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Lower Limb Morel-Lavallée Lesion Treated With Short-Stretch Compression Bandaging

Article Type
Changed
Thu, 09/19/2019 - 13:21
Display Headline
Lower Limb Morel-Lavallée Lesion Treated With Short-Stretch Compression Bandaging

Take-Home Points

  • Have a high-index of suspicion for MLLs and initiate treatment early.
  • Compression needs to occur through short-stretch bandaging over a conventional Ace wrap in order to be successful.
  • Apply the short-stretch compression with care to avoid shearing underlying tissue.
  • Nonoperative treatment modalities require high patient compliance.
  • MLLs need close monitoring until final healing occurs.

Morel-Lavallée lesions (MLLs) are traumatic degloving injuries resulting from separation of subcutaneous fat from underlying fascia. MLLs occur in association with acetabular fractures and are also associated with low-velocity crush injuries.1,2 Shearing creates a “false” space that is filled with hemorrhaged blood, fat, and lymphatic tissue.3 Disruption of the lymphatics leads to cavity formation and, eventually, a fibrotic pseudocapsule.4The pseudocapsule prevents resorption, leading to a chronic fluid collection, which potentiates the risk of infection or tissue necrosis.3,5,6 Skin necrosis may occur through direct-pressure compromise of the dermal vascular plexus.4 Necrotic skin may require multiple débridements, negative-pressure wound therapy or soft-tissue coverage, and may ultimately result in infection. MLLs classically occur in the greater trochanteric region, lateral thigh, buttocks, and back but also appear in the prepatellar region.1,3 Patients present with soft-tissue swelling, bruising, bulging, decreased cutaneous sensation over the region, and a palpable, fluctuant subcutaneous fluid collection with mobile skin.2,4,7 The mechanism of injury may cause a concomitant fracture. Magnetic resonance imaging (MRI), the preferred imaging modality, shows a discrete fluid collection between subcutaneous fat and underlying fascia. Ultrasonography may reveal a thickened capsule surrounding either a hypoechoic area or an anechoic area but its accuracy is user-dependent.7

Large MLLs may be treated with open serial débridement and healing by secondary intention; infection rates, however, are high. Authors have described several other treatment modalities, including percutaneous débridement with a brush followed by use of a large-bore drain and antibiotics; open débridement with meticulous dead-space closure; elastic compression bandaging; aspiration; and doxycycline sclerodesis.1,5,6,8,9 Modifications of short-stretch compression bandaging were recently described in edema control for hindfoot trauma, ankle trauma, and total ankle arthroplasty, but not for MLLs.10,11 Nickerson and colleagues4 retrospectively reviewed 87 MLLs, found that fluid aspirate of >50 mL predicted recurrence and failure with conservative measures, and recommended operative intervention for any MLL with >50 mL of fluid aspirated.

We report the case of an MLL that occurred in an unusual anatomical region, and we describe a novel application of a conservative treatment, which was selected on the basis of its success in lymphedema management. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old man was injured when a parked vehicle began moving, pulled him under, and ran over his lower right leg. In the emergency department, no fractures or major injuries were noted (Figures 1A, 1B), and the patient was discharged.

Figure 1.

About 10 days after injury, profuse ecchymosis and swelling were noted running from the distal medial thigh to the proximal medial calf (Figures 2A-2C).

Figure 2.
The leg had a palpable continuous fluid wave extending from the medial proximal thigh to the distal calf. The skin was hypermobile, and clinically an MLL was evident. Ultrasonography (Figure 3) and aspiration from interventional radiology 2 weeks after injury yielded 130 mL of blood-tinged fluid.

Given the size of the MLL, the fluid collection reaccumulated. The patient was evaluated by an orthopedic traumatologist 3 days after the aspiration (17 days after injury).
Figure 3.
The treating physician suggested several options, including open débridement with cornrow stitching over a drain; minimally invasive débridement and irrigation over a drain; and compression. Nonoperative management was considered of limited success secondary to the size of the MLL. However, the patient selected nonoperative management with compression wrapping.

Another orthopedic traumatologist confirmed the low likelihood that compression would resolve the MLL, given its size (Figures 4A, 4B).
Figure 4.
Another aspiration, 29 days after injury, yielded 235 mL of serous fluid (Figure 5). As expected, the lesion had reaccumulated. Compression wraps were continued for 2.5 weeks.
Figure 5.
The patient continued to have swelling in the foot, discomfort, and sleep disturbance as a result of bandage pressure. Maintaining the wrap’s position and pressure throughout the day was also proving difficult; he had to continually retighten the bandage.

After the second orthopedic consultation, the patient saw a physical therapist trained in complete decongestive therapy. The therapist suggested placing short-stretch bandage wraps over the conventional long-stretch Ace bandage currently being used—a treatment common in lymphedema. The patient was wrapped from toe to groin without an initial layer of padding (Figures 6A, 6B), and the response was immediate.
Figure 6.
Given the improvement with short-stretch wraps, nonoperative treatment with monitoring was continued by the orthopedic surgeon.

Nine weeks after injury, the leg was significantly improved, and clinical signs resolved (Figure 7).
Figure 7.
MRI with and without contrast showed no evidence of the MLL (Figures 8A-8D). Despite persistent discomfort, the swelling had subsided, and the traumatologist canceled the surgery. The patient was advised to start weaning off the wraps by going wrap-free a couple of hours each day. The trauma team was confident the infection risk was low, and the wraps were discontinued once the patient was pain-free, 7 months after injury.

Discussion

Short-stretch bandaging has been performed mainly in lymphedema and ulcer management.

Figure 8.
The bandage consists of woven cotton fibers that stretch to only 30% to 60% of the original length.12,13 By contrast, long-stretch bandages, such as conventional Ace wraps, are made of elastic fibers that stretch to 140% to 300%.12,13 Long-stretch bandages did not effectively control our patient’s swelling and had to be continually adjusted and retightened. Short-stretch bandages provide high working pressures and low resting pressures; Ace wraps work in opposite fashion.12-14 High working pressures occur from intermittent peaks in pressure with walking, creating a massage effect that results in reduced filtration of fluid from capillaries into surrounding tissue, promoting spontaneous contractions of lymphangions.13 These pressures decrease at rest and can improve patient comfort, especially at night.15 Although optimal pressures have yet to be determined, they have been estimated at 50 mm Hg to 60 mm Hg (supine) and 70 mm HG to 80 mm Hg (standing, with multilayer wrapping).13,15 Short-stretch bandages promote calf muscle pumping, provide edema containment, and improve peripheral venous and arterial flow.12 The efficacy of the bandages derives from the relationship of working and resting pressures, of containment and recoil.12 Used correctly, short-stretch bandages are applied in multiple layers and create an external force against calf muscle contraction, preventing the muscle from bulging outward as the bandages contract, thus forcing it to compress and pump the venous system.12 By contrast, long-stretch Ace wraps stretch with the muscle and, as edema increases, fail to provide adequate edema control.12 In addition, Ace wraps must be applied at a higher resting pressure to help effectively reduce venous reflux. Thus, patients experience continuous high pressures even when supine.14

Compression bandaging reduces volume in lymphedematous limbs by reducing capillary filtration, shifting fluid into noncompressed parts of the body, increasing lymphatic reabsorption and lymphatic transport stimulation, improving venous pumping, and breaking down fibrosclerotic tissue.15 We think containment, improved venous flow, and enhanced muscle contraction contributed to the effectiveness of short-stretch bandaging as treatment for our patient’s MLL. Because MLLs also contain disrupted lymphatics, lymphedema management strategies (eg, short-stretch bandages) can be used. Our patient rapidly improved after conversion to short-stretch bandages.

These bandages are applied with 50% overlap to ensure even pressures throughout.16 Multiple layers are applied using a combination of spiral and figure-of-8 techniques, first clockwise and then counterclockwise, to avoid shearing underlying tissue.17 This method is very important in MLL treatment, given the degloving involved and the highly mobile skin and subcutaneous fat.

