumentation in achieving knot security. Arthroscopy. 2005;21(1):69-76.
25. Lieurance RK, Pflaster DS, Abbott D, Nottage WM. Failure characteristics of various arthroscopically tied knots. Clin Orthop. 2003;(408):311-318.
26. Abbi G, Espinoza L, Odell T, Mahar A, Pedowitz R. Evaluation of 5 knots and 2 suture materials for arthroscopic rotator cuff repair: very strong sutures can still slip. Arthroscopy. 2006;22(1):38-43.
27. Wüst DM, Meyer DC, Favre P, Gerber C. Mechanical and handling properties of braided polyblend polyethylene sutures in comparison to braided polyester and monofilament polydioxanone sutures. Arthroscopy. 2006;22(11):1146-1153.
28. Mahar AT, Moezzi DM, Serra-Hsu F, Pedowitz RA. Comparison and performance characteristics of 3 different knots when tied with 2 suture materials used for shoulder arthroscopy. Arthroscopy. 2006;22(6):614.e1-e2.
Open-surgery knot tying is easily learned and performed, but knot tying during arthroscopic procedures can be both challenging and frustrating. According to Burkhart and colleagues,1,2 knot security is defined as the effectiveness of the knot in resisting slippage when load is applied, whereas loop security is the effectiveness in maintaining a tight suture loop while a knot is being tied. Arthroscopic knots commonly begin with an initial slipknot locked in place with a series of half-hitches. During arthroscopic surgery, the surgeon usually must tie an arthroscopic knot to obtain secure tissue fixation, an essential component of soft-tissue repair. A secure knot provides optimal tissue apposition for healing, which will ultimately improve functional outcome. For a knot to be effective, it must have both knot security and loop security. Knot security depends on knot configuration, the coefficient of friction, ductility, handling properties, solubility and diameter of suture material, internal interference, slack between throws, and surgeon experience. Tissue fluid and tissue reaction to suture material may affect knot and loop security.
The ideal knot would be easy to tie and reproducible and would not slip or stretch before tissue is healed. The ideal suture material should provide adequate strength to hold soft tissue in an anatomically correct position until healing can occur. It should also be easily and efficiently manipulated by arthroscopic means when tissues are being secured with knots and secure suture loops. Studies have been conducted to evaluate the security of knots tied with arthroscopic techniques, knot configurations, and suture materials, and these investigations have often evaluated knot performance under single load-to-failure (LTF) test scenarios and cyclic loading in vitro (dry environment) in a room-temperature environment.2-10 To our knowledge, few if any attempts have been made to simulate in situ conditions at body temperature when testing knot security. The fluid environment and the temperature could potentially affect the effectiveness of knots, as knot security depends on friction, internal interference, and slack between throws.1
We conducted a study to evaluate biomechanical performance (knot security, loop security) during destructive testing of several different suture materials with various arthroscopic knot configurations. The study was performed under in vitro (dry environment) and in situ (wet environment) conditions by surgeons with different levels of experience.
Materials and Methods
This investigation was conducted at the Orthopaedic Research Institute at Via Christi Health in Wichita, Kansas. The study compared 4 different suture materials tied with 3 different commonly used arthroscopic knots by 3 surgeons with different levels of experience. The 4 types of braided polyblend polyethylene sutures were Fiberwire (Arthrex, Naples, Florida), ForceFiber (Stryker, San Jose, California), Orthocord (DePuy-Mitek, Warsaw, Indiana), and Ultrabraid (Smith & Nephew, Memphis, Tennessee). Each suture material was tied with 3 arthroscopic knots—static surgeon’s knot, Weston knot,11 Tennessee slider12—and a series of 3 reversing half-hitches on alternating posts (RHAPs) (Figure 1). These knots were chosen based on studies showing they have a higher maximum force to failure when combined with 3 RHAPs.1,2,5,9,13-17
We evaluated performer variability with the help of 3 investigator-surgeons who differed in their level of experience tying arthroscopic knots. This experience was defined on the basis of total number of arthroscopies performed—one of the most important factors predicting basic arthroscopic skills. Our surgeon A was a sports medicine fellowship–trained surgeon with 10 years of experience and a significant number of arthroscopies performed annually (350); surgeon B was a sports medicine fellowship–trained surgeon with 3 years of experience and an annual arthroscopy volume of more than 250 procedures; and surgeon C was a third-year orthopedic resident with about 100 arthroscopies performed.
All knots were tied on a standardized post 30 mm in circumference, which provided a consistent starting circumference for each knot and replicated the suture loop created during arthroscopic rotator cuff repair. All knots were tied using standard arthroscopic techniques, with a standard knot pusher and a modified arthroscopic cannula, in a dry environment (Figure 2). Servohydraulic materials testing system instruments (model 810; MTS Systems, Eden Prairie, Minnesota) were used to test the knot security and loop security of each combination of knots and suture types. Two round hooks (diameter, 3.9 mm) were attached to the actuator and the load cell (Figure 3). Loops were preloaded to 6 N to avoid potential errors caused by slack in the loops or by stretching of suture materials and to provide a well-defined starting point for data recording.
LTF testing was performed for both in vitro and in situ conditions using 10 samples of each suture–knot configuration for each mechanical testing. Each type of testing was conducted for a total of 240 suture–knot combinations per investigator. For the in vitro condition, each suture loop was initiated with 5 preconditioning loading cycles, from 6 N to 30 N at 1 Hz. The load was then applied continuously at a crosshead speed of 1 mm/s until “clinical failure” (3 mm crosshead displacement). We used this criterion for clinical failure, as studies have indicated that 3 mm is the point at which tissue apposition is lost.15,18-21 After the crosshead reached the 3-mm displacement, the loads (under load control) were held for 5 minutes at maximum load, and then load was applied continuously at a crosshead speed of 1 mm/s until complete structure failure. Load and displacement data were collected at a frequency of 20 Hz.
For the in situ condition, the same test parameters were used, except that each combination of the suture loop was preloaded to 6 N and soaked in physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing in an effort to simulate the aqueous medium in vivo after surgery. The in situ tests were performed under physiologic solution maintained at 37°C to approximate postoperative physical conditions.
Statistical Analysis
Means and standard deviations of the knot security and loop security achieved by the surgeons (different experience levels) were calculated for each test configuration and each test condition. These values were used to determine the statistical relevance of the difference in arthroscopic loop security and knot security in each configuration. One-way analysis of variance (ANOVA) performed with SPSS Version 19.0 software (SPSS, Chicago, Illinois) with the least significant difference (LSD) multiple comparisons post hoc analysis was used to determine if any observed differences between the types of braided polyblend sutures, the types of sliding knots, the test conditions (in vitro, in situ), and the levels of surgeon experience were significant for each knot configuration. The level of significance of differences was set at P < .001.
Results
Figure 4 shows the mean maximum clinical failure load (3 mm of displacement) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. In the comparison of biomechanical performance (knot and loop security) under in vitro and in situ conditions, no significant difference was detected when Ultrabraid suture material was used, regardless of surgeon experience, for all knot configurations. For surgeon B, there was no significant difference between in vitro and in situ conditions for any knot configurations or suture materials. When Orthocord suture material was used, Weston knots tied by surgeon A, and static surgeon’s knots by surgeons A and C, resulted in a significant difference between the in vitro and in situ conditions. When ForceFiber suture material was used, only Weston knots and Tennessee slider knots by surgeon A had a significant difference between in vitro and in situ conditions. Weston knots by surgeon A exhibited a significant difference between in vitro and in situ conditions, except when Ultrabraid suture material was used.
Surgeon C’s Tennessee slider knots with all polyblend sutures showed significantly lower loads at clinical failure compared with all the other knot configurations and with knots tied by the other 2 surgeons under both in vitro and in situ conditions. Overall, knots tied by surgeon B had higher clinical failure load than knots tied by the other 2 surgeons.
Figure 5 shows the mean ultimate failure load (complete structural failure) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. Knots tied with Orthocord suture material had the overall lower ultimate failure load compared with other suture materials, whereas knots tied with Ultrabraid suture material had the overall highest ultimate failure load. However, the ultimate failure loads for all the knots tied using any suture material, regardless of surgeon experience, were more than 61 N, which is the estimated minimum required ultimate load per suture during a maximum muscle contraction.1
Figure 6 shows the percentage of knot slipping at constant clinical failure load. Orthocord and Fiberwire suture materials had the lowest incidence of knot slippage. Surgeon C had complete knot slippage at constant clinical failure load using ForceFiber with the Weston knot and Ultrabraid with the Tennessee slider knot. When using Ultrabraid or ForceFiber, surgeons A and C had at least 2 knots slip for all knot configurations.
Discussion
Optimization of knot security for any given knot configuration, suture material, and surgeon experience level during arthroscopic knot tying is crucial.1-10 Our study results showed that, under single LTF test scenarios, there was a significant difference between in vitro and in situ conditions with respect to both knot configuration and surgeon experience level, except when Ultrabraid suture material was used. Arthroscopic sliding knots are lockable or nonlockable.7,12 With lockable sliding knots, slippage may be prevented by tensioning the wrapping limb, which distorts the post in the distal part of the knot, resulting in a kink in the post, thereby increasing the internal interference that increases the resistance of the knot from backing off. With nonlockable sliding knots, slippage may be prevented by the tight grip of the wrappings around the initial post.7 The static surgeon’s knot and the Tennessee slider knot are nonlockable, whereas the Weston knot is a distal lockable sliding knot. Compared with nonlockable sliding knots, lockable sliding knots cause less suture loop enlargement. In 1976, Tera and Aberg22 studied the strength of knotted thread for 12 different types of suture knots combined with 11 types of suture material. They conducted their study 1 week after suture material was inserted into the subcutaneous tissue of rabbits. Their results show a greater propensity for certain suture materials to slip when tested in an aqueous environment. In 1998, Babetty and colleagues23 used Wistar rats to compare the in vivo strength, knot efficiency, and knot security of 4 types of sliding knots and to assess tissue reaction as a result of knot configuration, knot volume, and suture size. They found that 4/0 knots lost more strength than 2/0 knots did, and they concluded that the tissue response to all the knots, except 2/0 nylon, was similar. They indicated that the inflammatory sheath volume varied with knot volume, suture size, and knot configuration. Our results agree with observations that exposure to an aqueous environment alters the force to clinical failure of comparable suture and knot configurations.
In addition, our findings indicate that surgeon familiarity with certain knots has a major effect on knot security. The difference in our 3 surgeons’ levels of familiarity with certain knots was somewhat minimized by the knot tying they practiced before submitting knots for testing. The findings contrast with those of Milia and colleagues,24 who conducted a biomechanical study to determine the effect of experience level on knot security. They compared an experienced arthroscopic shoulder surgeon with a junior-level orthopedic resident surgeon and concluded that experience did not affect knot security. However, the knots in their study were tied by hand, not through an arthroscopic cannula with instruments. Our findings suggest that both experienced and less experienced orthopedic residents should be encouraged to practice arthroscopic knot tying in a nonsurgical environment in order to become comfortable tying arthroscopic knots.
Braided nonabsorbable polyester suture traditionally has been found to be stronger than monofilament absorbable polydioxanone (PDS) and to have less slippage potential.8,9,25 Several studies have determined that the braided polyblend sutures now commonly used for arthroscopic knots have better strength profiles over more traditional materials.12,26,27 Orthocord has a dyed absorbable core (PDS, 68%), an undyed nonabsorbable ultrahigh-molecular-weight polyethylene (UHMWPE, 32%) sleeve, and a polyglactin coating.9,10 Both Ultrabraid and ForceFiber are made with braided UHMWPE and have just a few variations in weave patterns. Fiberwire has a multifiber UHMWPE core covered with braided polyester suture material. Several biomechanical studies25,26,28 have evaluated different arthroscopic sliding knot configurations with different suture materials, and all concluded that a surgeon who is choosing an arthroscopic repair technique should know the differences in suture materials and the knot strengths afforded by different knot configurations, as suture material is an important aspect of loop security. Our findings agree with their findings, that suture materials have a major effect on knot security, even with a series of 3 RHAPs, as in theory the RHAPs should minimize suture friction, internal interference, and slack between knot loops—emphasizing the effect of material selection. Furthermore, our findings also indicated that suture materials with a core in their design (Fiberwire, Orthocord) tend to have the lowest incidence of knot slippage. We had suspected that suture surface characteristics and suture construction could be important factors in knot slippage.
Our experimental design had its limitations. First, although we simulated factors such as temperature, plasma environment, and surgeon experience, tying a knot on a standardized post (30 mm in circumference) differed from what is typically done clinically. Second, the metal hooks used in this study were not compressible and did not interpose in the substance of the knot as soft tissue does in the clinical setting. Third, knots were tied with no tension against the sutures, whereas clinically knots are tied under tension as tissues are pulled together in reconstructions. Fourth, it was assumed that soaking in a physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing was sufficient to simulate the aqueous medium in vivo after surgery, but these parameters may not represent conditions in a patient who has just undergone an arthroscopic shoulder repair and adheres to a passive motion protocol. Fifth, there was no blinding of knot type, and there was no randomization of tying order or testing order. Sixth, only a single LTF test was performed, and incremental cyclic loading can be more useful, as it has long been recognized as a leading source of failure in orthopedic repairs.
Conclusion
These study results advance our overall understanding of the biomechanics of the different knot configurations and loop security levels of the different braided polyblend sutures used in arthroscopic procedures through LTF in both in vitro and in situ conditions. Overall, no suture material was superior to any other in a fluid environment, as the combination of aqueous environment and surgeon level of experience with arthroscopic knot tying has a major effect on knot security under single LTF test scenarios. However, our data showed that Ultrabraid suture material had no effect on knot effectiveness over the fluid environment and the temperature. Furthermore, the study showed that the Tennessee slider knot had the steepest learning curve. This study may provide an alternative arthroscopic knots option for soft-tissue repair in which use of certain suture materials is limited.
Open-surgery knot tying is easily learned and performed, but knot tying during arthroscopic procedures can be both challenging and frustrating. According to Burkhart and colleagues,1,2 knot security is defined as the effectiveness of the knot in resisting slippage when load is applied, whereas loop security is the effectiveness in maintaining a tight suture loop while a knot is being tied. Arthroscopic knots commonly begin with an initial slipknot locked in place with a series of half-hitches. During arthroscopic surgery, the surgeon usually must tie an arthroscopic knot to obtain secure tissue fixation, an essential component of soft-tissue repair. A secure knot provides optimal tissue apposition for healing, which will ultimately improve functional outcome. For a knot to be effective, it must have both knot security and loop security. Knot security depends on knot configuration, the coefficient of friction, ductility, handling properties, solubility and diameter of suture material, internal interference, slack between throws, and surgeon experience. Tissue fluid and tissue reaction to suture material may affect knot and loop security.
The ideal knot would be easy to tie and reproducible and would not slip or stretch before tissue is healed. The ideal suture material should provide adequate strength to hold soft tissue in an anatomically correct position until healing can occur. It should also be easily and efficiently manipulated by arthroscopic means when tissues are being secured with knots and secure suture loops. Studies have been conducted to evaluate the security of knots tied with arthroscopic techniques, knot configurations, and suture materials, and these investigations have often evaluated knot performance under single load-to-failure (LTF) test scenarios and cyclic loading in vitro (dry environment) in a room-temperature environment.2-10 To our knowledge, few if any attempts have been made to simulate in situ conditions at body temperature when testing knot security. The fluid environment and the temperature could potentially affect the effectiveness of knots, as knot security depends on friction, internal interference, and slack between throws.1
We conducted a study to evaluate biomechanical performance (knot security, loop security) during destructive testing of several different suture materials with various arthroscopic knot configurations. The study was performed under in vitro (dry environment) and in situ (wet environment) conditions by surgeons with different levels of experience.
Materials and Methods
This investigation was conducted at the Orthopaedic Research Institute at Via Christi Health in Wichita, Kansas. The study compared 4 different suture materials tied with 3 different commonly used arthroscopic knots by 3 surgeons with different levels of experience. The 4 types of braided polyblend polyethylene sutures were Fiberwire (Arthrex, Naples, Florida), ForceFiber (Stryker, San Jose, California), Orthocord (DePuy-Mitek, Warsaw, Indiana), and Ultrabraid (Smith & Nephew, Memphis, Tennessee). Each suture material was tied with 3 arthroscopic knots—static surgeon’s knot, Weston knot,11 Tennessee slider12—and a series of 3 reversing half-hitches on alternating posts (RHAPs) (Figure 1). These knots were chosen based on studies showing they have a higher maximum force to failure when combined with 3 RHAPs.1,2,5,9,13-17
We evaluated performer variability with the help of 3 investigator-surgeons who differed in their level of experience tying arthroscopic knots. This experience was defined on the basis of total number of arthroscopies performed—one of the most important factors predicting basic arthroscopic skills. Our surgeon A was a sports medicine fellowship–trained surgeon with 10 years of experience and a significant number of arthroscopies performed annually (350); surgeon B was a sports medicine fellowship–trained surgeon with 3 years of experience and an annual arthroscopy volume of more than 250 procedures; and surgeon C was a third-year orthopedic resident with about 100 arthroscopies performed.
All knots were tied on a standardized post 30 mm in circumference, which provided a consistent starting circumference for each knot and replicated the suture loop created during arthroscopic rotator cuff repair. All knots were tied using standard arthroscopic techniques, with a standard knot pusher and a modified arthroscopic cannula, in a dry environment (Figure 2). Servohydraulic materials testing system instruments (model 810; MTS Systems, Eden Prairie, Minnesota) were used to test the knot security and loop security of each combination of knots and suture types. Two round hooks (diameter, 3.9 mm) were attached to the actuator and the load cell (Figure 3). Loops were preloaded to 6 N to avoid potential errors caused by slack in the loops or by stretching of suture materials and to provide a well-defined starting point for data recording.
LTF testing was performed for both in vitro and in situ conditions using 10 samples of each suture–knot configuration for each mechanical testing. Each type of testing was conducted for a total of 240 suture–knot combinations per investigator. For the in vitro condition, each suture loop was initiated with 5 preconditioning loading cycles, from 6 N to 30 N at 1 Hz. The load was then applied continuously at a crosshead speed of 1 mm/s until “clinical failure” (3 mm crosshead displacement). We used this criterion for clinical failure, as studies have indicated that 3 mm is the point at which tissue apposition is lost.15,18-21 After the crosshead reached the 3-mm displacement, the loads (under load control) were held for 5 minutes at maximum load, and then load was applied continuously at a crosshead speed of 1 mm/s until complete structure failure. Load and displacement data were collected at a frequency of 20 Hz.
For the in situ condition, the same test parameters were used, except that each combination of the suture loop was preloaded to 6 N and soaked in physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing in an effort to simulate the aqueous medium in vivo after surgery. The in situ tests were performed under physiologic solution maintained at 37°C to approximate postoperative physical conditions.
Statistical Analysis
Means and standard deviations of the knot security and loop security achieved by the surgeons (different experience levels) were calculated for each test configuration and each test condition. These values were used to determine the statistical relevance of the difference in arthroscopic loop security and knot security in each configuration. One-way analysis of variance (ANOVA) performed with SPSS Version 19.0 software (SPSS, Chicago, Illinois) with the least significant difference (LSD) multiple comparisons post hoc analysis was used to determine if any observed differences between the types of braided polyblend sutures, the types of sliding knots, the test conditions (in vitro, in situ), and the levels of surgeon experience were significant for each knot configuration. The level of significance of differences was set at P < .001.
Results
Figure 4 shows the mean maximum clinical failure load (3 mm of displacement) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. In the comparison of biomechanical performance (knot and loop security) under in vitro and in situ conditions, no significant difference was detected when Ultrabraid suture material was used, regardless of surgeon experience, for all knot configurations. For surgeon B, there was no significant difference between in vitro and in situ conditions for any knot configurations or suture materials. When Orthocord suture material was used, Weston knots tied by surgeon A, and static surgeon’s knots by surgeons A and C, resulted in a significant difference between the in vitro and in situ conditions. When ForceFiber suture material was used, only Weston knots and Tennessee slider knots by surgeon A had a significant difference between in vitro and in situ conditions. Weston knots by surgeon A exhibited a significant difference between in vitro and in situ conditions, except when Ultrabraid suture material was used.
Surgeon C’s Tennessee slider knots with all polyblend sutures showed significantly lower loads at clinical failure compared with all the other knot configurations and with knots tied by the other 2 surgeons under both in vitro and in situ conditions. Overall, knots tied by surgeon B had higher clinical failure load than knots tied by the other 2 surgeons.
Figure 5 shows the mean ultimate failure load (complete structural failure) of different arthroscopic knot configurations for different braided polyblend sutures by surgeons of different levels of experience. Knots tied with Orthocord suture material had the overall lower ultimate failure load compared with other suture materials, whereas knots tied with Ultrabraid suture material had the overall highest ultimate failure load. However, the ultimate failure loads for all the knots tied using any suture material, regardless of surgeon experience, were more than 61 N, which is the estimated minimum required ultimate load per suture during a maximum muscle contraction.1
Figure 6 shows the percentage of knot slipping at constant clinical failure load. Orthocord and Fiberwire suture materials had the lowest incidence of knot slippage. Surgeon C had complete knot slippage at constant clinical failure load using ForceFiber with the Weston knot and Ultrabraid with the Tennessee slider knot. When using Ultrabraid or ForceFiber, surgeons A and C had at least 2 knots slip for all knot configurations.
Discussion
Optimization of knot security for any given knot configuration, suture material, and surgeon experience level during arthroscopic knot tying is crucial.1-10 Our study results showed that, under single LTF test scenarios, there was a significant difference between in vitro and in situ conditions with respect to both knot configuration and surgeon experience level, except when Ultrabraid suture material was used. Arthroscopic sliding knots are lockable or nonlockable.7,12 With lockable sliding knots, slippage may be prevented by tensioning the wrapping limb, which distorts the post in the distal part of the knot, resulting in a kink in the post, thereby increasing the internal interference that increases the resistance of the knot from backing off. With nonlockable sliding knots, slippage may be prevented by the tight grip of the wrappings around the initial post.7 The static surgeon’s knot and the Tennessee slider knot are nonlockable, whereas the Weston knot is a distal lockable sliding knot. Compared with nonlockable sliding knots, lockable sliding knots cause less suture loop enlargement. In 1976, Tera and Aberg22 studied the strength of knotted thread for 12 different types of suture knots combined with 11 types of suture material. They conducted their study 1 week after suture material was inserted into the subcutaneous tissue of rabbits. Their results show a greater propensity for certain suture materials to slip when tested in an aqueous environment. In 1998, Babetty and colleagues23 used Wistar rats to compare the in vivo strength, knot efficiency, and knot security of 4 types of sliding knots and to assess tissue reaction as a result of knot configuration, knot volume, and suture size. They found that 4/0 knots lost more strength than 2/0 knots did, and they concluded that the tissue response to all the knots, except 2/0 nylon, was similar. They indicated that the inflammatory sheath volume varied with knot volume, suture size, and knot configuration. Our results agree with observations that exposure to an aqueous environment alters the force to clinical failure of comparable suture and knot configurations.
In addition, our findings indicate that surgeon familiarity with certain knots has a major effect on knot security. The difference in our 3 surgeons’ levels of familiarity with certain knots was somewhat minimized by the knot tying they practiced before submitting knots for testing. The findings contrast with those of Milia and colleagues,24 who conducted a biomechanical study to determine the effect of experience level on knot security. They compared an experienced arthroscopic shoulder surgeon with a junior-level orthopedic resident surgeon and concluded that experience did not affect knot security. However, the knots in their study were tied by hand, not through an arthroscopic cannula with instruments. Our findings suggest that both experienced and less experienced orthopedic residents should be encouraged to practice arthroscopic knot tying in a nonsurgical environment in order to become comfortable tying arthroscopic knots.
Braided nonabsorbable polyester suture traditionally has been found to be stronger than monofilament absorbable polydioxanone (PDS) and to have less slippage potential.8,9,25 Several studies have determined that the braided polyblend sutures now commonly used for arthroscopic knots have better strength profiles over more traditional materials.12,26,27 Orthocord has a dyed absorbable core (PDS, 68%), an undyed nonabsorbable ultrahigh-molecular-weight polyethylene (UHMWPE, 32%) sleeve, and a polyglactin coating.9,10 Both Ultrabraid and ForceFiber are made with braided UHMWPE and have just a few variations in weave patterns. Fiberwire has a multifiber UHMWPE core covered with braided polyester suture material. Several biomechanical studies25,26,28 have evaluated different arthroscopic sliding knot configurations with different suture materials, and all concluded that a surgeon who is choosing an arthroscopic repair technique should know the differences in suture materials and the knot strengths afforded by different knot configurations, as suture material is an important aspect of loop security. Our findings agree with their findings, that suture materials have a major effect on knot security, even with a series of 3 RHAPs, as in theory the RHAPs should minimize suture friction, internal interference, and slack between knot loops—emphasizing the effect of material selection. Furthermore, our findings also indicated that suture materials with a core in their design (Fiberwire, Orthocord) tend to have the lowest incidence of knot slippage. We had suspected that suture surface characteristics and suture construction could be important factors in knot slippage.
Our experimental design had its limitations. First, although we simulated factors such as temperature, plasma environment, and surgeon experience, tying a knot on a standardized post (30 mm in circumference) differed from what is typically done clinically. Second, the metal hooks used in this study were not compressible and did not interpose in the substance of the knot as soft tissue does in the clinical setting. Third, knots were tied with no tension against the sutures, whereas clinically knots are tied under tension as tissues are pulled together in reconstructions. Fourth, it was assumed that soaking in a physiologic solution bath (human blood plasma) at 37°C (body temperature) for 24 hours before testing was sufficient to simulate the aqueous medium in vivo after surgery, but these parameters may not represent conditions in a patient who has just undergone an arthroscopic shoulder repair and adheres to a passive motion protocol. Fifth, there was no blinding of knot type, and there was no randomization of tying order or testing order. Sixth, only a single LTF test was performed, and incremental cyclic loading can be more useful, as it has long been recognized as a leading source of failure in orthopedic repairs.
Conclusion
These study results advance our overall understanding of the biomechanics of the different knot configurations and loop security levels of the different braided polyblend sutures used in arthroscopic procedures through LTF in both in vitro and in situ conditions. Overall, no suture material was superior to any other in a fluid environment, as the combination of aqueous environment and surgeon level of experience with arthroscopic knot tying has a major effect on knot security under single LTF test scenarios. However, our data showed that Ultrabraid suture material had no effect on knot effectiveness over the fluid environment and the temperature. Furthermore, the study showed that the Tennessee slider knot had the steepest learning curve. This study may provide an alternative arthroscopic knots option for soft-tissue repair in which use of certain suture materials is limited.
1. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Knot security in simple sliding knots and its relationship to rotator cuff repair: how secure must the knot be? Arthroscopy. 2000;16(2):202-207.
2. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Loop security as a determinant of tissue fixation security. Arthroscopy. 1998;14(7):773-776.
3. Elkousy H, Hammerman SM, Edwards TB, et al. The arthroscopic square knot: a biomechanical comparison with open and arthroscopic knots. Arthroscopy. 2006;22(7):736-741.
4. Elkousy HA, Sekiya JK, Stabile KJ, McMahon PJ. A biomechanical comparison of arthroscopic sliding and sliding-locking knots. Arthroscopy. 2005;21(2):204-210.
5. Ilahi OA, Younas SA, Alexander J, Noble PC. Cyclic testing of arthroscopic knot security. Arthroscopy. 2004;20(1):62-68.
6. Loutzenheiser TD, Harryman DT 2nd, Ziegler DW, Yung SW. Optimizing arthroscopic knots using braided or monofilament suture. Arthroscopy. 1998;14(1):57-65.
7. Chan KC, Burkhart SS, Thiagarajan P, Goh JC. Optimization of stacked half-hitch knots for arthroscopic surgery. Arthroscopy. 2001;17(7):752-759.
8. Lee TQ, Matsuura PA, Fogolin RP, Lin AC, Kim D, McMahon PJ. Arthroscopic suture tying: a comparison of knot types and suture materials. Arthroscopy. 2001;17(4):348-352.
9. Mishra DK, Cannon WD Jr, Lucas DJ, Belzer JP. Elongation of arthroscopically tied knots. Am J Sports Med. 1997;25(1):113-117.
10. Kim SH, Ha KI, Kim SH, Kim JS. Significance of the internal locking mechanism for loop security enhancement in the arthroscopic knot. Arthroscopy. 2001;17(8):850-855.
11. Weston PV. A new clinch knot. Obstet Gynecol. 1991;78(1):144-147.
12. Lo IK, Burkhart SS, Chan KC, Athanasiou K. Arthroscopic knots: determining the optimal balance of loop security and knot security. Arthroscopy. 2004;20(5):489-502.
13. Lo IK, Burkhart SS, Athanasiou K. Abrasion resistance of two types of nonabsorbable braided suture. Arthroscopy. 2004;20(4):407-413.
14. De Beer JF, van Rooyen K, Boezaart AP. Nicky’s knot—a new slip knot for arthroscopic surgery. Arthroscopy. 1998;14(1):109-110.
15. Loutzenheiser TD, Harryman DT 2nd, Yung SW, France MP, Sidles JA. Optimizing arthroscopic knots. Arthroscopy. 1995;11(2):199-206.
16. Wetzler MJ, Bartolozzi AR, Gillespie MJ, et al. Fatigue properties of suture anchors in anterior shoulder reconstructions: Mitek GII. Arthroscopy. 1996;12(6):687-693.
17. Barber FA, Herbert MA, Beavis RC. Cyclic load and failure behavior of arthroscopic knots and high strength sutures. Arthroscopy. 2009;25(2):192-199.
18. Richmond JC. A comparison of ultrasonic suture welding and traditional knot tying. Am J Sports Med. 200;29(3):297-299.
19. James JD, Wu MM, Batra EK, Rodeheaver GT, Edlich RF. Technical considerations in manual and instrument tying techniques. J Emerg Med. 1992;10(4):469-480.
20. Batra EK, Franz DA, Towler MA, et al. Influence of emergency physician’s tying technique on knot security. J Emerg Med. 1992;10(3):309-316.
21. Livermore RW, Chong AC, Prohaska DJ, Cooke FW, Jones TL. Knot security, loop security and elongation of braided polyblend sutures used for arthroscopic knots. Am J Orthop. 2010;39(12):569-576.
22. Tera H, Aberg C. The strength of suture knots after one week in vivo. Acta Chir Scand. 1976;142(4):301-307.
23. Babetty Z, Sümer A, Altintaş S, Ergüney S, Göksel S. Changes in knot-holding capacity of sliding knots in vivo and tissue reaction. Arch Surg. 1998;133(7):727-734.
24. Milia MJ, Peindl RD, Connor PM. Arthroscopic knot tying: the role of instrumentation in achieving knot security. Arthroscopy. 2005;21(1):69-76.
25. Lieurance RK, Pflaster DS, Abbott D, Nottage WM. Failure characteristics of various arthroscopically tied knots. Clin Orthop. 2003;(408):311-318.
26. Abbi G, Espinoza L, Odell T, Mahar A, Pedowitz R. Evaluation of 5 knots and 2 suture materials for arthroscopic rotator cuff repair: very strong sutures can still slip. Arthroscopy. 2006;22(1):38-43.
27. Wüst DM, Meyer DC, Favre P, Gerber C. Mechanical and handling properties of braided polyblend polyethylene sutures in comparison to braided polyester and monofilament polydioxanone sutures. Arthroscopy. 2006;22(11):1146-1153.
28. Mahar AT, Moezzi DM, Serra-Hsu F, Pedowitz RA. Comparison and performance characteristics of 3 different knots when tied with 2 suture materials used for shoulder arthroscopy. Arthroscopy. 2006;22(6):614.e1-e2.
1. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Knot security in simple sliding knots and its relationship to rotator cuff repair: how secure must the knot be? Arthroscopy. 2000;16(2):202-207.
2. Burkhart SS, Wirth MA, Simonich M, Salem D, Lanctot D, Athanasiou K. Loop security as a determinant of tissue fixation security. Arthroscopy. 1998;14(7):773-776.
3. Elkousy H, Hammerman SM, Edwards TB, et al. The arthroscopic square knot: a biomechanical comparison with open and arthroscopic knots. Arthroscopy. 2006;22(7):736-741.
4. Elkousy HA, Sekiya JK, Stabile KJ, McMahon PJ. A biomechanical comparison of arthroscopic sliding and sliding-locking knots. Arthroscopy. 2005;21(2):204-210.
5. Ilahi OA, Younas SA, Alexander J, Noble PC. Cyclic testing of arthroscopic knot security. Arthroscopy. 2004;20(1):62-68.
6. Loutzenheiser TD, Harryman DT 2nd, Ziegler DW, Yung SW. Optimizing arthroscopic knots using braided or monofilament suture. Arthroscopy. 1998;14(1):57-65.
7. Chan KC, Burkhart SS, Thiagarajan P, Goh JC. Optimization of stacked half-hitch knots for arthroscopic surgery. Arthroscopy. 2001;17(7):752-759.
8. Lee TQ, Matsuura PA, Fogolin RP, Lin AC, Kim D, McMahon PJ. Arthroscopic suture tying: a comparison of knot types and suture materials. Arthroscopy. 2001;17(4):348-352.
9. Mishra DK, Cannon WD Jr, Lucas DJ, Belzer JP. Elongation of arthroscopically tied knots. Am J Sports Med. 1997;25(1):113-117.
10. Kim SH, Ha KI, Kim SH, Kim JS. Significance of the internal locking mechanism for loop security enhancement in the arthroscopic knot. Arthroscopy. 2001;17(8):850-855.
11. Weston PV. A new clinch knot. Obstet Gynecol. 1991;78(1):144-147.
12. Lo IK, Burkhart SS, Chan KC, Athanasiou K. Arthroscopic knots: determining the optimal balance of loop security and knot security. Arthroscopy. 2004;20(5):489-502.
13. Lo IK, Burkhart SS, Athanasiou K. Abrasion resistance of two types of nonabsorbable braided suture. Arthroscopy. 2004;20(4):407-413.
14. De Beer JF, van Rooyen K, Boezaart AP. Nicky’s knot—a new slip knot for arthroscopic surgery. Arthroscopy. 1998;14(1):109-110.
15. Loutzenheiser TD, Harryman DT 2nd, Yung SW, France MP, Sidles JA. Optimizing arthroscopic knots. Arthroscopy. 1995;11(2):199-206.
16. Wetzler MJ, Bartolozzi AR, Gillespie MJ, et al. Fatigue properties of suture anchors in anterior shoulder reconstructions: Mitek GII. Arthroscopy. 1996;12(6):687-693.
17. Barber FA, Herbert MA, Beavis RC. Cyclic load and failure behavior of arthroscopic knots and high strength sutures. Arthroscopy. 2009;25(2):192-199.
18. Richmond JC. A comparison of ultrasonic suture welding and traditional knot tying. Am J Sports Med. 200;29(3):297-299.
19. James JD, Wu MM, Batra EK, Rodeheaver GT, Edlich RF. Technical considerations in manual and instrument tying techniques. J Emerg Med. 1992;10(4):469-480.
20. Batra EK, Franz DA, Towler MA, et al. Influence of emergency physician’s tying technique on knot security. J Emerg Med. 1992;10(3):309-316.
21. Livermore RW, Chong AC, Prohaska DJ, Cooke FW, Jones TL. Knot security, loop security and elongation of braided polyblend sutures used for arthroscopic knots. Am J Orthop. 2010;39(12):569-576.
22. Tera H, Aberg C. The strength of suture knots after one week in vivo. Acta Chir Scand. 1976;142(4):301-307.
23. Babetty Z, Sümer A, Altintaş S, Ergüney S, Göksel S. Changes in knot-holding capacity of sliding knots in vivo and tissue reaction. Arch Surg. 1998;133(7):727-734.
24. Milia MJ, Peindl RD, Connor PM. Arthroscopic knot tying: the role of instrumentation in achieving knot security. Arthroscopy. 2005;21(1):69-76.
25. Lieurance RK, Pflaster DS, Abbott D, Nottage WM. Failure characteristics of various arthroscopically tied knots. Clin Orthop. 2003;(408):311-318.
26. Abbi G, Espinoza L, Odell T, Mahar A, Pedowitz R. Evaluation of 5 knots and 2 suture materials for arthroscopic rotator cuff repair: very strong sutures can still slip. Arthroscopy. 2006;22(1):38-43.
27. Wüst DM, Meyer DC, Favre P, Gerber C. Mechanical and handling properties of braided polyblend polyethylene sutures in comparison to braided polyester and monofilament polydioxanone sutures. Arthroscopy. 2006;22(11):1146-1153.
28. Mahar AT, Moezzi DM, Serra-Hsu F, Pedowitz RA. Comparison and performance characteristics of 3 different knots when tied with 2 suture materials used for shoulder arthroscopy. Arthroscopy. 2006;22(6):614.e1-e2.
Arthroscopic Anterior Cruciate Ligament Reconstruction Using a Flexible Guide Pin With a Rigid Reamer
Anterior cruciate ligament (ACL) injuries are common, and arthroscopic ACL reconstruction is a routine procedure. Successful ACL reconstruction requires correct placement of the graft within the anatomical insertion of the native ACL.1-3 Errors in surgical technique—specifically, improper femoral tunnel placement—are the most common cause of graft failure in patients who present with recurrent instability after ACL reconstruction.4 There has been much emphasis on placing the tunnel more centrally in the ACL footprint as well as in a more horizontal position, which is thought to provide better rotational control and anterior-to-posterior translational stability.5-7
Two common techniques for creating the femoral tunnel, transtibial and anteromedial drilling, have their unique limitations. Transtibial drilling can place the tunnel high in the notch, resulting in nonanatomical, vertical graft placement.8,9 This technique can be modified to obtain a more anatomical tunnel, but the risk is the tunnel will be short and close to the joint line.10 To avoid these difficulties, surgeons began using an anteromedial portal.11,12 Although anteromedial drilling places the tunnel in a more anatomical position, it too has drawbacks, including the need to hyperflex the knee, a short tunnel, damage to articular cartilage, proximity to neurovascular structures, and difficulty in visualization during drilling.13-16
Femoral tunnel drilling techniques using flexible guide pins and reamers have been developed to address the limitations of rigid instruments. When we first started using flexible instruments through anteromedial portals, there were multiple incidents of reamer breakage during drilling. We therefore developed a technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position. The patient described in this article provided written informed consent for print and electronic publication of this report.
Technique
We begin with our standard arthroscopic portals, including superolateral outflow, lateral parapatellar, and medial parapatellar portals. The medial parapatellar portal is placed under direct visualization with insertion of an 18-gauge spinal needle, ensuring the trajectory reaches the anatomical location of the native ACL on the lateral femoral condyle (LFC). The ACL stump is débrided with a shaver and a radiofrequency ablator, leaving a remnant of tissue to assist with tunnel placement. We do not routinely perform a notchplasty unless there is a concern about possible graft impingement, or the notch is abnormally small. The anatomical footprint is marked with a small awl (Figure 1), and the arthroscope is moved into the anteromedial portal to confirm anatomical placement of the awl mark (Figure 2).
With the knee flexed to 100° to 110°, a flexible 2.7-mm nitonol guide pin (Smith & Nephew, Memphis, Tennessee) is placed freehand through the anteromedial portal into the anatomical footprint of the ACL, marked by the awl, and is passed through the femur before exiting the lateral skin. In most cases, we prefer freehand placement of the awl and pin; however, a femoral drill guide may be used to place the pin into the anatomical footprint of the ACL (Figure 3). The flexible pin allows for knee hyperflexion, clearance of the medial femoral condyle, central placement of the pin between the footprints of the anteromedial and posterolateral bundles for anatomical single-bundle reconstruction, and drilling of a long tunnel (average, 35-40 mm). The pin has a black laser marking that should be placed at the edge of the articular surface of the LFC to ensure appropriate depth of insertion (Figure 4).
A small incision is then made around the guide wire on the lateral thigh, and an outside-in depth gauge is used to obtain an accurate length for the femoral tunnel. The gauge must abut the femoral cortex for accurate assessment of tunnel length. We use an Endobutton (Smith & Nephew) for fixation of the graft in the tunnel. The measured length of the tunnel is used to select an Endobutton of appropriate size and the proper reaming depth for suspension. We routinely use a 10- or 15-mm Endobutton, which provides an average 20 to 25 mm of graft inside the bony tunnel. The knee may then be relaxed to a normal resting flexion angle off the side of the bed, and the arthroscope is inserted into a medial portal or an accessory anteromedial portal to ensure anatomical placement of the pin. Using a flexible guide pin allows the knee to be relatively extended, providing good visualization of overall positioning in relation to the posterior wall of the LFC, whereas keeping the knee in a flexed position (as with a rigid guide pin) can often compromise this visualization.
Using a solid reamer corresponding to the size of the graft, we drill over the guide pin to the appropriate depth, again with the knee hyperflexed (Figure 5), making sure not to breach the lateral femoral cortex, which would compromise fixation with the Endobutton. After drilling with the rigid reamer is completed, placement of the tunnel in an anatomical position is again confirmed with the knee in the normal resting flexion angle (Figure 6). Once the tibial tunnel is drilled at the anatomical footprint, the graft is passed with the proper-length Endobutton and is fixed on the tibial side with a bioabsorbable interference screw 1 to 2 mm larger than the soft-tissue graft and tibial tunnel size. The knee is flexed to 30° while the tibial screw is placed. Graft tension and impingement are then checked (Figure 7). Postoperative anteroposterior and lateral radiographs of the knee may be obtained to confirm anatomical placement of the tunnels as well as proper positioning of the Endobutton (Figures 8A, 8B).
Discussion
Successful ACL reconstruction depends heavily on anatomical tunnel positioning. Failure to place the femoral tunnel in the anatomical footprint of the native ACL results in incomplete restoration of knee kinematics, rotational instability, and graft failure.1-7 Two common techniques for creating this tunnel, transtibial and anteromedial drilling, can reliably place it in an anatomical position. Each technique, however, has limitations. Transtibial drilling can place the tunnel too vertical and high in the notch, or produce a short tibial tunnel close to the joint line.8-10 Anteromedial drilling requires knee hyperflexion, risks damaging the articular cartilage and nearby neurovascular structures, and makes visualization difficult.13-16
One option for addressing some of the difficulties and limitations with anteromedial drilling is to use flexible guide pins and reamers, as first introduced by Cain and Clancy.1 In a cadaveric study, Silver and colleagues17 demonstrated that interosseous tunnels drilled with flexible guide pins were on average more than 6 mm longer than those drilled with rigid pins and consistently were 40 mm or longer. In addition, all tunnels drilled with flexible guide pins were on average 42.3 mm away from the peroneal nerve and 26.1 mm away from the femoral origin of the lateral collateral ligament—safe distances.
Steiner and Smart18 compared flexible and rigid instruments used to drill transtibial and anteromedial (without hyperflexion) anatomical femoral tunnels in ACL reconstruction in cadaveric knees. Although transtibial drilling with flexible pins produced anatomical tunnels, the tunnels were shorter, and the pins exited more posterior in comparison with anteromedial drilling with flexible pins. Transtibial tunnels drilled with rigid pins were nonanatomical and exited more superior and anterior on the femur, resulting in longer tunnels. Anteromedial tunnels drilled with rigid and flexible pins were placed anatomically, but flexible pins produced longer tunnels, did not require hyperflexion (120°), could easily be placed with the knee in 90° of flexion, and did not violate the posterior femoral cortex.
Five times in our early experience with flexible guide pins and reamers, the reamer broke when LFC reaming was initiated. In each case, the broken reamer was retrieved. However, these complications resulted in increased surgical time and cost. In addition, an unretrievable reamer could have caused further injury and suboptimal outcomes. We subsequently developed an anteromedial technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position (Figure 9). The flexible pin provides consistent placement of anatomical tunnels averaging 35 to 40 mm in length. Use of the flexible pin does not require constant hyperflexion of the knee, and it allows for better visualization of the posterior wall of the LFC, ensures anatomical graft placement, and decreases the risk of damaging articular cartilage and causing neurovascular injury. Use of the rigid reamer negates the risks and additional costs associated with reamer breakage. It is unclear why 5 flexible reamers broke during our early use of flexible guide pins and reamers, but it is possible that, because of the patients’ anatomy, placement of the pin in the correct anatomical position in the ACL footprint put a significant amount of abnormal stress on the reamer during tunnel reaming, leading to breakage and failure.
A short femoral tunnel is a common complication of using an anteromedial portal for tunnel drilling.13-16 With the technique we have been using, tunnel lengths average 35 to 40 mm. To address the occasional shorter tunnel, we use Endobutton Direct (Smith & Nephew), which allows for direct fixation of the graft on the button, maximizing the amount of graft in the femoral tunnel and minimizing graft–tunnel length mismatch. In the event there is a lateral wall breach during overdrilling with the reamer, the femoral graft may be secured with screw and post, with interference screw, or with the larger Xtendobuton (Smith & Nephew).
We have successfully used this technique with bone–patellar tendon–bone (BPTB) and hamstring autografts, as well as allografts. Complications, such as graft–tunnel length mismatch, have been uncommon, but, when using BPTB grafts, passing the bone block into the femoral tunnel can be difficult because of the sharp turn required.
Conclusion
Successful ACL reconstruction depends heavily on placement of the graft within the anatomical insertion of the native ACL. With the development of techniques that use flexible guide pins and reamers, it has become possible to place longer anatomical femoral tunnels without the need for hyperflexion. Use of a flexible guide pin with a rigid reamer allows placement of longer anatomical tunnels through an anteromedial portal, reduces time spent with the knee in hyperflexion, provides better viewing, poses less risk of damage to the articular cartilage and neurovascular structures, and at a lower cost with less risk of reamer breakage. In addition, this technique can be used with a variety of graft options, including BPTB grafts, hamstring autografts, and allografts.
1. Cain EL Jr, Clancy WG Jr. Anatomic endoscopic anterior cruciate ligament reconstruction with patella tendon autograft. Orthop Clin North Am. 2002;33(4):717-725.
2. Chhabra A, Starman JS, Ferretti M, Vidal AF, Zantop T, Fu FH. Anatomic, radiographic, biomechanical, and kinematic evaluation of the anterior cruciate ligament and its two functional bundles. J Bone Joint Surg Am. 2006;88(suppl 4):2-10.
3. Christel P, Sahasrabudhe A, Basdekis G. Anatomic double-bundle anterior cruciate ligament reconstruction with anatomic aimers. Arthroscopy. 2008;24(10):1146-1151.
4. Allen CR, Giffin JR, Harner CD. Revision anterior cruciate ligament reconstruction. Orthop Clin North Am. 2003;34(1):79-98.
5. Miller CD, Gerdeman AC, Hart JM, et al. A comparison of 2 drilling techniques on the femoral tunnel for anterior cruciate ligament reconstruction. Arthroscopy. 2011;27(3):372-379.
6. Seon JK, Park SJ, Lee KB, Seo HY, Kim MS, Song EK. In vivo stability and clinical comparison of anterior cruciate ligament reconstruction using low or high femoral tunnel positions. Am J Sports Med. 2011;39(1):127-133.
7. Steiner ME, Battaglia TC, Heming JF, Rand JD, Festa A, Baria M. Independent drilling outperforms conventional transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2009;37(10):1912-1919.
8. Kopf S, Forsythe B, Wong AK, et al. Nonanatomic tunnel position in traditional transtibial single-bundle anterior cruciate ligament reconstruction evaluated by three-dimensional computed tomography. J Bone Joint Surg Am. 2010;92(6):1427-1431.
9. Tompkins M, Milewski MD, Brockmeier SF, Gaskin CM, Hart JM, Miller MD. Anatomic femoral tunnel drilling in anterior cruciate ligament reconstruction: use of an accessory medial portal versus traditional transtibial drilling. Am J Sports Med. 2012;40(6):1313-1321.
10. Heming JF, Rand J, Steiner ME. Anatomical limitations of transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2007;35(10):1708-1715.
11. Harner CD, Honkamp NJ, Ranawat AS. Anteromedial portal technique for creating the anterior cruciate ligament femoral tunnel. Arthroscopy. 2008;24(1):113-115.
12. Lubowitz JH. Anteromedial portal technique for the anterior cruciate ligament femoral socket: pitfalls and solutions. Arthroscopy. 2009;25(1):95-101.
13. Basdekis G, Abisafi C, Christel P. Influence of knee flexion angle on femoral tunnel characteristics when drilled through the anteromedial portal during anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(4):459-464.
14. Zantop T, Haase AK, Fu FH, Petersen W. Potential risk of cartilage damage in double bundle ACL reconstruction: impact of knee flexion angle and portal location on the femoral PL bundle tunnel. Arch Orthop Trauma Surg. 2008;128(5):509-513.
15. Farrow LD, Parker RD. The relationship of lateral anatomic structures to exiting guide pins during femoral tunnel preparation utilizing an accessory medial portal. Knee Surg Sports Traumatol Arthrosc. 2010;18(6):747-753.
16. Nakamura M, Deie M, Shibuya H, et al. Potential risks of femoral tunnel drilling through the far anteromedial portal: a cadaveric study. Arthroscopy. 2009;25(5):481-487.
17. Silver AG, Kaar SG, Grisell MK, Reagan JM, Farrow LD. Comparison between rigid and flexible systems for drilling the femoral tunnel through an anteromedial portal in anterior cruciate ligament reconstruction. Arthroscopy. 2010;26(6):790-795.
18. Steiner ME, Smart LR. Flexible instruments outperform rigid instruments to place anatomic anterior cruciate ligament femoral tunnels without hyperflexion. Arthroscopy. 2012;28(6):835-843.
Anterior cruciate ligament (ACL) injuries are common, and arthroscopic ACL reconstruction is a routine procedure. Successful ACL reconstruction requires correct placement of the graft within the anatomical insertion of the native ACL.1-3 Errors in surgical technique—specifically, improper femoral tunnel placement—are the most common cause of graft failure in patients who present with recurrent instability after ACL reconstruction.4 There has been much emphasis on placing the tunnel more centrally in the ACL footprint as well as in a more horizontal position, which is thought to provide better rotational control and anterior-to-posterior translational stability.5-7
Two common techniques for creating the femoral tunnel, transtibial and anteromedial drilling, have their unique limitations. Transtibial drilling can place the tunnel high in the notch, resulting in nonanatomical, vertical graft placement.8,9 This technique can be modified to obtain a more anatomical tunnel, but the risk is the tunnel will be short and close to the joint line.10 To avoid these difficulties, surgeons began using an anteromedial portal.11,12 Although anteromedial drilling places the tunnel in a more anatomical position, it too has drawbacks, including the need to hyperflex the knee, a short tunnel, damage to articular cartilage, proximity to neurovascular structures, and difficulty in visualization during drilling.13-16
Femoral tunnel drilling techniques using flexible guide pins and reamers have been developed to address the limitations of rigid instruments. When we first started using flexible instruments through anteromedial portals, there were multiple incidents of reamer breakage during drilling. We therefore developed a technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position. The patient described in this article provided written informed consent for print and electronic publication of this report.
Technique
We begin with our standard arthroscopic portals, including superolateral outflow, lateral parapatellar, and medial parapatellar portals. The medial parapatellar portal is placed under direct visualization with insertion of an 18-gauge spinal needle, ensuring the trajectory reaches the anatomical location of the native ACL on the lateral femoral condyle (LFC). The ACL stump is débrided with a shaver and a radiofrequency ablator, leaving a remnant of tissue to assist with tunnel placement. We do not routinely perform a notchplasty unless there is a concern about possible graft impingement, or the notch is abnormally small. The anatomical footprint is marked with a small awl (Figure 1), and the arthroscope is moved into the anteromedial portal to confirm anatomical placement of the awl mark (Figure 2).
With the knee flexed to 100° to 110°, a flexible 2.7-mm nitonol guide pin (Smith & Nephew, Memphis, Tennessee) is placed freehand through the anteromedial portal into the anatomical footprint of the ACL, marked by the awl, and is passed through the femur before exiting the lateral skin. In most cases, we prefer freehand placement of the awl and pin; however, a femoral drill guide may be used to place the pin into the anatomical footprint of the ACL (Figure 3). The flexible pin allows for knee hyperflexion, clearance of the medial femoral condyle, central placement of the pin between the footprints of the anteromedial and posterolateral bundles for anatomical single-bundle reconstruction, and drilling of a long tunnel (average, 35-40 mm). The pin has a black laser marking that should be placed at the edge of the articular surface of the LFC to ensure appropriate depth of insertion (Figure 4).
A small incision is then made around the guide wire on the lateral thigh, and an outside-in depth gauge is used to obtain an accurate length for the femoral tunnel. The gauge must abut the femoral cortex for accurate assessment of tunnel length. We use an Endobutton (Smith & Nephew) for fixation of the graft in the tunnel. The measured length of the tunnel is used to select an Endobutton of appropriate size and the proper reaming depth for suspension. We routinely use a 10- or 15-mm Endobutton, which provides an average 20 to 25 mm of graft inside the bony tunnel. The knee may then be relaxed to a normal resting flexion angle off the side of the bed, and the arthroscope is inserted into a medial portal or an accessory anteromedial portal to ensure anatomical placement of the pin. Using a flexible guide pin allows the knee to be relatively extended, providing good visualization of overall positioning in relation to the posterior wall of the LFC, whereas keeping the knee in a flexed position (as with a rigid guide pin) can often compromise this visualization.
Using a solid reamer corresponding to the size of the graft, we drill over the guide pin to the appropriate depth, again with the knee hyperflexed (Figure 5), making sure not to breach the lateral femoral cortex, which would compromise fixation with the Endobutton. After drilling with the rigid reamer is completed, placement of the tunnel in an anatomical position is again confirmed with the knee in the normal resting flexion angle (Figure 6). Once the tibial tunnel is drilled at the anatomical footprint, the graft is passed with the proper-length Endobutton and is fixed on the tibial side with a bioabsorbable interference screw 1 to 2 mm larger than the soft-tissue graft and tibial tunnel size. The knee is flexed to 30° while the tibial screw is placed. Graft tension and impingement are then checked (Figure 7). Postoperative anteroposterior and lateral radiographs of the knee may be obtained to confirm anatomical placement of the tunnels as well as proper positioning of the Endobutton (Figures 8A, 8B).
Discussion
Successful ACL reconstruction depends heavily on anatomical tunnel positioning. Failure to place the femoral tunnel in the anatomical footprint of the native ACL results in incomplete restoration of knee kinematics, rotational instability, and graft failure.1-7 Two common techniques for creating this tunnel, transtibial and anteromedial drilling, can reliably place it in an anatomical position. Each technique, however, has limitations. Transtibial drilling can place the tunnel too vertical and high in the notch, or produce a short tibial tunnel close to the joint line.8-10 Anteromedial drilling requires knee hyperflexion, risks damaging the articular cartilage and nearby neurovascular structures, and makes visualization difficult.13-16
One option for addressing some of the difficulties and limitations with anteromedial drilling is to use flexible guide pins and reamers, as first introduced by Cain and Clancy.1 In a cadaveric study, Silver and colleagues17 demonstrated that interosseous tunnels drilled with flexible guide pins were on average more than 6 mm longer than those drilled with rigid pins and consistently were 40 mm or longer. In addition, all tunnels drilled with flexible guide pins were on average 42.3 mm away from the peroneal nerve and 26.1 mm away from the femoral origin of the lateral collateral ligament—safe distances.
Steiner and Smart18 compared flexible and rigid instruments used to drill transtibial and anteromedial (without hyperflexion) anatomical femoral tunnels in ACL reconstruction in cadaveric knees. Although transtibial drilling with flexible pins produced anatomical tunnels, the tunnels were shorter, and the pins exited more posterior in comparison with anteromedial drilling with flexible pins. Transtibial tunnels drilled with rigid pins were nonanatomical and exited more superior and anterior on the femur, resulting in longer tunnels. Anteromedial tunnels drilled with rigid and flexible pins were placed anatomically, but flexible pins produced longer tunnels, did not require hyperflexion (120°), could easily be placed with the knee in 90° of flexion, and did not violate the posterior femoral cortex.
Five times in our early experience with flexible guide pins and reamers, the reamer broke when LFC reaming was initiated. In each case, the broken reamer was retrieved. However, these complications resulted in increased surgical time and cost. In addition, an unretrievable reamer could have caused further injury and suboptimal outcomes. We subsequently developed an anteromedial technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position (Figure 9). The flexible pin provides consistent placement of anatomical tunnels averaging 35 to 40 mm in length. Use of the flexible pin does not require constant hyperflexion of the knee, and it allows for better visualization of the posterior wall of the LFC, ensures anatomical graft placement, and decreases the risk of damaging articular cartilage and causing neurovascular injury. Use of the rigid reamer negates the risks and additional costs associated with reamer breakage. It is unclear why 5 flexible reamers broke during our early use of flexible guide pins and reamers, but it is possible that, because of the patients’ anatomy, placement of the pin in the correct anatomical position in the ACL footprint put a significant amount of abnormal stress on the reamer during tunnel reaming, leading to breakage and failure.
A short femoral tunnel is a common complication of using an anteromedial portal for tunnel drilling.13-16 With the technique we have been using, tunnel lengths average 35 to 40 mm. To address the occasional shorter tunnel, we use Endobutton Direct (Smith & Nephew), which allows for direct fixation of the graft on the button, maximizing the amount of graft in the femoral tunnel and minimizing graft–tunnel length mismatch. In the event there is a lateral wall breach during overdrilling with the reamer, the femoral graft may be secured with screw and post, with interference screw, or with the larger Xtendobuton (Smith & Nephew).
We have successfully used this technique with bone–patellar tendon–bone (BPTB) and hamstring autografts, as well as allografts. Complications, such as graft–tunnel length mismatch, have been uncommon, but, when using BPTB grafts, passing the bone block into the femoral tunnel can be difficult because of the sharp turn required.
Conclusion
Successful ACL reconstruction depends heavily on placement of the graft within the anatomical insertion of the native ACL. With the development of techniques that use flexible guide pins and reamers, it has become possible to place longer anatomical femoral tunnels without the need for hyperflexion. Use of a flexible guide pin with a rigid reamer allows placement of longer anatomical tunnels through an anteromedial portal, reduces time spent with the knee in hyperflexion, provides better viewing, poses less risk of damage to the articular cartilage and neurovascular structures, and at a lower cost with less risk of reamer breakage. In addition, this technique can be used with a variety of graft options, including BPTB grafts, hamstring autografts, and allografts.
Anterior cruciate ligament (ACL) injuries are common, and arthroscopic ACL reconstruction is a routine procedure. Successful ACL reconstruction requires correct placement of the graft within the anatomical insertion of the native ACL.1-3 Errors in surgical technique—specifically, improper femoral tunnel placement—are the most common cause of graft failure in patients who present with recurrent instability after ACL reconstruction.4 There has been much emphasis on placing the tunnel more centrally in the ACL footprint as well as in a more horizontal position, which is thought to provide better rotational control and anterior-to-posterior translational stability.5-7
Two common techniques for creating the femoral tunnel, transtibial and anteromedial drilling, have their unique limitations. Transtibial drilling can place the tunnel high in the notch, resulting in nonanatomical, vertical graft placement.8,9 This technique can be modified to obtain a more anatomical tunnel, but the risk is the tunnel will be short and close to the joint line.10 To avoid these difficulties, surgeons began using an anteromedial portal.11,12 Although anteromedial drilling places the tunnel in a more anatomical position, it too has drawbacks, including the need to hyperflex the knee, a short tunnel, damage to articular cartilage, proximity to neurovascular structures, and difficulty in visualization during drilling.13-16
Femoral tunnel drilling techniques using flexible guide pins and reamers have been developed to address the limitations of rigid instruments. When we first started using flexible instruments through anteromedial portals, there were multiple incidents of reamer breakage during drilling. We therefore developed a technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position. The patient described in this article provided written informed consent for print and electronic publication of this report.
Technique
We begin with our standard arthroscopic portals, including superolateral outflow, lateral parapatellar, and medial parapatellar portals. The medial parapatellar portal is placed under direct visualization with insertion of an 18-gauge spinal needle, ensuring the trajectory reaches the anatomical location of the native ACL on the lateral femoral condyle (LFC). The ACL stump is débrided with a shaver and a radiofrequency ablator, leaving a remnant of tissue to assist with tunnel placement. We do not routinely perform a notchplasty unless there is a concern about possible graft impingement, or the notch is abnormally small. The anatomical footprint is marked with a small awl (Figure 1), and the arthroscope is moved into the anteromedial portal to confirm anatomical placement of the awl mark (Figure 2).
With the knee flexed to 100° to 110°, a flexible 2.7-mm nitonol guide pin (Smith & Nephew, Memphis, Tennessee) is placed freehand through the anteromedial portal into the anatomical footprint of the ACL, marked by the awl, and is passed through the femur before exiting the lateral skin. In most cases, we prefer freehand placement of the awl and pin; however, a femoral drill guide may be used to place the pin into the anatomical footprint of the ACL (Figure 3). The flexible pin allows for knee hyperflexion, clearance of the medial femoral condyle, central placement of the pin between the footprints of the anteromedial and posterolateral bundles for anatomical single-bundle reconstruction, and drilling of a long tunnel (average, 35-40 mm). The pin has a black laser marking that should be placed at the edge of the articular surface of the LFC to ensure appropriate depth of insertion (Figure 4).
A small incision is then made around the guide wire on the lateral thigh, and an outside-in depth gauge is used to obtain an accurate length for the femoral tunnel. The gauge must abut the femoral cortex for accurate assessment of tunnel length. We use an Endobutton (Smith & Nephew) for fixation of the graft in the tunnel. The measured length of the tunnel is used to select an Endobutton of appropriate size and the proper reaming depth for suspension. We routinely use a 10- or 15-mm Endobutton, which provides an average 20 to 25 mm of graft inside the bony tunnel. The knee may then be relaxed to a normal resting flexion angle off the side of the bed, and the arthroscope is inserted into a medial portal or an accessory anteromedial portal to ensure anatomical placement of the pin. Using a flexible guide pin allows the knee to be relatively extended, providing good visualization of overall positioning in relation to the posterior wall of the LFC, whereas keeping the knee in a flexed position (as with a rigid guide pin) can often compromise this visualization.
Using a solid reamer corresponding to the size of the graft, we drill over the guide pin to the appropriate depth, again with the knee hyperflexed (Figure 5), making sure not to breach the lateral femoral cortex, which would compromise fixation with the Endobutton. After drilling with the rigid reamer is completed, placement of the tunnel in an anatomical position is again confirmed with the knee in the normal resting flexion angle (Figure 6). Once the tibial tunnel is drilled at the anatomical footprint, the graft is passed with the proper-length Endobutton and is fixed on the tibial side with a bioabsorbable interference screw 1 to 2 mm larger than the soft-tissue graft and tibial tunnel size. The knee is flexed to 30° while the tibial screw is placed. Graft tension and impingement are then checked (Figure 7). Postoperative anteroposterior and lateral radiographs of the knee may be obtained to confirm anatomical placement of the tunnels as well as proper positioning of the Endobutton (Figures 8A, 8B).
Discussion
Successful ACL reconstruction depends heavily on anatomical tunnel positioning. Failure to place the femoral tunnel in the anatomical footprint of the native ACL results in incomplete restoration of knee kinematics, rotational instability, and graft failure.1-7 Two common techniques for creating this tunnel, transtibial and anteromedial drilling, can reliably place it in an anatomical position. Each technique, however, has limitations. Transtibial drilling can place the tunnel too vertical and high in the notch, or produce a short tibial tunnel close to the joint line.8-10 Anteromedial drilling requires knee hyperflexion, risks damaging the articular cartilage and nearby neurovascular structures, and makes visualization difficult.13-16
One option for addressing some of the difficulties and limitations with anteromedial drilling is to use flexible guide pins and reamers, as first introduced by Cain and Clancy.1 In a cadaveric study, Silver and colleagues17 demonstrated that interosseous tunnels drilled with flexible guide pins were on average more than 6 mm longer than those drilled with rigid pins and consistently were 40 mm or longer. In addition, all tunnels drilled with flexible guide pins were on average 42.3 mm away from the peroneal nerve and 26.1 mm away from the femoral origin of the lateral collateral ligament—safe distances.
Steiner and Smart18 compared flexible and rigid instruments used to drill transtibial and anteromedial (without hyperflexion) anatomical femoral tunnels in ACL reconstruction in cadaveric knees. Although transtibial drilling with flexible pins produced anatomical tunnels, the tunnels were shorter, and the pins exited more posterior in comparison with anteromedial drilling with flexible pins. Transtibial tunnels drilled with rigid pins were nonanatomical and exited more superior and anterior on the femur, resulting in longer tunnels. Anteromedial tunnels drilled with rigid and flexible pins were placed anatomically, but flexible pins produced longer tunnels, did not require hyperflexion (120°), could easily be placed with the knee in 90° of flexion, and did not violate the posterior femoral cortex.
Five times in our early experience with flexible guide pins and reamers, the reamer broke when LFC reaming was initiated. In each case, the broken reamer was retrieved. However, these complications resulted in increased surgical time and cost. In addition, an unretrievable reamer could have caused further injury and suboptimal outcomes. We subsequently developed an anteromedial technique that uses a flexible guide pin with a rigid reamer to place the femoral tunnel in an anatomical position (Figure 9). The flexible pin provides consistent placement of anatomical tunnels averaging 35 to 40 mm in length. Use of the flexible pin does not require constant hyperflexion of the knee, and it allows for better visualization of the posterior wall of the LFC, ensures anatomical graft placement, and decreases the risk of damaging articular cartilage and causing neurovascular injury. Use of the rigid reamer negates the risks and additional costs associated with reamer breakage. It is unclear why 5 flexible reamers broke during our early use of flexible guide pins and reamers, but it is possible that, because of the patients’ anatomy, placement of the pin in the correct anatomical position in the ACL footprint put a significant amount of abnormal stress on the reamer during tunnel reaming, leading to breakage and failure.
A short femoral tunnel is a common complication of using an anteromedial portal for tunnel drilling.13-16 With the technique we have been using, tunnel lengths average 35 to 40 mm. To address the occasional shorter tunnel, we use Endobutton Direct (Smith & Nephew), which allows for direct fixation of the graft on the button, maximizing the amount of graft in the femoral tunnel and minimizing graft–tunnel length mismatch. In the event there is a lateral wall breach during overdrilling with the reamer, the femoral graft may be secured with screw and post, with interference screw, or with the larger Xtendobuton (Smith & Nephew).
We have successfully used this technique with bone–patellar tendon–bone (BPTB) and hamstring autografts, as well as allografts. Complications, such as graft–tunnel length mismatch, have been uncommon, but, when using BPTB grafts, passing the bone block into the femoral tunnel can be difficult because of the sharp turn required.