In standard lymphedema management, a foam padding layer is applied before the short-stretch bandage in order to reshape the limb and avoid proximal constrictions.13 In our patient’s case, the short-stretch wrap was applied without padding. Because his condition was acute, and the limb contour was preserved, limb reshaping and thus padding were not necessary.

Given the rapid, high-volume reduction that occurs within the first 1 to 2 weeks, bandages are reapplied daily to effectively adjust for the decreased swelling and altered limb shape.17 Most improvement is expected within the first few weeks—consistent with our patient’s case. Bandages usually are applied to the entire limb. For partial cases, the bandaging must extend past the area of swelling and incorporate the knee to prevent displacement of fluid into the joint.17 Feet and ankles are bandaged in dorsiflexion.17Several factors must be considered with short-stretch wraps. For example, pressure may need to be adjusted in patients with peripheral vascular disease. In patients with ankle-brachial indexes >0.5, it is safe to apply pressure up to 40 mm Hg.12 Reduced pressure is recommended for patients with arterial disease, sensory disturbance, lipoedema, poor mobility, frailty, or palliative needs.13The unusual location of our patient’s MLL accounts for the delay in diagnosis. To our knowledge, no other authors have reported such a large MLL in this location. A few series and case reports have listed MLLs in the calf near the gastrocnemius muscle, in the ankle, in the prepatellar area, and in the suprapatellar region, including the thigh,1,3,18-20 but there are no reports of MLLs running from medial thigh to proximal calf. MLLs of this size classically are treated surgically, but our patient selected nonoperative management.

To our knowledge, there are no earlier reports of using this nonoperative technique to treat MLLs. Conservative treatment with compression has been discussed, but no case involved short-stretch bandages. Large MLLs are thought to require surgery plus some type of drainage. The success of using short-stretch bandages in our patient’s case should prompt further investigation of use in adherent patients—which could ultimately result in reduced surgical needs, improved wound care (surgery is avoided), and a maintained low risk of infection. Although more work is needed to come to a more definitive verdict on this treatment method, it is a promising option that warrants consideration.

Am J Orthop. 2017;46(4):E213-E218. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.

2. Tsur A, Galin A, Kogan L, Loberant N. Morel-Lavallee syndrome after crush injury [in Hebrew]. Harefuah. 2006;145(2):111-113.

3. Ciaschini M, Sundaram M. Radiologic case study. Prepatellar Morel-Lavallée lesion. Orthopedics. 2008;31(7):626, 719-721.

4. Nickerson TP, Zielinski MD, Jenkins DH, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014;76(2):493-497.

5. Bansal A, Bhatia N, Singh A, Singh AK. Doxycycline sclerodesis as a treatment option for persistent Morel-Lavallée lesions. Injury. 2013;44(1):66-69.

6. Carlson DA, Simmons J, Sando W, Weber T, Clements B. Morel-Lavalée lesions treated with debridement and meticulous dead space closure: surgical technique. J Orthop Trauma. 2007;21(2):140-144.

7. Miller J, Daggett J, Ambay R, Payne WG. Morel-Lavallée lesion. Eplasty. 2014;14:ic12.

8. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

9. Harma A, Inan M, Ertem K. The Morel-Lavallée lesion: a conservative approach to closed degloving injuries [in Turkish]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

10. Hsu A, Franceschina D, Haddad SL. A novel method of postoperative wound care following total ankle arthroplasty. Foot Ankle Int. 2014;35(7):719-724.

11. Rohner-Spengler M, Frotzler A, Honigmann P, Babst R. Effective treatment of posttraumatic and postoperative edema in patients with ankle and hindfoot fractures: a randomized controlled trial comparing multilayer compression therapy and intermittent impulse compression with the standard treatment with ice. J Bone Joint Surg Am. 2014;96(15):1263-1271.

12. Bjork R. The long and short of it: understanding compression bandaging. Wound Care Advisor. 2013;2(6):12-15.

13. Partsch H. Assessing the effectiveness of multilayer inelastic bandaging. J Lymphoedema. 2007;2(2):55-61.

14. Hafner J, Botonakis I, Burg G. A comparison of multilayer bandage systems during rest, exercise, and over 2 days of wear time. Arch Dermatol. 2000;136(7):857-863.

15. Földi E, Jünger M, Partsch H. The science of lymphoedema bandaging. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:2-4.

16. King TI, Droessler JL. Physical properties of short-stretch compression bandages used to treat lymphedema. Am J Occup Ther. 2001;55(5):573-576.

17. Williams AF, Keller M. Practical guidance on lymphoedema bandaging of the upper and lower limbs. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:10-14.

18. Moriarty JM, Borrero CG, Kavanagh EC. A rare cause of calf swelling: the Morel-Lavallee lesion. Ir J Med Sci. 2011;180(1):265-268.

19. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Knee Morel-Lavallee lesion after a football injury in an 11-year-old boy: case report and review of the literature. Univ Pa Orthop J. 2011;21:56-58.

20. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.

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Take-Home Points

  • Have a high-index of suspicion for MLLs and initiate treatment early.
  • Compression needs to occur through short-stretch bandaging over a conventional Ace wrap in order to be successful.
  • Apply the short-stretch compression with care to avoid shearing underlying tissue.
  • Nonoperative treatment modalities require high patient compliance.
  • MLLs need close monitoring until final healing occurs.

Morel-Lavallée lesions (MLLs) are traumatic degloving injuries resulting from separation of subcutaneous fat from underlying fascia. MLLs occur in association with acetabular fractures and are also associated with low-velocity crush injuries.1,2 Shearing creates a “false” space that is filled with hemorrhaged blood, fat, and lymphatic tissue.3 Disruption of the lymphatics leads to cavity formation and, eventually, a fibrotic pseudocapsule.4The pseudocapsule prevents resorption, leading to a chronic fluid collection, which potentiates the risk of infection or tissue necrosis.3,5,6 Skin necrosis may occur through direct-pressure compromise of the dermal vascular plexus.4 Necrotic skin may require multiple débridements, negative-pressure wound therapy or soft-tissue coverage, and may ultimately result in infection. MLLs classically occur in the greater trochanteric region, lateral thigh, buttocks, and back but also appear in the prepatellar region.1,3 Patients present with soft-tissue swelling, bruising, bulging, decreased cutaneous sensation over the region, and a palpable, fluctuant subcutaneous fluid collection with mobile skin.2,4,7 The mechanism of injury may cause a concomitant fracture. Magnetic resonance imaging (MRI), the preferred imaging modality, shows a discrete fluid collection between subcutaneous fat and underlying fascia. Ultrasonography may reveal a thickened capsule surrounding either a hypoechoic area or an anechoic area but its accuracy is user-dependent.7

Large MLLs may be treated with open serial débridement and healing by secondary intention; infection rates, however, are high. Authors have described several other treatment modalities, including percutaneous débridement with a brush followed by use of a large-bore drain and antibiotics; open débridement with meticulous dead-space closure; elastic compression bandaging; aspiration; and doxycycline sclerodesis.1,5,6,8,9 Modifications of short-stretch compression bandaging were recently described in edema control for hindfoot trauma, ankle trauma, and total ankle arthroplasty, but not for MLLs.10,11 Nickerson and colleagues4 retrospectively reviewed 87 MLLs, found that fluid aspirate of >50 mL predicted recurrence and failure with conservative measures, and recommended operative intervention for any MLL with >50 mL of fluid aspirated.

We report the case of an MLL that occurred in an unusual anatomical region, and we describe a novel application of a conservative treatment, which was selected on the basis of its success in lymphedema management. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old man was injured when a parked vehicle began moving, pulled him under, and ran over his lower right leg. In the emergency department, no fractures or major injuries were noted (Figures 1A, 1B), and the patient was discharged.

Figure 1.

About 10 days after injury, profuse ecchymosis and swelling were noted running from the distal medial thigh to the proximal medial calf (Figures 2A-2C).

Figure 2.
The leg had a palpable continuous fluid wave extending from the medial proximal thigh to the distal calf. The skin was hypermobile, and clinically an MLL was evident. Ultrasonography (Figure 3) and aspiration from interventional radiology 2 weeks after injury yielded 130 mL of blood-tinged fluid.