Conclusion
Successful ACL reconstruction depends heavily on placement of the graft within the anatomical insertion of the native ACL. With the development of techniques that use flexible guide pins and reamers, it has become possible to place longer anatomical femoral tunnels without the need for hyperflexion. Use of a flexible guide pin with a rigid reamer allows placement of longer anatomical tunnels through an anteromedial portal, reduces time spent with the knee in hyperflexion, provides better viewing, poses less risk of damage to the articular cartilage and neurovascular structures, and at a lower cost with less risk of reamer breakage. In addition, this technique can be used with a variety of graft options, including BPTB grafts, hamstring autografts, and allografts.
1. Cain EL Jr, Clancy WG Jr. Anatomic endoscopic anterior cruciate ligament reconstruction with patella tendon autograft. Orthop Clin North Am. 2002;33(4):717-725.
2. Chhabra A, Starman JS, Ferretti M, Vidal AF, Zantop T, Fu FH. Anatomic, radiographic, biomechanical, and kinematic evaluation of the anterior cruciate ligament and its two functional bundles. J Bone Joint Surg Am. 2006;88(suppl 4):2-10.
3. Christel P, Sahasrabudhe A, Basdekis G. Anatomic double-bundle anterior cruciate ligament reconstruction with anatomic aimers. Arthroscopy. 2008;24(10):1146-1151.
4. Allen CR, Giffin JR, Harner CD. Revision anterior cruciate ligament reconstruction. Orthop Clin North Am. 2003;34(1):79-98.
5. Miller CD, Gerdeman AC, Hart JM, et al. A comparison of 2 drilling techniques on the femoral tunnel for anterior cruciate ligament reconstruction. Arthroscopy. 2011;27(3):372-379.
6. Seon JK, Park SJ, Lee KB, Seo HY, Kim MS, Song EK. In vivo stability and clinical comparison of anterior cruciate ligament reconstruction using low or high femoral tunnel positions. Am J Sports Med. 2011;39(1):127-133.
7. Steiner ME, Battaglia TC, Heming JF, Rand JD, Festa A, Baria M. Independent drilling outperforms conventional transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2009;37(10):1912-1919.
8. Kopf S, Forsythe B, Wong AK, et al. Nonanatomic tunnel position in traditional transtibial single-bundle anterior cruciate ligament reconstruction evaluated by three-dimensional computed tomography. J Bone Joint Surg Am. 2010;92(6):1427-1431.
9. Tompkins M, Milewski MD, Brockmeier SF, Gaskin CM, Hart JM, Miller MD. Anatomic femoral tunnel drilling in anterior cruciate ligament reconstruction: use of an accessory medial portal versus traditional transtibial drilling. Am J Sports Med. 2012;40(6):1313-1321.
10. Heming JF, Rand J, Steiner ME. Anatomical limitations of transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2007;35(10):1708-1715.
11. Harner CD, Honkamp NJ, Ranawat AS. Anteromedial portal technique for creating the anterior cruciate ligament femoral tunnel. Arthroscopy. 2008;24(1):113-115.
12. Lubowitz JH. Anteromedial portal technique for the anterior cruciate ligament femoral socket: pitfalls and solutions. Arthroscopy. 2009;25(1):95-101.
13. Basdekis G, Abisafi C, Christel P. Influence of knee flexion angle on femoral tunnel characteristics when drilled through the anteromedial portal during anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(4):459-464.
14. Zantop T, Haase AK, Fu FH, Petersen W. Potential risk of cartilage damage in double bundle ACL reconstruction: impact of knee flexion angle and portal location on the femoral PL bundle tunnel. Arch Orthop Trauma Surg. 2008;128(5):509-513.
15. Farrow LD, Parker RD. The relationship of lateral anatomic structures to exiting guide pins during femoral tunnel preparation utilizing an accessory medial portal. Knee Surg Sports Traumatol Arthrosc. 2010;18(6):747-753.
16. Nakamura M, Deie M, Shibuya H, et al. Potential risks of femoral tunnel drilling through the far anteromedial portal: a cadaveric study. Arthroscopy. 2009;25(5):481-487.
17. Silver AG, Kaar SG, Grisell MK, Reagan JM, Farrow LD. Comparison between rigid and flexible systems for drilling the femoral tunnel through an anteromedial portal in anterior cruciate ligament reconstruction. Arthroscopy. 2010;26(6):790-795.
18. Steiner ME, Smart LR. Flexible instruments outperform rigid instruments to place anatomic anterior cruciate ligament femoral tunnels without hyperflexion. Arthroscopy. 2012;28(6):835-843.
1. Cain EL Jr, Clancy WG Jr. Anatomic endoscopic anterior cruciate ligament reconstruction with patella tendon autograft. Orthop Clin North Am. 2002;33(4):717-725.
2. Chhabra A, Starman JS, Ferretti M, Vidal AF, Zantop T, Fu FH. Anatomic, radiographic, biomechanical, and kinematic evaluation of the anterior cruciate ligament and its two functional bundles. J Bone Joint Surg Am. 2006;88(suppl 4):2-10.
3. Christel P, Sahasrabudhe A, Basdekis G. Anatomic double-bundle anterior cruciate ligament reconstruction with anatomic aimers. Arthroscopy. 2008;24(10):1146-1151.
4. Allen CR, Giffin JR, Harner CD. Revision anterior cruciate ligament reconstruction. Orthop Clin North Am. 2003;34(1):79-98.
5. Miller CD, Gerdeman AC, Hart JM, et al. A comparison of 2 drilling techniques on the femoral tunnel for anterior cruciate ligament reconstruction. Arthroscopy. 2011;27(3):372-379.
6. Seon JK, Park SJ, Lee KB, Seo HY, Kim MS, Song EK. In vivo stability and clinical comparison of anterior cruciate ligament reconstruction using low or high femoral tunnel positions. Am J Sports Med. 2011;39(1):127-133.
7. Steiner ME, Battaglia TC, Heming JF, Rand JD, Festa A, Baria M. Independent drilling outperforms conventional transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2009;37(10):1912-1919.
8. Kopf S, Forsythe B, Wong AK, et al. Nonanatomic tunnel position in traditional transtibial single-bundle anterior cruciate ligament reconstruction evaluated by three-dimensional computed tomography. J Bone Joint Surg Am. 2010;92(6):1427-1431.
9. Tompkins M, Milewski MD, Brockmeier SF, Gaskin CM, Hart JM, Miller MD. Anatomic femoral tunnel drilling in anterior cruciate ligament reconstruction: use of an accessory medial portal versus traditional transtibial drilling. Am J Sports Med. 2012;40(6):1313-1321.
10. Heming JF, Rand J, Steiner ME. Anatomical limitations of transtibial drilling in anterior cruciate ligament reconstruction. Am J Sports Med. 2007;35(10):1708-1715.
11. Harner CD, Honkamp NJ, Ranawat AS. Anteromedial portal technique for creating the anterior cruciate ligament femoral tunnel. Arthroscopy. 2008;24(1):113-115.
12. Lubowitz JH. Anteromedial portal technique for the anterior cruciate ligament femoral socket: pitfalls and solutions. Arthroscopy. 2009;25(1):95-101.
13. Basdekis G, Abisafi C, Christel P. Influence of knee flexion angle on femoral tunnel characteristics when drilled through the anteromedial portal during anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(4):459-464.
14. Zantop T, Haase AK, Fu FH, Petersen W. Potential risk of cartilage damage in double bundle ACL reconstruction: impact of knee flexion angle and portal location on the femoral PL bundle tunnel. Arch Orthop Trauma Surg. 2008;128(5):509-513.
15. Farrow LD, Parker RD. The relationship of lateral anatomic structures to exiting guide pins during femoral tunnel preparation utilizing an accessory medial portal. Knee Surg Sports Traumatol Arthrosc. 2010;18(6):747-753.
16. Nakamura M, Deie M, Shibuya H, et al. Potential risks of femoral tunnel drilling through the far anteromedial portal: a cadaveric study. Arthroscopy. 2009;25(5):481-487.
17. Silver AG, Kaar SG, Grisell MK, Reagan JM, Farrow LD. Comparison between rigid and flexible systems for drilling the femoral tunnel through an anteromedial portal in anterior cruciate ligament reconstruction. Arthroscopy. 2010;26(6):790-795.
18. Steiner ME, Smart LR. Flexible instruments outperform rigid instruments to place anatomic anterior cruciate ligament femoral tunnels without hyperflexion. Arthroscopy. 2012;28(6):835-843.
Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?
Letter to the Editor
Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?
We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.1 We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.2P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.3 Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).4
Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.5 The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.5 Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.
In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.4 The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues6 reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues7 recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.8 We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.9,10
According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).8 Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues11 (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.12
To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.
Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD
Nantes University Hospital, Microbiology Laboratory, Nantes, France
Authors’ Response
Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.
Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,1 which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.
The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.
In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.1 Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions.
In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.
Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY
Letter to the Editor
1. Nodzo SR, Hohman DW, Crane JK, Duquin TR. Hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection. Am J Orthop. 2014;43(5):E93-E97.
2. Portillo ME, Corvec S, Borens O, Trampuz A. Propionibacterium acnes: an underestimated pathogen in implant-associated infections. BioMed Res Int. 2013;2013:804391.
3. Corvec S, Portillo ME, Pasticci BM, Borens O, Trampuz A. Epidemiology and new developments in the diagnosis of prosthetic joint infection. Int J Artif Organs. 2012;35(10):923-934.
4. Aubin GG, Portillo ME, Trampuz A, Corvec S. Propionibacterium acnes, an emerging pathogen: from acne to implant-infections, from phylotype to resistance. Médecine Mal Infect. 2014;44(6):241-250.
5. Hoeffler U. Enzymatic and hemolytic properties of Propionibacterium acnes and related bacteria. J Clin Microbiol. 1977;6(6):555-558.
6. McDowell A, Perry AL, Lambert PA, Patrick S. A new phylogenetic group of Propionibacterium acnes. J Med Microbiol. 2008;57(Pt 2):218-224.
7. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
8. Lomholt HB, Kilian M. Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne. PloS One. 2010;5(8):e12277.
9. Furustrand Tafin U, Corvec S, Betrisey B, Zimmerli W, Trampuz A. Role of rifampin against Propionibacterium acnes biofilm in vitro and in an experimental foreign-body infection model. Antimicrob Agents Chemother. 2012;56(4):1885-1891.
10. Holmberg A, Lood R, Mörgelin M, et al. Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates. Clin Microbiol Infect. 2009;15(8):787-795.
11. Valanne S, McDowell A, Ramage G, et al. CAMP factor homologues in Propionibacterium acnes: a new protein family differentially expressed by types I and II. Microbiol. 2005;151(Pt 5):1369-1379.
12. Sörensen M, Mak TN, Hurwitz R, et al. Mutagenesis of Propionibacterium acnes and analysis of two CAMP factor knock-out mutants. J Microbiol Methods. 2010;83(2):211-216.
Authors' Response Reference
1. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
Letter to the Editor
Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?
We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.1 We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.2P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.3 Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).4
Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.5 The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.5 Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.
In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.4 The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues6 reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues7 recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.8 We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.9,10
According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).8 Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues11 (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.12
To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.
Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD
Nantes University Hospital, Microbiology Laboratory, Nantes, France
Authors’ Response
Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.
Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,1 which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.
The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.
In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.1 Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions.
In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.
Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY
Letter to the Editor
Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?
We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.1 We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.2P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.3 Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).4
Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.5 The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.5 Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.
In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.4 The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues6 reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues7 recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.8 We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.9,10
According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).8 Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues11 (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.12
To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.
Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD
Nantes University Hospital, Microbiology Laboratory, Nantes, France
Authors’ Response
Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.
Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,1 which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.
The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.
In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.1 Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions.
In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.
Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY
Letter to the Editor
1. Nodzo SR, Hohman DW, Crane JK, Duquin TR. Hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection. Am J Orthop. 2014;43(5):E93-E97.
2. Portillo ME, Corvec S, Borens O, Trampuz A. Propionibacterium acnes: an underestimated pathogen in implant-associated infections. BioMed Res Int. 2013;2013:804391.
3. Corvec S, Portillo ME, Pasticci BM, Borens O, Trampuz A. Epidemiology and new developments in the diagnosis of prosthetic joint infection. Int J Artif Organs. 2012;35(10):923-934.
4. Aubin GG, Portillo ME, Trampuz A, Corvec S. Propionibacterium acnes, an emerging pathogen: from acne to implant-infections, from phylotype to resistance. Médecine Mal Infect. 2014;44(6):241-250.
5. Hoeffler U. Enzymatic and hemolytic properties of Propionibacterium acnes and related bacteria. J Clin Microbiol. 1977;6(6):555-558.
6. McDowell A, Perry AL, Lambert PA, Patrick S. A new phylogenetic group of Propionibacterium acnes. J Med Microbiol. 2008;57(Pt 2):218-224.
7. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
8. Lomholt HB, Kilian M. Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne. PloS One. 2010;5(8):e12277.
9. Furustrand Tafin U, Corvec S, Betrisey B, Zimmerli W, Trampuz A. Role of rifampin against Propionibacterium acnes biofilm in vitro and in an experimental foreign-body infection model. Antimicrob Agents Chemother. 2012;56(4):1885-1891.
10. Holmberg A, Lood R, Mörgelin M, et al. Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates. Clin Microbiol Infect. 2009;15(8):787-795.
11. Valanne S, McDowell A, Ramage G, et al. CAMP factor homologues in Propionibacterium acnes: a new protein family differentially expressed by types I and II. Microbiol. 2005;151(Pt 5):1369-1379.
12. Sörensen M, Mak TN, Hurwitz R, et al. Mutagenesis of Propionibacterium acnes and analysis of two CAMP factor knock-out mutants. J Microbiol Methods. 2010;83(2):211-216.
Authors' Response Reference
1. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
Letter to the Editor
1. Nodzo SR, Hohman DW, Crane JK, Duquin TR. Hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection. Am J Orthop. 2014;43(5):E93-E97.
2. Portillo ME, Corvec S, Borens O, Trampuz A. Propionibacterium acnes: an underestimated pathogen in implant-associated infections. BioMed Res Int. 2013;2013:804391.
3. Corvec S, Portillo ME, Pasticci BM, Borens O, Trampuz A. Epidemiology and new developments in the diagnosis of prosthetic joint infection. Int J Artif Organs. 2012;35(10):923-934.
4. Aubin GG, Portillo ME, Trampuz A, Corvec S. Propionibacterium acnes, an emerging pathogen: from acne to implant-infections, from phylotype to resistance. Médecine Mal Infect. 2014;44(6):241-250.
5. Hoeffler U. Enzymatic and hemolytic properties of Propionibacterium acnes and related bacteria. J Clin Microbiol. 1977;6(6):555-558.
6. McDowell A, Perry AL, Lambert PA, Patrick S. A new phylogenetic group of Propionibacterium acnes. J Med Microbiol. 2008;57(Pt 2):218-224.
7. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
8. Lomholt HB, Kilian M. Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne. PloS One. 2010;5(8):e12277.
9. Furustrand Tafin U, Corvec S, Betrisey B, Zimmerli W, Trampuz A. Role of rifampin against Propionibacterium acnes biofilm in vitro and in an experimental foreign-body infection model. Antimicrob Agents Chemother. 2012;56(4):1885-1891.
10. Holmberg A, Lood R, Mörgelin M, et al. Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates. Clin Microbiol Infect. 2009;15(8):787-795.
11. Valanne S, McDowell A, Ramage G, et al. CAMP factor homologues in Propionibacterium acnes: a new protein family differentially expressed by types I and II. Microbiol. 2005;151(Pt 5):1369-1379.
12. Sörensen M, Mak TN, Hurwitz R, et al. Mutagenesis of Propionibacterium acnes and analysis of two CAMP factor knock-out mutants. J Microbiol Methods. 2010;83(2):211-216.
Authors' Response Reference
1. Sampedro MF, Piper KE, McDowell A, et al. Species of Propionibacterium and Propionibacterium acnes phylotypes associated with orthopedic implants. Diagn Microbiol Infect Dis. 2009;64(2):138-145.
Nanotechnology: Why Should We Care?
The orthopedic community is increasingly deluged with advancements in the basic sciences. With each step, we must evaluate the necessity of new information and the relevance of these topics for clinical practice. Since the late 1990s, the promise of nanotechnology to effect significant changes in the medical field has been heralded. However, in this coming decade, we as a profession will see unprecedented advances in the movement of this technology “from the bench to the bedside.” Not unlike many other basic science advancements in our field, nanotechnology is poorly understood among clinicians and residents. As the use of biologics and drug delivery systems expands in orthopedics, nanoparticle-based devices will become more prevalent and have a momentous impact on the way we treat and diagnose orthopedic patients.
A nanoparticle is generally defined as a particle in which at least 1 dimension is between 1 to 100 nanometers and has material properties consistent with quantum mechanics.1 Nanomaterials can be composed of organic and inorganic chemical elements that enable basic chemical processes to create more complex systems. Individual nanoparticle units can be synthesized to form nanostructures, including nanotubes, nanoscaffolds, nanofibers, and even nanodiamonds.2-4 Nanoparticles at this scale display unique optical, chemical, and physical properties that can be manipulated to create specific end-use applications. Such uses may include glass fabrication, optical probes, television screens, drug delivery, gene delivery, and multiplex diagnostic assays.5-7 By crossing disciplines of physics, engineering, and medical sciences, we can create novel technology that includes nanomanufacturing, targeted drug delivery, nanorobotics in conjunction with artificial intelligence, and point-of-care diagnostics.7-9
The field of orthopedics has benefited from nanotechnologic advances, such as new therapeutics and implant-related technology. Nanotubes are hollow nanosized cylinders that are commonly created from titania, silica, or carbon-based substrates. They have garnered significant interest for their high tensile and shear strength, favorable microstructure for bony ingrowth, and their capacity to hold antibiotics or growth factors, such as bone morphogenic proteins (BMPs).10 The current local delivery limitations of BMPs via a collagen sponge have the potential to be maximized and better controlled with a nanotechnology-based approach. The size, internal structure, and shape of the nanoparticle can be manipulated to control the release of these growth factors, and certain nanoparticles can be dual-layered, allowing for release of multiple growth factors at once or in succession.11,12 A more powerful and targeted delivery system of these types of growth factors may result in improved or more robust outcomes, and further research is warranted.
It is possible that carbon-based nanotubes can be categorized as a biomedical implant secondary to their mechanical properties.13 Their strength and ability to be augmented with osteogenic materials has made them an attractive area of research as alternative implant surfaces and stand-alone implants. Nanotubes are capable of acting as a scaffold for antibiotic-loaded, carbon-based nanodiamonds for localized treatment of periprosthetic infection, and research has been directed toward controlled release of the nanodiamond-antibiotic construct from these scaffolds or hydrogels.4,14 Technologies like this may allow the clinician to treat periprosthetic infections locally and minimize the use of systemic antibiotics. The perfection of this type of delivery system may augment the role of antibiotic-laden cement and improve our treatment success rates, even in traditionally hard-to-treat organisms.
Nanoscaffolds and nanofibers are created from nanosized polymers and rendered into a 3-dimensional structure that can be loaded with biologic particles or acting as a scaffold/template for tissue or bone ingrowth. Nanofibers created using biodegradable substrates such as poly(lactic-co-glycolic acid) (PLGA) and chitosan have been extensively studied for their delayed-release properties and biocompatibility.15 These scaffolds are often soaked or loaded with chondrogenic, osteogenic, or antibacterial agents, and have been evaluated in both in vitro and in vivo studies with promising results.15,16 They have been an exciting area of research in tissue engineering, and have been accepted as an adjunct in tendon-repair treatments and local bone regeneration.3,17 As this technology is perfected, the potential to treat more effectively massive rotator cuff tears or tears with poor tissue integrity will dramatically improve and expand the indications for rotator cuff repair.
Augmentation of implant surfaces with nanomaterials that improve osseointegration, or that act as antimicrobial agents have also been a focus of research in hopes of decreasing the rates of aseptic failure and periprosthetic infection in arthroplasty procedures. Nanocrystalline surfaces made of hydroxyapatite and cobalt chromium have been evaluated for their enhanced osteoconductive properties, and may replace standard surfaces.18-20 Recent work evaluating nanoparticle-antibiotic constructs that have been covalently bound to implant surfaces for delayed release of antibiotics during the perioperative period has shown promise, and may allow a more targeted and localized treatment strategy for periprosthetic infection.21,22
Major limitations regarding successful clinical implementation of nanotechnology include both cost and regulatory processes. Currently, pharmaceutical companies estimate that, on average, successful clinical trials from phase 1 to completion for new drugs can cost hundreds of millions of dollars.23 Such high costs result partially from the laborious and capital-intensive process of conducting clinical trials that meet US Food and Drug Administration (FDA) requirements. These regulations would apply to both surface-coated implants and nanoparticle-based drug delivery systems. These types of implants would not be expedited into the market secondary to their drug delivery component and would likely require lengthy clinical studies. Implant companies may be reluctant to invest millions of dollars in multiple FDA trials when they have lucrative implants on the market.
Other limitations include the particles’ complex 3-dimensional structure, which can present challenges for mass production. Producing large quantities of nanoparticles at a consistent quality may be a major limitation to the more unique and target-based nanotherapies. Recent concerns with the toxicity profile of nanotechnology-based medicines have resulted in more intense scrutiny of the nanotechnology safety profile.24,25 Currently, nanoparticle technology is evaluated case by case with each technology requiring its own toxicology and safety profile testing if it is intended for human use. These tests can be cost-prohibitive and require extensive private and government capital for successful market entry. Despite these limitations, nanotechnology will impact the next generation of orthopedic surgeons. Current estimates project the nanomedicine market to be worth $177.6 billion by 2019.26
Advances in nanobased orthopedic technologies have expanded dramatically in the past decade, and we, as the treating physicians, must make educated decisions on how and when to use nanoparticle-based therapies and treatment options. Nanotechnology’s basic science is confusing and often burdensome, but contemporary review articles may be helpful in keeping the orthopedic resident and clinician current with advancements.10,27,28 The more we educate ourselves about evolving nanotechnologies, the less reluctance we will have when evaluating new diagnostic and therapeutic treatment modalities.
1. Hewakuruppu YL, Dombrovsky LA, Chen C, et al. Plasmonic “pump-probe” method to study semi-transparent nanofluids. Appl Opt. 2013;52(24):6041-6050.
2. Balasundaram G, Webster TJ. An overview of nano-polymers for orthopedic applications. Macromol Biosci. 2007;7(5):635-642.
3. Zhang Z, Hu J, Ma PX. Nanofiber-based delivery of bioactive agents and stem cells to bone sites. Adv Drug Deliv Rev. 2012;64(12):1129-1141.
4. Mochalin VN, Shenderova O, Ho D, Gogotsi Y. The properties and applications of nanodiamonds. Nat Nanotechnol. 2012;7(1):11-23.
5. Kneipp J, Kneipp H, Rice WL, Kneipp K. Optical probes for biological applications based on surface-enhanced Raman scattering from indocyanine green on gold nanoparticles. Anal Chem. 2005;77(8):2381-2385.
6. Wang L, O’Donoghue MB, Tan W. Nanoparticles for multiplex diagnostics and imaging. Nanomedicine (Lond). 2006;1(4):413-426.
7. Krebs MD, Salter E, Chen E, Sutter KA, Alsberg E. Calcium phosphate-DNA nanoparticle gene delivery from alginate hydrogels induces in vivo osteogenesis. J Biomed Mater Res A. 2010;92(3):1131-1138.
8. Myers FB, Lee LP. Innovations in optical microfluidic technologies for point-of-care diagnostics. Lab Chip. 2008;8(12):2015-2031.
9. Sacha GM, Varona P. Artificial intelligence in nanotechnology. Nanotechnology. 2013;24(45):452002.
10. Ganguly DY, Shahbazian R, Shokuhfar T. Recent advances in nanotubes for orthopedic implants. J Nanotech Smart Mater. 2014;1:1-10.
11. Srivastava S, Kotov NA. Composite Layer-by-Layer (LBL) assembly with inorganic nanoparticles and nanowires. Acc Chem Res. 2008;41(12):1831-1841.
12. Panda HS, Srivastava R, Bahadur D. Shape and size control of nano dispersed Mg/Al layered double hydroxide. J Nanosci Nanotechnol. 2008;8(8):4218-4223.
13. Wang X, Li Q, Xie J, et al. Fabrication of ultralong and electrically uniform single-walled carbon nanotubes on clean substrates. Nano Lett. 2009;9(9):3137-3141.
14. Zhu Y, Li J, Li W, et al. The biocompatibility of nanodiamonds and their application in drug delivery systems. Theranostics. 2012;2(3):302-312.
15. Wu L, Ding J. In vitro degradation of three-dimensional porous poly(D,L-lactide-co-glycolide) scaffolds for tissue engineering. Biomaterials. 2004;25(2):5821-5830.
16. Wu X, Rabkin-Aikawa E, Guleserian KJ, et al. Tissue-engineered microvessels on three-dimensional biodegradable scaffolds using human endothelial progenitor cells. Am J Physiol Heart Circ Physiol. 2004;287(2):H480-H487.
17. Xia W, Liu W, Cui L, et al. Tissue engineering of cartilage with the use of chitosan-gelatin complex scaffolds. J Biomed Mater Res B Appl Biomater. 2004;71(2):373-380.
18. Laurencin CT, Kumbar SG, Nukavarapu SP. Nanotechnology and orthopedics: a personal perspective. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2009;1(1):6-10.
19. Webster TJ, Ejiofor JU. Increased osteoblast adhesion on nanophase metals: Ti, Ti6Al4V, and CoCrMo. Biomaterials. 2004;25(19):4731-4739.
20. Webster TJ, Ergun C, Doremus RH, Siegel RW, Bizios R. Enhanced functions of osteoblasts on nanophase ceramics. Biomaterials. 2000;21(17):1803-1810.
21. Stewart S, Barr S, Engiles J, et al. Vancomycin-modified implant surface inhibits biofilm formation and supports bone-healing in an infected osteotomy model in sheep: a proof-of-concept study. J Bone Joint Surg Am. 2012;94(15):1406-1415.
22. Hickok NJ, Shapiro IM. Immobilized antibiotics to prevent orthopaedic implant infections. Adv Drug Deliv Rev. 2012;64(12):1165-1176.
23. DiMasi JA, Hansen RW, Grabowski HG. The price of innovation: new estimates of drug development costs. J Health Econ. 2003;22(2):151-185.
24. Vines T, Faunce T. Assessing the safety and cost-effectiveness of early nanodrugs. J Law Med. 2009;16(5):822-845.
25. Nel A, Xia T, Mädler L, Li N. Toxic potential of materials at the nanolevel. Science. 2006;311(5761):622-627.
26. Nanomedicine Market (Neurology, Cardiovascular, Anti-Inflammatory, Anti-Infective, and Oncology Applications): Global Industry Analysis, Size, Share, Growth, Trends and Forecast, 2013-2019. Transparency Market Research website. http://www.transparencymarketresearch.com/nanomedicine-market.html. Published August 1, 2014. Accessed January 20, 2015.
27. Sullivan MP, McHale KJ, Parvizi J, Mehta S. Nanotechnology: current concepts in orthopaedic surgery and future directions. Bone Joint J. 2014;96-B(5):569-573.
28. Pleshko N, Grande DA, Myers KR. Nanotechnology in orthopaedics. J Am Acad Orthop Surg. 2012;20(1):60-62.
The orthopedic community is increasingly deluged with advancements in the basic sciences. With each step, we must evaluate the necessity of new information and the relevance of these topics for clinical practice. Since the late 1990s, the promise of nanotechnology to effect significant changes in the medical field has been heralded. However, in this coming decade, we as a profession will see unprecedented advances in the movement of this technology “from the bench to the bedside.” Not unlike many other basic science advancements in our field, nanotechnology is poorly understood among clinicians and residents. As the use of biologics and drug delivery systems expands in orthopedics, nanoparticle-based devices will become more prevalent and have a momentous impact on the way we treat and diagnose orthopedic patients.
A nanoparticle is generally defined as a particle in which at least 1 dimension is between 1 to 100 nanometers and has material properties consistent with quantum mechanics.1 Nanomaterials can be composed of organic and inorganic chemical elements that enable basic chemical processes to create more complex systems. Individual nanoparticle units can be synthesized to form nanostructures, including nanotubes, nanoscaffolds, nanofibers, and even nanodiamonds.2-4 Nanoparticles at this scale display unique optical, chemical, and physical properties that can be manipulated to create specific end-use applications. Such uses may include glass fabrication, optical probes, television screens, drug delivery, gene delivery, and multiplex diagnostic assays.5-7 By crossing disciplines of physics, engineering, and medical sciences, we can create novel technology that includes nanomanufacturing, targeted drug delivery, nanorobotics in conjunction with artificial intelligence, and point-of-care diagnostics.7-9
The field of orthopedics has benefited from nanotechnologic advances, such as new therapeutics and implant-related technology. Nanotubes are hollow nanosized cylinders that are commonly created from titania, silica, or carbon-based substrates. They have garnered significant interest for their high tensile and shear strength, favorable microstructure for bony ingrowth, and their capacity to hold antibiotics or growth factors, such as bone morphogenic proteins (BMPs).10 The current local delivery limitations of BMPs via a collagen sponge have the potential to be maximized and better controlled with a nanotechnology-based approach. The size, internal structure, and shape of the nanoparticle can be manipulated to control the release of these growth factors, and certain nanoparticles can be dual-layered, allowing for release of multiple growth factors at once or in succession.11,12 A more powerful and targeted delivery system of these types of growth factors may result in improved or more robust outcomes, and further research is warranted.
It is possible that carbon-based nanotubes can be categorized as a biomedical implant secondary to their mechanical properties.13 Their strength and ability to be augmented with osteogenic materials has made them an attractive area of research as alternative implant surfaces and stand-alone implants. Nanotubes are capable of acting as a scaffold for antibiotic-loaded, carbon-based nanodiamonds for localized treatment of periprosthetic infection, and research has been directed toward controlled release of the nanodiamond-antibiotic construct from these scaffolds or hydrogels.4,14 Technologies like this may allow the clinician to treat periprosthetic infections locally and minimize the use of systemic antibiotics. The perfection of this type of delivery system may augment the role of antibiotic-laden cement and improve our treatment success rates, even in traditionally hard-to-treat organisms.
Nanoscaffolds and nanofibers are created from nanosized polymers and rendered into a 3-dimensional structure that can be loaded with biologic particles or acting as a scaffold/template for tissue or bone ingrowth. Nanofibers created using biodegradable substrates such as poly(lactic-co-glycolic acid) (PLGA) and chitosan have been extensively studied for their delayed-release properties and biocompatibility.15 These scaffolds are often soaked or loaded with chondrogenic, osteogenic, or antibacterial agents, and have been evaluated in both in vitro and in vivo studies with promising results.15,16 They have been an exciting area of research in tissue engineering, and have been accepted as an adjunct in tendon-repair treatments and local bone regeneration.3,17 As this technology is perfected, the potential to treat more effectively massive rotator cuff tears or tears with poor tissue integrity will dramatically improve and expand the indications for rotator cuff repair.
Augmentation of implant surfaces with nanomaterials that improve osseointegration, or that act as antimicrobial agents have also been a focus of research in hopes of decreasing the rates of aseptic failure and periprosthetic infection in arthroplasty procedures. Nanocrystalline surfaces made of hydroxyapatite and cobalt chromium have been evaluated for their enhanced osteoconductive properties, and may replace standard surfaces.18-20 Recent work evaluating nanoparticle-antibiotic constructs that have been covalently bound to implant surfaces for delayed release of antibiotics during the perioperative period has shown promise, and may allow a more targeted and localized treatment strategy for periprosthetic infection.21,22
Major limitations regarding successful clinical implementation of nanotechnology include both cost and regulatory processes. Currently, pharmaceutical companies estimate that, on average, successful clinical trials from phase 1 to completion for new drugs can cost hundreds of millions of dollars.23 Such high costs result partially from the laborious and capital-intensive process of conducting clinical trials that meet US Food and Drug Administration (FDA) requirements. These regulations would apply to both surface-coated implants and nanoparticle-based drug delivery systems. These types of implants would not be expedited into the market secondary to their drug delivery component and would likely require lengthy clinical studies. Implant companies may be reluctant to invest millions of dollars in multiple FDA trials when they have lucrative implants on the market.
Other limitations include the particles’ complex 3-dimensional structure, which can present challenges for mass production. Producing large quantities of nanoparticles at a consistent quality may be a major limitation to the more unique and target-based nanotherapies. Recent concerns with the toxicity profile of nanotechnology-based medicines have resulted in more intense scrutiny of the nanotechnology safety profile.24,25 Currently, nanoparticle technology is evaluated case by case with each technology requiring its own toxicology and safety profile testing if it is intended for human use. These tests can be cost-prohibitive and require extensive private and government capital for successful market entry. Despite these limitations, nanotechnology will impact the next generation of orthopedic surgeons. Current estimates project the nanomedicine market to be worth $177.6 billion by 2019.26
Advances in nanobased orthopedic technologies have expanded dramatically in the past decade, and we, as the treating physicians, must make educated decisions on how and when to use nanoparticle-based therapies and treatment options. Nanotechnology’s basic science is confusing and often burdensome, but contemporary review articles may be helpful in keeping the orthopedic resident and clinician current with advancements.10,27,28 The more we educate ourselves about evolving nanotechnologies, the less reluctance we will have when evaluating new diagnostic and therapeutic treatment modalities.
The orthopedic community is increasingly deluged with advancements in the basic sciences. With each step, we must evaluate the necessity of new information and the relevance of these topics for clinical practice. Since the late 1990s, the promise of nanotechnology to effect significant changes in the medical field has been heralded. However, in this coming decade, we as a profession will see unprecedented advances in the movement of this technology “from the bench to the bedside.” Not unlike many other basic science advancements in our field, nanotechnology is poorly understood among clinicians and residents. As the use of biologics and drug delivery systems expands in orthopedics, nanoparticle-based devices will become more prevalent and have a momentous impact on the way we treat and diagnose orthopedic patients.
A nanoparticle is generally defined as a particle in which at least 1 dimension is between 1 to 100 nanometers and has material properties consistent with quantum mechanics.1 Nanomaterials can be composed of organic and inorganic chemical elements that enable basic chemical processes to create more complex systems. Individual nanoparticle units can be synthesized to form nanostructures, including nanotubes, nanoscaffolds, nanofibers, and even nanodiamonds.2-4 Nanoparticles at this scale display unique optical, chemical, and physical properties that can be manipulated to create specific end-use applications. Such uses may include glass fabrication, optical probes, television screens, drug delivery, gene delivery, and multiplex diagnostic assays.5-7 By crossing disciplines of physics, engineering, and medical sciences, we can create novel technology that includes nanomanufacturing, targeted drug delivery, nanorobotics in conjunction with artificial intelligence, and point-of-care diagnostics.7-9
The field of orthopedics has benefited from nanotechnologic advances, such as new therapeutics and implant-related technology. Nanotubes are hollow nanosized cylinders that are commonly created from titania, silica, or carbon-based substrates. They have garnered significant interest for their high tensile and shear strength, favorable microstructure for bony ingrowth, and their capacity to hold antibiotics or growth factors, such as bone morphogenic proteins (BMPs).10 The current local delivery limitations of BMPs via a collagen sponge have the potential to be maximized and better controlled with a nanotechnology-based approach. The size, internal structure, and shape of the nanoparticle can be manipulated to control the release of these growth factors, and certain nanoparticles can be dual-layered, allowing for release of multiple growth factors at once or in succession.11,12 A more powerful and targeted delivery system of these types of growth factors may result in improved or more robust outcomes, and further research is warranted.
It is possible that carbon-based nanotubes can be categorized as a biomedical implant secondary to their mechanical properties.13 Their strength and ability to be augmented with osteogenic materials has made them an attractive area of research as alternative implant surfaces and stand-alone implants. Nanotubes are capable of acting as a scaffold for antibiotic-loaded, carbon-based nanodiamonds for localized treatment of periprosthetic infection, and research has been directed toward controlled release of the nanodiamond-antibiotic construct from these scaffolds or hydrogels.4,14 Technologies like this may allow the clinician to treat periprosthetic infections locally and minimize the use of systemic antibiotics. The perfection of this type of delivery system may augment the role of antibiotic-laden cement and improve our treatment success rates, even in traditionally hard-to-treat organisms.
Nanoscaffolds and nanofibers are created from nanosized polymers and rendered into a 3-dimensional structure that can be loaded with biologic particles or acting as a scaffold/template for tissue or bone ingrowth. Nanofibers created using biodegradable substrates such as poly(lactic-co-glycolic acid) (PLGA) and chitosan have been extensively studied for their delayed-release properties and biocompatibility.15 These scaffolds are often soaked or loaded with chondrogenic, osteogenic, or antibacterial agents, and have been evaluated in both in vitro and in vivo studies with promising results.15,16 They have been an exciting area of research in tissue engineering, and have been accepted as an adjunct in tendon-repair treatments and local bone regeneration.3,17 As this technology is perfected, the potential to treat more effectively massive rotator cuff tears or tears with poor tissue integrity will dramatically improve and expand the indications for rotator cuff repair.
Augmentation of implant surfaces with nanomaterials that improve osseointegration, or that act as antimicrobial agents have also been a focus of research in hopes of decreasing the rates of aseptic failure and periprosthetic infection in arthroplasty procedures. Nanocrystalline surfaces made of hydroxyapatite and cobalt chromium have been evaluated for their enhanced osteoconductive properties, and may replace standard surfaces.18-20 Recent work evaluating nanoparticle-antibiotic constructs that have been covalently bound to implant surfaces for delayed release of antibiotics during the perioperative period has shown promise, and may allow a more targeted and localized treatment strategy for periprosthetic infection.21,22
Major limitations regarding successful clinical implementation of nanotechnology include both cost and regulatory processes. Currently, pharmaceutical companies estimate that, on average, successful clinical trials from phase 1 to completion for new drugs can cost hundreds of millions of dollars.23 Such high costs result partially from the laborious and capital-intensive process of conducting clinical trials that meet US Food and Drug Administration (FDA) requirements. These regulations would apply to both surface-coated implants and nanoparticle-based drug delivery systems. These types of implants would not be expedited into the market secondary to their drug delivery component and would likely require lengthy clinical studies. Implant companies may be reluctant to invest millions of dollars in multiple FDA trials when they have lucrative implants on the market.
Other limitations include the particles’ complex 3-dimensional structure, which can present challenges for mass production. Producing large quantities of nanoparticles at a consistent quality may be a major limitation to the more unique and target-based nanotherapies. Recent concerns with the toxicity profile of nanotechnology-based medicines have resulted in more intense scrutiny of the nanotechnology safety profile.24,25 Currently, nanoparticle technology is evaluated case by case with each technology requiring its own toxicology and safety profile testing if it is intended for human use. These tests can be cost-prohibitive and require extensive private and government capital for successful market entry. Despite these limitations, nanotechnology will impact the next generation of orthopedic surgeons. Current estimates project the nanomedicine market to be worth $177.6 billion by 2019.26
Advances in nanobased orthopedic technologies have expanded dramatically in the past decade, and we, as the treating physicians, must make educated decisions on how and when to use nanoparticle-based therapies and treatment options. Nanotechnology’s basic science is confusing and often burdensome, but contemporary review articles may be helpful in keeping the orthopedic resident and clinician current with advancements.10,27,28 The more we educate ourselves about evolving nanotechnologies, the less reluctance we will have when evaluating new diagnostic and therapeutic treatment modalities.
1. Hewakuruppu YL, Dombrovsky LA, Chen C, et al. Plasmonic “pump-probe” method to study semi-transparent nanofluids. Appl Opt. 2013;52(24):6041-6050.
2. Balasundaram G, Webster TJ. An overview of nano-polymers for orthopedic applications. Macromol Biosci. 2007;7(5):635-642.
3. Zhang Z, Hu J, Ma PX. Nanofiber-based delivery of bioactive agents and stem cells to bone sites. Adv Drug Deliv Rev. 2012;64(12):1129-1141.
4. Mochalin VN, Shenderova O, Ho D, Gogotsi Y. The properties and applications of nanodiamonds. Nat Nanotechnol. 2012;7(1):11-23.
5. Kneipp J, Kneipp H, Rice WL, Kneipp K. Optical probes for biological applications based on surface-enhanced Raman scattering from indocyanine green on gold nanoparticles. Anal Chem. 2005;77(8):2381-2385.
6. Wang L, O’Donoghue MB, Tan W. Nanoparticles for multiplex diagnostics and imaging. Nanomedicine (Lond). 2006;1(4):413-426.
7. Krebs MD, Salter E, Chen E, Sutter KA, Alsberg E. Calcium phosphate-DNA nanoparticle gene delivery from alginate hydrogels induces in vivo osteogenesis. J Biomed Mater Res A. 2010;92(3):1131-1138.
8. Myers FB, Lee LP. Innovations in optical microfluidic technologies for point-of-care diagnostics. Lab Chip. 2008;8(12):2015-2031.
9. Sacha GM, Varona P. Artificial intelligence in nanotechnology. Nanotechnology. 2013;24(45):452002.
10. Ganguly DY, Shahbazian R, Shokuhfar T. Recent advances in nanotubes for orthopedic implants. J Nanotech Smart Mater. 2014;1:1-10.
11. Srivastava S, Kotov NA. Composite Layer-by-Layer (LBL) assembly with inorganic nanoparticles and nanowires. Acc Chem Res. 2008;41(12):1831-1841.
12. Panda HS, Srivastava R, Bahadur D. Shape and size control of nano dispersed Mg/Al layered double hydroxide. J Nanosci Nanotechnol. 2008;8(8):4218-4223.
13. Wang X, Li Q, Xie J, et al. Fabrication of ultralong and electrically uniform single-walled carbon nanotubes on clean substrates. Nano Lett. 2009;9(9):3137-3141.
14. Zhu Y, Li J, Li W, et al. The biocompatibility of nanodiamonds and their application in drug delivery systems. Theranostics. 2012;2(3):302-312.
15. Wu L, Ding J. In vitro degradation of three-dimensional porous poly(D,L-lactide-co-glycolide) scaffolds for tissue engineering. Biomaterials. 2004;25(2):5821-5830.
16. Wu X, Rabkin-Aikawa E, Guleserian KJ, et al. Tissue-engineered microvessels on three-dimensional biodegradable scaffolds using human endothelial progenitor cells. Am J Physiol Heart Circ Physiol. 2004;287(2):H480-H487.
17. Xia W, Liu W, Cui L, et al. Tissue engineering of cartilage with the use of chitosan-gelatin complex scaffolds. J Biomed Mater Res B Appl Biomater. 2004;71(2):373-380.
18. Laurencin CT, Kumbar SG, Nukavarapu SP. Nanotechnology and orthopedics: a personal perspective. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2009;1(1):6-10.
19. Webster TJ, Ejiofor JU. Increased osteoblast adhesion on nanophase metals: Ti, Ti6Al4V, and CoCrMo. Biomaterials. 2004;25(19):4731-4739.
20. Webster TJ, Ergun C, Doremus RH, Siegel RW, Bizios R. Enhanced functions of osteoblasts on nanophase ceramics. Biomaterials. 2000;21(17):1803-1810.
21. Stewart S, Barr S, Engiles J, et al. Vancomycin-modified implant surface inhibits biofilm formation and supports bone-healing in an infected osteotomy model in sheep: a proof-of-concept study. J Bone Joint Surg Am. 2012;94(15):1406-1415.
22. Hickok NJ, Shapiro IM. Immobilized antibiotics to prevent orthopaedic implant infections. Adv Drug Deliv Rev. 2012;64(12):1165-1176.
23. DiMasi JA, Hansen RW, Grabowski HG. The price of innovation: new estimates of drug development costs. J Health Econ. 2003;22(2):151-185.
24. Vines T, Faunce T. Assessing the safety and cost-effectiveness of early nanodrugs. J Law Med. 2009;16(5):822-845.
25. Nel A, Xia T, Mädler L, Li N. Toxic potential of materials at the nanolevel. Science. 2006;311(5761):622-627.
26. Nanomedicine Market (Neurology, Cardiovascular, Anti-Inflammatory, Anti-Infective, and Oncology Applications): Global Industry Analysis, Size, Share, Growth, Trends and Forecast, 2013-2019. Transparency Market Research website. http://www.transparencymarketresearch.com/nanomedicine-market.html. Published August 1, 2014. Accessed January 20, 2015.
27. Sullivan MP, McHale KJ, Parvizi J, Mehta S. Nanotechnology: current concepts in orthopaedic surgery and future directions. Bone Joint J. 2014;96-B(5):569-573.
28. Pleshko N, Grande DA, Myers KR. Nanotechnology in orthopaedics. J Am Acad Orthop Surg. 2012;20(1):60-62.
1. Hewakuruppu YL, Dombrovsky LA, Chen C, et al. Plasmonic “pump-probe” method to study semi-transparent nanofluids. Appl Opt. 2013;52(24):6041-6050.
2. Balasundaram G, Webster TJ. An overview of nano-polymers for orthopedic applications. Macromol Biosci. 2007;7(5):635-642.
3. Zhang Z, Hu J, Ma PX. Nanofiber-based delivery of bioactive agents and stem cells to bone sites. Adv Drug Deliv Rev. 2012;64(12):1129-1141.
4. Mochalin VN, Shenderova O, Ho D, Gogotsi Y. The properties and applications of nanodiamonds. Nat Nanotechnol. 2012;7(1):11-23.
5. Kneipp J, Kneipp H, Rice WL, Kneipp K. Optical probes for biological applications based on surface-enhanced Raman scattering from indocyanine green on gold nanoparticles. Anal Chem. 2005;77(8):2381-2385.
6. Wang L, O’Donoghue MB, Tan W. Nanoparticles for multiplex diagnostics and imaging. Nanomedicine (Lond). 2006;1(4):413-426.
7. Krebs MD, Salter E, Chen E, Sutter KA, Alsberg E. Calcium phosphate-DNA nanoparticle gene delivery from alginate hydrogels induces in vivo osteogenesis. J Biomed Mater Res A. 2010;92(3):1131-1138.
8. Myers FB, Lee LP. Innovations in optical microfluidic technologies for point-of-care diagnostics. Lab Chip. 2008;8(12):2015-2031.
9. Sacha GM, Varona P. Artificial intelligence in nanotechnology. Nanotechnology. 2013;24(45):452002.
10. Ganguly DY, Shahbazian R, Shokuhfar T. Recent advances in nanotubes for orthopedic implants. J Nanotech Smart Mater. 2014;1:1-10.
11. Srivastava S, Kotov NA. Composite Layer-by-Layer (LBL) assembly with inorganic nanoparticles and nanowires. Acc Chem Res. 2008;41(12):1831-1841.
12. Panda HS, Srivastava R, Bahadur D. Shape and size control of nano dispersed Mg/Al layered double hydroxide. J Nanosci Nanotechnol. 2008;8(8):4218-4223.
13. Wang X, Li Q, Xie J, et al. Fabrication of ultralong and electrically uniform single-walled carbon nanotubes on clean substrates. Nano Lett. 2009;9(9):3137-3141.
14. Zhu Y, Li J, Li W, et al. The biocompatibility of nanodiamonds and their application in drug delivery systems. Theranostics. 2012;2(3):302-312.
15. Wu L, Ding J. In vitro degradation of three-dimensional porous poly(D,L-lactide-co-glycolide) scaffolds for tissue engineering. Biomaterials. 2004;25(2):5821-5830.
16. Wu X, Rabkin-Aikawa E, Guleserian KJ, et al. Tissue-engineered microvessels on three-dimensional biodegradable scaffolds using human endothelial progenitor cells. Am J Physiol Heart Circ Physiol. 2004;287(2):H480-H487.
17. Xia W, Liu W, Cui L, et al. Tissue engineering of cartilage with the use of chitosan-gelatin complex scaffolds. J Biomed Mater Res B Appl Biomater. 2004;71(2):373-380.
18. Laurencin CT, Kumbar SG, Nukavarapu SP. Nanotechnology and orthopedics: a personal perspective. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2009;1(1):6-10.
19. Webster TJ, Ejiofor JU. Increased osteoblast adhesion on nanophase metals: Ti, Ti6Al4V, and CoCrMo. Biomaterials. 2004;25(19):4731-4739.
20. Webster TJ, Ergun C, Doremus RH, Siegel RW, Bizios R. Enhanced functions of osteoblasts on nanophase ceramics. Biomaterials. 2000;21(17):1803-1810.
21. Stewart S, Barr S, Engiles J, et al. Vancomycin-modified implant surface inhibits biofilm formation and supports bone-healing in an infected osteotomy model in sheep: a proof-of-concept study. J Bone Joint Surg Am. 2012;94(15):1406-1415.
22. Hickok NJ, Shapiro IM. Immobilized antibiotics to prevent orthopaedic implant infections. Adv Drug Deliv Rev. 2012;64(12):1165-1176.
23. DiMasi JA, Hansen RW, Grabowski HG. The price of innovation: new estimates of drug development costs. J Health Econ. 2003;22(2):151-185.
24. Vines T, Faunce T. Assessing the safety and cost-effectiveness of early nanodrugs. J Law Med. 2009;16(5):822-845.
25. Nel A, Xia T, Mädler L, Li N. Toxic potential of materials at the nanolevel. Science. 2006;311(5761):622-627.
26. Nanomedicine Market (Neurology, Cardiovascular, Anti-Inflammatory, Anti-Infective, and Oncology Applications): Global Industry Analysis, Size, Share, Growth, Trends and Forecast, 2013-2019. Transparency Market Research website. http://www.transparencymarketresearch.com/nanomedicine-market.html. Published August 1, 2014. Accessed January 20, 2015.
27. Sullivan MP, McHale KJ, Parvizi J, Mehta S. Nanotechnology: current concepts in orthopaedic surgery and future directions. Bone Joint J. 2014;96-B(5):569-573.
28. Pleshko N, Grande DA, Myers KR. Nanotechnology in orthopaedics. J Am Acad Orthop Surg. 2012;20(1):60-62.
Intragrade Intramedullary Nailing of an Open Tibial Shaft Fracture in a Patient With Concomitant Ipsilateral Total Knee Arthroplasty
Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.3,4
Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.
The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.
Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).
The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.
Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal.
The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.
Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.
In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.
At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7).
Discussion
We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.8 Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.14
If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible.
Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.20 However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.8 Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.21 Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.
A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.22 An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.23 However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure.
Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple reoperations.14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.26-28
Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.
Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.
Conclusion
We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.
1. Patzakis MJ, Wilkins J. Factors influencing infection rate in open fracture wounds. Clin Orthop. 1989;243:36-40.
2. Court-Brown CM, McBirnie J. The epidemiology of tibial fractures. J Bone Joint Surg Br. 1995;77(3):417-421.
3. Puno RM, Teynor JT, Nagano J, Gustilo RB. Critical analysis of results of treatment of 201 tibial shaft fractures. Clin Orthop. 1986;212:113-121.
4. Melvin JS, Dombroski DG, Torbert JT, Kovach SJ, Esterhal JL, Mehta S. Open tibial shaft fractures: I. Evaluation and initial wound management. J Am Acad Orthop Surg. 2010;18(1):10-19.
5. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
6. SPRINT Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Study to prospectively evaluate reamed intramedually nails in patients with tibial fractures (S.P.R.I.N.T.): study rationale and design. BMC Musculoskelet Disord. 2008;9:91.
7. Study to Prospectively Evaluate Reamed Intramedullary Nails in Patients with Tibial Fractures Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures. J Bone Joint Surg Am. 2008;90(12):2567-2578.
8. Burr DB, Milgrom C, Fyhrie D, et al. In vivo measurement of human tibial strains during vigorous activity. Bone. 1996;18(5):405-410.
9. Edwards P. Fracture of the shaft of the tibia: 492 consecutive cases in adults: Importance of soft tissue injury. Acta Orthop Scand (Suppl). 1965;76(suppl 76):1-82.
10. Papakostidis C, Kanakaris NK, Pretel J, Faour O, Morell DJ, Giannoudis PV. Prevalence of complications of open tibial shaft fractures stratified as per the Gustilo–Anderson classification. Injury. 2011;42(12):1408-1415.
11. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma. 1984;24(8):742-746.
12. DeLong WG Jr, Born CT, Wei SY, Petrik ME, Ponzio R, Schwab CW. Aggressive treatment of 119 open fracture wounds. J Trauma. 1999;46(6):1049-1054.
13. Tielinen L, Lindahl JE, Tukiainen EJ. Acute unreamed intramedullary nailing and soft tissue reconstruction with muscle flaps for the treatment of severe open tibial shaft fractures. Injury. 2007;38(8):906-912.
14. Georgiadis GM, Behrens FF, Joyce MJ, Earle AS, Simmons AL. Open tibial fractures with severe soft-tissue loss. Limb salvage compared with below-the-knee amputation. J Bone Joint Surg Am. 1993;75(10):1431-1441.
15. Hansen M, Mehler D, Hessmann MH, Blum J, Rommens PM. Intramedullary stabilization of extraarticular proximal tibial fractures: a biomechanical comparison of intramedullary and extramedullary implants including a new proximal tibia nail (PTN). J Orthop Trauma. 2007;21(10):701-709.
16. Hoegel FW, Hoffmann S, Weninger P, Bühren V, Augat P. Biomechanical comparison of locked plate osteosynthesis, reamed and unreamed nailing in conventional interlocking technique, and unreamed angle stable nailing in distal tibia fractures. J Trauma Acute Care Surg. 2012;73(4):933-938.
17. Brumback RJ, Reilly JP, Poka A, Lakatos RP, Bathon GH, Burgess AR. Intramedullary nailing of femoral shaft fractures. Part 1: Decision-making errors with interlocking fixation. J Bone Joint Surg Am. 1988;70(10):1441-1452.
18. Hooper GJ, Keddell RG, Penny ID. Conservative management or closed nailing for tibial shaft fractures. A randomised prospective trial. J Bone Joint Surg Br. 1991;73(1):83-85.
19. Karladani AH, Granhed H, Edshage B, Jerre R, Styf J. Displaced tibial shaft fractures: a prospective randomized study of closed intramedullary nailing versus cast treatment in 53 patients. Acta Orthop Scand. 2000;71(12):160-167.
20. Kenwright J, Richardson JB, Goodship AE, et al. Effect of controlled axial micromovement on healing of tibial fractures. Lancet. 1986;22(8517):1185-1187.
21. Im GI, Tae SK. Distal metaphyseal fractures of tibia: a prospective randomized trial of closed reduction and intramedullary nail versus open reduction and plate and screws fixation. J Trauma. 2005;59(5):1219-1223.
22. Henley MB, Chapman JR, Agel J, Harvey EJ, Whorton AM, Swiontkowski MF. Treatment of type II, IIIA, and IIIB open fractures of the tibial shaft: a prospective comparison of unreamed interlocking intramedullary nails and half-pin external fixators. J Orthop Trauma. 1998;12(1):1-7.
23. Ramos T, Ekholm C, Eriksson BI, Karlsson J, Nistor L. The Ilizarov external fixator - a useful alternative for the treatment of proximal tibial fractures. A prospective observational study of 30 consecutive patients. BMC Musculoskelet Disord. 2013;14:11.
24. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
25. Webb LX, Bosse MJ, Castillo RC, MacKenzie EJ; LEAP Study Group. Analysis of surgeon-controlled variables in the treatment of limb-threatening type-III open tibial diaphyseal fractures. J Bone Joint Surg Am. 2007;89(5):923-928.
26. Bondurant FJ, Cotler HB, Buckle R, Miller-Crotchett P, Browner BD. The medical and economic impact of severely injured lower extremities. J Trauma. 1988;28(8):1270-1273.
27. Bosse MJ, MacKenzie EJ, Kellam JF, et al. An analysis of outcomes of reconstruction or amputation of leg-threatening injuries. N Engl J Med. 2002;347(24):1924-1931.
28. MacKenzie EJ, Bosse MJ, Pollak AN, et al. Long-term persistence of disability following severe lower-limb trauma. Results of a seven-year follow-up. J Bone Joint Surg Am. 2005;87(8):1801-1809.
29. Doulens KM, Joshi AB, Wagner RA. Tibial fracture after total knee arthroplasty treated with retrograde intramedullary fixation. Am J Orthop. 2007;36(7):E111-E113.
30. Zafra-Jiménez JA, Pretell-Mazzini J, Resines-Erasun C. Distal tibial fracture below a total knee arthroplasty: retrograde intramedullary nailing as an alternative method of treatment: a case report. J Orthop Trauma. 2011;25(7):e74-e76.
31. Loosen S, Preuss S, Zelle BA, Pape HC, Tarken IS. Multimorbid patients with poor soft tissue conditions: Treatment of distal tibia fractures with retrograde intramedullary nailing. Unfallchirurg. 2012;116(6):553-558.
32. Kessler SB, Hallfeldt KJ, Perren SM, Schweiberer L. The effects of reaming and intramedullary nailing on fracture healing. Clin Orthop. 1986;212:18-25.
33. Klein MP, Rahn BA, Frigg R, Kessler S, Perren SM. Reaming versus non-reaming in medullary nailing: interference with cortical circulation of the canine tibia. Arch Orthop Trauma Surg. 1990;109(6):314-316.
34. Reichert IL, McCarthy ID, Hughes SP. The acute vascular response to intramedullary reaming. Microsphere estimation of blood flow in the intact ovine tibia. J Bone Joint Surg Br. 1995;77(3):490-493.
Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.3,4
Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.
The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.
Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).
The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.
Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal.
The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.
Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.
In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.
At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7).
Discussion
We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.8 Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.14
If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible.
Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.20 However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.8 Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.21 Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.
A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.22 An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.23 However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure.
Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple reoperations.14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.26-28
Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.
Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.
Conclusion
We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.
Fracture of the tibial shaft below an ipsilateral total knee arthroplasty (TKA) is an infrequently occurring injury pattern that presents a unique treatment scenario. The high predilection for open wounds associated with these diaphyseal fractures further complicates the treatment algorithm.1,2 The standard principles of treatment for open tibial shaft fractures entail open fracture débridement followed by adequate fracture reduction and stable skeletal fixation in a manner that limits adverse complications of this injury, which include nonunion, malunion, infection, soft-tissue compromise, and reoperation.3,4
Antegrade intramedullary (IM) tibial nailing has become standard treatment for tibial shaft fractures.5-7 This minimally invasive method of fixation limits damage to the soft-tissue envelope, provides superior neutralization of the mechanical forces to provide a template for biologic fracture healing, and allows the best options for revision procedures in the event of inadequate healing. This case report examines treatment options for an open tibial shaft fracture of an ipsilateral TKA, complicating the standard treatment of antegrade tibial nailing. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 66-year-old woman became light-headed and fell down a flight of stairs at her home. She was taken to the local emergency room where she presented with left leg pain, deformity, and a skin wound. The wound was dressed with sterile gauze and the extremity immobilized in a temporary plaster splint after which the patient was transferred to our level I trauma center. The accident occurred shortly after dawn, and she received definitive evaluation at the level I trauma center before noon the same day, making the time from injury to evaluation less than 6 hours.
The patient’s medical history was significant for depressive and anxiety disorders, fibromyalgia, hypertension, peripheral vascular disease, and lymphedema. Her surgical history was significant for a remote left TKA and remote open reduction with internal fixation of a left lateral malleolus fracture. She was prescribed antidepressant and anti-anxiolytic medications, narcotic medication, and antihypertensive therapy. She smoked 1 pack of cigarettes per day for approximately 20 years and denied alcohol consumption or illicit drug use. Her body mass index was 37.5, and she ambulated independently in the community.
Upon presentation at our hospital, the patient was hemodynamically stable with no discernable systemic compromise from the extremity injury. An examination of the left lower extremity showed a large longitudinal skin wound over the anteromedial surface of the lower leg measuring roughly 10 cm in length with obvious periosteal stripping and protrusion of the proximal fracture segment. Neurologic motor and sensory function was intact in the lower extremities and pulses were strong. Lower leg compartments were soft. Radiographic imaging confirmed a short oblique fracture of the distal third of the tibial diaphysis. The left TKA was intact with no signs of component loosening or periprosthetic fracture (Figures 1A, 1B).
The patient urgently received broad-spectrum antibiotics with intravenous (IV) cefazolin and IV gentamicin as well as tetanus vaccination. Her fracture was temporarily stabilized in a long-leg splint before she was transported to the operating room. Based upon the characteristics of the patient and the open fracture, we had an extensive discussion with the patient regarding the severity of her injury and treatment options, including nonoperative treatment, operative irrigation and débridement with skeletal stabilization, or below-knee amputation. The patient was adamant that limb salvage be attempted despite adequate understanding that she was exposing herself to risk of multiple reoperations from potential complications, as well as systemic medical compromise. Thus, we considered possible techniques for internal fixation of the tibial shaft fracture and treatment of the open wound.
Two primary technical concerns were addressed in the preoperative planning phase: the first was the need for primary closure of the open wound. This patient had a large wound over the anteromedial surface of the distal third of the tibia with scant soft-tissue coverage. Consequently, skin graft alone would not be adequate. While a muscle flap is another option, it would be prone to failure because of the patient’s age and comorbidities, including hypertension, peripheral vascular disease, lymphedema, and tobacco use. Therefore, we hoped to achieve primary closure. Our second major concern was that the method of fixation must be biomechanically sound without impeding our first goal of primary wound closure. In the setting of an ipsilateral TKA, standard antegrade IM nail fixation would not be possible. While we considered plate fixation, it is biomechanically less stable than an IM nail, and we had great concerns about wound complications. External fixation—uniplanar and mutliplanar (eg, Ilizarov)—was limited by issues of long-term fracture stability and risk of pin-site infection. Both methods appeared less desirable compared with IM nail fixation. Thus, we devised an innovative technique to implant an IM nail into the tibial canal.
The operative procedure first entailed standard open fracture care comprising débridement of nonviable soft tissue from the traumatic anteromedial tibial wound, curettage of the fractured bone ends, and irrigation with pulse-jet lavage. Then, we turned to reduction and internal fixation of the bony injury. The large traumatic wound was not extended and was used as the primary surgical approach to permit introduction of the IM nail into the canal. Through the traumatic wound, we performed limited reaming of the proximal and distal fracture segments. Using a cannulated technique over guide wires, we reamed to 11 mm (Figure 2). The tourniquet was not used during the IM reaming. We determined the maximum nail length (approximately 22 cm) by measuring the distance from the fracture to the bone interface with the tibial component. We used a 10×200-mm femoral retrograde Synthes nail (Synthes, Inc, West Chester, Pennsylvania) for the procedure, although we considered an IM humerus nail. Through the traumatic wound, the nail was advanced in its entirety into the proximal tibial segment (Figure 3). The fracture was reduced anatomically and held with a bone tenaculum (Figures 4A, 4B). A medial cortical window proximal to the proximal extent of the IM nail was created through which the Synthes IM reduction tool (aluminum femoral finger) was advanced to impact the IM nail antegrade through the fracture site into the distal segment (Figure 5). After placement of the nail was complete, the excised fragment of bone was reinserted into the cortical window. The Synthes IM reduction tool was chosen for its diameter, length, and, most important, its relative flexibility. While maintaining reduction of the fracture, cross-locking of the nail was performed at the distal and proximal ends with perfect circle technique through stab incisions. Length, alignment, and rotation of the affected tibia were deemed symmetric to the contralateral side based on preoperative clinical measurements. Final fluoroscopic images showed appropriate alignment and proper implant placement.
Following open reduction and internal fixation of the fracture, the traumatic and surgical wounds were closed in a layered fashion. A subcutaneous drain and an incisional vacuum-assisted closure (VAC) device were applied to the closed traumatic wound, and a second subcutaneous drain was placed at the site of the cortical window. The patient tolerated the procedure well without perioperative complications.
In the acute period after surgery, the patient’s neurologic and vascular status remained stable. Her muscular compartments remained soft and compressible on physical examination, and her pain was well controlled. The incisional VAC and the 2 Hemovac drains were removed within a few days of the operation. Intravenous cefazolin was continued through her hospital stay and she was transitioned to oral cephalexin at discharge as recommended by our infectious disease colleagues to complete a 10-day course of antibiotic therapy.
At the time of discharge—within 1 week of her initial injury—the patient’s wounds were dry and she was ambulatory with a walker. She was instructed to remain non-weight-bearing and to keep her wounds clean and dry with follow-up in 2 weeks. Over 6 to 8 weeks after surgery, the patient’s weight-bearing status was gradually advanced to full weight-bearing, and she achieved union of the fracture and uneventful healing of the traumatic wound (Figures 6A, 6B, 7).
Discussion
We have presented a case of an open distal-third tibial shaft fracture in a 66-year-old obese woman with an ipsilateral TKA. Open fracture of the tibial shaft is potentially limb-threatening because of the challenging management of the bone and soft-tissue injury. The presence of an ipsilateral TKA adds a degree of complexity. From a biomechanical standpoint, the lower interdigitation of cortical bone, coupled with weight-bearing of the lower extremity, subjects the tibia diaphysis to issues of rotation, length, and angular control.8 Due to the diaphyseal nature of the fracture, consisting of cortical bone with comparably lower vascularity and a small soft-tissue envelope, these fractures heal very slowly and often take as many as 6 to 9 months to achieve union.9,10 Furthermore, as was the case here, short oblique fractures of the tibial shaft often occur under bending stresses that also cause significant damage to the tibial soft-tissue envelope and periosteum, as indicated by the open wound. This disruption deprives the fracture and soft tissues of important vascular supply that is critical to healing and to avoiding infection and soft-tissue necrosis.11-13 The effects of treatment may magnify these biomechanical and biologic consequences. Ideal fixation serves to minimize potential complications by neutralizing the biomechanical forces to permit fracture healing while also limiting the amount of soft-tissue trauma and tension. Because the challenges associated with treatment of open tibial shaft fractures make it a limb-threatening injury in a patient with poor peripheral circulation, it is appropriate to consider primary amputation.14
If circumstances warrant an attempt at limb salvage, IM nailing with static interlocking screws would typically be the standard of care for treatment of an open fracture of the tibia shaft. This provides stable internal fixation that controls tibial alignment in 6° of freedom and neutralizes bending forces with less strain on the implant because of the IM position.15,16 In addition to superior neutralization of the biomechanical forces, IM nailing is also a minimally invasive approach that limits further trauma to the periosteum and soft-tissue envelope surrounding the fracture site. This optimizes biologic fracture healing and minimizes complications of malunion, infection, and nonunion.17-19 Moreover, by limiting further damage to the surrounding soft tissue, there is a diminished need for a plastic surgery procedure to reestablish soft-tissue integrity overlying the fracture site. This is particularly advantageous in patients with medical comorbidities that make skin grafts and muscle flaps less likely to succeed. For these reasons, IM nailing was our preferred method of fixation in our patient; however, the presence of an ipsilateral TKA made this standard treatment through an antegrade approach impossible.