Given the size of the MLL, the fluid collection reaccumulated. The patient was evaluated by an orthopedic traumatologist 3 days after the aspiration (17 days after injury).
Figure 3.
The treating physician suggested several options, including open débridement with cornrow stitching over a drain; minimally invasive débridement and irrigation over a drain; and compression. Nonoperative management was considered of limited success secondary to the size of the MLL. However, the patient selected nonoperative management with compression wrapping.

Another orthopedic traumatologist confirmed the low likelihood that compression would resolve the MLL, given its size (Figures 4A, 4B).
Figure 4.
Another aspiration, 29 days after injury, yielded 235 mL of serous fluid (Figure 5). As expected, the lesion had reaccumulated. Compression wraps were continued for 2.5 weeks.
Figure 5.
The patient continued to have swelling in the foot, discomfort, and sleep disturbance as a result of bandage pressure. Maintaining the wrap’s position and pressure throughout the day was also proving difficult; he had to continually retighten the bandage.

After the second orthopedic consultation, the patient saw a physical therapist trained in complete decongestive therapy. The therapist suggested placing short-stretch bandage wraps over the conventional long-stretch Ace bandage currently being used—a treatment common in lymphedema. The patient was wrapped from toe to groin without an initial layer of padding (Figures 6A, 6B), and the response was immediate.
Figure 6.
Given the improvement with short-stretch wraps, nonoperative treatment with monitoring was continued by the orthopedic surgeon.

Nine weeks after injury, the leg was significantly improved, and clinical signs resolved (Figure 7).
Figure 7.
MRI with and without contrast showed no evidence of the MLL (Figures 8A-8D). Despite persistent discomfort, the swelling had subsided, and the traumatologist canceled the surgery. The patient was advised to start weaning off the wraps by going wrap-free a couple of hours each day. The trauma team was confident the infection risk was low, and the wraps were discontinued once the patient was pain-free, 7 months after injury.

Discussion

Short-stretch bandaging has been performed mainly in lymphedema and ulcer management.

Figure 8.
The bandage consists of woven cotton fibers that stretch to only 30% to 60% of the original length.12,13 By contrast, long-stretch bandages, such as conventional Ace wraps, are made of elastic fibers that stretch to 140% to 300%.12,13 Long-stretch bandages did not effectively control our patient’s swelling and had to be continually adjusted and retightened. Short-stretch bandages provide high working pressures and low resting pressures; Ace wraps work in opposite fashion.12-14 High working pressures occur from intermittent peaks in pressure with walking, creating a massage effect that results in reduced filtration of fluid from capillaries into surrounding tissue, promoting spontaneous contractions of lymphangions.13 These pressures decrease at rest and can improve patient comfort, especially at night.15 Although optimal pressures have yet to be determined, they have been estimated at 50 mm Hg to 60 mm Hg (supine) and 70 mm HG to 80 mm Hg (standing, with multilayer wrapping).13,15 Short-stretch bandages promote calf muscle pumping, provide edema containment, and improve peripheral venous and arterial flow.12 The efficacy of the bandages derives from the relationship of working and resting pressures, of containment and recoil.12 Used correctly, short-stretch bandages are applied in multiple layers and create an external force against calf muscle contraction, preventing the muscle from bulging outward as the bandages contract, thus forcing it to compress and pump the venous system.12 By contrast, long-stretch Ace wraps stretch with the muscle and, as edema increases, fail to provide adequate edema control.12 In addition, Ace wraps must be applied at a higher resting pressure to help effectively reduce venous reflux. Thus, patients experience continuous high pressures even when supine.14

Compression bandaging reduces volume in lymphedematous limbs by reducing capillary filtration, shifting fluid into noncompressed parts of the body, increasing lymphatic reabsorption and lymphatic transport stimulation, improving venous pumping, and breaking down fibrosclerotic tissue.15 We think containment, improved venous flow, and enhanced muscle contraction contributed to the effectiveness of short-stretch bandaging as treatment for our patient’s MLL. Because MLLs also contain disrupted lymphatics, lymphedema management strategies (eg, short-stretch bandages) can be used. Our patient rapidly improved after conversion to short-stretch bandages.

These bandages are applied with 50% overlap to ensure even pressures throughout.16 Multiple layers are applied using a combination of spiral and figure-of-8 techniques, first clockwise and then counterclockwise, to avoid shearing underlying tissue.17 This method is very important in MLL treatment, given the degloving involved and the highly mobile skin and subcutaneous fat.

In standard lymphedema management, a foam padding layer is applied before the short-stretch bandage in order to reshape the limb and avoid proximal constrictions.13 In our patient’s case, the short-stretch wrap was applied without padding. Because his condition was acute, and the limb contour was preserved, limb reshaping and thus padding were not necessary.

Given the rapid, high-volume reduction that occurs within the first 1 to 2 weeks, bandages are reapplied daily to effectively adjust for the decreased swelling and altered limb shape.17 Most improvement is expected within the first few weeks—consistent with our patient’s case. Bandages usually are applied to the entire limb. For partial cases, the bandaging must extend past the area of swelling and incorporate the knee to prevent displacement of fluid into the joint.17 Feet and ankles are bandaged in dorsiflexion.17Several factors must be considered with short-stretch wraps. For example, pressure may need to be adjusted in patients with peripheral vascular disease. In patients with ankle-brachial indexes >0.5, it is safe to apply pressure up to 40 mm Hg.12 Reduced pressure is recommended for patients with arterial disease, sensory disturbance, lipoedema, poor mobility, frailty, or palliative needs.13The unusual location of our patient’s MLL accounts for the delay in diagnosis. To our knowledge, no other authors have reported such a large MLL in this location. A few series and case reports have listed MLLs in the calf near the gastrocnemius muscle, in the ankle, in the prepatellar area, and in the suprapatellar region, including the thigh,1,3,18-20 but there are no reports of MLLs running from medial thigh to proximal calf. MLLs of this size classically are treated surgically, but our patient selected nonoperative management.

To our knowledge, there are no earlier reports of using this nonoperative technique to treat MLLs. Conservative treatment with compression has been discussed, but no case involved short-stretch bandages. Large MLLs are thought to require surgery plus some type of drainage. The success of using short-stretch bandages in our patient’s case should prompt further investigation of use in adherent patients—which could ultimately result in reduced surgical needs, improved wound care (surgery is avoided), and a maintained low risk of infection. Although more work is needed to come to a more definitive verdict on this treatment method, it is a promising option that warrants consideration.

Am J Orthop. 2017;46(4):E213-E218. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Have a high-index of suspicion for MLLs and initiate treatment early.
  • Compression needs to occur through short-stretch bandaging over a conventional Ace wrap in order to be successful.
  • Apply the short-stretch compression with care to avoid shearing underlying tissue.
  • Nonoperative treatment modalities require high patient compliance.
  • MLLs need close monitoring until final healing occurs.

Morel-Lavallée lesions (MLLs) are traumatic degloving injuries resulting from separation of subcutaneous fat from underlying fascia. MLLs occur in association with acetabular fractures and are also associated with low-velocity crush injuries.1,2 Shearing creates a “false” space that is filled with hemorrhaged blood, fat, and lymphatic tissue.3 Disruption of the lymphatics leads to cavity formation and, eventually, a fibrotic pseudocapsule.4The pseudocapsule prevents resorption, leading to a chronic fluid collection, which potentiates the risk of infection or tissue necrosis.3,5,6 Skin necrosis may occur through direct-pressure compromise of the dermal vascular plexus.4 Necrotic skin may require multiple débridements, negative-pressure wound therapy or soft-tissue coverage, and may ultimately result in infection. MLLs classically occur in the greater trochanteric region, lateral thigh, buttocks, and back but also appear in the prepatellar region.1,3 Patients present with soft-tissue swelling, bruising, bulging, decreased cutaneous sensation over the region, and a palpable, fluctuant subcutaneous fluid collection with mobile skin.2,4,7 The mechanism of injury may cause a concomitant fracture. Magnetic resonance imaging (MRI), the preferred imaging modality, shows a discrete fluid collection between subcutaneous fat and underlying fascia. Ultrasonography may reveal a thickened capsule surrounding either a hypoechoic area or an anechoic area but its accuracy is user-dependent.7

Large MLLs may be treated with open serial débridement and healing by secondary intention; infection rates, however, are high. Authors have described several other treatment modalities, including percutaneous débridement with a brush followed by use of a large-bore drain and antibiotics; open débridement with meticulous dead-space closure; elastic compression bandaging; aspiration; and doxycycline sclerodesis.1,5,6,8,9 Modifications of short-stretch compression bandaging were recently described in edema control for hindfoot trauma, ankle trauma, and total ankle arthroplasty, but not for MLLs.10,11 Nickerson and colleagues4 retrospectively reviewed 87 MLLs, found that fluid aspirate of >50 mL predicted recurrence and failure with conservative measures, and recommended operative intervention for any MLL with >50 mL of fluid aspirated.