Consequently, we considered other methods of fixation, including internal fixation with plate application or external fixation with a multiplanar construct, such as an Ilizarov frame. Some orthopedists consider plate application a superior technique for achieving fracture union because it results in interfragmentary compression, which promotes primary healing. Interestingly, some would argue that the absolute stability provided by the plate may be too rigid a construct to enable optimal fracture healing biology if compression is not achieved.20 However, to allow primary healing to complete fracture union, absolute stability with rigid and strong fixation must be provided. In the tibial shaft, with large bending forces and rotational moments, this is difficult to achieve with plate fixation alone.8 Furthermore, plate application often requires relatively extensive soft-tissue dissection and may impede biologic factors in healing of the bone and soft tissue, increasing the likelihood of infection.21 Finally, adequate plate fixation would significantly increase the soft-tissue volume at this location, further compromising the soft tissues and impeding our goal of primary wound closure.
A uniplanar or mutliplanar external fixator would be an appealing option for definitive fixation because of minimal additional soft-tissue damage that is created during its application. However, it is difficult to achieve adequate stability to encourage either primary, or more commonly, secondary healing in the adult or elderly population.22 An Ilizarov frame is a multiplanar external construct, which allows reconstructive applications because of multiple points of fixation in bone.23 However, the multiple fixation points result in burdensome size of the implant for the patient and requires patient compliance to minimize risk of pin-site infection, which is magnified in a patient with multiple medical comorbid conditions. Furthermore, when comparing treatment options that aim to minimize additional soft-tissue trauma at the site of injury, there is little evidence to show a lower risk of infection at the open fracture site compared with IM nailing.24,25 Thus, in our patient, customary treatment of an open tibial shaft fracture using antegrade IM nailing was not possible, while plate application and external fixation, though potential treatment options, would be relatively contraindicated due to a higher likelihood of failure.
Consequently, primary amputation may be the most appropriate treatment option in a patient with multiple comorbid medical conditions, including peripheral vascular disease. Primary amputation prevents morbidity and mortality associated with complications related to the aforementioned treatment options, as well as limiting risks associated with multiple reoperations.14,25 Studies illustrate that patient functional outcomes after primary amputation are equal to and, in some cases, superior to those patients undergoing limb salvage procedures for open tibial shaft fractures.26-28
Despite the appropriateness of primary amputation in this case, the patient requested limb salvage. Therefore, other innovative treatment options were explored to achieve our goals of primary wound closure and stable internal fixation. Previous case reports have examined retrograde IM nailing as a means of rigidly fixing tibial shaft fractures in the setting of poor soft tissues or ipsilateral knee arthroplasty.29-31 However, the retrograde approach to IM nailing requires passage of reamers through the subtalar and ankle joints, leading to associated arthritis in these joints or, more commonly, rigidity because the final nail position often crosses these joints in addition to the fracture site. Therefore, a novel approach for IM nailing was performed using the large open-fracture wound. Through the traumatic wound, open-fracture débridement was first performed, followed by placement of a nail into the medullary canal with little additional disruption of the surrounding periosteum or soft tissue.
Possible complications of this novel method for IM nail passage warrant discussion. First, potentially unfavorable aspects associated with IM reaming include impairment of endosteal blood circulation in the subacute postoperative period.32-34 If the patient develops complications, such as deep infection, nonunion, hardware failure, or periprosthetic fracture, treatment options that require removal of the nail would be very difficult to execute because this nail was passed “intragrade,” or through the fracture site, not from the knee or the calcaneus. However, unique to this case of intragrade nailing, complications associated with the proximal cortical window may occur. In particular, unintended cortical fracture may happen during impaction of the nail into the distal segment of the fracture after reduction. However, this complication may be avoided with the use of a 1-cm wide and 2-cm long window and the use of the malleable aluminum femoral finger (Synthes). Furthermore, use of a femoral nail is recommended because the Herzog curve of a tibial nail cannot be inserted in the proximal tibial segment using an “intragrade” nailing technique. However, fracture may occur intraoperatively or during rehabilitation after surgery because the cortical window creates a region of high stress distal to the tibial arthroplasty component. Likewise, the area of bone between the proximal extent of the IM nail and tibial component of the TKA represents an area of high stress susceptible to periprosthetic fracture.
Conclusion
We have presented a case of a high-energy open distal tibial diaphyseal fracture in a 66-year-old woman with medical comorbidities and treatment complicated by the presence of an ipsilateral TKA. Intramedullary nailing has become the standard of care for open fractures of the tibial diaphysis because of the high rate of union with little additional soft-tissue damage at the fracture site. Despite these advantages, the ipsilateral TKA complicated the placement of an antegrade tibial nail. An alternative treatment, such as an external fixation using an Ilizarov frame, would present equally challenging treatment aspects, including patient compliance, with little proven benefit over an IM nail. Application of a plate would be less desirable because of increased risk of infection at the fracture site, soft-tissue and periosteum disruption, and muscle necrosis compared with other treatment options. Primary amputation was an appropriate consideration for this patient given her comorbid medical circumstances, but the patient refused this treatment option. Therefore, we created a novel approach to place an IM nail, using the traumatic wound to achieve access to the medullary canal proximally and distally.
1. Patzakis MJ, Wilkins J. Factors influencing infection rate in open fracture wounds. Clin Orthop. 1989;243:36-40.
2. Court-Brown CM, McBirnie J. The epidemiology of tibial fractures. J Bone Joint Surg Br. 1995;77(3):417-421.
3. Puno RM, Teynor JT, Nagano J, Gustilo RB. Critical analysis of results of treatment of 201 tibial shaft fractures. Clin Orthop. 1986;212:113-121.
4. Melvin JS, Dombroski DG, Torbert JT, Kovach SJ, Esterhal JL, Mehta S. Open tibial shaft fractures: I. Evaluation and initial wound management. J Am Acad Orthop Surg. 2010;18(1):10-19.
5. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
6. SPRINT Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Study to prospectively evaluate reamed intramedually nails in patients with tibial fractures (S.P.R.I.N.T.): study rationale and design. BMC Musculoskelet Disord. 2008;9:91.
7. Study to Prospectively Evaluate Reamed Intramedullary Nails in Patients with Tibial Fractures Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures. J Bone Joint Surg Am. 2008;90(12):2567-2578.
8. Burr DB, Milgrom C, Fyhrie D, et al. In vivo measurement of human tibial strains during vigorous activity. Bone. 1996;18(5):405-410.
9. Edwards P. Fracture of the shaft of the tibia: 492 consecutive cases in adults: Importance of soft tissue injury. Acta Orthop Scand (Suppl). 1965;76(suppl 76):1-82.
10. Papakostidis C, Kanakaris NK, Pretel J, Faour O, Morell DJ, Giannoudis PV. Prevalence of complications of open tibial shaft fractures stratified as per the Gustilo–Anderson classification. Injury. 2011;42(12):1408-1415.
11. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma. 1984;24(8):742-746.
12. DeLong WG Jr, Born CT, Wei SY, Petrik ME, Ponzio R, Schwab CW. Aggressive treatment of 119 open fracture wounds. J Trauma. 1999;46(6):1049-1054.
13. Tielinen L, Lindahl JE, Tukiainen EJ. Acute unreamed intramedullary nailing and soft tissue reconstruction with muscle flaps for the treatment of severe open tibial shaft fractures. Injury. 2007;38(8):906-912.
14. Georgiadis GM, Behrens FF, Joyce MJ, Earle AS, Simmons AL. Open tibial fractures with severe soft-tissue loss. Limb salvage compared with below-the-knee amputation. J Bone Joint Surg Am. 1993;75(10):1431-1441.
15. Hansen M, Mehler D, Hessmann MH, Blum J, Rommens PM. Intramedullary stabilization of extraarticular proximal tibial fractures: a biomechanical comparison of intramedullary and extramedullary implants including a new proximal tibia nail (PTN). J Orthop Trauma. 2007;21(10):701-709.
16. Hoegel FW, Hoffmann S, Weninger P, Bühren V, Augat P. Biomechanical comparison of locked plate osteosynthesis, reamed and unreamed nailing in conventional interlocking technique, and unreamed angle stable nailing in distal tibia fractures. J Trauma Acute Care Surg. 2012;73(4):933-938.
17. Brumback RJ, Reilly JP, Poka A, Lakatos RP, Bathon GH, Burgess AR. Intramedullary nailing of femoral shaft fractures. Part 1: Decision-making errors with interlocking fixation. J Bone Joint Surg Am. 1988;70(10):1441-1452.
18. Hooper GJ, Keddell RG, Penny ID. Conservative management or closed nailing for tibial shaft fractures. A randomised prospective trial. J Bone Joint Surg Br. 1991;73(1):83-85.
19. Karladani AH, Granhed H, Edshage B, Jerre R, Styf J. Displaced tibial shaft fractures: a prospective randomized study of closed intramedullary nailing versus cast treatment in 53 patients. Acta Orthop Scand. 2000;71(12):160-167.
20. Kenwright J, Richardson JB, Goodship AE, et al. Effect of controlled axial micromovement on healing of tibial fractures. Lancet. 1986;22(8517):1185-1187.
21. Im GI, Tae SK. Distal metaphyseal fractures of tibia: a prospective randomized trial of closed reduction and intramedullary nail versus open reduction and plate and screws fixation. J Trauma. 2005;59(5):1219-1223.
22. Henley MB, Chapman JR, Agel J, Harvey EJ, Whorton AM, Swiontkowski MF. Treatment of type II, IIIA, and IIIB open fractures of the tibial shaft: a prospective comparison of unreamed interlocking intramedullary nails and half-pin external fixators. J Orthop Trauma. 1998;12(1):1-7.
23. Ramos T, Ekholm C, Eriksson BI, Karlsson J, Nistor L. The Ilizarov external fixator - a useful alternative for the treatment of proximal tibial fractures. A prospective observational study of 30 consecutive patients. BMC Musculoskelet Disord. 2013;14:11.
24. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
25. Webb LX, Bosse MJ, Castillo RC, MacKenzie EJ; LEAP Study Group. Analysis of surgeon-controlled variables in the treatment of limb-threatening type-III open tibial diaphyseal fractures. J Bone Joint Surg Am. 2007;89(5):923-928.
26. Bondurant FJ, Cotler HB, Buckle R, Miller-Crotchett P, Browner BD. The medical and economic impact of severely injured lower extremities. J Trauma. 1988;28(8):1270-1273.
27. Bosse MJ, MacKenzie EJ, Kellam JF, et al. An analysis of outcomes of reconstruction or amputation of leg-threatening injuries. N Engl J Med. 2002;347(24):1924-1931.
28. MacKenzie EJ, Bosse MJ, Pollak AN, et al. Long-term persistence of disability following severe lower-limb trauma. Results of a seven-year follow-up. J Bone Joint Surg Am. 2005;87(8):1801-1809.
29. Doulens KM, Joshi AB, Wagner RA. Tibial fracture after total knee arthroplasty treated with retrograde intramedullary fixation. Am J Orthop. 2007;36(7):E111-E113.
30. Zafra-Jiménez JA, Pretell-Mazzini J, Resines-Erasun C. Distal tibial fracture below a total knee arthroplasty: retrograde intramedullary nailing as an alternative method of treatment: a case report. J Orthop Trauma. 2011;25(7):e74-e76.
31. Loosen S, Preuss S, Zelle BA, Pape HC, Tarken IS. Multimorbid patients with poor soft tissue conditions: Treatment of distal tibia fractures with retrograde intramedullary nailing. Unfallchirurg. 2012;116(6):553-558.
32. Kessler SB, Hallfeldt KJ, Perren SM, Schweiberer L. The effects of reaming and intramedullary nailing on fracture healing. Clin Orthop. 1986;212:18-25.
33. Klein MP, Rahn BA, Frigg R, Kessler S, Perren SM. Reaming versus non-reaming in medullary nailing: interference with cortical circulation of the canine tibia. Arch Orthop Trauma Surg. 1990;109(6):314-316.
34. Reichert IL, McCarthy ID, Hughes SP. The acute vascular response to intramedullary reaming. Microsphere estimation of blood flow in the intact ovine tibia. J Bone Joint Surg Br. 1995;77(3):490-493.
1. Patzakis MJ, Wilkins J. Factors influencing infection rate in open fracture wounds. Clin Orthop. 1989;243:36-40.
2. Court-Brown CM, McBirnie J. The epidemiology of tibial fractures. J Bone Joint Surg Br. 1995;77(3):417-421.
3. Puno RM, Teynor JT, Nagano J, Gustilo RB. Critical analysis of results of treatment of 201 tibial shaft fractures. Clin Orthop. 1986;212:113-121.
4. Melvin JS, Dombroski DG, Torbert JT, Kovach SJ, Esterhal JL, Mehta S. Open tibial shaft fractures: I. Evaluation and initial wound management. J Am Acad Orthop Surg. 2010;18(1):10-19.
5. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
6. SPRINT Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Study to prospectively evaluate reamed intramedually nails in patients with tibial fractures (S.P.R.I.N.T.): study rationale and design. BMC Musculoskelet Disord. 2008;9:91.
7. Study to Prospectively Evaluate Reamed Intramedullary Nails in Patients with Tibial Fractures Investigators, Bhandari M, Guyatt G, Tornetta P 3rd, et al. Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures. J Bone Joint Surg Am. 2008;90(12):2567-2578.
8. Burr DB, Milgrom C, Fyhrie D, et al. In vivo measurement of human tibial strains during vigorous activity. Bone. 1996;18(5):405-410.
9. Edwards P. Fracture of the shaft of the tibia: 492 consecutive cases in adults: Importance of soft tissue injury. Acta Orthop Scand (Suppl). 1965;76(suppl 76):1-82.
10. Papakostidis C, Kanakaris NK, Pretel J, Faour O, Morell DJ, Giannoudis PV. Prevalence of complications of open tibial shaft fractures stratified as per the Gustilo–Anderson classification. Injury. 2011;42(12):1408-1415.
11. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma. 1984;24(8):742-746.
12. DeLong WG Jr, Born CT, Wei SY, Petrik ME, Ponzio R, Schwab CW. Aggressive treatment of 119 open fracture wounds. J Trauma. 1999;46(6):1049-1054.
13. Tielinen L, Lindahl JE, Tukiainen EJ. Acute unreamed intramedullary nailing and soft tissue reconstruction with muscle flaps for the treatment of severe open tibial shaft fractures. Injury. 2007;38(8):906-912.
14. Georgiadis GM, Behrens FF, Joyce MJ, Earle AS, Simmons AL. Open tibial fractures with severe soft-tissue loss. Limb salvage compared with below-the-knee amputation. J Bone Joint Surg Am. 1993;75(10):1431-1441.
15. Hansen M, Mehler D, Hessmann MH, Blum J, Rommens PM. Intramedullary stabilization of extraarticular proximal tibial fractures: a biomechanical comparison of intramedullary and extramedullary implants including a new proximal tibia nail (PTN). J Orthop Trauma. 2007;21(10):701-709.
16. Hoegel FW, Hoffmann S, Weninger P, Bühren V, Augat P. Biomechanical comparison of locked plate osteosynthesis, reamed and unreamed nailing in conventional interlocking technique, and unreamed angle stable nailing in distal tibia fractures. J Trauma Acute Care Surg. 2012;73(4):933-938.
17. Brumback RJ, Reilly JP, Poka A, Lakatos RP, Bathon GH, Burgess AR. Intramedullary nailing of femoral shaft fractures. Part 1: Decision-making errors with interlocking fixation. J Bone Joint Surg Am. 1988;70(10):1441-1452.
18. Hooper GJ, Keddell RG, Penny ID. Conservative management or closed nailing for tibial shaft fractures. A randomised prospective trial. J Bone Joint Surg Br. 1991;73(1):83-85.
19. Karladani AH, Granhed H, Edshage B, Jerre R, Styf J. Displaced tibial shaft fractures: a prospective randomized study of closed intramedullary nailing versus cast treatment in 53 patients. Acta Orthop Scand. 2000;71(12):160-167.
20. Kenwright J, Richardson JB, Goodship AE, et al. Effect of controlled axial micromovement on healing of tibial fractures. Lancet. 1986;22(8517):1185-1187.
21. Im GI, Tae SK. Distal metaphyseal fractures of tibia: a prospective randomized trial of closed reduction and intramedullary nail versus open reduction and plate and screws fixation. J Trauma. 2005;59(5):1219-1223.
22. Henley MB, Chapman JR, Agel J, Harvey EJ, Whorton AM, Swiontkowski MF. Treatment of type II, IIIA, and IIIB open fractures of the tibial shaft: a prospective comparison of unreamed interlocking intramedullary nails and half-pin external fixators. J Orthop Trauma. 1998;12(1):1-7.
23. Ramos T, Ekholm C, Eriksson BI, Karlsson J, Nistor L. The Ilizarov external fixator - a useful alternative for the treatment of proximal tibial fractures. A prospective observational study of 30 consecutive patients. BMC Musculoskelet Disord. 2013;14:11.
24. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment of open fractures of the shaft of the tibia. J Bone Joint Surg Br. 2001;83(1):62-68.
25. Webb LX, Bosse MJ, Castillo RC, MacKenzie EJ; LEAP Study Group. Analysis of surgeon-controlled variables in the treatment of limb-threatening type-III open tibial diaphyseal fractures. J Bone Joint Surg Am. 2007;89(5):923-928.
26. Bondurant FJ, Cotler HB, Buckle R, Miller-Crotchett P, Browner BD. The medical and economic impact of severely injured lower extremities. J Trauma. 1988;28(8):1270-1273.
27. Bosse MJ, MacKenzie EJ, Kellam JF, et al. An analysis of outcomes of reconstruction or amputation of leg-threatening injuries. N Engl J Med. 2002;347(24):1924-1931.
28. MacKenzie EJ, Bosse MJ, Pollak AN, et al. Long-term persistence of disability following severe lower-limb trauma. Results of a seven-year follow-up. J Bone Joint Surg Am. 2005;87(8):1801-1809.
29. Doulens KM, Joshi AB, Wagner RA. Tibial fracture after total knee arthroplasty treated with retrograde intramedullary fixation. Am J Orthop. 2007;36(7):E111-E113.
30. Zafra-Jiménez JA, Pretell-Mazzini J, Resines-Erasun C. Distal tibial fracture below a total knee arthroplasty: retrograde intramedullary nailing as an alternative method of treatment: a case report. J Orthop Trauma. 2011;25(7):e74-e76.
31. Loosen S, Preuss S, Zelle BA, Pape HC, Tarken IS. Multimorbid patients with poor soft tissue conditions: Treatment of distal tibia fractures with retrograde intramedullary nailing. Unfallchirurg. 2012;116(6):553-558.
32. Kessler SB, Hallfeldt KJ, Perren SM, Schweiberer L. The effects of reaming and intramedullary nailing on fracture healing. Clin Orthop. 1986;212:18-25.
33. Klein MP, Rahn BA, Frigg R, Kessler S, Perren SM. Reaming versus non-reaming in medullary nailing: interference with cortical circulation of the canine tibia. Arch Orthop Trauma Surg. 1990;109(6):314-316.
34. Reichert IL, McCarthy ID, Hughes SP. The acute vascular response to intramedullary reaming. Microsphere estimation of blood flow in the intact ovine tibia. J Bone Joint Surg Br. 1995;77(3):490-493.
Glenoid Damage From Articular Protrusion of Metal Suture Anchor After Arthroscopic Rotator Cuff Repair
Complications with the use of anchor screws in shoulder surgery have been well-documented1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.
Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.3 However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.
Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.
Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.
A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.
After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.
The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.
Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.
After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).
Discussion
Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.3,4 Zuckerman and Matsen4 divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.5 In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.
Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues5 performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.
The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.
This case has shown the importance of obtaining postoperative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.1
Conclusion
Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.
1. Park HB, Keyurapan E, Gill HS, Selhi HS, McFarland EG. Suture anchors and tacks for shoulder surgery. Part II: The prevention and treatment of complications. Am J Sports Med. 2006;34(1):136-144.
2. McFarland EG, Park HB, Keyurapan E, Gill HS, Selhi HS. Suture anchors and tacks for shoulder surgery. Part I: Biology and biomechanics. Am J Sports Med. 2005;33(12):1918-1923.
3. Rhee YG, Lee DH, Chun IH, Bae SC. Glenohumeral arthropathy after arthroscopic anterior shoulder stabilization. Arthroscopy. 2004;20(4):402-406.
4. Zuckerman JD, Matsen FA III. Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am. 1984;66(2):175-180.
5. Wong AS, Kokkalis ZT, Schmidt CC. Proper insertion angle is essential to prevent intra-articular protrusion of a knotless suture anchor in shoulder rotator cuff repair. Arthroscopy. 2010;26(2):286-290.
6. Grutter PW, McFarland EG, Zikria BA, Dai Z, Petersen SA. Techniques for suture anchor removal in shoulder surgery. Am J Sports Med. 2010;38(8):1706-1710.
Complications with the use of anchor screws in shoulder surgery have been well-documented1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.
Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.3 However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.
Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.
Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.
A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.
After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.
The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.
Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.
After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).
Discussion
Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.3,4 Zuckerman and Matsen4 divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.5 In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.
Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues5 performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.
The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.
This case has shown the importance of obtaining postoperative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.1
Conclusion
Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.
Complications with the use of anchor screws in shoulder surgery have been well-documented1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.
Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.3 However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.
Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.
Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.
A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.
After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.
The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.
Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.
After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).
Discussion
Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.3,4 Zuckerman and Matsen4 divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.5 In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.
Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues5 performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.
The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.
This case has shown the importance of obtaining postoperative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.1
Conclusion
Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.
1. Park HB, Keyurapan E, Gill HS, Selhi HS, McFarland EG. Suture anchors and tacks for shoulder surgery. Part II: The prevention and treatment of complications. Am J Sports Med. 2006;34(1):136-144.
2. McFarland EG, Park HB, Keyurapan E, Gill HS, Selhi HS. Suture anchors and tacks for shoulder surgery. Part I: Biology and biomechanics. Am J Sports Med. 2005;33(12):1918-1923.
3. Rhee YG, Lee DH, Chun IH, Bae SC. Glenohumeral arthropathy after arthroscopic anterior shoulder stabilization. Arthroscopy. 2004;20(4):402-406.
4. Zuckerman JD, Matsen FA III. Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am. 1984;66(2):175-180.
5. Wong AS, Kokkalis ZT, Schmidt CC. Proper insertion angle is essential to prevent intra-articular protrusion of a knotless suture anchor in shoulder rotator cuff repair. Arthroscopy. 2010;26(2):286-290.
6. Grutter PW, McFarland EG, Zikria BA, Dai Z, Petersen SA. Techniques for suture anchor removal in shoulder surgery. Am J Sports Med. 2010;38(8):1706-1710.
1. Park HB, Keyurapan E, Gill HS, Selhi HS, McFarland EG. Suture anchors and tacks for shoulder surgery. Part II: The prevention and treatment of complications. Am J Sports Med. 2006;34(1):136-144.
2. McFarland EG, Park HB, Keyurapan E, Gill HS, Selhi HS. Suture anchors and tacks for shoulder surgery. Part I: Biology and biomechanics. Am J Sports Med. 2005;33(12):1918-1923.
3. Rhee YG, Lee DH, Chun IH, Bae SC. Glenohumeral arthropathy after arthroscopic anterior shoulder stabilization. Arthroscopy. 2004;20(4):402-406.
4. Zuckerman JD, Matsen FA III. Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am. 1984;66(2):175-180.
5. Wong AS, Kokkalis ZT, Schmidt CC. Proper insertion angle is essential to prevent intra-articular protrusion of a knotless suture anchor in shoulder rotator cuff repair. Arthroscopy. 2010;26(2):286-290.
6. Grutter PW, McFarland EG, Zikria BA, Dai Z, Petersen SA. Techniques for suture anchor removal in shoulder surgery. Am J Sports Med. 2010;38(8):1706-1710.
Harrington Rod Revision After Failed Total Hip Arthroplasty Due to Missed Acetabular Metastasis
We report the case of a patient who was treated with total hip arthroplasty (THA) for osteoarthritis but was found to have a large acetabular defect caused by pulmonary metastasis. She was promptly referred to our orthopedic oncology clinic for revision because she had experienced no improvement in her symptoms. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman was referred to us for evaluation of a large right supra-acetabular lesion after undergoing a right THA at another hospital 3 weeks earlier. Preoperative radiographs showed severe osteoarthritis of the right hip but there was no diagnosis of an acetabular lesion in her medical history. During the operation, the surgeon noted poor acetabulum bone quality and sent acetabular reamings for histopathologic analysis, which revealed adenocarcinoma. The arthroplasty was completed in a normal fashion, and the patient was discharged. Postoperatively, her pain did not resolve, and her functional status deteriorated from ambulating with a walker to very limited activity and weight-bearing.
When the patient came to our clinic, we learned she underwent a lobectomy in 2011 for lung cancer resulting from her 40-pack-year history of smoking and had a strong family history of breast cancer. She also had a history of coronary artery disease, hypertension, hyperlipidemia, morbid obesity, and depression. We obtained plain films and a computed tomography (CT) scan that showed a 6.5×7.1×6.5-cm lytic lesion arising from the right acetabulum with cortical penetration and an extraosseous soft-tissue component. Two smaller 10-mm to 12-mm lesions were also found superior and medial to the large lesion. These radiographs and CT images are shown in Figures 1-3.
We discussed nonoperative and operative options for treatment with the patient and her family, and she elected to undergo palliative surgical curettage and fixation. Significant bone erosion of the acetabulum and a resultant lack of mechanical support for the acetabular cup were found intraoperatively. An unusual surgical approach was selected in order to minimize morbidity and avoid performing a revision acetabular component if the cup was found to be stable from the standpoint of osseointegration. We approached from the superior side of the ilium, removing the abductors in the superperiosteal fashion extending down from the supra-acetabular ilium, sparing the hip capsule. When the acetabular component was exposed and stressed under fluoroscopy, there was no evidence of loosening. We decided to reconstruct the mechanical defect without revision of the acetabular component and to leave the screw in place. After partial excision of the right supra-acetabular ilium, specimens were sent to pathology. We placed five 4.8-mm and four 4.0-mm threaded Steinmann pins intraosseously through the iliac wing to abut the acetabular cup. In this way, the Steinmann pins provided a stable roof to the cup for weight-bearing and scaffolding for methylmethacrylate cement impregnated with tobramycin. A postoperative radiograph of the patient’s pelvis is shown in Figure 4.
Immediately after her surgery, the patient was bearing weight as tolerated and participating in physical therapy 3 times a day. Two months postoperatively, she was able to walk 1 block with use of a walker, and her pain was controlled with oral pain medication. At her 1-year visit, she was walking without pain for prolonged distances. She had a mild limp but did not need ambulatory aids. She had full range of motion, was able to perform all of her desired activities, and was quite pleased with her result. One-year postoperative radiographs (Figure 5) show stable placement of her acetabular cup with her pins and cement in an unchanged position without recurrence of her destructive lesion. There was no evidence of progression of her cancer, although she had some heterotopic bone in her lateral soft tissues.
Discussion
Many cases have been reported in the literature of metastases to the pelvis and acetabulum; almost 10% of bone metastases are in the pelvis.1 Although many are seen on radiographs, pelvic metastases, especially if they involve the acetabulum, can present with hip pain, decreased joint range of motion, and reduced ambulatory function, all symptoms that are similar to osteoarthritis. While the presence of metastases indicates late-stage disease, many patients still live for years with hip symptoms before succumbing to cancer.1 Palliative treatment initially consists of protected weight-bearing, analgesics, antineoplastic medications ,and radiation. When these first-line therapies fail, palliative operative treatment can be considered, with goals to maintain stability and to preserve mobility, independence, and comfort.2 Patients should be offered this only if there is a reasonable chance that structural stability can be achieved via reconstruction and if the patient will live long enough to realize the functional improvement.3 Harrington4 described patterns of acetabular metastases and surgical treatments in his classic series of 58 patients. For class II and III lesions, he concluded it was necessary to provide additional structural support to the acetabular component of a THA, either in the form of a protrusion shell or with Steinmann pins and bone cement.4 Antiprotrusion cages combined with arthroplasty have been used with modest success for cases where implant bone integration is unlikely.5-6 Several studies since Harrington have shown that constructs with cement reinforced with Steinmann pins can provide reduced pain and improved mobility with a low failure rate for the remainder of the patient’s life.7-9
In addition, a few cases have been reported of metastases to endoprostheses, which were implanted long before the diagnosis of cancer.10 To an unsuspecting surgeon, the lytic periprosthetic metastases may look like osteolysis or pseudotumor. Fabbri and colleagues11 presented 4 cases showing how sarcoma around a joint endoprosthesis can easily be mistaken for pseudotumor. A patient considering primary or revision THA for bone loss caused by osteolysis would be given different options than if the bone loss were secondary to metastases. Revision techniques in the setting of acetabular osteolysis include acetabular liner exchanges, cementless hemispherical components and jumbo cups, structural allografts, metal augments, impaction grafting, and acetabular cages and cup-cage constructs. Rarely are “Harrington” reconstructions performed for this reason.12
This case is unusual because the diagnosis of metastatic disease was missed and THA was performed under the presumptive diagnosis of osteoarthritis. While a malignant process was recognized intraoperatively, the joint replacement was completed nonetheless, with revision surgery inevitably occurring within a few weeks. Our patient’s history of lung cancer reinforces the importance of preoperative history taking, and the missed diagnosis highlights the need for clinicians to maintain a broad differential, even in seemingly simple arthritis cases. Proper preoperative imaging, biopsies, and cultures are also paramount. Lesions that are painful, involve the whole cortex, appear soon after implementation, and are rapidly progressing should raise concern for malignancy.10 If there is concern for osteolysis, quantitative CT with 3-dimensional reconstructions can help visualize the lesions and help in planning surgery.13 Had a timely diagnosis been made, the proper reconstruction could have been planned before the index procedure, and our patient could have been spared the pain, risk, and morbidity of a second operation.
The second lesson of this case is that, as long as the cup was stable, the etiology of the hip pain was lack of mechanical support. Once corrected, the total hip functioned as planned. A minimally invasive approach that allowed for observation of the cup without exposing the entire hip saved a patient a significant amount of morbidity and led to an acceptable outcome.
1. Ho L, Ahlmann ER, Menendez LR. Modified Harrington reconstruction for advanced periacetabular metastatic disease. J Surg Oncol. 2010;101(2):170-174.
2. Papagelopoulos PJ, Mavrogenis AF, Soucacos PN. Evaluation and treatment of pelvic metastases. Injury. 2007;38(4):509-520.
3. Allan DG, Bell RS, Davis A, Langer F. Complex acetabular reconstruction for metastatic tumor. J Arthroplasty. 1995;10(3):301-306.
4. Harrington KD. The management of acetabular insufficiency secondary to metastatic malignant disease. J Bone Joint Surg Am. 1981;63(4):653-64.
5. Hoell S, Dedy N, Gosheger G, Dieckmann R, Daniilidis K, Hardes J. The Burch-Schneider cage for reconstruction after metastatic destruction of the acetabulum: outcome and complications. Arch Orthop Trauma Surg. 2012;132(3):405-410.
6. Clayer M. The survivorship of protrusio cages for metastatic disease involving the acetabulum. Clin Orthop. 2010;468(11):2980-2984.
7. Marco RA, Sheth DS, Boland PJ, Wunder JS, Siegel JA, Healey JH. Functional and oncological outcome of acetabular reconstruction for the treatment of metastatic disease. J Bone Joint Surg Am. 2000;82(5):642-651.
8. Tillman RM, Myers GJ, Abudu AT, Carter SR, Grimer RJ. The three-pin modified ‘Harrington’ procedure for advanced metastatic destruction of the acetabulum. J Bone Joint Surg Br. 2008;90(1):84-87.
9. Walker RH. Pelvic reconstruction/total hip arthroplasty for metastatic acetabular insufficiency. Clin Orthop. 1993;294:170-175.
10. Dramis A, Desai AS, Board TN, Hekal WE, Panezai JR. Periprosthetic osteolysis due to metastatic renal cell carcinoma: a case report. Cases J. 2008;1(1):297.
11. Fabbri N, Rustemi E, Masetti C, et al. Severe osteolysis and soft tissue mass around total hip arthroplasty: description of four cases and review of the literature with respect to clinico-radiographic and pathologic differential diagnosis. Eur J Radiol. 2011;77(1):43-50.
12. Deirmengian GK, Zmistowski B, O’Neil JT, Hozack WJ. Management of acetabular bone loss in revision total hip arthroplasty. J Bone Joint Surg Am. 2011;93(19):1842-1852.
13. Kitamura N, Leung SB, Engh CA Sr. Characteristics of pelvic osteolysis on computed tomography after total hip arthroplasty. Clin Orthop. 2005;441:291-297.
We report the case of a patient who was treated with total hip arthroplasty (THA) for osteoarthritis but was found to have a large acetabular defect caused by pulmonary metastasis. She was promptly referred to our orthopedic oncology clinic for revision because she had experienced no improvement in her symptoms. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman was referred to us for evaluation of a large right supra-acetabular lesion after undergoing a right THA at another hospital 3 weeks earlier. Preoperative radiographs showed severe osteoarthritis of the right hip but there was no diagnosis of an acetabular lesion in her medical history. During the operation, the surgeon noted poor acetabulum bone quality and sent acetabular reamings for histopathologic analysis, which revealed adenocarcinoma. The arthroplasty was completed in a normal fashion, and the patient was discharged. Postoperatively, her pain did not resolve, and her functional status deteriorated from ambulating with a walker to very limited activity and weight-bearing.
When the patient came to our clinic, we learned she underwent a lobectomy in 2011 for lung cancer resulting from her 40-pack-year history of smoking and had a strong family history of breast cancer. She also had a history of coronary artery disease, hypertension, hyperlipidemia, morbid obesity, and depression. We obtained plain films and a computed tomography (CT) scan that showed a 6.5×7.1×6.5-cm lytic lesion arising from the right acetabulum with cortical penetration and an extraosseous soft-tissue component. Two smaller 10-mm to 12-mm lesions were also found superior and medial to the large lesion. These radiographs and CT images are shown in Figures 1-3.
We discussed nonoperative and operative options for treatment with the patient and her family, and she elected to undergo palliative surgical curettage and fixation. Significant bone erosion of the acetabulum and a resultant lack of mechanical support for the acetabular cup were found intraoperatively. An unusual surgical approach was selected in order to minimize morbidity and avoid performing a revision acetabular component if the cup was found to be stable from the standpoint of osseointegration. We approached from the superior side of the ilium, removing the abductors in the superperiosteal fashion extending down from the supra-acetabular ilium, sparing the hip capsule. When the acetabular component was exposed and stressed under fluoroscopy, there was no evidence of loosening. We decided to reconstruct the mechanical defect without revision of the acetabular component and to leave the screw in place. After partial excision of the right supra-acetabular ilium, specimens were sent to pathology. We placed five 4.8-mm and four 4.0-mm threaded Steinmann pins intraosseously through the iliac wing to abut the acetabular cup. In this way, the Steinmann pins provided a stable roof to the cup for weight-bearing and scaffolding for methylmethacrylate cement impregnated with tobramycin. A postoperative radiograph of the patient’s pelvis is shown in Figure 4.
Immediately after her surgery, the patient was bearing weight as tolerated and participating in physical therapy 3 times a day. Two months postoperatively, she was able to walk 1 block with use of a walker, and her pain was controlled with oral pain medication. At her 1-year visit, she was walking without pain for prolonged distances. She had a mild limp but did not need ambulatory aids. She had full range of motion, was able to perform all of her desired activities, and was quite pleased with her result. One-year postoperative radiographs (Figure 5) show stable placement of her acetabular cup with her pins and cement in an unchanged position without recurrence of her destructive lesion. There was no evidence of progression of her cancer, although she had some heterotopic bone in her lateral soft tissues.
Discussion
Many cases have been reported in the literature of metastases to the pelvis and acetabulum; almost 10% of bone metastases are in the pelvis.1 Although many are seen on radiographs, pelvic metastases, especially if they involve the acetabulum, can present with hip pain, decreased joint range of motion, and reduced ambulatory function, all symptoms that are similar to osteoarthritis. While the presence of metastases indicates late-stage disease, many patients still live for years with hip symptoms before succumbing to cancer.1 Palliative treatment initially consists of protected weight-bearing, analgesics, antineoplastic medications ,and radiation. When these first-line therapies fail, palliative operative treatment can be considered, with goals to maintain stability and to preserve mobility, independence, and comfort.2 Patients should be offered this only if there is a reasonable chance that structural stability can be achieved via reconstruction and if the patient will live long enough to realize the functional improvement.3 Harrington4 described patterns of acetabular metastases and surgical treatments in his classic series of 58 patients. For class II and III lesions, he concluded it was necessary to provide additional structural support to the acetabular component of a THA, either in the form of a protrusion shell or with Steinmann pins and bone cement.4 Antiprotrusion cages combined with arthroplasty have been used with modest success for cases where implant bone integration is unlikely.5-6 Several studies since Harrington have shown that constructs with cement reinforced with Steinmann pins can provide reduced pain and improved mobility with a low failure rate for the remainder of the patient’s life.7-9
In addition, a few cases have been reported of metastases to endoprostheses, which were implanted long before the diagnosis of cancer.10 To an unsuspecting surgeon, the lytic periprosthetic metastases may look like osteolysis or pseudotumor. Fabbri and colleagues11 presented 4 cases showing how sarcoma around a joint endoprosthesis can easily be mistaken for pseudotumor. A patient considering primary or revision THA for bone loss caused by osteolysis would be given different options than if the bone loss were secondary to metastases. Revision techniques in the setting of acetabular osteolysis include acetabular liner exchanges, cementless hemispherical components and jumbo cups, structural allografts, metal augments, impaction grafting, and acetabular cages and cup-cage constructs. Rarely are “Harrington” reconstructions performed for this reason.12
This case is unusual because the diagnosis of metastatic disease was missed and THA was performed under the presumptive diagnosis of osteoarthritis. While a malignant process was recognized intraoperatively, the joint replacement was completed nonetheless, with revision surgery inevitably occurring within a few weeks. Our patient’s history of lung cancer reinforces the importance of preoperative history taking, and the missed diagnosis highlights the need for clinicians to maintain a broad differential, even in seemingly simple arthritis cases. Proper preoperative imaging, biopsies, and cultures are also paramount. Lesions that are painful, involve the whole cortex, appear soon after implementation, and are rapidly progressing should raise concern for malignancy.10 If there is concern for osteolysis, quantitative CT with 3-dimensional reconstructions can help visualize the lesions and help in planning surgery.13 Had a timely diagnosis been made, the proper reconstruction could have been planned before the index procedure, and our patient could have been spared the pain, risk, and morbidity of a second operation.
The second lesson of this case is that, as long as the cup was stable, the etiology of the hip pain was lack of mechanical support. Once corrected, the total hip functioned as planned. A minimally invasive approach that allowed for observation of the cup without exposing the entire hip saved a patient a significant amount of morbidity and led to an acceptable outcome.
We report the case of a patient who was treated with total hip arthroplasty (THA) for osteoarthritis but was found to have a large acetabular defect caused by pulmonary metastasis. She was promptly referred to our orthopedic oncology clinic for revision because she had experienced no improvement in her symptoms. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 61-year-old woman was referred to us for evaluation of a large right supra-acetabular lesion after undergoing a right THA at another hospital 3 weeks earlier. Preoperative radiographs showed severe osteoarthritis of the right hip but there was no diagnosis of an acetabular lesion in her medical history. During the operation, the surgeon noted poor acetabulum bone quality and sent acetabular reamings for histopathologic analysis, which revealed adenocarcinoma. The arthroplasty was completed in a normal fashion, and the patient was discharged. Postoperatively, her pain did not resolve, and her functional status deteriorated from ambulating with a walker to very limited activity and weight-bearing.
When the patient came to our clinic, we learned she underwent a lobectomy in 2011 for lung cancer resulting from her 40-pack-year history of smoking and had a strong family history of breast cancer. She also had a history of coronary artery disease, hypertension, hyperlipidemia, morbid obesity, and depression. We obtained plain films and a computed tomography (CT) scan that showed a 6.5×7.1×6.5-cm lytic lesion arising from the right acetabulum with cortical penetration and an extraosseous soft-tissue component. Two smaller 10-mm to 12-mm lesions were also found superior and medial to the large lesion. These radiographs and CT images are shown in Figures 1-3.
We discussed nonoperative and operative options for treatment with the patient and her family, and she elected to undergo palliative surgical curettage and fixation. Significant bone erosion of the acetabulum and a resultant lack of mechanical support for the acetabular cup were found intraoperatively. An unusual surgical approach was selected in order to minimize morbidity and avoid performing a revision acetabular component if the cup was found to be stable from the standpoint of osseointegration. We approached from the superior side of the ilium, removing the abductors in the superperiosteal fashion extending down from the supra-acetabular ilium, sparing the hip capsule. When the acetabular component was exposed and stressed under fluoroscopy, there was no evidence of loosening. We decided to reconstruct the mechanical defect without revision of the acetabular component and to leave the screw in place. After partial excision of the right supra-acetabular ilium, specimens were sent to pathology. We placed five 4.8-mm and four 4.0-mm threaded Steinmann pins intraosseously through the iliac wing to abut the acetabular cup. In this way, the Steinmann pins provided a stable roof to the cup for weight-bearing and scaffolding for methylmethacrylate cement impregnated with tobramycin. A postoperative radiograph of the patient’s pelvis is shown in Figure 4.
Immediately after her surgery, the patient was bearing weight as tolerated and participating in physical therapy 3 times a day. Two months postoperatively, she was able to walk 1 block with use of a walker, and her pain was controlled with oral pain medication. At her 1-year visit, she was walking without pain for prolonged distances. She had a mild limp but did not need ambulatory aids. She had full range of motion, was able to perform all of her desired activities, and was quite pleased with her result. One-year postoperative radiographs (Figure 5) show stable placement of her acetabular cup with her pins and cement in an unchanged position without recurrence of her destructive lesion. There was no evidence of progression of her cancer, although she had some heterotopic bone in her lateral soft tissues.
Discussion
Many cases have been reported in the literature of metastases to the pelvis and acetabulum; almost 10% of bone metastases are in the pelvis.1 Although many are seen on radiographs, pelvic metastases, especially if they involve the acetabulum, can present with hip pain, decreased joint range of motion, and reduced ambulatory function, all symptoms that are similar to osteoarthritis. While the presence of metastases indicates late-stage disease, many patients still live for years with hip symptoms before succumbing to cancer.1 Palliative treatment initially consists of protected weight-bearing, analgesics, antineoplastic medications ,and radiation. When these first-line therapies fail, palliative operative treatment can be considered, with goals to maintain stability and to preserve mobility, independence, and comfort.2 Patients should be offered this only if there is a reasonable chance that structural stability can be achieved via reconstruction and if the patient will live long enough to realize the functional improvement.3 Harrington4 described patterns of acetabular metastases and surgical treatments in his classic series of 58 patients. For class II and III lesions, he concluded it was necessary to provide additional structural support to the acetabular component of a THA, either in the form of a protrusion shell or with Steinmann pins and bone cement.4 Antiprotrusion cages combined with arthroplasty have been used with modest success for cases where implant bone integration is unlikely.5-6 Several studies since Harrington have shown that constructs with cement reinforced with Steinmann pins can provide reduced pain and improved mobility with a low failure rate for the remainder of the patient’s life.7-9
In addition, a few cases have been reported of metastases to endoprostheses, which were implanted long before the diagnosis of cancer.10 To an unsuspecting surgeon, the lytic periprosthetic metastases may look like osteolysis or pseudotumor. Fabbri and colleagues11 presented 4 cases showing how sarcoma around a joint endoprosthesis can easily be mistaken for pseudotumor. A patient considering primary or revision THA for bone loss caused by osteolysis would be given different options than if the bone loss were secondary to metastases. Revision techniques in the setting of acetabular osteolysis include acetabular liner exchanges, cementless hemispherical components and jumbo cups, structural allografts, metal augments, impaction grafting, and acetabular cages and cup-cage constructs. Rarely are “Harrington” reconstructions performed for this reason.12
This case is unusual because the diagnosis of metastatic disease was missed and THA was performed under the presumptive diagnosis of osteoarthritis. While a malignant process was recognized intraoperatively, the joint replacement was completed nonetheless, with revision surgery inevitably occurring within a few weeks. Our patient’s history of lung cancer reinforces the importance of preoperative history taking, and the missed diagnosis highlights the need for clinicians to maintain a broad differential, even in seemingly simple arthritis cases. Proper preoperative imaging, biopsies, and cultures are also paramount. Lesions that are painful, involve the whole cortex, appear soon after implementation, and are rapidly progressing should raise concern for malignancy.10 If there is concern for osteolysis, quantitative CT with 3-dimensional reconstructions can help visualize the lesions and help in planning surgery.13 Had a timely diagnosis been made, the proper reconstruction could have been planned before the index procedure, and our patient could have been spared the pain, risk, and morbidity of a second operation.
The second lesson of this case is that, as long as the cup was stable, the etiology of the hip pain was lack of mechanical support. Once corrected, the total hip functioned as planned. A minimally invasive approach that allowed for observation of the cup without exposing the entire hip saved a patient a significant amount of morbidity and led to an acceptable outcome.
1. Ho L, Ahlmann ER, Menendez LR. Modified Harrington reconstruction for advanced periacetabular metastatic disease. J Surg Oncol. 2010;101(2):170-174.
2. Papagelopoulos PJ, Mavrogenis AF, Soucacos PN. Evaluation and treatment of pelvic metastases. Injury. 2007;38(4):509-520.
3. Allan DG, Bell RS, Davis A, Langer F. Complex acetabular reconstruction for metastatic tumor. J Arthroplasty. 1995;10(3):301-306.
4. Harrington KD. The management of acetabular insufficiency secondary to metastatic malignant disease. J Bone Joint Surg Am. 1981;63(4):653-64.
5. Hoell S, Dedy N, Gosheger G, Dieckmann R, Daniilidis K, Hardes J. The Burch-Schneider cage for reconstruction after metastatic destruction of the acetabulum: outcome and complications. Arch Orthop Trauma Surg. 2012;132(3):405-410.
6. Clayer M. The survivorship of protrusio cages for metastatic disease involving the acetabulum. Clin Orthop. 2010;468(11):2980-2984.
7. Marco RA, Sheth DS, Boland PJ, Wunder JS, Siegel JA, Healey JH. Functional and oncological outcome of acetabular reconstruction for the treatment of metastatic disease. J Bone Joint Surg Am. 2000;82(5):642-651.
8. Tillman RM, Myers GJ, Abudu AT, Carter SR, Grimer RJ. The three-pin modified ‘Harrington’ procedure for advanced metastatic destruction of the acetabulum. J Bone Joint Surg Br. 2008;90(1):84-87.
9. Walker RH. Pelvic reconstruction/total hip arthroplasty for metastatic acetabular insufficiency. Clin Orthop. 1993;294:170-175.
10. Dramis A, Desai AS, Board TN, Hekal WE, Panezai JR. Periprosthetic osteolysis due to metastatic renal cell carcinoma: a case report. Cases J. 2008;1(1):297.
11. Fabbri N, Rustemi E, Masetti C, et al. Severe osteolysis and soft tissue mass around total hip arthroplasty: description of four cases and review of the literature with respect to clinico-radiographic and pathologic differential diagnosis. Eur J Radiol. 2011;77(1):43-50.
12. Deirmengian GK, Zmistowski B, O’Neil JT, Hozack WJ. Management of acetabular bone loss in revision total hip arthroplasty. J Bone Joint Surg Am. 2011;93(19):1842-1852.
13. Kitamura N, Leung SB, Engh CA Sr. Characteristics of pelvic osteolysis on computed tomography after total hip arthroplasty. Clin Orthop. 2005;441:291-297.
1. Ho L, Ahlmann ER, Menendez LR. Modified Harrington reconstruction for advanced periacetabular metastatic disease. J Surg Oncol. 2010;101(2):170-174.
2. Papagelopoulos PJ, Mavrogenis AF, Soucacos PN. Evaluation and treatment of pelvic metastases. Injury. 2007;38(4):509-520.
3. Allan DG, Bell RS, Davis A, Langer F. Complex acetabular reconstruction for metastatic tumor. J Arthroplasty. 1995;10(3):301-306.
4. Harrington KD. The management of acetabular insufficiency secondary to metastatic malignant disease. J Bone Joint Surg Am. 1981;63(4):653-64.
5. Hoell S, Dedy N, Gosheger G, Dieckmann R, Daniilidis K, Hardes J. The Burch-Schneider cage for reconstruction after metastatic destruction of the acetabulum: outcome and complications. Arch Orthop Trauma Surg. 2012;132(3):405-410.
6. Clayer M. The survivorship of protrusio cages for metastatic disease involving the acetabulum. Clin Orthop. 2010;468(11):2980-2984.
7. Marco RA, Sheth DS, Boland PJ, Wunder JS, Siegel JA, Healey JH. Functional and oncological outcome of acetabular reconstruction for the treatment of metastatic disease. J Bone Joint Surg Am. 2000;82(5):642-651.
8. Tillman RM, Myers GJ, Abudu AT, Carter SR, Grimer RJ. The three-pin modified ‘Harrington’ procedure for advanced metastatic destruction of the acetabulum. J Bone Joint Surg Br. 2008;90(1):84-87.
9. Walker RH. Pelvic reconstruction/total hip arthroplasty for metastatic acetabular insufficiency. Clin Orthop. 1993;294:170-175.
10. Dramis A, Desai AS, Board TN, Hekal WE, Panezai JR. Periprosthetic osteolysis due to metastatic renal cell carcinoma: a case report. Cases J. 2008;1(1):297.
11. Fabbri N, Rustemi E, Masetti C, et al. Severe osteolysis and soft tissue mass around total hip arthroplasty: description of four cases and review of the literature with respect to clinico-radiographic and pathologic differential diagnosis. Eur J Radiol. 2011;77(1):43-50.
12. Deirmengian GK, Zmistowski B, O’Neil JT, Hozack WJ. Management of acetabular bone loss in revision total hip arthroplasty. J Bone Joint Surg Am. 2011;93(19):1842-1852.
13. Kitamura N, Leung SB, Engh CA Sr. Characteristics of pelvic osteolysis on computed tomography after total hip arthroplasty. Clin Orthop. 2005;441:291-297.
Atypical Presentation of Fat Embolism Syndrome After Gunshot Wound to the Foot
Fat embolism syndrome (FES) is a rare complication reported primarily after long bone fractures, with an incidence of 0.3% to 2.2%.1-3 It is most commonly caused by trauma and is thought to result from movement of bone fragments or to occur during intramedullary reaming.1 Both of these factors lead to a distortion of the bone marrow cavity, allowing marrow and fat to enter the circulatory system.1
Although the true pathophysiology remains poorly understood, it is possible that, once in systemic circulation, the fat particles become lodged in the vascular system, inciting an inflammatory response, leading to organ dysfunction via mechanical or biochemical processes.4 Typically, the diagnosis is made after clinical features are observed, including hypoxemia, petechial rash, and cerebral signs not related to a head injury or other conditions.5,6
Although FES is an uncommon complication after traumatic injuries, mortality after FES in a recent study was reported to be 10%.1 FES is most commonly seen after fractures of the femur and tibia, although cases have been described involving fractures of the radius, ulna, and humerus.1,3 We present an atypical case of cerebral FES after multiple fractures of the foot; to our knowledge, such a case has not been reported in the English-language literature. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 42-year-old man was hunting with his son when he was accidentally shot in the left foot with a .270-caliber rifle bullet at close range. The patient sought care at a local hospital and, in the ensuing 3 hours, his mentation appeared normal. He reported pain and numbness distal to the injury in the tibial nerve distribution, but he remained vascularly intact, alert, and oriented. He was given 7 mg of hydromorphone hydrochloride over 2 hours for pain control and was transferred to our hospital via ambulance approximately 6 hours after injury. Upon arrival, he was noted to be extremely sedated and obtunded, responding only to pain with spontaneous eye opening. He was unable to follow commands. He was given
1.2 mg of naloxone intravenously to reverse what was presumed to be acute opioid intoxication; however, his mental status did not improve.
On examination, the patient was noted to have a small entrance wound through the Achilles tendon (Figures 1A, 1B) and an exit wound on the plantar aspect of the foot near the heads of the first and second metatarsals (Figures 1C, 1D) with minimal bleeding and no gross contamination. There was significant edema on the medial and proximal aspects of the left foot, 3+ dorsalis pedis pulse, and a capillary refill of 4 seconds. Radiographs showed traumatic fracture deformities of the calcaneus, navicular, medial cuneiform, and first and second metatarsal bases, as well as an intra-articular fracture deformity of the left talus extending to the talar dome (Figures 2A-2C). Neurologic examination could not be reliably obtained because of the patient’s mental status. He was determined to be unstable for immediate surgery, and his left leg was splinted pending neurologic evaluation.
The patient’s oxygen saturation was 94%, and his temperature was 38.2°C (100.76°F). Although his heart rate was in the 90s upon arrival, he became tachycardic over the next 4 hours, with heart rate ranging from the 110s to 130s; he remained tachycardic for approximately 72 hours. Laboratory values upon arrival showed a hemoglobin value of 12.8 g/dL and platelets of 249,000/μL. He developed anemia and thrombocytopenia within 72 hours of the injury, with a low of 6.6 g/dL and 88,000/μL, respectively, by postinjury day 4. Computed tomography of the head, electroencephalography, urine drug screen, and lumbar puncture were unremarkable. The patient never became hypoxemic. Within 14 hours after injury, he was completely comatose with extensor posturing. In the intensive care unit (ICU), the patient was intubated for airway protection.
The next day, the patient underwent magnetic resonance imaging (MRI) of the brain, which showed innumerable tiny infarcts throughout cerebral hemispheres, cerebellum, and brainstem in a characteristic “starfield” pattern on T2-weighted images (Figure 3). This was radiographically consistent with fat emboli related to the left lower extremity gunshot wound. An echocardiogram showed small right-to-left shunt and a possible intrapulmonary shunt, although this was never confirmed. The echocardiogram was technically challenging secondary to his persistent tachycardia. He also developed a subtle petechial rash (Figure 4A).
The patient underwent percutaneous gastrostomy-tube placement for nutrition on postinjury day 4 and remained intubated, unable to protect his airway, and nonresponsive with extensor posturing (Figure 4B). He was also taken to the operating room for spanning external fixator placement on postinjury day 3 to restore calcaneal height and length as well as foot stability (Figures 5A, 5B).
The patient was treated with supportive care and was discharged from the hospital in a comatose state on hospital day 17 to a rehabilitation facility. He began to emerge from the coma 6 weeks after injury, and his external fixator was removed and a cast applied to his lower extremity. His entrance and exit wounds healed as expected. Initial agitation was treated with propranolol and quetiapine. Because he continued to have difficulty with spasticity and increased tone, he was given botulinum toxin type A injections in the pectoral muscles, biceps, and forearms. He made continued and rapid improvement in response to intensive multidisciplinary therapy and returned home 4½ months after injury. Eight months after the injury, he is now walking independently with a cane and independent with his activities of daily living. Unfortunately, he has substantial pain in his foot, which appears to be a combination of both neuropathic and posttraumatic arthrosis causes. He is undergoing consultation for a possible amputation. Radiographs show consolidation of the hind and midfoot fractures with retained bullet fragments (Figures 6A-6C). He continues to receive multidisciplinary care to address cognitive limitations and is making progress.
Discussion
FES is a life-threatening disease affecting multiple organ systems.7 Classically, the pulmonary, central nervous, and dermatologic systems are affected.5,6,8 While FES is most recognizable after long bone fractures and orthopedic procedures involving the intramedullary canal, to our knowledge, FES after gunshot wound and concomitant fractures of the foot has never been reported.
The syndrome is defined by major and minor criteria as outlined by Gurd.5 Major criteria include hypoxia, deteriorating mental status, and petechiae. This case represents a somewhat atypical presentation of FES, because dermatologic manifestations and pulmonary compromise were subtle. The minor criteria consisting of tachycardia, fever, anemia, and thrombocytopenia were present in our patient, although at different phases during the progression of the syndrome. This emphasizes the difficulty in diagnosing FES because the symptoms do not occur simultaneously.
In the classic syndrome, after an initial asymptomatic interval of 12 to 72 hours, pulmonary, neurologic, and/or dermatologic changes usually ensue.9 Altered mental status, including headache, confusion, stupor, coma, rigidity, or convulsions, has been documented in 86% of patients.10 In our case, the neurologic symptoms presented earlier, at around 6 hours after injury, and respiratory symptoms, including hypoxia, tachypnea, and dyspnea, reported in 75% of cases,2,11 did not occur at all. In fact, continued intubation was only required in this case for neuromuscular airway protection. Classic dermatologic manifestations, a reddish-brown nonpalpable petechial rash diffusely covering the upper torso and extremities, normally appears within 12 to 36 hours.12,13 Nevertheless, in our case, these findings were subtle compared with others previously reported.14,15 In fact, despite being seen by numerous physicians, including neurologists and ICU intensivists, only the orthopedists’ notes made reference to this modest finding (Figure 4A).
Further complicating the diagnosis is that, during the onset of symptoms, patients are typically victims of polytrauma and/or routinely given narcotics to help with significant pain. Therefore, it is appropriate to rule out opioid overdose and other metabolic sources of mental-status change. This can be done fairly expeditiously with laboratory testing and narcotic reversal. After these have been eliminated, FES should be considered in a patient with rapid neurologic deterioration, because a delay in treatment can affect outcomes.2,4,16
Because continuous showering of emboli to the brain and other organs occurs without fracture stabilization, rapid diagnosis with high clinical suspicion of FES is essential and can be aided immensely with MRI. In fact, MRI is the most sensitive test for this diagnosis and correlates with clinical severity of brain injury.17 T2-weighted images show regions of high-signal intensity and “starfield” pattern, which are sensitive markers for FES (Figure 3).18 These tests can be done concomitantly with a well-splinted extremity, and definitive stabilization should be carried out promptly because early splinting and fixation of orthopedic fractures improves outcomes.17
Perhaps the most important reason to make an expeditious diagnosis is to help counsel families, who are undoubtedly in shock and disbelief. Recovery times can vary widely, with the patient often continuing to regain cognitive and motor function over the course of months to years.2 Without knowledge of signs of improvement in neurologic outcome, families cannot be accurately counseled regarding potential for recovery. The practicing orthopedist should be aware of this disorder, because initial neurologic deterioration may seem hopeless. Furthermore, supportive care should be initiated early with multidisciplinary teams and extensive rehabilitation because these offer the best outcomes in patients with FES.4,18 Although our patient continues to have cognitive impairment, his recovery in the preceding 8 months has been aided by rapid diagnosis and multidisciplinary care and should offer hope to other patients faced with this situation.
1. Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27(3):533-550.
2. Müller C, Rahn BA, Pfister U, Meinig RP. The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev. 1994;23(2):107-117.
3. Stein PD, Yaekoub AY, Matta F, Kleerekoper M. Fat embolism syndrome. Am J Med Sci. 2008;336(6):472-477.
4. Parisi DM, Koval K, Egol K. Fat embolism syndrome. Am J Orthop. 2002;31(9):507-512.
5. Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surb Br. 1970;52(4):732-737.
6. Lee SC, Yoon JY, Nam CH, Kim TK, Jung KA, Lee DW. Cerebral fat embolism syndrome after simultaneous bilateral total knee arthroplasty: a case series. J Arthroplasty. 2012;27(3):409-414.
7. Gurd AR, Wilson RI. Fat-embolism syndrome. Lancet. 1972;2(7770):
231-232.
8. Habashi NM, Andrews PL, Scalea TM. Therapeutic aspects of fat embolism syndrome. Injury. 2006;37(Suppl 4):S68-S73.
9. Weiss W, Bardana D, Yen D. Delayed presentation of fat embolism syndrome after intramedullary nailing of a fractured femur: a case report. J Trauma. 2009;66(3):E42-E45.
10. Byrick RJ. Fat embolism and postoperative coagulopathy. Can J Anaesth. 2001;48(7):618-621.
11. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56(3):408-416.
12. Burgher LW. Fat embolism syndrome. Chest. 1981;79(2):131-132.
13. Burgher LW, Dines DE, Linscheid RL, Didier EP. Fat embolism and the adult respiratory distress syndrome. Mayo Clin Proc. 1974;49(2):107-109.
14. Liu DD, Hsieh NK, Chen HI. Histopathological and biochemical changes following fat embolism with administration of corn oil micelles: a new animal model for fat embolism syndrome. J Bone Joint Surg Br. 2008;90(11):
1517-1521.
15. Liu HK, Chen WC. Images in clinical medicine. Fat embolism syndrome. N Engl J Med. 2011;364(18):1761.
16. Pinney SJ, Keating JF, Meek RN. Fat embolism syndrome in isolated femoral fractures: does timing of nailing influence incidence? Injury. 1998;29(2):
131-133.
17. Takahashi M, Suzuki R, Osakabe Y, et al. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. J Trauma. 1999;46(2):324-327.
18. Parizel PM, Demey HE, Veeckmans G, et al. Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI (starfield pattern). Stroke. 2001;32(12):2942-2944.
Fat embolism syndrome (FES) is a rare complication reported primarily after long bone fractures, with an incidence of 0.3% to 2.2%.1-3 It is most commonly caused by trauma and is thought to result from movement of bone fragments or to occur during intramedullary reaming.1 Both of these factors lead to a distortion of the bone marrow cavity, allowing marrow and fat to enter the circulatory system.1
Although the true pathophysiology remains poorly understood, it is possible that, once in systemic circulation, the fat particles become lodged in the vascular system, inciting an inflammatory response, leading to organ dysfunction via mechanical or biochemical processes.4 Typically, the diagnosis is made after clinical features are observed, including hypoxemia, petechial rash, and cerebral signs not related to a head injury or other conditions.5,6
Although FES is an uncommon complication after traumatic injuries, mortality after FES in a recent study was reported to be 10%.1 FES is most commonly seen after fractures of the femur and tibia, although cases have been described involving fractures of the radius, ulna, and humerus.1,3 We present an atypical case of cerebral FES after multiple fractures of the foot; to our knowledge, such a case has not been reported in the English-language literature. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 42-year-old man was hunting with his son when he was accidentally shot in the left foot with a .270-caliber rifle bullet at close range. The patient sought care at a local hospital and, in the ensuing 3 hours, his mentation appeared normal. He reported pain and numbness distal to the injury in the tibial nerve distribution, but he remained vascularly intact, alert, and oriented. He was given 7 mg of hydromorphone hydrochloride over 2 hours for pain control and was transferred to our hospital via ambulance approximately 6 hours after injury. Upon arrival, he was noted to be extremely sedated and obtunded, responding only to pain with spontaneous eye opening. He was unable to follow commands. He was given
1.2 mg of naloxone intravenously to reverse what was presumed to be acute opioid intoxication; however, his mental status did not improve.
On examination, the patient was noted to have a small entrance wound through the Achilles tendon (Figures 1A, 1B) and an exit wound on the plantar aspect of the foot near the heads of the first and second metatarsals (Figures 1C, 1D) with minimal bleeding and no gross contamination. There was significant edema on the medial and proximal aspects of the left foot, 3+ dorsalis pedis pulse, and a capillary refill of 4 seconds. Radiographs showed traumatic fracture deformities of the calcaneus, navicular, medial cuneiform, and first and second metatarsal bases, as well as an intra-articular fracture deformity of the left talus extending to the talar dome (Figures 2A-2C). Neurologic examination could not be reliably obtained because of the patient’s mental status. He was determined to be unstable for immediate surgery, and his left leg was splinted pending neurologic evaluation.
The patient’s oxygen saturation was 94%, and his temperature was 38.2°C (100.76°F). Although his heart rate was in the 90s upon arrival, he became tachycardic over the next 4 hours, with heart rate ranging from the 110s to 130s; he remained tachycardic for approximately 72 hours. Laboratory values upon arrival showed a hemoglobin value of 12.8 g/dL and platelets of 249,000/μL. He developed anemia and thrombocytopenia within 72 hours of the injury, with a low of 6.6 g/dL and 88,000/μL, respectively, by postinjury day 4. Computed tomography of the head, electroencephalography, urine drug screen, and lumbar puncture were unremarkable. The patient never became hypoxemic. Within 14 hours after injury, he was completely comatose with extensor posturing. In the intensive care unit (ICU), the patient was intubated for airway protection.
The next day, the patient underwent magnetic resonance imaging (MRI) of the brain, which showed innumerable tiny infarcts throughout cerebral hemispheres, cerebellum, and brainstem in a characteristic “starfield” pattern on T2-weighted images (Figure 3). This was radiographically consistent with fat emboli related to the left lower extremity gunshot wound. An echocardiogram showed small right-to-left shunt and a possible intrapulmonary shunt, although this was never confirmed. The echocardiogram was technically challenging secondary to his persistent tachycardia. He also developed a subtle petechial rash (Figure 4A).
The patient underwent percutaneous gastrostomy-tube placement for nutrition on postinjury day 4 and remained intubated, unable to protect his airway, and nonresponsive with extensor posturing (Figure 4B). He was also taken to the operating room for spanning external fixator placement on postinjury day 3 to restore calcaneal height and length as well as foot stability (Figures 5A, 5B).
The patient was treated with supportive care and was discharged from the hospital in a comatose state on hospital day 17 to a rehabilitation facility. He began to emerge from the coma 6 weeks after injury, and his external fixator was removed and a cast applied to his lower extremity. His entrance and exit wounds healed as expected. Initial agitation was treated with propranolol and quetiapine. Because he continued to have difficulty with spasticity and increased tone, he was given botulinum toxin type A injections in the pectoral muscles, biceps, and forearms. He made continued and rapid improvement in response to intensive multidisciplinary therapy and returned home 4½ months after injury. Eight months after the injury, he is now walking independently with a cane and independent with his activities of daily living. Unfortunately, he has substantial pain in his foot, which appears to be a combination of both neuropathic and posttraumatic arthrosis causes. He is undergoing consultation for a possible amputation. Radiographs show consolidation of the hind and midfoot fractures with retained bullet fragments (Figures 6A-6C). He continues to receive multidisciplinary care to address cognitive limitations and is making progress.
Discussion
FES is a life-threatening disease affecting multiple organ systems.7 Classically, the pulmonary, central nervous, and dermatologic systems are affected.5,6,8 While FES is most recognizable after long bone fractures and orthopedic procedures involving the intramedullary canal, to our knowledge, FES after gunshot wound and concomitant fractures of the foot has never been reported.
The syndrome is defined by major and minor criteria as outlined by Gurd.5 Major criteria include hypoxia, deteriorating mental status, and petechiae. This case represents a somewhat atypical presentation of FES, because dermatologic manifestations and pulmonary compromise were subtle. The minor criteria consisting of tachycardia, fever, anemia, and thrombocytopenia were present in our patient, although at different phases during the progression of the syndrome. This emphasizes the difficulty in diagnosing FES because the symptoms do not occur simultaneously.