We report the case of an MLL that occurred in an unusual anatomical region, and we describe a novel application of a conservative treatment, which was selected on the basis of its success in lymphedema management. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 66-year-old man was injured when a parked vehicle began moving, pulled him under, and ran over his lower right leg. In the emergency department, no fractures or major injuries were noted (Figures 1A, 1B), and the patient was discharged.

Figure 1.

About 10 days after injury, profuse ecchymosis and swelling were noted running from the distal medial thigh to the proximal medial calf (Figures 2A-2C).

Figure 2.
The leg had a palpable continuous fluid wave extending from the medial proximal thigh to the distal calf. The skin was hypermobile, and clinically an MLL was evident. Ultrasonography (Figure 3) and aspiration from interventional radiology 2 weeks after injury yielded 130 mL of blood-tinged fluid.

Given the size of the MLL, the fluid collection reaccumulated. The patient was evaluated by an orthopedic traumatologist 3 days after the aspiration (17 days after injury).
Figure 3.
The treating physician suggested several options, including open débridement with cornrow stitching over a drain; minimally invasive débridement and irrigation over a drain; and compression. Nonoperative management was considered of limited success secondary to the size of the MLL. However, the patient selected nonoperative management with compression wrapping.

Another orthopedic traumatologist confirmed the low likelihood that compression would resolve the MLL, given its size (Figures 4A, 4B).
Figure 4.
Another aspiration, 29 days after injury, yielded 235 mL of serous fluid (Figure 5). As expected, the lesion had reaccumulated. Compression wraps were continued for 2.5 weeks.
Figure 5.
The patient continued to have swelling in the foot, discomfort, and sleep disturbance as a result of bandage pressure. Maintaining the wrap’s position and pressure throughout the day was also proving difficult; he had to continually retighten the bandage.

After the second orthopedic consultation, the patient saw a physical therapist trained in complete decongestive therapy. The therapist suggested placing short-stretch bandage wraps over the conventional long-stretch Ace bandage currently being used—a treatment common in lymphedema. The patient was wrapped from toe to groin without an initial layer of padding (Figures 6A, 6B), and the response was immediate.
Figure 6.
Given the improvement with short-stretch wraps, nonoperative treatment with monitoring was continued by the orthopedic surgeon.

Nine weeks after injury, the leg was significantly improved, and clinical signs resolved (Figure 7).
Figure 7.
MRI with and without contrast showed no evidence of the MLL (Figures 8A-8D). Despite persistent discomfort, the swelling had subsided, and the traumatologist canceled the surgery. The patient was advised to start weaning off the wraps by going wrap-free a couple of hours each day. The trauma team was confident the infection risk was low, and the wraps were discontinued once the patient was pain-free, 7 months after injury.

Discussion

Short-stretch bandaging has been performed mainly in lymphedema and ulcer management.

Figure 8.
The bandage consists of woven cotton fibers that stretch to only 30% to 60% of the original length.12,13 By contrast, long-stretch bandages, such as conventional Ace wraps, are made of elastic fibers that stretch to 140% to 300%.12,13 Long-stretch bandages did not effectively control our patient’s swelling and had to be continually adjusted and retightened. Short-stretch bandages provide high working pressures and low resting pressures; Ace wraps work in opposite fashion.12-14 High working pressures occur from intermittent peaks in pressure with walking, creating a massage effect that results in reduced filtration of fluid from capillaries into surrounding tissue, promoting spontaneous contractions of lymphangions.13 These pressures decrease at rest and can improve patient comfort, especially at night.15 Although optimal pressures have yet to be determined, they have been estimated at 50 mm Hg to 60 mm Hg (supine) and 70 mm HG to 80 mm Hg (standing, with multilayer wrapping).13,15 Short-stretch bandages promote calf muscle pumping, provide edema containment, and improve peripheral venous and arterial flow.12 The efficacy of the bandages derives from the relationship of working and resting pressures, of containment and recoil.12 Used correctly, short-stretch bandages are applied in multiple layers and create an external force against calf muscle contraction, preventing the muscle from bulging outward as the bandages contract, thus forcing it to compress and pump the venous system.12 By contrast, long-stretch Ace wraps stretch with the muscle and, as edema increases, fail to provide adequate edema control.12 In addition, Ace wraps must be applied at a higher resting pressure to help effectively reduce venous reflux. Thus, patients experience continuous high pressures even when supine.14

Compression bandaging reduces volume in lymphedematous limbs by reducing capillary filtration, shifting fluid into noncompressed parts of the body, increasing lymphatic reabsorption and lymphatic transport stimulation, improving venous pumping, and breaking down fibrosclerotic tissue.15 We think containment, improved venous flow, and enhanced muscle contraction contributed to the effectiveness of short-stretch bandaging as treatment for our patient’s MLL. Because MLLs also contain disrupted lymphatics, lymphedema management strategies (eg, short-stretch bandages) can be used. Our patient rapidly improved after conversion to short-stretch bandages.

These bandages are applied with 50% overlap to ensure even pressures throughout.16 Multiple layers are applied using a combination of spiral and figure-of-8 techniques, first clockwise and then counterclockwise, to avoid shearing underlying tissue.17 This method is very important in MLL treatment, given the degloving involved and the highly mobile skin and subcutaneous fat.

In standard lymphedema management, a foam padding layer is applied before the short-stretch bandage in order to reshape the limb and avoid proximal constrictions.13 In our patient’s case, the short-stretch wrap was applied without padding. Because his condition was acute, and the limb contour was preserved, limb reshaping and thus padding were not necessary.

Given the rapid, high-volume reduction that occurs within the first 1 to 2 weeks, bandages are reapplied daily to effectively adjust for the decreased swelling and altered limb shape.17 Most improvement is expected within the first few weeks—consistent with our patient’s case. Bandages usually are applied to the entire limb. For partial cases, the bandaging must extend past the area of swelling and incorporate the knee to prevent displacement of fluid into the joint.17 Feet and ankles are bandaged in dorsiflexion.17Several factors must be considered with short-stretch wraps. For example, pressure may need to be adjusted in patients with peripheral vascular disease. In patients with ankle-brachial indexes >0.5, it is safe to apply pressure up to 40 mm Hg.12 Reduced pressure is recommended for patients with arterial disease, sensory disturbance, lipoedema, poor mobility, frailty, or palliative needs.13The unusual location of our patient’s MLL accounts for the delay in diagnosis. To our knowledge, no other authors have reported such a large MLL in this location. A few series and case reports have listed MLLs in the calf near the gastrocnemius muscle, in the ankle, in the prepatellar area, and in the suprapatellar region, including the thigh,1,3,18-20 but there are no reports of MLLs running from medial thigh to proximal calf. MLLs of this size classically are treated surgically, but our patient selected nonoperative management.

To our knowledge, there are no earlier reports of using this nonoperative technique to treat MLLs. Conservative treatment with compression has been discussed, but no case involved short-stretch bandages. Large MLLs are thought to require surgery plus some type of drainage. The success of using short-stretch bandages in our patient’s case should prompt further investigation of use in adherent patients—which could ultimately result in reduced surgical needs, improved wound care (surgery is avoided), and a maintained low risk of infection. Although more work is needed to come to a more definitive verdict on this treatment method, it is a promising option that warrants consideration.

Am J Orthop. 2017;46(4):E213-E218. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.

2. Tsur A, Galin A, Kogan L, Loberant N. Morel-Lavallee syndrome after crush injury [in Hebrew]. Harefuah. 2006;145(2):111-113.

3. Ciaschini M, Sundaram M. Radiologic case study. Prepatellar Morel-Lavallée lesion. Orthopedics. 2008;31(7):626, 719-721.

4. Nickerson TP, Zielinski MD, Jenkins DH, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014;76(2):493-497.

5. Bansal A, Bhatia N, Singh A, Singh AK. Doxycycline sclerodesis as a treatment option for persistent Morel-Lavallée lesions. Injury. 2013;44(1):66-69.

6. Carlson DA, Simmons J, Sando W, Weber T, Clements B. Morel-Lavalée lesions treated with debridement and meticulous dead space closure: surgical technique. J Orthop Trauma. 2007;21(2):140-144.

7. Miller J, Daggett J, Ambay R, Payne WG. Morel-Lavallée lesion. Eplasty. 2014;14:ic12.

8. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

9. Harma A, Inan M, Ertem K. The Morel-Lavallée lesion: a conservative approach to closed degloving injuries [in Turkish]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

10. Hsu A, Franceschina D, Haddad SL. A novel method of postoperative wound care following total ankle arthroplasty. Foot Ankle Int. 2014;35(7):719-724.

11. Rohner-Spengler M, Frotzler A, Honigmann P, Babst R. Effective treatment of posttraumatic and postoperative edema in patients with ankle and hindfoot fractures: a randomized controlled trial comparing multilayer compression therapy and intermittent impulse compression with the standard treatment with ice. J Bone Joint Surg Am. 2014;96(15):1263-1271.

12. Bjork R. The long and short of it: understanding compression bandaging. Wound Care Advisor. 2013;2(6):12-15.

13. Partsch H. Assessing the effectiveness of multilayer inelastic bandaging. J Lymphoedema. 2007;2(2):55-61.

14. Hafner J, Botonakis I, Burg G. A comparison of multilayer bandage systems during rest, exercise, and over 2 days of wear time. Arch Dermatol. 2000;136(7):857-863.

15. Földi E, Jünger M, Partsch H. The science of lymphoedema bandaging. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:2-4.

16. King TI, Droessler JL. Physical properties of short-stretch compression bandages used to treat lymphedema. Am J Occup Ther. 2001;55(5):573-576.

17. Williams AF, Keller M. Practical guidance on lymphoedema bandaging of the upper and lower limbs. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:10-14.

18. Moriarty JM, Borrero CG, Kavanagh EC. A rare cause of calf swelling: the Morel-Lavallee lesion. Ir J Med Sci. 2011;180(1):265-268.

19. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Knee Morel-Lavallee lesion after a football injury in an 11-year-old boy: case report and review of the literature. Univ Pa Orthop J. 2011;21:56-58.

20. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.

References

1. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallee lesion of the knee: twenty-seven cases in the National Football League. Am J Sports Med. 2007;35(7):1162-1167.

2. Tsur A, Galin A, Kogan L, Loberant N. Morel-Lavallee syndrome after crush injury [in Hebrew]. Harefuah. 2006;145(2):111-113.

3. Ciaschini M, Sundaram M. Radiologic case study. Prepatellar Morel-Lavallée lesion. Orthopedics. 2008;31(7):626, 719-721.

4. Nickerson TP, Zielinski MD, Jenkins DH, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014;76(2):493-497.

5. Bansal A, Bhatia N, Singh A, Singh AK. Doxycycline sclerodesis as a treatment option for persistent Morel-Lavallée lesions. Injury. 2013;44(1):66-69.

6. Carlson DA, Simmons J, Sando W, Weber T, Clements B. Morel-Lavalée lesions treated with debridement and meticulous dead space closure: surgical technique. J Orthop Trauma. 2007;21(2):140-144.

7. Miller J, Daggett J, Ambay R, Payne WG. Morel-Lavallée lesion. Eplasty. 2014;14:ic12.

8. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96.

9. Harma A, Inan M, Ertem K. The Morel-Lavallée lesion: a conservative approach to closed degloving injuries [in Turkish]. Acta Orthop Traumatol Turc. 2004;38(4):270-273.

10. Hsu A, Franceschina D, Haddad SL. A novel method of postoperative wound care following total ankle arthroplasty. Foot Ankle Int. 2014;35(7):719-724.

11. Rohner-Spengler M, Frotzler A, Honigmann P, Babst R. Effective treatment of posttraumatic and postoperative edema in patients with ankle and hindfoot fractures: a randomized controlled trial comparing multilayer compression therapy and intermittent impulse compression with the standard treatment with ice. J Bone Joint Surg Am. 2014;96(15):1263-1271.

12. Bjork R. The long and short of it: understanding compression bandaging. Wound Care Advisor. 2013;2(6):12-15.

13. Partsch H. Assessing the effectiveness of multilayer inelastic bandaging. J Lymphoedema. 2007;2(2):55-61.

14. Hafner J, Botonakis I, Burg G. A comparison of multilayer bandage systems during rest, exercise, and over 2 days of wear time. Arch Dermatol. 2000;136(7):857-863.

15. Földi E, Jünger M, Partsch H. The science of lymphoedema bandaging. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:2-4.

16. King TI, Droessler JL. Physical properties of short-stretch compression bandages used to treat lymphedema. Am J Occup Ther. 2001;55(5):573-576.

17. Williams AF, Keller M. Practical guidance on lymphoedema bandaging of the upper and lower limbs. In: Lymphoedema Bandaging in Practice [European Wound Management Association focus document]. London, England: Medical Education Partnership; 2005:10-14.

18. Moriarty JM, Borrero CG, Kavanagh EC. A rare cause of calf swelling: the Morel-Lavallee lesion. Ir J Med Sci. 2011;180(1):265-268.

19. Anakwenze OA, Trivedi V, Goodman AM, Ganley TJ. Knee Morel-Lavallee lesion after a football injury in an 11-year-old boy: case report and review of the literature. Univ Pa Orthop J. 2011;21:56-58.

20. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg. 1992;89(5):853-855.

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Biceps Tenodesis: An Evolution of Treatment

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Biceps Tenodesis: An Evolution of Treatment

Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

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Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

References

1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

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The American Journal of Orthopedics - 46(4)
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The American Journal of Orthopedics - 46(4)
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Knotless Arthroscopic Reduction and Internal Fixation of a Displaced Anterior Cruciate Ligament Tibial Eminence Avulsion Fracture

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Knotless Arthroscopic Reduction and Internal Fixation of a Displaced Anterior Cruciate Ligament Tibial Eminence Avulsion Fracture

Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

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Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Technique provides optimal fixation while simultaneously protecting open growth plates.
  • Self tensioning feature insures both optimal ACL tension and fracture reduction.
  • No need for future hardware removal.
  • 10Cross suture configuration optimizes strength of fixation for highly consistent results.
  • Use fluoroscopy to avoid violation of tibial physis.

Generally occurring in the 8- to 14-year-old population, tibial eminence avulsion (TEA) fractures are a common variant of anterior cruciate ligament (ACL) ruptures and represent 2% to 5% of all knee injuries in skeletally immature individuals.1,2 Compared with adults, children likely experience this anomaly more often because of the weakness of their incompletely ossified tibial plateau relative to the strength of their native ACL.3

The open repair techniques that have been described have multiple disadvantages, including open incisions, difficult visualization of the fracture owing to the location of the fat pad, and increased risk for arthrofibrosis. Arthroscopic fixation is considered the treatment of choice for TEA fractures because it allows for direct visualization of injury, accurate reduction of fracture fragments, removal of loose fragments, and easy treatment of associated soft-tissue injuries.4-6Several fixation techniques for ACL-TEA fractures were recently described: arthroscopic reduction and internal fixation (ARIF) with Kirschner wires,7 cannulated screws,4 the Meniscus Arrow device (Bionx Implants),8 pull-out sutures,9,10 bioabsorbable nails,11 Herbert screws,12 TightRope fixation (Arthrex),13 and various other rotator cuff and meniscal repair systems.14,15 These approaches tend to have good outcomes for TEA fractures, but there are risks associated with ACL tensioning and potential tibial growth plate violation or hardware problems. Likewise, there are no studies with large numbers of patients treated with these new techniques, so the optimal method of reduction and fixation is still unknown.