In the classic syndrome, after an initial asymptomatic interval of 12 to 72 hours, pulmonary, neurologic, and/or dermatologic changes usually ensue.9 Altered mental status, including headache, confusion, stupor, coma, rigidity, or convulsions, has been documented in 86% of patients.10 In our case, the neurologic symptoms presented earlier, at around 6 hours after injury, and respiratory symptoms, including hypoxia, tachypnea, and dyspnea, reported in 75% of cases,2,11 did not occur at all. In fact, continued intubation was only required in this case for neuromuscular airway protection. Classic dermatologic manifestations, a reddish-brown nonpalpable petechial rash diffusely covering the upper torso and extremities, normally appears within 12 to 36 hours.12,13 Nevertheless, in our case, these findings were subtle compared with others previously reported.14,15 In fact, despite being seen by numerous physicians, including neurologists and ICU intensivists, only the orthopedists’ notes made reference to this modest finding (Figure 4A).
Further complicating the diagnosis is that, during the onset of symptoms, patients are typically victims of polytrauma and/or routinely given narcotics to help with significant pain. Therefore, it is appropriate to rule out opioid overdose and other metabolic sources of mental-status change. This can be done fairly expeditiously with laboratory testing and narcotic reversal. After these have been eliminated, FES should be considered in a patient with rapid neurologic deterioration, because a delay in treatment can affect outcomes.2,4,16
Because continuous showering of emboli to the brain and other organs occurs without fracture stabilization, rapid diagnosis with high clinical suspicion of FES is essential and can be aided immensely with MRI. In fact, MRI is the most sensitive test for this diagnosis and correlates with clinical severity of brain injury.17 T2-weighted images show regions of high-signal intensity and “starfield” pattern, which are sensitive markers for FES (Figure 3).18 These tests can be done concomitantly with a well-splinted extremity, and definitive stabilization should be carried out promptly because early splinting and fixation of orthopedic fractures improves outcomes.17
Perhaps the most important reason to make an expeditious diagnosis is to help counsel families, who are undoubtedly in shock and disbelief. Recovery times can vary widely, with the patient often continuing to regain cognitive and motor function over the course of months to years.2 Without knowledge of signs of improvement in neurologic outcome, families cannot be accurately counseled regarding potential for recovery. The practicing orthopedist should be aware of this disorder, because initial neurologic deterioration may seem hopeless. Furthermore, supportive care should be initiated early with multidisciplinary teams and extensive rehabilitation because these offer the best outcomes in patients with FES.4,18 Although our patient continues to have cognitive impairment, his recovery in the preceding 8 months has been aided by rapid diagnosis and multidisciplinary care and should offer hope to other patients faced with this situation.
Fat embolism syndrome (FES) is a rare complication reported primarily after long bone fractures, with an incidence of 0.3% to 2.2%.1-3 It is most commonly caused by trauma and is thought to result from movement of bone fragments or to occur during intramedullary reaming.1 Both of these factors lead to a distortion of the bone marrow cavity, allowing marrow and fat to enter the circulatory system.1
Although the true pathophysiology remains poorly understood, it is possible that, once in systemic circulation, the fat particles become lodged in the vascular system, inciting an inflammatory response, leading to organ dysfunction via mechanical or biochemical processes.4 Typically, the diagnosis is made after clinical features are observed, including hypoxemia, petechial rash, and cerebral signs not related to a head injury or other conditions.5,6
Although FES is an uncommon complication after traumatic injuries, mortality after FES in a recent study was reported to be 10%.1 FES is most commonly seen after fractures of the femur and tibia, although cases have been described involving fractures of the radius, ulna, and humerus.1,3 We present an atypical case of cerebral FES after multiple fractures of the foot; to our knowledge, such a case has not been reported in the English-language literature. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 42-year-old man was hunting with his son when he was accidentally shot in the left foot with a .270-caliber rifle bullet at close range. The patient sought care at a local hospital and, in the ensuing 3 hours, his mentation appeared normal. He reported pain and numbness distal to the injury in the tibial nerve distribution, but he remained vascularly intact, alert, and oriented. He was given 7 mg of hydromorphone hydrochloride over 2 hours for pain control and was transferred to our hospital via ambulance approximately 6 hours after injury. Upon arrival, he was noted to be extremely sedated and obtunded, responding only to pain with spontaneous eye opening. He was unable to follow commands. He was given
1.2 mg of naloxone intravenously to reverse what was presumed to be acute opioid intoxication; however, his mental status did not improve.
On examination, the patient was noted to have a small entrance wound through the Achilles tendon (Figures 1A, 1B) and an exit wound on the plantar aspect of the foot near the heads of the first and second metatarsals (Figures 1C, 1D) with minimal bleeding and no gross contamination. There was significant edema on the medial and proximal aspects of the left foot, 3+ dorsalis pedis pulse, and a capillary refill of 4 seconds. Radiographs showed traumatic fracture deformities of the calcaneus, navicular, medial cuneiform, and first and second metatarsal bases, as well as an intra-articular fracture deformity of the left talus extending to the talar dome (Figures 2A-2C). Neurologic examination could not be reliably obtained because of the patient’s mental status. He was determined to be unstable for immediate surgery, and his left leg was splinted pending neurologic evaluation.
The patient’s oxygen saturation was 94%, and his temperature was 38.2°C (100.76°F). Although his heart rate was in the 90s upon arrival, he became tachycardic over the next 4 hours, with heart rate ranging from the 110s to 130s; he remained tachycardic for approximately 72 hours. Laboratory values upon arrival showed a hemoglobin value of 12.8 g/dL and platelets of 249,000/μL. He developed anemia and thrombocytopenia within 72 hours of the injury, with a low of 6.6 g/dL and 88,000/μL, respectively, by postinjury day 4. Computed tomography of the head, electroencephalography, urine drug screen, and lumbar puncture were unremarkable. The patient never became hypoxemic. Within 14 hours after injury, he was completely comatose with extensor posturing. In the intensive care unit (ICU), the patient was intubated for airway protection.
The next day, the patient underwent magnetic resonance imaging (MRI) of the brain, which showed innumerable tiny infarcts throughout cerebral hemispheres, cerebellum, and brainstem in a characteristic “starfield” pattern on T2-weighted images (Figure 3). This was radiographically consistent with fat emboli related to the left lower extremity gunshot wound. An echocardiogram showed small right-to-left shunt and a possible intrapulmonary shunt, although this was never confirmed. The echocardiogram was technically challenging secondary to his persistent tachycardia. He also developed a subtle petechial rash (Figure 4A).
The patient underwent percutaneous gastrostomy-tube placement for nutrition on postinjury day 4 and remained intubated, unable to protect his airway, and nonresponsive with extensor posturing (Figure 4B). He was also taken to the operating room for spanning external fixator placement on postinjury day 3 to restore calcaneal height and length as well as foot stability (Figures 5A, 5B).
The patient was treated with supportive care and was discharged from the hospital in a comatose state on hospital day 17 to a rehabilitation facility. He began to emerge from the coma 6 weeks after injury, and his external fixator was removed and a cast applied to his lower extremity. His entrance and exit wounds healed as expected. Initial agitation was treated with propranolol and quetiapine. Because he continued to have difficulty with spasticity and increased tone, he was given botulinum toxin type A injections in the pectoral muscles, biceps, and forearms. He made continued and rapid improvement in response to intensive multidisciplinary therapy and returned home 4½ months after injury. Eight months after the injury, he is now walking independently with a cane and independent with his activities of daily living. Unfortunately, he has substantial pain in his foot, which appears to be a combination of both neuropathic and posttraumatic arthrosis causes. He is undergoing consultation for a possible amputation. Radiographs show consolidation of the hind and midfoot fractures with retained bullet fragments (Figures 6A-6C). He continues to receive multidisciplinary care to address cognitive limitations and is making progress.
Discussion
FES is a life-threatening disease affecting multiple organ systems.7 Classically, the pulmonary, central nervous, and dermatologic systems are affected.5,6,8 While FES is most recognizable after long bone fractures and orthopedic procedures involving the intramedullary canal, to our knowledge, FES after gunshot wound and concomitant fractures of the foot has never been reported.
The syndrome is defined by major and minor criteria as outlined by Gurd.5 Major criteria include hypoxia, deteriorating mental status, and petechiae. This case represents a somewhat atypical presentation of FES, because dermatologic manifestations and pulmonary compromise were subtle. The minor criteria consisting of tachycardia, fever, anemia, and thrombocytopenia were present in our patient, although at different phases during the progression of the syndrome. This emphasizes the difficulty in diagnosing FES because the symptoms do not occur simultaneously.
In the classic syndrome, after an initial asymptomatic interval of 12 to 72 hours, pulmonary, neurologic, and/or dermatologic changes usually ensue.9 Altered mental status, including headache, confusion, stupor, coma, rigidity, or convulsions, has been documented in 86% of patients.10 In our case, the neurologic symptoms presented earlier, at around 6 hours after injury, and respiratory symptoms, including hypoxia, tachypnea, and dyspnea, reported in 75% of cases,2,11 did not occur at all. In fact, continued intubation was only required in this case for neuromuscular airway protection. Classic dermatologic manifestations, a reddish-brown nonpalpable petechial rash diffusely covering the upper torso and extremities, normally appears within 12 to 36 hours.12,13 Nevertheless, in our case, these findings were subtle compared with others previously reported.14,15 In fact, despite being seen by numerous physicians, including neurologists and ICU intensivists, only the orthopedists’ notes made reference to this modest finding (Figure 4A).
Further complicating the diagnosis is that, during the onset of symptoms, patients are typically victims of polytrauma and/or routinely given narcotics to help with significant pain. Therefore, it is appropriate to rule out opioid overdose and other metabolic sources of mental-status change. This can be done fairly expeditiously with laboratory testing and narcotic reversal. After these have been eliminated, FES should be considered in a patient with rapid neurologic deterioration, because a delay in treatment can affect outcomes.2,4,16
Because continuous showering of emboli to the brain and other organs occurs without fracture stabilization, rapid diagnosis with high clinical suspicion of FES is essential and can be aided immensely with MRI. In fact, MRI is the most sensitive test for this diagnosis and correlates with clinical severity of brain injury.17 T2-weighted images show regions of high-signal intensity and “starfield” pattern, which are sensitive markers for FES (Figure 3).18 These tests can be done concomitantly with a well-splinted extremity, and definitive stabilization should be carried out promptly because early splinting and fixation of orthopedic fractures improves outcomes.17
Perhaps the most important reason to make an expeditious diagnosis is to help counsel families, who are undoubtedly in shock and disbelief. Recovery times can vary widely, with the patient often continuing to regain cognitive and motor function over the course of months to years.2 Without knowledge of signs of improvement in neurologic outcome, families cannot be accurately counseled regarding potential for recovery. The practicing orthopedist should be aware of this disorder, because initial neurologic deterioration may seem hopeless. Furthermore, supportive care should be initiated early with multidisciplinary teams and extensive rehabilitation because these offer the best outcomes in patients with FES.4,18 Although our patient continues to have cognitive impairment, his recovery in the preceding 8 months has been aided by rapid diagnosis and multidisciplinary care and should offer hope to other patients faced with this situation.
1. Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27(3):533-550.
2. Müller C, Rahn BA, Pfister U, Meinig RP. The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev. 1994;23(2):107-117.
3. Stein PD, Yaekoub AY, Matta F, Kleerekoper M. Fat embolism syndrome. Am J Med Sci. 2008;336(6):472-477.
4. Parisi DM, Koval K, Egol K. Fat embolism syndrome. Am J Orthop. 2002;31(9):507-512.
5. Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surb Br. 1970;52(4):732-737.
6. Lee SC, Yoon JY, Nam CH, Kim TK, Jung KA, Lee DW. Cerebral fat embolism syndrome after simultaneous bilateral total knee arthroplasty: a case series. J Arthroplasty. 2012;27(3):409-414.
7. Gurd AR, Wilson RI. Fat-embolism syndrome. Lancet. 1972;2(7770):
231-232.
8. Habashi NM, Andrews PL, Scalea TM. Therapeutic aspects of fat embolism syndrome. Injury. 2006;37(Suppl 4):S68-S73.
9. Weiss W, Bardana D, Yen D. Delayed presentation of fat embolism syndrome after intramedullary nailing of a fractured femur: a case report. J Trauma. 2009;66(3):E42-E45.
10. Byrick RJ. Fat embolism and postoperative coagulopathy. Can J Anaesth. 2001;48(7):618-621.
11. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56(3):408-416.
12. Burgher LW. Fat embolism syndrome. Chest. 1981;79(2):131-132.
13. Burgher LW, Dines DE, Linscheid RL, Didier EP. Fat embolism and the adult respiratory distress syndrome. Mayo Clin Proc. 1974;49(2):107-109.
14. Liu DD, Hsieh NK, Chen HI. Histopathological and biochemical changes following fat embolism with administration of corn oil micelles: a new animal model for fat embolism syndrome. J Bone Joint Surg Br. 2008;90(11):
1517-1521.
15. Liu HK, Chen WC. Images in clinical medicine. Fat embolism syndrome. N Engl J Med. 2011;364(18):1761.
16. Pinney SJ, Keating JF, Meek RN. Fat embolism syndrome in isolated femoral fractures: does timing of nailing influence incidence? Injury. 1998;29(2):
131-133.
17. Takahashi M, Suzuki R, Osakabe Y, et al. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. J Trauma. 1999;46(2):324-327.
18. Parizel PM, Demey HE, Veeckmans G, et al. Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI (starfield pattern). Stroke. 2001;32(12):2942-2944.
1. Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27(3):533-550.
2. Müller C, Rahn BA, Pfister U, Meinig RP. The incidence, pathogenesis, diagnosis, and treatment of fat embolism. Orthop Rev. 1994;23(2):107-117.
3. Stein PD, Yaekoub AY, Matta F, Kleerekoper M. Fat embolism syndrome. Am J Med Sci. 2008;336(6):472-477.
4. Parisi DM, Koval K, Egol K. Fat embolism syndrome. Am J Orthop. 2002;31(9):507-512.
5. Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surb Br. 1970;52(4):732-737.
6. Lee SC, Yoon JY, Nam CH, Kim TK, Jung KA, Lee DW. Cerebral fat embolism syndrome after simultaneous bilateral total knee arthroplasty: a case series. J Arthroplasty. 2012;27(3):409-414.
7. Gurd AR, Wilson RI. Fat-embolism syndrome. Lancet. 1972;2(7770):
231-232.
8. Habashi NM, Andrews PL, Scalea TM. Therapeutic aspects of fat embolism syndrome. Injury. 2006;37(Suppl 4):S68-S73.
9. Weiss W, Bardana D, Yen D. Delayed presentation of fat embolism syndrome after intramedullary nailing of a fractured femur: a case report. J Trauma. 2009;66(3):E42-E45.
10. Byrick RJ. Fat embolism and postoperative coagulopathy. Can J Anaesth. 2001;48(7):618-621.
11. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br. 1974;56(3):408-416.
12. Burgher LW. Fat embolism syndrome. Chest. 1981;79(2):131-132.
13. Burgher LW, Dines DE, Linscheid RL, Didier EP. Fat embolism and the adult respiratory distress syndrome. Mayo Clin Proc. 1974;49(2):107-109.
14. Liu DD, Hsieh NK, Chen HI. Histopathological and biochemical changes following fat embolism with administration of corn oil micelles: a new animal model for fat embolism syndrome. J Bone Joint Surg Br. 2008;90(11):
1517-1521.
15. Liu HK, Chen WC. Images in clinical medicine. Fat embolism syndrome. N Engl J Med. 2011;364(18):1761.
16. Pinney SJ, Keating JF, Meek RN. Fat embolism syndrome in isolated femoral fractures: does timing of nailing influence incidence? Injury. 1998;29(2):
131-133.
17. Takahashi M, Suzuki R, Osakabe Y, et al. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. J Trauma. 1999;46(2):324-327.
18. Parizel PM, Demey HE, Veeckmans G, et al. Early diagnosis of cerebral fat embolism syndrome by diffusion-weighted MRI (starfield pattern). Stroke. 2001;32(12):2942-2944.
Aneurysmal Bone Cyst Involving the Metacarpal Bone in a Child
Less than 5% of aneurysmal bone cysts (ABCs) are located in the hand,1 and only a few cases have been reported in the literature.2-7 Unfortunately, it is impossible to predict when an ABC will exhibit aggressive behavior.4,8 Aneurysmal bone cysts and giant cell bone tumors have been considered benign9 lesions that can behave in a locally aggressive fashion.1 Optimal treatment has not been established because treatment is variable depending on the condition of the lesion. Several authors have recommended more radical treatment modalities, such as en bloc resection or excision diaphysectomy followed by strut bone grafting, which had a relatively low rate of recurrence. A relatively low rate of recurrence and other complications indicate that those techniques would serve as a good strategy for patients with expansile hand ABCs in terms of safety, simplicity, and reduced number of reoperations.3,7,10
This article reports a case of an ABC of the second metacarpal bone of the right hand in a 12-year-old boy treated with curettage and autologous morselized iliac bone grafting. The patient’s guardian provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right hand–dominant 12-year-old-boy, who noticed the development of a lump in the dorsum of his right hand. On examination, we found a large, firm swelling of the dorsum of his right hand over the second metacarpal. Radiographic examination showed a symmetrical expansile lytic lesion (22×24×25 mm) involving the entire second metacarpal bone (Figure 1A). Magnetic resonance imaging (MRI) showed a well-defined expansile intramedullary lesion with preservation of the epiphyseal plate, shell-like periosteal reaction, and a multilocular appearance with a hemorrhagic compartment (fluid-fluid levels) (Figure 1B).
At surgery, we found a blood-filled cyst, and the cortex was very thin. The lesion extended to the distal two-thirds of the bone to the level of the physeal plate. We had considered using allograft or other bone substitutes. However, we did not have confidence in the bone-induction potential and power of osteogenesis of bone substitutes or allograft compared with autologous bone graft. Consequently, we performed autologous bone grafting, despite its being an invasive procedure, on the immature iliac crest. We performed thorough curettage of the intramedullary material without damaging the physeal plate, followed by impact morselized autologous bone grafting. Histologic examination confirmed that the final diagnosis was identical to the provisional diagnosis shown on MRI (Figure 1C). A thumb spica cast was applied for 4 weeks after surgery, and regular follow-up radiographs were taken for 3 years and 6 months until confirmation of complete normalization of the lesion without recurrence (Figures 2A-2C).
Discussion
Primary ABCs in the small tubular bones of the hands are rare. Less than 5% of aneurysmal cysts are located in the hand.1 Only a few small cases of this condition have been reported in the literature.2-7 Radiographic examination showed that, in all cases, the lesion was both expansile and completely lucent.7 Although radiographic finding of ABC in short tubular bone characteristically shows central symmetry with expansion into the diaphysis and subarticular bone, the appearance of an ABC on radiographs and angiograms is usually not diagnostic.8 Even though fluid-fluid levels are highly suggestive of ABC, only pathologic study confirms the diagnosis. MRI may be a good tool for postsurgery follow-up. On the basis of these ideas, we performed histological examination and confirmed the diagnosis of ABC of the metacarpus by radiograph and MRI.
The goals in the treatment of primary ABCs are preservation of function and avoidance of recurrence. Unfortunately, it is impossible to predict the possible aggressive behavior in ABCs. Active or aggressive character in certain localizations of ABC in children requires either curettage, which has a considerable recurrence rate, or radical segmental excision, which raises complex reconstructive challenges. Frassica and colleagues7 reported no recurrences in 3 patients treated by complete excision and bone grafting. Curettage and bone grafting in 7 cases were associated with 4 recurrences.7
Because optimal treatment has not been established,3 current recommendations vary, depending on the condition of the lesion. Several authors recommend more radical treatment modalities, such as en bloc resection, excision diaphysectomy, cryotherapy, and strut bone grafting, and a relatively low rate of recurrence and other complications indicates that those techniques would serve as a good strategy for patients with expansile ABCs in the hand.3,7,10 On the other hand, successful results with less aggressive procedures, such as curettage and autologous bone grafting, have been reported.4,5,8
In pediatric patients, surgery to preserve the growth plate is recommended.5 Ropars and colleagues4 suggested that aggressive treatment approaches, such as cryotherapy and resection with reconstruction, should be used only in cases when the articular surface is involved, when full-bone invasion of the phalanx or metacarpal has occurred, or in cases of more than 1 recurrence.
In conclusion, despite the high risk of recurrence of ABC treated with curettage with bone grafting, the findings of the present case show that ABC of the metacarpal bone in children can be treated successfully with curettage followed by morselized autologous bone grafting without recurrence.
1. Athanasian EA. Aneurysmal bone cyst and giant cell tumor of bone of the hand and distal radius. Hand Clin. 2004;20(3):269-281, vi.
2. Tarazona-Velutini P, Romo-Rodriguez R, Saleme-Cruz J. Aneurysmatic bone cyst in the proximal phalanx of a finger. Case report and literature review. Acta Ortop Mex. 2012;26(4):245-249.
3. Jafari D, Jamshidi K, Najdmazhar F, Shariatzade H, Liaghat O. Expansile aneurysmal bone cyst in the tubular bones of the hand treated with en bloc excision and autograft reconstruction: a report of 12 cases. J Hand Surg Eur Vol. 2011;36(8):648-655.
4. Ropars M, Kaila R, Briggs T, Cannon S. Aneurysmal bone cysts of the metacarpals and phalanges of the hand. A 6 case series and literature review. Chir Main. 2007;26(4-5):214-217.
5. Sproule JA, Salmo E, Mortimer G, O’Sullivan M. Aneursymal bone cyst of the proximal phalanx of the thumb in a child. Hand Surg. 2002;7(1):147-150.
6. Schwartz GB, Hammerman MZ. Aneurysmal bone cyst of the fifth metacarpal. Orthop Rev. 1989;18(12):1309-1314.
7. Frassica FJ, Amadio PC, Wold LE, Beabout JW. Aneurysmal bone cyst: clinicopathologic features and treatment of ten cases involving the hand. J Hand Surg Am. 1988;13(5):676-683.
8. Louahem D, Kouyoumdjian P, Ghanem I, et al. Active aneurysmal bone cysts in children: possible evolution after biopsy. J Child Orthop. 2012;6(4):333-338.
9. Lindfors NC. Treatment of a recurrent aneurysmal bone cyst with bioactive glass in a child allows for good bone remodelling and growth. Bone. 2009;45(2):398-400.
10. Salon A, Rémi J, Brunelle F, Drapé JL, Glorion Ch. Total replacement of a middle phalanx by free non-vascularized chondral graft, after failure of sclerotherapy for treatment of an aneurysmal bone cyst. Chir Main. 2005;24(3-4):187-192.
Less than 5% of aneurysmal bone cysts (ABCs) are located in the hand,1 and only a few cases have been reported in the literature.2-7 Unfortunately, it is impossible to predict when an ABC will exhibit aggressive behavior.4,8 Aneurysmal bone cysts and giant cell bone tumors have been considered benign9 lesions that can behave in a locally aggressive fashion.1 Optimal treatment has not been established because treatment is variable depending on the condition of the lesion. Several authors have recommended more radical treatment modalities, such as en bloc resection or excision diaphysectomy followed by strut bone grafting, which had a relatively low rate of recurrence. A relatively low rate of recurrence and other complications indicate that those techniques would serve as a good strategy for patients with expansile hand ABCs in terms of safety, simplicity, and reduced number of reoperations.3,7,10
This article reports a case of an ABC of the second metacarpal bone of the right hand in a 12-year-old boy treated with curettage and autologous morselized iliac bone grafting. The patient’s guardian provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right hand–dominant 12-year-old-boy, who noticed the development of a lump in the dorsum of his right hand. On examination, we found a large, firm swelling of the dorsum of his right hand over the second metacarpal. Radiographic examination showed a symmetrical expansile lytic lesion (22×24×25 mm) involving the entire second metacarpal bone (Figure 1A). Magnetic resonance imaging (MRI) showed a well-defined expansile intramedullary lesion with preservation of the epiphyseal plate, shell-like periosteal reaction, and a multilocular appearance with a hemorrhagic compartment (fluid-fluid levels) (Figure 1B).
At surgery, we found a blood-filled cyst, and the cortex was very thin. The lesion extended to the distal two-thirds of the bone to the level of the physeal plate. We had considered using allograft or other bone substitutes. However, we did not have confidence in the bone-induction potential and power of osteogenesis of bone substitutes or allograft compared with autologous bone graft. Consequently, we performed autologous bone grafting, despite its being an invasive procedure, on the immature iliac crest. We performed thorough curettage of the intramedullary material without damaging the physeal plate, followed by impact morselized autologous bone grafting. Histologic examination confirmed that the final diagnosis was identical to the provisional diagnosis shown on MRI (Figure 1C). A thumb spica cast was applied for 4 weeks after surgery, and regular follow-up radiographs were taken for 3 years and 6 months until confirmation of complete normalization of the lesion without recurrence (Figures 2A-2C).
Discussion
Primary ABCs in the small tubular bones of the hands are rare. Less than 5% of aneurysmal cysts are located in the hand.1 Only a few small cases of this condition have been reported in the literature.2-7 Radiographic examination showed that, in all cases, the lesion was both expansile and completely lucent.7 Although radiographic finding of ABC in short tubular bone characteristically shows central symmetry with expansion into the diaphysis and subarticular bone, the appearance of an ABC on radiographs and angiograms is usually not diagnostic.8 Even though fluid-fluid levels are highly suggestive of ABC, only pathologic study confirms the diagnosis. MRI may be a good tool for postsurgery follow-up. On the basis of these ideas, we performed histological examination and confirmed the diagnosis of ABC of the metacarpus by radiograph and MRI.
The goals in the treatment of primary ABCs are preservation of function and avoidance of recurrence. Unfortunately, it is impossible to predict the possible aggressive behavior in ABCs. Active or aggressive character in certain localizations of ABC in children requires either curettage, which has a considerable recurrence rate, or radical segmental excision, which raises complex reconstructive challenges. Frassica and colleagues7 reported no recurrences in 3 patients treated by complete excision and bone grafting. Curettage and bone grafting in 7 cases were associated with 4 recurrences.7
Because optimal treatment has not been established,3 current recommendations vary, depending on the condition of the lesion. Several authors recommend more radical treatment modalities, such as en bloc resection, excision diaphysectomy, cryotherapy, and strut bone grafting, and a relatively low rate of recurrence and other complications indicates that those techniques would serve as a good strategy for patients with expansile ABCs in the hand.3,7,10 On the other hand, successful results with less aggressive procedures, such as curettage and autologous bone grafting, have been reported.4,5,8
In pediatric patients, surgery to preserve the growth plate is recommended.5 Ropars and colleagues4 suggested that aggressive treatment approaches, such as cryotherapy and resection with reconstruction, should be used only in cases when the articular surface is involved, when full-bone invasion of the phalanx or metacarpal has occurred, or in cases of more than 1 recurrence.
In conclusion, despite the high risk of recurrence of ABC treated with curettage with bone grafting, the findings of the present case show that ABC of the metacarpal bone in children can be treated successfully with curettage followed by morselized autologous bone grafting without recurrence.
Less than 5% of aneurysmal bone cysts (ABCs) are located in the hand,1 and only a few cases have been reported in the literature.2-7 Unfortunately, it is impossible to predict when an ABC will exhibit aggressive behavior.4,8 Aneurysmal bone cysts and giant cell bone tumors have been considered benign9 lesions that can behave in a locally aggressive fashion.1 Optimal treatment has not been established because treatment is variable depending on the condition of the lesion. Several authors have recommended more radical treatment modalities, such as en bloc resection or excision diaphysectomy followed by strut bone grafting, which had a relatively low rate of recurrence. A relatively low rate of recurrence and other complications indicate that those techniques would serve as a good strategy for patients with expansile hand ABCs in terms of safety, simplicity, and reduced number of reoperations.3,7,10
This article reports a case of an ABC of the second metacarpal bone of the right hand in a 12-year-old boy treated with curettage and autologous morselized iliac bone grafting. The patient’s guardian provided written informed consent for print and electronic publication of this case report.
Case Report
The patient was a right hand–dominant 12-year-old-boy, who noticed the development of a lump in the dorsum of his right hand. On examination, we found a large, firm swelling of the dorsum of his right hand over the second metacarpal. Radiographic examination showed a symmetrical expansile lytic lesion (22×24×25 mm) involving the entire second metacarpal bone (Figure 1A). Magnetic resonance imaging (MRI) showed a well-defined expansile intramedullary lesion with preservation of the epiphyseal plate, shell-like periosteal reaction, and a multilocular appearance with a hemorrhagic compartment (fluid-fluid levels) (Figure 1B).
At surgery, we found a blood-filled cyst, and the cortex was very thin. The lesion extended to the distal two-thirds of the bone to the level of the physeal plate. We had considered using allograft or other bone substitutes. However, we did not have confidence in the bone-induction potential and power of osteogenesis of bone substitutes or allograft compared with autologous bone graft. Consequently, we performed autologous bone grafting, despite its being an invasive procedure, on the immature iliac crest. We performed thorough curettage of the intramedullary material without damaging the physeal plate, followed by impact morselized autologous bone grafting. Histologic examination confirmed that the final diagnosis was identical to the provisional diagnosis shown on MRI (Figure 1C). A thumb spica cast was applied for 4 weeks after surgery, and regular follow-up radiographs were taken for 3 years and 6 months until confirmation of complete normalization of the lesion without recurrence (Figures 2A-2C).
Discussion
Primary ABCs in the small tubular bones of the hands are rare. Less than 5% of aneurysmal cysts are located in the hand.1 Only a few small cases of this condition have been reported in the literature.2-7 Radiographic examination showed that, in all cases, the lesion was both expansile and completely lucent.7 Although radiographic finding of ABC in short tubular bone characteristically shows central symmetry with expansion into the diaphysis and subarticular bone, the appearance of an ABC on radiographs and angiograms is usually not diagnostic.8 Even though fluid-fluid levels are highly suggestive of ABC, only pathologic study confirms the diagnosis. MRI may be a good tool for postsurgery follow-up. On the basis of these ideas, we performed histological examination and confirmed the diagnosis of ABC of the metacarpus by radiograph and MRI.
The goals in the treatment of primary ABCs are preservation of function and avoidance of recurrence. Unfortunately, it is impossible to predict the possible aggressive behavior in ABCs. Active or aggressive character in certain localizations of ABC in children requires either curettage, which has a considerable recurrence rate, or radical segmental excision, which raises complex reconstructive challenges. Frassica and colleagues7 reported no recurrences in 3 patients treated by complete excision and bone grafting. Curettage and bone grafting in 7 cases were associated with 4 recurrences.7
Because optimal treatment has not been established,3 current recommendations vary, depending on the condition of the lesion. Several authors recommend more radical treatment modalities, such as en bloc resection, excision diaphysectomy, cryotherapy, and strut bone grafting, and a relatively low rate of recurrence and other complications indicates that those techniques would serve as a good strategy for patients with expansile ABCs in the hand.3,7,10 On the other hand, successful results with less aggressive procedures, such as curettage and autologous bone grafting, have been reported.4,5,8
In pediatric patients, surgery to preserve the growth plate is recommended.5 Ropars and colleagues4 suggested that aggressive treatment approaches, such as cryotherapy and resection with reconstruction, should be used only in cases when the articular surface is involved, when full-bone invasion of the phalanx or metacarpal has occurred, or in cases of more than 1 recurrence.
In conclusion, despite the high risk of recurrence of ABC treated with curettage with bone grafting, the findings of the present case show that ABC of the metacarpal bone in children can be treated successfully with curettage followed by morselized autologous bone grafting without recurrence.
1. Athanasian EA. Aneurysmal bone cyst and giant cell tumor of bone of the hand and distal radius. Hand Clin. 2004;20(3):269-281, vi.
2. Tarazona-Velutini P, Romo-Rodriguez R, Saleme-Cruz J. Aneurysmatic bone cyst in the proximal phalanx of a finger. Case report and literature review. Acta Ortop Mex. 2012;26(4):245-249.
3. Jafari D, Jamshidi K, Najdmazhar F, Shariatzade H, Liaghat O. Expansile aneurysmal bone cyst in the tubular bones of the hand treated with en bloc excision and autograft reconstruction: a report of 12 cases. J Hand Surg Eur Vol. 2011;36(8):648-655.
4. Ropars M, Kaila R, Briggs T, Cannon S. Aneurysmal bone cysts of the metacarpals and phalanges of the hand. A 6 case series and literature review. Chir Main. 2007;26(4-5):214-217.
5. Sproule JA, Salmo E, Mortimer G, O’Sullivan M. Aneursymal bone cyst of the proximal phalanx of the thumb in a child. Hand Surg. 2002;7(1):147-150.
6. Schwartz GB, Hammerman MZ. Aneurysmal bone cyst of the fifth metacarpal. Orthop Rev. 1989;18(12):1309-1314.
7. Frassica FJ, Amadio PC, Wold LE, Beabout JW. Aneurysmal bone cyst: clinicopathologic features and treatment of ten cases involving the hand. J Hand Surg Am. 1988;13(5):676-683.
8. Louahem D, Kouyoumdjian P, Ghanem I, et al. Active aneurysmal bone cysts in children: possible evolution after biopsy. J Child Orthop. 2012;6(4):333-338.
9. Lindfors NC. Treatment of a recurrent aneurysmal bone cyst with bioactive glass in a child allows for good bone remodelling and growth. Bone. 2009;45(2):398-400.
10. Salon A, Rémi J, Brunelle F, Drapé JL, Glorion Ch. Total replacement of a middle phalanx by free non-vascularized chondral graft, after failure of sclerotherapy for treatment of an aneurysmal bone cyst. Chir Main. 2005;24(3-4):187-192.