In this article, we describe a new ARIF technique that involves 2 absorbable anchors with adjustable suture-tensioning technology. This technique optimizes reduction and helps surgeons avoid proximal tibial physeal damage, procedure-related morbidity, and additional surgery.

Case Report

History

The patient, an 8-year-old boy, sustained a noncontact twisting injury of the left knee during a cutting maneuver in a flag football game. He experienced immediate pain and subsequent swelling. Clinical examination revealed a moderate effusion with motion limitations secondary to swelling and irritability. The patient’s Lachman test result was 2+. Pivot shift testing was not possible because of guarding. The knee was stable to varus and valgus stress at 0° and 30° of flexion. Limited knee flexion prohibited placement of the patient in the position needed for anterior and posterior drawer testing. His patella was stable on lateral stress testing at 20° of flexion with no apprehension. Neurovascular status was intact throughout the lower extremity.

Anteroposterior and lateral radiographs showed a minimally displaced Meyers-McKeever type II TEA fracture (Figures 1A, 1B).

Figure 1.
Distal femoral and proximal tibial growth plates were wide open. Magnetic resonance imaging confirmed the displaced type II TEA fracture and showed good signal quality in the attached ACL (Figures 2A, 2B).
Figure 2.
The remaining ligamentous structures appeared without injury or signal change. No tear signal was seen in the imaging sequences of the medial and lateral meniscus.

After discussing potential treatment options with the parents, Dr. Smith proceeded with arthroscopic surgery for definitive reduction and internal fixation of the patient’s left knee displaced ACL-TEA fracture. The new adjustable suture-tensioning fixation technique was used. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Examination Under Anesthesia

Examination with the patient under general anesthesia revealed 3+ Lachman, 2+ pivot shift with foot in internal and external rotation, and 1+ anterior drawer with foot in neutral and internal rotation. The knee was stable to varus and valgus stress testing.

Surgical Technique

Proper patient positioning and padding of bony prominences were ensured, and the limb was sterilely prepared and draped.

Figure 3.
A standard lateral parapatellar portal was established for arthroscope placement; a medial parapatellar working portal was established as well. Thorough joint inspection revealed normal articular surfaces of patella, femur, and tibial plateau. Similarly, both menisci were intact without evidence of injury.
Figure 4.
With use of the probe, the ACL-TEA fracture could be elevated up to 2 cm toward the top of the notch (Figure 3). Further inspection of the ACL fibers revealed minimal hemorrhaging and no frank tearing (Figure 4).

Given the young age of the patient, it was imperative to avoid the open proximal tibial growth plate. The surgical plan for stabilization involved use of two 3.0-mm BioComposite Knotless SutureTak anchors (Arthrex). This anchor configuration is based on a No. 2 FiberWire suture shuttled through itself to create a locking splice mechanism that allows for adjustable tensioning. The anchors were placed on each side of the tibial bony avulsion site with two No. 2 FiberWire sutures and were then crossed about the avulsion fracture fragment in an “x-type” configuration to secure the ACL back down to the bony bed.

First, a curette was used to débride fibrous tissue on the underside of the fracture fragment and on the fracture bed. Minimal amounts of cancellous bone were débrided from the tibial fracture bed to optimize fracture reduction by slightly recessing the fracture fragment to ensure optimal ACL tensioning (Figure 5).

Figure 5.
Next, an 18-gauge needle was used to establish an accessory superior medial percutaneous portal to ensure a satisfactory drilling trajectory just medial to the fracture site. Under fluoroscopic guidance, a drill guide was placed, and a 2.4-mm bit was used to drill to a depth of 16 mm to accommodate the 12.7-mm anchor. Avoidance of the proximal tibial physis was confirmed with fluoroscopy (Figure 6).
Figure 6.
One of the SutureTak anchors was secured in this drill hole along the anteromedial avulsion fracture site. From the anteromedial portal, a curved needle tip suture passer was placed medially through the ACL fibers and bone, with the wire retrieved out of the superior medial accessory portal. Then, the drill guide was introduced through the lateral portal and positioned just lateral to the tibial avulsion site, a hole was drilled 16 mm deep, and fluoroscopy was used to confirm the physis was not violated. The second SutureTak anchor was placed in this anterolateral location. From the anterolateral portal, the curved needle tip suture passer was placed laterally through the ACL fibers and avulsion fragment, and the wire was passed and retrieved out the anteromedial portal and shuttled back to the anterolateral portal.

Next, from the accessory superior medial portal, the end of the wire that had been passed through the medial aspect of the bony avulsion was retrieved through the lateral portal. This wire was used to shuttle the repair suture from the laterally positioned SutureTak anchor over and through the medial aspect of the bony fragment out of the accessory superior medial (Figure 7).
Figure 7.
This suture was passed through the shuttling loop of the medially positioned SutureTak anchor to create the splice in the anchor for the adjustable fixation. This process was repeated through the lateral aspect of the bony fragment—the medial SutureTak repair suture was passed over the bone here. Thus, the lateral suture was over and through the bony fragment secured to the medial SutureTak anchor, and the medial suture was crossed over and through bone to the lateral SutureTak anchor. With the knee held in full extension, the bony avulsion fracture was easily reduced by alternating tension on the SutureTak limbs, which enabled controlled reduction of the TEA fracture (Figures 8A, 8B).
Figure 8.
An arthroscopic knot pusher was used for final tightening of the SutureTak fixation. An arthroscopic probe was used to confirm anatomical reduction of the fracture and restoration of ACL fiber tension (Figure 9).
Figure 9.
The knee was ranged from 0° to 120° of flexion with visual affirmation of the construct and maintenance of the reduction. Fluoroscopy confirmed anatomical reduction of the TEA fracture. The patient was immobilized in a long leg brace locked in 30° of flexion.

 

 

Follow-Up

Two weeks after surgery, the patient returned to clinic for suture removal. Four weeks after surgery, radiographs confirmed anatomical reduction of the TEA fracture, and outpatient physical therapy (range-of-motion exercises as tolerated) and isometric quadriceps strengthening were instituted. Twelve weeks after surgery, examination revealed full knee motion, negative Lachman and pivot shift test results, and residual quadriceps muscle atrophy, and radiographs confirmed complete fracture healing with maintenance of a normal proximal tibial growth plate (Figures 10A, 10B).

Figure 10.
Sixteen weeks after surgery, ligamentous examination findings were normal, and quadriceps muscle mass was good. In addition, on KT-1000 testing, the surgically repaired knee had only 1 more millimeter of laxity at the 30-pound pull, and equal displacement on the manual maximum test. The patient was allowed to return to full activities as tolerated.

Discussion

The highlight of this case is the simplicity of an excellent reduction of a displaced ACL-TEA fracture. Minimally invasive absorbable implants did not violate the proximal tibial physis, and the unique adjustable suture-tensioning technology allowed the degree of reduction and ACL tension to be “dialed in.” SutureTak implants have strong No. 2 FiberWire suture for excellent stability with an overall small suture load, and their small size avoids the risk of violating the proximal tibial physis and avoids potential growth disturbances.

Despite the obvious risks it poses to the open proximal tibial physis, surgical reduction of Meyers-McKeever type II and type III fractures is the norm for restoring ACL stability. Screws and suture fixation are the most common and reliable methods of TEA fracture reduction.16,17 In recent systematic reviews, however, Osti and colleagues17 and Gans and colleagues18 noted there is not enough evidence to warrant a “gold standard” in pediatric tibial avulsion cases.