1. Athanasian EA. Aneurysmal bone cyst and giant cell tumor of bone of the hand and distal radius. Hand Clin. 2004;20(3):269-281, vi.
2. Tarazona-Velutini P, Romo-Rodriguez R, Saleme-Cruz J. Aneurysmatic bone cyst in the proximal phalanx of a finger. Case report and literature review. Acta Ortop Mex. 2012;26(4):245-249.
3. Jafari D, Jamshidi K, Najdmazhar F, Shariatzade H, Liaghat O. Expansile aneurysmal bone cyst in the tubular bones of the hand treated with en bloc excision and autograft reconstruction: a report of 12 cases. J Hand Surg Eur Vol. 2011;36(8):648-655.
4. Ropars M, Kaila R, Briggs T, Cannon S. Aneurysmal bone cysts of the metacarpals and phalanges of the hand. A 6 case series and literature review. Chir Main. 2007;26(4-5):214-217.
5. Sproule JA, Salmo E, Mortimer G, O’Sullivan M. Aneursymal bone cyst of the proximal phalanx of the thumb in a child. Hand Surg. 2002;7(1):147-150.
6. Schwartz GB, Hammerman MZ. Aneurysmal bone cyst of the fifth metacarpal. Orthop Rev. 1989;18(12):1309-1314.
7. Frassica FJ, Amadio PC, Wold LE, Beabout JW. Aneurysmal bone cyst: clinicopathologic features and treatment of ten cases involving the hand. J Hand Surg Am. 1988;13(5):676-683.
8. Louahem D, Kouyoumdjian P, Ghanem I, et al. Active aneurysmal bone cysts in children: possible evolution after biopsy. J Child Orthop. 2012;6(4):333-338.
9. Lindfors NC. Treatment of a recurrent aneurysmal bone cyst with bioactive glass in a child allows for good bone remodelling and growth. Bone. 2009;45(2):398-400.
10. Salon A, Rémi J, Brunelle F, Drapé JL, Glorion Ch. Total replacement of a middle phalanx by free non-vascularized chondral graft, after failure of sclerotherapy for treatment of an aneurysmal bone cyst. Chir Main. 2005;24(3-4):187-192.
Assessment of Medical School Musculoskeletal Education
A basic understanding of the clinical components of musculoskeletal medicine is necessary in many medical fields. Musculoskeletal injuries represent the second most common presentation in US emergency departments, account for 49 million visits to orthopedic surgeon offices, and cost the United States an estimated $950 billion annually.1-3 Despite the staggering need for competency in musculoskeletal medicine, Freedman and Bernstein4 in 1998 demonstrated that musculoskeletal knowledge is inadequate among medical school graduates.
In 2005, the United States Bone and Joint Decade (now the United States Bone and Joint Initiative) announced Project 100, which recommended that 100% of US medical schools begin requiring a musculoskeletal course by the end of the decade.5 This project was intended to increase musculoskeletal understanding among medical students. Optimal curriculum reform, however, remains controversial. Many studies have found that medical schools continue to provide inadequate musculoskeletal education.4,6-9 For example, an integrated musculoskeletal curriculum with increased lecture time was found to improve clinical confidence but not musculoskeletal knowledge.6 In contrast, a 2-week intensive musculoskeletal module and a 6-week course involving orthopedic resident and faculty education has been shown to improve understanding.10,11
We conducted a study to determine the adequacy of musculoskeletal knowledge in medical school students, to determine musculoskeletal competency after curriculum reform through increased lecture and laboratory time, and to draw conclusions about factors leading to increased musculoskeletal competency to guide future curriculum reforms. We hypothesized that musculoskeletal knowledge would increase as a result of increased lecture and laboratory time.
Materials and Methods
The Tufts University School of Medicine Institutional Review Board approved this study. The medical school curriculum at our institution was redesigned to include a dedicated musculoskeletal module to improve medical student education (Table). The study compared medical students given the old musculoskeletal module (premodule group) and those given the new musculoskeletal module (postmodule group). The premodule group received 8.5 hours of physical diagnosis skills training and 30 hours of clinical anatomy training (12 lecture hours, 18 laboratory hours), and the postmodule group received 10 hours of physical diagnosis training and 41.5 hours of clinical anatomy training (18.5 lecture hours, 23 laboratory hours).
The lecture material for the postmodule group covered all topics/questions addressed on the validated musculoskeletal adequacy assessment. The new module specifically added 6 hours of dedicated clinically based musculoskeletal lecture time during the anatomy course and concurrent with the physical diagnosis course. The topics covered with case-based scenarios were orthopedic emergencies, adult hip and back, knee, pediatric hip and back, elbow/wrist/hand, and shoulder. A validated musculoskeletal competency examination was given to the premodule group at the end of the musculoskeletal anatomy and physical diagnosis lectures. The postmodule group took the competency examination at the end of the “new” 6 hours of musculoskeletal education.
We used the Freedman and Bernstein4 basic competency examination for musculoskeletal education assessment to assess knowledge. This examination is the only validated tool for assessing basic clinical musculoskeletal knowledge. All students were also asked whether they had experience rotating in orthopedic surgery or in a related musculoskeletal field (rheumatology, physiatry, neurology) during the medical school “selective” period that allowed 1 afternoon per week of elective time. Duration of exposure was assessed. The examination was given to 109 students in the premodule group 1 year before the curriculum changes. The examination was then given to the students for the first 2 years after the curriculum changes were implemented, with 296 students in the postmodule group. All questions on the examination were addressed within the 6 lecture hours in the new module. A single reviewer anonymously scored the examinations according to the validated scoring system over a 2-week period.4 Independent t tests were used to compare examination scores between the premodule and postmodule groups. Statistical significance was set at P < .05. Equal variance between groups was not assumed.
Results
The examination was given to 405 medical students (109 premodule, 296 postmodule) Mean examination score was 40%, significantly below the recommended mean passing score of 73.1%.4 Only 1 student achieved a passing score. Independent t tests were used to compare examination scores of the premodule and postmodule groups. Mean (SD) scores were higher (P < .05) for the premodule group, 42.1 (13.6), than the postmodule group, 39.1 (11.4) (Figure 1).
Independent t tests were used to compare examination scores of students with either orthopedics or rheumatology experience and students without this experience. Mean (SD) scores were higher (P < .05) for students with experience, 44.4 (11.9), than students without experience, 39.6 (12.1) (Figure 2). Students with neurology or physiatry experience did not score significantly higher than students without this experience. Statistical significance was set as P < .05. SAS 9.0 software (SAS Institute, Cary, North Carolina) was used for statistical analysis.
Discussion
Our students’ mean examination score was significantly lower than the passing (competency) score of 73.1%. Although Project 100 acknowledged many medical schools for implementing a required musculoskeletal course, our study results showed that adequate competency as indicated by a passing score on the Freedman and Bernstein examination was not achieved in medical school despite devoted musculoskeletal lecture time. Our postmodule group had lower scores than our premodule group despite being exposed to more lecture and laboratory material that systematically addressed every examination question. Similarly, Day and colleagues6 found that medical students scored a mean of 45% on the Freedman and Bernstein examination despite increased lecture and laboratory time.6 Lecture and laboratory exposure does not result in long-term information retention. Medical school competency is not significantly higher than what Freedman and Bernstein4 found for musculoskeletal education almost a decade earlier.
Musculoskeletal medicine typically is not revisited during medical school unless a student opts for an elective with a musculoskeletal basis. This specialty differs from others, such as neurology, which requires a 1-month clinical rotation before graduation. As increasing lecture and laboratory time did little to increase competency, adding a required clinical rotation in a musculoskeletal field or integrated musculoskeletal modules for anatomy and clinical training may be the best option for educational reform.
Our study found significantly higher Freedman and Bernstein examination scores for students with orthopedic surgery or rheumatology experience than for students without this experience. First- and second-year medical students are allowed to do a “selective” rotation—1 afternoon a week in an elective rotation of their choice. Students with orthopedics or rheumatology experience in this setting tended to score higher on the examination, possibly a result of both exposure to and interest in musculoskeletal issues. Many other studies have found that clinical exposure within a musculoskeletal field resulted in significantly higher musculoskeletal knowledge.8,12-16 Skelley and colleagues12 found that musculoskeletal clinical exposure of as short as 15 days significantly increased understanding among medical students. Grunfeld and colleagues15 found that students interested in orthopedics also had significantly more musculoskeletal knowledge. Musculoskeletal clinical exposure should be considered in medical school reform. As coordinating a curriculum with orthopedic resident and faculty involvement can set up educational barriers at some medical schools, dedicated musculoskeletal modules with a mock clinical skills component may be a useful consideration, and these have been shown to improve musculoskeletal knowledge.10,11
There are limitations to our study. The musculoskeletal examination was not given to an equal number of medical students in each group. The study also did not control for attendance, and therefore some students who took the musculoskeletal examination may not have attended all musculoskeletal module lectures. The validated examination used for basic competency is another possible limitation. The Freedman and Bernstein examination is the only validated examination used for basic competency, but it may not accurately assess meaningful development of clinical skills applicable to a patient musculoskeletal setting. No studies have assessed the correlation between musculoskeletal competency based on the Freedman and Bernstein examination and patient outcomes.
We conclude that increasing dedicated musculoskeletal lecture hours does not improve musculoskeletal knowledge. Future considerations should include incorporating further hands-on training through clinical skills workshops or rotations in orthopedic surgery or rheumatology.
1. Centers for Disease Control and Prevention, National Center for Health Statistics, Ambulatory and Hospital Care Statistics Branch. National Hospital Ambulatory Medical Care Survey: 2009 outpatient department summary tables. http://www.cdc.gov/nchs/data/ahcd/nhamcs_outpatient/2009_opd_web_tables.pdf. Accessed January 8, 2015.
2. Pitts SR, Niska RW, Xu J, Burt CW. National Hospital Ambulatory Medical Care Survey: 2006 emergency department summary. Natl Health Stat Report. 2008 Aug 6;(7):1-38.
3. United States Bone and Joint Initiative. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Costs. Rosemont, IL: United States Bone and Joint Initiative; 2008. http://www.boneandjointburden.org. Accessed January 9, 2015.
4. Freedman KB, Bernstein J. The adequacy of medical school education in musculoskeletal medicine. J Bone Joint Surg Am. 1998;80(10):1421-1427.
5. United States Bone and Joint Initiative. Project 100—Undergraduate Musculoskeletal Education. Rosemont, IL: United States Bone and Joint Initiative; 2005. www.usbjd.org/projects/project_op.cfm?dirID=127. Accessed January 9, 2015.
6. Day CS, Ahn CS, Yeh AC, Tabrizi S. Early assessment of a new integrated preclinical musculoskeletal curriculum at a medical school. Am J Orthop. 2011;40(1):14-18.
7. Day CS, Yeh AC, Franko O, Ramirez M, Krupat E. Musculoskeletal medicine: an assessment of the attitudes and knowledge of medical students at Harvard Medical School. Acad Med. 2007;82(5):452-457.
8. Matzkin E, Smith EL, Freccero D, Richardson AB. Adequacy of education in musculoskeletal medicine. J Bone Joint Surg Am. 2005;87(2):310-314.
9. Freedman KB, Bernstein J. Educational deficiencies in musculoskeletal medicine. J Bone Joint Surg Am. 2002;84(4):604-608.
10. Bilderback K, Eggerstedt J, Sadasivan KK, et al. Design and implementation of a system-based course in musculoskeletal medicine for medical students. J Bone Joint Surg Am. 2008;90(10):2292-2300.
11. Queally JM, Cummins F, Brennan SA, Shelly MJ, O’Byrne JM. Assessment of a new undergraduate module in musculoskeletal medicine. J Bone Joint Surg Am. 2011;93(3):e9.
12. Skelley NW, Tanaka MJ, Skelley LM, LaPorte DM. Medical student musculoskeletal education: an institutional survey. J Bone Joint Surg Am. 2012;94(19):e146(1-7).
13. DiGiovanni BF, Chu JY, Mooney CJ, Lambert DR. Maturation of medical student musculoskeletal medicine knowledge and clinical confidence. Med Educ Online. 2012;17. doi:10.3402/meo.v17i0.17092. Epub 2012 Jul 23.
14. Schmale GA. More evidence of educational inadequacies in musculoskeletal medicine. Clin Orthop. 2005;(437):251-259.
15. Grunfeld R, Banks S, Fox E, Levy BA, Craig C, Black K. An assessment of musculoskeletal knowledge in graduating medical and physician assistant students and implications for musculoskeletal care providers. J Bone Joint Surg Am. 2012;94(4):343-348.
16. Yeh AC, Franko O, Day CS. Impact of clinical electives and residency interest on medical students’ education in musculoskeletal medicine. J Bone Joint Surg Am. 2008;90(2):307-315.
A basic understanding of the clinical components of musculoskeletal medicine is necessary in many medical fields. Musculoskeletal injuries represent the second most common presentation in US emergency departments, account for 49 million visits to orthopedic surgeon offices, and cost the United States an estimated $950 billion annually.1-3 Despite the staggering need for competency in musculoskeletal medicine, Freedman and Bernstein4 in 1998 demonstrated that musculoskeletal knowledge is inadequate among medical school graduates.
In 2005, the United States Bone and Joint Decade (now the United States Bone and Joint Initiative) announced Project 100, which recommended that 100% of US medical schools begin requiring a musculoskeletal course by the end of the decade.5 This project was intended to increase musculoskeletal understanding among medical students. Optimal curriculum reform, however, remains controversial. Many studies have found that medical schools continue to provide inadequate musculoskeletal education.4,6-9 For example, an integrated musculoskeletal curriculum with increased lecture time was found to improve clinical confidence but not musculoskeletal knowledge.6 In contrast, a 2-week intensive musculoskeletal module and a 6-week course involving orthopedic resident and faculty education has been shown to improve understanding.10,11
We conducted a study to determine the adequacy of musculoskeletal knowledge in medical school students, to determine musculoskeletal competency after curriculum reform through increased lecture and laboratory time, and to draw conclusions about factors leading to increased musculoskeletal competency to guide future curriculum reforms. We hypothesized that musculoskeletal knowledge would increase as a result of increased lecture and laboratory time.
Materials and Methods
The Tufts University School of Medicine Institutional Review Board approved this study. The medical school curriculum at our institution was redesigned to include a dedicated musculoskeletal module to improve medical student education (Table). The study compared medical students given the old musculoskeletal module (premodule group) and those given the new musculoskeletal module (postmodule group). The premodule group received 8.5 hours of physical diagnosis skills training and 30 hours of clinical anatomy training (12 lecture hours, 18 laboratory hours), and the postmodule group received 10 hours of physical diagnosis training and 41.5 hours of clinical anatomy training (18.5 lecture hours, 23 laboratory hours).
The lecture material for the postmodule group covered all topics/questions addressed on the validated musculoskeletal adequacy assessment. The new module specifically added 6 hours of dedicated clinically based musculoskeletal lecture time during the anatomy course and concurrent with the physical diagnosis course. The topics covered with case-based scenarios were orthopedic emergencies, adult hip and back, knee, pediatric hip and back, elbow/wrist/hand, and shoulder. A validated musculoskeletal competency examination was given to the premodule group at the end of the musculoskeletal anatomy and physical diagnosis lectures. The postmodule group took the competency examination at the end of the “new” 6 hours of musculoskeletal education.
We used the Freedman and Bernstein4 basic competency examination for musculoskeletal education assessment to assess knowledge. This examination is the only validated tool for assessing basic clinical musculoskeletal knowledge. All students were also asked whether they had experience rotating in orthopedic surgery or in a related musculoskeletal field (rheumatology, physiatry, neurology) during the medical school “selective” period that allowed 1 afternoon per week of elective time. Duration of exposure was assessed. The examination was given to 109 students in the premodule group 1 year before the curriculum changes. The examination was then given to the students for the first 2 years after the curriculum changes were implemented, with 296 students in the postmodule group. All questions on the examination were addressed within the 6 lecture hours in the new module. A single reviewer anonymously scored the examinations according to the validated scoring system over a 2-week period.4 Independent t tests were used to compare examination scores between the premodule and postmodule groups. Statistical significance was set at P < .05. Equal variance between groups was not assumed.
Results
The examination was given to 405 medical students (109 premodule, 296 postmodule) Mean examination score was 40%, significantly below the recommended mean passing score of 73.1%.4 Only 1 student achieved a passing score. Independent t tests were used to compare examination scores of the premodule and postmodule groups. Mean (SD) scores were higher (P < .05) for the premodule group, 42.1 (13.6), than the postmodule group, 39.1 (11.4) (Figure 1).
Independent t tests were used to compare examination scores of students with either orthopedics or rheumatology experience and students without this experience. Mean (SD) scores were higher (P < .05) for students with experience, 44.4 (11.9), than students without experience, 39.6 (12.1) (Figure 2). Students with neurology or physiatry experience did not score significantly higher than students without this experience. Statistical significance was set as P < .05. SAS 9.0 software (SAS Institute, Cary, North Carolina) was used for statistical analysis.
Discussion
Our students’ mean examination score was significantly lower than the passing (competency) score of 73.1%. Although Project 100 acknowledged many medical schools for implementing a required musculoskeletal course, our study results showed that adequate competency as indicated by a passing score on the Freedman and Bernstein examination was not achieved in medical school despite devoted musculoskeletal lecture time. Our postmodule group had lower scores than our premodule group despite being exposed to more lecture and laboratory material that systematically addressed every examination question. Similarly, Day and colleagues6 found that medical students scored a mean of 45% on the Freedman and Bernstein examination despite increased lecture and laboratory time.6 Lecture and laboratory exposure does not result in long-term information retention. Medical school competency is not significantly higher than what Freedman and Bernstein4 found for musculoskeletal education almost a decade earlier.
Musculoskeletal medicine typically is not revisited during medical school unless a student opts for an elective with a musculoskeletal basis. This specialty differs from others, such as neurology, which requires a 1-month clinical rotation before graduation. As increasing lecture and laboratory time did little to increase competency, adding a required clinical rotation in a musculoskeletal field or integrated musculoskeletal modules for anatomy and clinical training may be the best option for educational reform.
Our study found significantly higher Freedman and Bernstein examination scores for students with orthopedic surgery or rheumatology experience than for students without this experience. First- and second-year medical students are allowed to do a “selective” rotation—1 afternoon a week in an elective rotation of their choice. Students with orthopedics or rheumatology experience in this setting tended to score higher on the examination, possibly a result of both exposure to and interest in musculoskeletal issues. Many other studies have found that clinical exposure within a musculoskeletal field resulted in significantly higher musculoskeletal knowledge.8,12-16 Skelley and colleagues12 found that musculoskeletal clinical exposure of as short as 15 days significantly increased understanding among medical students. Grunfeld and colleagues15 found that students interested in orthopedics also had significantly more musculoskeletal knowledge. Musculoskeletal clinical exposure should be considered in medical school reform. As coordinating a curriculum with orthopedic resident and faculty involvement can set up educational barriers at some medical schools, dedicated musculoskeletal modules with a mock clinical skills component may be a useful consideration, and these have been shown to improve musculoskeletal knowledge.10,11
There are limitations to our study. The musculoskeletal examination was not given to an equal number of medical students in each group. The study also did not control for attendance, and therefore some students who took the musculoskeletal examination may not have attended all musculoskeletal module lectures. The validated examination used for basic competency is another possible limitation. The Freedman and Bernstein examination is the only validated examination used for basic competency, but it may not accurately assess meaningful development of clinical skills applicable to a patient musculoskeletal setting. No studies have assessed the correlation between musculoskeletal competency based on the Freedman and Bernstein examination and patient outcomes.
We conclude that increasing dedicated musculoskeletal lecture hours does not improve musculoskeletal knowledge. Future considerations should include incorporating further hands-on training through clinical skills workshops or rotations in orthopedic surgery or rheumatology.
A basic understanding of the clinical components of musculoskeletal medicine is necessary in many medical fields. Musculoskeletal injuries represent the second most common presentation in US emergency departments, account for 49 million visits to orthopedic surgeon offices, and cost the United States an estimated $950 billion annually.1-3 Despite the staggering need for competency in musculoskeletal medicine, Freedman and Bernstein4 in 1998 demonstrated that musculoskeletal knowledge is inadequate among medical school graduates.
In 2005, the United States Bone and Joint Decade (now the United States Bone and Joint Initiative) announced Project 100, which recommended that 100% of US medical schools begin requiring a musculoskeletal course by the end of the decade.5 This project was intended to increase musculoskeletal understanding among medical students. Optimal curriculum reform, however, remains controversial. Many studies have found that medical schools continue to provide inadequate musculoskeletal education.4,6-9 For example, an integrated musculoskeletal curriculum with increased lecture time was found to improve clinical confidence but not musculoskeletal knowledge.6 In contrast, a 2-week intensive musculoskeletal module and a 6-week course involving orthopedic resident and faculty education has been shown to improve understanding.10,11
We conducted a study to determine the adequacy of musculoskeletal knowledge in medical school students, to determine musculoskeletal competency after curriculum reform through increased lecture and laboratory time, and to draw conclusions about factors leading to increased musculoskeletal competency to guide future curriculum reforms. We hypothesized that musculoskeletal knowledge would increase as a result of increased lecture and laboratory time.
Materials and Methods
The Tufts University School of Medicine Institutional Review Board approved this study. The medical school curriculum at our institution was redesigned to include a dedicated musculoskeletal module to improve medical student education (Table). The study compared medical students given the old musculoskeletal module (premodule group) and those given the new musculoskeletal module (postmodule group). The premodule group received 8.5 hours of physical diagnosis skills training and 30 hours of clinical anatomy training (12 lecture hours, 18 laboratory hours), and the postmodule group received 10 hours of physical diagnosis training and 41.5 hours of clinical anatomy training (18.5 lecture hours, 23 laboratory hours).
The lecture material for the postmodule group covered all topics/questions addressed on the validated musculoskeletal adequacy assessment. The new module specifically added 6 hours of dedicated clinically based musculoskeletal lecture time during the anatomy course and concurrent with the physical diagnosis course. The topics covered with case-based scenarios were orthopedic emergencies, adult hip and back, knee, pediatric hip and back, elbow/wrist/hand, and shoulder. A validated musculoskeletal competency examination was given to the premodule group at the end of the musculoskeletal anatomy and physical diagnosis lectures. The postmodule group took the competency examination at the end of the “new” 6 hours of musculoskeletal education.
We used the Freedman and Bernstein4 basic competency examination for musculoskeletal education assessment to assess knowledge. This examination is the only validated tool for assessing basic clinical musculoskeletal knowledge. All students were also asked whether they had experience rotating in orthopedic surgery or in a related musculoskeletal field (rheumatology, physiatry, neurology) during the medical school “selective” period that allowed 1 afternoon per week of elective time. Duration of exposure was assessed. The examination was given to 109 students in the premodule group 1 year before the curriculum changes. The examination was then given to the students for the first 2 years after the curriculum changes were implemented, with 296 students in the postmodule group. All questions on the examination were addressed within the 6 lecture hours in the new module. A single reviewer anonymously scored the examinations according to the validated scoring system over a 2-week period.4 Independent t tests were used to compare examination scores between the premodule and postmodule groups. Statistical significance was set at P < .05. Equal variance between groups was not assumed.
Results
The examination was given to 405 medical students (109 premodule, 296 postmodule) Mean examination score was 40%, significantly below the recommended mean passing score of 73.1%.4 Only 1 student achieved a passing score. Independent t tests were used to compare examination scores of the premodule and postmodule groups. Mean (SD) scores were higher (P < .05) for the premodule group, 42.1 (13.6), than the postmodule group, 39.1 (11.4) (Figure 1).
Independent t tests were used to compare examination scores of students with either orthopedics or rheumatology experience and students without this experience. Mean (SD) scores were higher (P < .05) for students with experience, 44.4 (11.9), than students without experience, 39.6 (12.1) (Figure 2). Students with neurology or physiatry experience did not score significantly higher than students without this experience. Statistical significance was set as P < .05. SAS 9.0 software (SAS Institute, Cary, North Carolina) was used for statistical analysis.
Discussion
Our students’ mean examination score was significantly lower than the passing (competency) score of 73.1%. Although Project 100 acknowledged many medical schools for implementing a required musculoskeletal course, our study results showed that adequate competency as indicated by a passing score on the Freedman and Bernstein examination was not achieved in medical school despite devoted musculoskeletal lecture time. Our postmodule group had lower scores than our premodule group despite being exposed to more lecture and laboratory material that systematically addressed every examination question. Similarly, Day and colleagues6 found that medical students scored a mean of 45% on the Freedman and Bernstein examination despite increased lecture and laboratory time.6 Lecture and laboratory exposure does not result in long-term information retention. Medical school competency is not significantly higher than what Freedman and Bernstein4 found for musculoskeletal education almost a decade earlier.
Musculoskeletal medicine typically is not revisited during medical school unless a student opts for an elective with a musculoskeletal basis. This specialty differs from others, such as neurology, which requires a 1-month clinical rotation before graduation. As increasing lecture and laboratory time did little to increase competency, adding a required clinical rotation in a musculoskeletal field or integrated musculoskeletal modules for anatomy and clinical training may be the best option for educational reform.
Our study found significantly higher Freedman and Bernstein examination scores for students with orthopedic surgery or rheumatology experience than for students without this experience. First- and second-year medical students are allowed to do a “selective” rotation—1 afternoon a week in an elective rotation of their choice. Students with orthopedics or rheumatology experience in this setting tended to score higher on the examination, possibly a result of both exposure to and interest in musculoskeletal issues. Many other studies have found that clinical exposure within a musculoskeletal field resulted in significantly higher musculoskeletal knowledge.8,12-16 Skelley and colleagues12 found that musculoskeletal clinical exposure of as short as 15 days significantly increased understanding among medical students. Grunfeld and colleagues15 found that students interested in orthopedics also had significantly more musculoskeletal knowledge. Musculoskeletal clinical exposure should be considered in medical school reform. As coordinating a curriculum with orthopedic resident and faculty involvement can set up educational barriers at some medical schools, dedicated musculoskeletal modules with a mock clinical skills component may be a useful consideration, and these have been shown to improve musculoskeletal knowledge.10,11
There are limitations to our study. The musculoskeletal examination was not given to an equal number of medical students in each group. The study also did not control for attendance, and therefore some students who took the musculoskeletal examination may not have attended all musculoskeletal module lectures. The validated examination used for basic competency is another possible limitation. The Freedman and Bernstein examination is the only validated examination used for basic competency, but it may not accurately assess meaningful development of clinical skills applicable to a patient musculoskeletal setting. No studies have assessed the correlation between musculoskeletal competency based on the Freedman and Bernstein examination and patient outcomes.
We conclude that increasing dedicated musculoskeletal lecture hours does not improve musculoskeletal knowledge. Future considerations should include incorporating further hands-on training through clinical skills workshops or rotations in orthopedic surgery or rheumatology.
1. Centers for Disease Control and Prevention, National Center for Health Statistics, Ambulatory and Hospital Care Statistics Branch. National Hospital Ambulatory Medical Care Survey: 2009 outpatient department summary tables. http://www.cdc.gov/nchs/data/ahcd/nhamcs_outpatient/2009_opd_web_tables.pdf. Accessed January 8, 2015.
2. Pitts SR, Niska RW, Xu J, Burt CW. National Hospital Ambulatory Medical Care Survey: 2006 emergency department summary. Natl Health Stat Report. 2008 Aug 6;(7):1-38.
3. United States Bone and Joint Initiative. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Costs. Rosemont, IL: United States Bone and Joint Initiative; 2008. http://www.boneandjointburden.org. Accessed January 9, 2015.
4. Freedman KB, Bernstein J. The adequacy of medical school education in musculoskeletal medicine. J Bone Joint Surg Am. 1998;80(10):1421-1427.
5. United States Bone and Joint Initiative. Project 100—Undergraduate Musculoskeletal Education. Rosemont, IL: United States Bone and Joint Initiative; 2005. www.usbjd.org/projects/project_op.cfm?dirID=127. Accessed January 9, 2015.
6. Day CS, Ahn CS, Yeh AC, Tabrizi S. Early assessment of a new integrated preclinical musculoskeletal curriculum at a medical school. Am J Orthop. 2011;40(1):14-18.
7. Day CS, Yeh AC, Franko O, Ramirez M, Krupat E. Musculoskeletal medicine: an assessment of the attitudes and knowledge of medical students at Harvard Medical School. Acad Med. 2007;82(5):452-457.
8. Matzkin E, Smith EL, Freccero D, Richardson AB. Adequacy of education in musculoskeletal medicine. J Bone Joint Surg Am. 2005;87(2):310-314.
9. Freedman KB, Bernstein J. Educational deficiencies in musculoskeletal medicine. J Bone Joint Surg Am. 2002;84(4):604-608.
10. Bilderback K, Eggerstedt J, Sadasivan KK, et al. Design and implementation of a system-based course in musculoskeletal medicine for medical students. J Bone Joint Surg Am. 2008;90(10):2292-2300.
11. Queally JM, Cummins F, Brennan SA, Shelly MJ, O’Byrne JM. Assessment of a new undergraduate module in musculoskeletal medicine. J Bone Joint Surg Am. 2011;93(3):e9.
12. Skelley NW, Tanaka MJ, Skelley LM, LaPorte DM. Medical student musculoskeletal education: an institutional survey. J Bone Joint Surg Am. 2012;94(19):e146(1-7).
13. DiGiovanni BF, Chu JY, Mooney CJ, Lambert DR. Maturation of medical student musculoskeletal medicine knowledge and clinical confidence. Med Educ Online. 2012;17. doi:10.3402/meo.v17i0.17092. Epub 2012 Jul 23.
14. Schmale GA. More evidence of educational inadequacies in musculoskeletal medicine. Clin Orthop. 2005;(437):251-259.
15. Grunfeld R, Banks S, Fox E, Levy BA, Craig C, Black K. An assessment of musculoskeletal knowledge in graduating medical and physician assistant students and implications for musculoskeletal care providers. J Bone Joint Surg Am. 2012;94(4):343-348.
16. Yeh AC, Franko O, Day CS. Impact of clinical electives and residency interest on medical students’ education in musculoskeletal medicine. J Bone Joint Surg Am. 2008;90(2):307-315.
1. Centers for Disease Control and Prevention, National Center for Health Statistics, Ambulatory and Hospital Care Statistics Branch. National Hospital Ambulatory Medical Care Survey: 2009 outpatient department summary tables. http://www.cdc.gov/nchs/data/ahcd/nhamcs_outpatient/2009_opd_web_tables.pdf. Accessed January 8, 2015.
2. Pitts SR, Niska RW, Xu J, Burt CW. National Hospital Ambulatory Medical Care Survey: 2006 emergency department summary. Natl Health Stat Report. 2008 Aug 6;(7):1-38.
3. United States Bone and Joint Initiative. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Costs. Rosemont, IL: United States Bone and Joint Initiative; 2008. http://www.boneandjointburden.org. Accessed January 9, 2015.
4. Freedman KB, Bernstein J. The adequacy of medical school education in musculoskeletal medicine. J Bone Joint Surg Am. 1998;80(10):1421-1427.
5. United States Bone and Joint Initiative. Project 100—Undergraduate Musculoskeletal Education. Rosemont, IL: United States Bone and Joint Initiative; 2005. www.usbjd.org/projects/project_op.cfm?dirID=127. Accessed January 9, 2015.
6. Day CS, Ahn CS, Yeh AC, Tabrizi S. Early assessment of a new integrated preclinical musculoskeletal curriculum at a medical school. Am J Orthop. 2011;40(1):14-18.
7. Day CS, Yeh AC, Franko O, Ramirez M, Krupat E. Musculoskeletal medicine: an assessment of the attitudes and knowledge of medical students at Harvard Medical School. Acad Med. 2007;82(5):452-457.
8. Matzkin E, Smith EL, Freccero D, Richardson AB. Adequacy of education in musculoskeletal medicine. J Bone Joint Surg Am. 2005;87(2):310-314.
9. Freedman KB, Bernstein J. Educational deficiencies in musculoskeletal medicine. J Bone Joint Surg Am. 2002;84(4):604-608.
10. Bilderback K, Eggerstedt J, Sadasivan KK, et al. Design and implementation of a system-based course in musculoskeletal medicine for medical students. J Bone Joint Surg Am. 2008;90(10):2292-2300.
11. Queally JM, Cummins F, Brennan SA, Shelly MJ, O’Byrne JM. Assessment of a new undergraduate module in musculoskeletal medicine. J Bone Joint Surg Am. 2011;93(3):e9.
12. Skelley NW, Tanaka MJ, Skelley LM, LaPorte DM. Medical student musculoskeletal education: an institutional survey. J Bone Joint Surg Am. 2012;94(19):e146(1-7).
13. DiGiovanni BF, Chu JY, Mooney CJ, Lambert DR. Maturation of medical student musculoskeletal medicine knowledge and clinical confidence. Med Educ Online. 2012;17. doi:10.3402/meo.v17i0.17092. Epub 2012 Jul 23.
14. Schmale GA. More evidence of educational inadequacies in musculoskeletal medicine. Clin Orthop. 2005;(437):251-259.
15. Grunfeld R, Banks S, Fox E, Levy BA, Craig C, Black K. An assessment of musculoskeletal knowledge in graduating medical and physician assistant students and implications for musculoskeletal care providers. J Bone Joint Surg Am. 2012;94(4):343-348.
16. Yeh AC, Franko O, Day CS. Impact of clinical electives and residency interest on medical students’ education in musculoskeletal medicine. J Bone Joint Surg Am. 2008;90(2):307-315.