Other fixation methods for TEA fractures must be investigated. Anderson and colleagues19 described the biomechanics of 4 different physeal-sparing avulsion fracture reduction techniques: an ultra-high-molecular-weight polyethylene (UHMWPE) suture-suture button, a suture anchor, a polydioxanone suture-suture button, and screw fixation. Using techniques described by Kocher and colleagues,4 Berg,20 Mah and colleagues,21 Vega and colleagues,22 and Lu and colleagues,23 Anderson and colleagues19 reduced TEA fractures in skeletally immature porcine knees. Compared with suture anchors, UHMWPE suture-suture buttons provided biomechanically superior cyclic and load-to-failure results as well as more consistent fixation.

Screw fixation has shown good results but has disadvantages. Incorrect positioning of a screw can lead to impingement and articular cartilage damage, and screw removal may be needed if discomfort at the fixation site persists.24,25 Likewise, screws generally are an option only for large fracture fragments, as there is an inherent risk of fracturing small TEA fractures, which can be common in skeletally immature patients.

Brunner and colleagues26 recently found that TEA fracture repair with absorbable sutures and distal bone bridge fixation yielded 3-month radiographic and clinical healing rates similar to those obtained with nonabsorbable sutures tied around a screw. However, other authors have reported growth disturbances with use of a similar technique, owing to a disturbance of the open proximal tibial growth plate.9 In that regard, a major advantage of this new knotless suturing technique is that distal fixation is not necessary.

The minimally invasive TEA fraction reduction technique described in this article has 6 advantages: It provides excellent fixation while avoiding proximal tibial growth plate injury; the degree of tensioning is easily controlled during reduction; it uses strong suture instead of metal screws or pins; the reduction construct is low-profile; distal fixation is unnecessary; and implant removal is unnecessary, thus limiting subsequent surgical intervention. With respect to long-term outcomes, however, it is not known how this procedure will compare with other commonly used ARIF methods in physeal-sparing techniques for TEA fracture fixation.

This case report highlights a novel pediatric displaced ACL-TEA fracture reduction technique that allows for adjustable reduction and resultant ACL tensioning with excellent strong suture fixation without violating the proximal tibial physis, which could make it invaluable in the surgical treatment of this injury in skeletally immature patients.

Am J Orthop. 2017;46(4):203-208. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

References

1. Eiskjaer S, Larsen ST, Schmidt MB. The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg. 1988;107(2):96-98.

2. Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23(2):199-202.

3. Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-225.

4. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19(10):1085-1090.

5. Lubowitz JH, Elson WS, Guttmann D. Part II: arthroscopic treatment of tibial plateau fractures: intercondylar eminence avulsion fractures. Arthroscopy. 2005;21(1):86-92.

6. Vargas B, Lutz N, Dutoit M, Zambelli PY. Nonunion after fracture of the anterior tibial spine: case report and review of the literature. J Pediatr Orthop B. 2009;18(2):90-92.

7. Sommerfeldt DW. Arthroscopically assisted internal fixation of avulsion fractures of the anterior cruciate ligament during childhood and adolescence [in German]. Oper Orthop Traumatol. 2008;20(4-5):310-320.

8. Wouters DB, de Graaf JS, Hemmer PH, Burgerhof JG, Kramer WL. The arthroscopic treatment of displaced tibial spine fractures in children and adolescents using Meniscus Arrows®. Knee Surg Sports Traumatol Arthrosc. 2011;19(5):736-739.

9. Ahn JH, Yoo JC. Clinical outcome of arthroscopic reduction and suture for displaced acute and chronic tibial spine fractures. Knee Surg Sports Traumatol Arthrosc. 2005;13(2):116-121.

10. Huang TW, Hsu KY, Cheng CY, et al. Arthroscopic suture fixation of tibial eminence avulsion fractures. Arthroscopy. 2008;24(11):1232-1238.

11. Liljeros K, Werner S, Janarv PM. Arthroscopic fixation of anterior tibial spine fractures with bioabsorbable nails in skeletally immature patients. Am J Sports Med. 2009;37(5):923-928.

12. Wiegand N, Naumov I, Vamhidy L, Not LG. Arthroscopic treatment of tibial spine fracture in children with a cannulated Herbert screw. Knee. 2014;21(2):481-485.

13. Faivre B, Benea H, Klouche S, Lespagnol F, Bauer T, Hardy P. An original arthroscopic fixation of adult’s tibial eminence fractures using the Tightrope® device: a report of 8 cases and review of literature. Knee. 2014;21(4):833-839.

14. Kluemper CT, Snyder GM, Coats AC, Johnson DL, Mair SD. Arthroscopic suture fixation of tibial eminence fractures. Orthopedics. 2013;36(11):e1401-e1406.

15. Ochiai S, Hagino T, Watanabe Y, Senga S, Haro H. One strategy for arthroscopic suture fixation of tibial intercondylar eminence fractures using the Meniscal Viper Repair System. Sports Med Arthrosc Rehabil Ther Technol. 2011;3:17.

16. Bogunovic L, Tarabichi M, Harris D, Wright R. Treatment of tibial eminence fractures: a systematic review. J Knee Surg. 2015;28(3):255-262.

17. Osti L, Buda M, Soldati F, Del Buono A, Osti R, Maffulli N. Arthroscopic treatment of tibial eminence fracture: a systematic review of different fixation methods. Br Med Bull. 2016;118(1):73-90.

18. Gans I, Baldwin KD, Ganley TJ. Treatment and management outcomes of tibial eminence fractures in pediatric patients: a systematic review. Am J Sports Med. 2014;42(7):1743-1750.

19. Anderson CN, Nyman JS, McCullough KA, et al. Biomechanical evaluation of physeal-sparing fixation methods in tibial eminence fractures. Am J Sports Med. 2013;41(7):1586-1594.

20. Berg EE. Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy. 1995;11(3):328-331.

21. Mah JY, Otsuka NY, McLean J. An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop. 1996;16(1):119-121.

22. Vega JR, Irribarra LA, Baar AK, Iniguez M, Salgado M, Gana N. Arthroscopic fixation of displaced tibial eminence fractures: a new growth plate-sparing method. Arthroscopy. 2008;24(11):1239-1243.

23. Lu XW, Hu XP, Jin C, Zhu T, Ding Y, Dai LY. Reduction and fixation of the avulsion fracture of the tibial eminence using mini-open technique. Knee Surg Sports Traumatol Arthrosc. 2010;18(11):1476-1480.

24. Bonin N, Jeunet L, Obert L, Dejour D. Adult tibial eminence fracture fixation: arthroscopic procedure using K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):857-862.

25. Senekovic V, Veselko M. Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy. 2003;19(1):54-61.

26. Brunner S, Vavken P, Kilger R, et al. Absorbable and non-absorbable suture fixation results in similar outcomes for tibial eminence fractures in children and adolescents. Knee Surg Sports Traumatol Arthrosc. 2016;24(3):723-729.

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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Authors’ Disclosure Statement: Dr. Miniaci reports that he receives financial support (consultant fees, speaker fees, honoraria, royalties, stock options) from Arthrosurface, Inc. Dr. Smucny reports no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Miniaci reports that he receives financial support (consultant fees, speaker fees, honoraria, royalties, stock options) from Arthrosurface, Inc. Dr. Smucny reports no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Miniaci reports that he receives financial support (consultant fees, speaker fees, honoraria, royalties, stock options) from Arthrosurface, Inc. Dr. Smucny reports no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Systematic Review of Novel Synovial Fluid Markers and Polymerase Chain Reaction in the Diagnosis of Prosthetic Joint Infection

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Systematic Review of Novel Synovial Fluid Markers and Polymerase Chain Reaction in the Diagnosis of Prosthetic Joint Infection

Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Maradit Kremers H, Larson DR, Crowson CS, et al. Prevalence of total hip and knee replacement in the United States. J Bone Joint Surg Am. 2015;97(17):1386-1397.

2. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

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Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Novel synovial markers and PCR have the potential to improve the detection of PJIs.
  • 10Difficult-to-detect infections of prosthetic joints pose a diagnostic problem to surgeons and can lead to suboptimal outcomes.
  • AD is a highly sensitive and specific synovial fluid marker for detecting PJIs.
  • AD has shown promising results in detecting low virulence organisms.
  • Studies are needed to determine how to best incorporate novel synovial markers and PCR to current diagnostic criteria in order to improve diagnostic accuracy.

Approximately 7 million Americans are living with a hip or knee replacement.1 According to projections, primary hip arthroplasties will increase by 174% and knee arthroplasties by 673% by 2030. Revision arthroplasties are projected to increase by 137% for hips and 601% for knees during the same time period.2 Infection and aseptic loosening are the most common causes of implant failure.3 The literature shows that infection is the most common cause of failure within 2 years after surgery and that aseptic loosening is the most common cause for late revision.3

Recent studies suggest that prosthetic joint infection (PJI) may be underreported because of difficulty making a diagnosis and that cases of aseptic loosening may in fact be attributable to infections with low-virulence organisms.2,3 These findings have led to new efforts to develop uniform criteria for diagnosing PJIs. In 2011, the Musculoskeletal Infection Society (MSIS) offered a new definition for PJI diagnosis, based on clinical and laboratory criteria, to increase the accuracy of PJI diagnosis.4 The MSIS committee acknowledged that PJI may be present even if these criteria are not met, particularly in the case of low-virulence organisms, as patients may not present with clinical signs of infection and may have normal inflammatory markers and joint aspirates. Reports of PJI cases misdiagnosed as aseptic loosening suggest that current screening and diagnostic tools are not sensitive enough to detect all infections and that PJI is likely underdiagnosed.

According to MSIS criteria, the diagnosis of PJI can be made when there is a sinus tract communicating with the prosthesis, when a pathogen is isolated by culture from 2 or more separate tissue or fluid samples obtained from the affected prosthetic joint, or when 4 of 6 criteria are met. The 6 criteria are (1) elevated serum erythrocyte sedimentation rate (ESR) (>30 mm/hour) and elevated C-reactive protein (CRP) level (>10 mg/L); (2) elevated synovial white blood cell (WBC) count (1100-4000 cells/μL); (3) elevated synovial polymorphonuclear leukocytes (>64%); (4) purulence in affected joint; (5) isolation of a microorganism in a culture of periprosthetic tissue or fluid; and (6) more than 5 neutrophils per high-power field in 5 high-power fields observed.

In this review article, we discuss recently developed novel synovial biomarkers and polymerase chain reaction (PCR) technologies that may help increase the sensitivity and specificity of diagnostic guidelines for PJI.

Methods

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), we performed a systematic review of specific synovial fluid markers and PCR used in PJI diagnosis. In May 2016, we searched the PubMed database for these criteria: ((((((PCR[Text Word]) OR IL-6[Text Word]) OR leukocyte esterase[Text Word]) OR alpha defensin[Text Word]) AND ((“infection/diagnosis”[MeSH Terms] OR “infection/surgery”[MeSH Terms])))) AND (prosthetic joint infection[MeSH Terms] OR periprosthetic joint infection[MeSH Terms]).

We included patients who had undergone total hip, knee, or shoulder arthroplasty (THA, TKA, TSA). Index tests were PCR and the synovial fluid markers α-defensin (AD), interleukin 6 (IL-6), and leukocyte esterase (LE). Reference tests included joint fluid/serum analysis or tissue analysis (ESR/CRP level, cell count, culture, frozen section), which defined the MSIS criteria for PJI. Primary outcomes of interest were sensitivity and specificity, and secondary outcomes of interest included positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (+LR), and negative likelihood ratio (–LR). Randomized controlled trials and controlled cohort studies in humans published within the past 10 years were included.

Results

Our full-text review yielded 15 papers that met our study inclusion criteria (Figure 1).

α-Defensin

One of the novel synovial biomarkers that has shown significant promise in diagnosing PJIs, even with difficult-to-detect organisms, is AD.

Figure 1.
Frangiamore and colleagues5 conducted a prospective study comparing patients with painful TSAs that required revision (n = 33). Patients were grouped based on objective clinical, laboratory, and histologic criteria of infection, which included preoperative clinical signs (swelling, sinus track, redness, drainage), elevated serum ESR or CRP, intraoperative gross findings (purulence, necrosis) and positive intraoperative frozen section. Synovial fluid aspiration was obtained preoperatively or intraoperatively. Of the 33 patients, 11 patients met the authors criteria for suspected PJI prior to final intraoperative culture results; 22 patients did not. Of the samples taken intraoperatively, Propionibacterium acnes was the most commonly isolated organism (9 cases), followed by coagulase-negative Staphylococcus (4 cases). AD demonstrated a sensitivity of 63%, specificity of 95%, +LR ratio of 12.1, and –LR ratio of 0.38. AD showed a strong association with growth of P acnes in the infected group (median signal-to-cutoff ratio, 4.45) compared with the noninfected group (median signal-to-cutoff ratio, 1.33) as well as strong associations with frozen section histology. Frangiamore and colleagues5 concluded that the use of AD in diagnosing PJIs with difficult-to-detect organisms was promising.

AD has shown even more impressive results as a biomarker for PJI in the hip and knee, where infection with low virulence organism is less common. In 2014, Deirmengian and colleagues6 conducted a prospective clinical study of 149 patients who underwent revision THA or TKA for aseptic loosening (n = 112) or PJI (n = 37) as defined by MSIS criteria. Aseptic loosening was diagnosed when there was no identifiable reason for pain, and MSIS criteria were not met. Synovial fluid aspirates were collected before or during surgery. AD correctly identified 143 of the 149 patients with confirmed infection with sensitivity of 97.3% (95% confidence interval [CI], 85.8%-99.6%) and specificity of 95.5% (95% CI, 89.9%-98.5%). Similarly, Bingham and colleagues7 conducted a retrospective clinical study of 61 assays done on 57 patients who underwent revision arthroplasty for PJI as defined by MSIS criteria. Synovial fluid aspirates were collected before or during surgery. AD correctly identified all 19 PJIs with sensitivity of 100% (95% CI, 79%-100%) and specificity of 95% (95% CI, 83%-99%). Sensitivity and specificity of the AD assay more accurately predicted infection than synovial cell count or serum ESR/CRP level did.

These results are supported by another prospective study by Deirmengian and colleagues8 differentiating aseptic failures and PJIs in THA or TKA. The sensitivity and specificity of AD in diagnosing PJI were 100% (95% CI, 85.05%-100%).

Table 1.
Synovial fluid was collected from 46 patients before and during surgery: 23 with PJI and 23 with aseptic failure as defined by MSIS criteria. All patients were tested for AD or LE. Of the 23 PJI cases, 18 were associated with a positive culture, with the most common organism being Staphylococcus epidermidis (n = 6). AD correctly diagnosed 100% of PJIs, whereas LE correctly diagnosed only 78%; the difference was statistically significant (P < 0.001).

In a prospective study of 102 patients who underwent revision THA or TKA secondary to aseptic loosening or PJI, Frangiamore and colleaguesalso demonstrated the value of AD as a diagnostic for PJI in primary and revision hip and knee arthroplasty.
Figure 2.
Based on MSIS criteria, 54 cases were classified as non-infected first-stage revision, 24 as infected first-stage revision, 35 as non-infected second-stage revision, and 3 as infected second-stage revision. For patients with first-stage revision THA or TKA, AD had sensitivity of 100% (95% CI, 86%-100%), specificity of 98% (95% CI, 90%-100%), PPV of 96% (95% CI, 80%-99%), and NPV of 100% (95% CI, 93%-100%). +LR was 54 (95% CI, 8-376), and –LR was 0. When combining all patients, AD outperformed serum ESR and CRP and synovial cell count as a biomarker for predicting PJI.

Table 1 and Figure 2 provide a concise review of the findings of each study.

Interleukin 6

Another synovial fluid biomarker that has shown promise in PJI diagnosis is IL-6. In 2015, Frangiamore and colleagues10 conducted a prospective clinical study of 32 patients who underwent revision TSA. Synovial fluid aspiration was obtained before or during surgery. MSIS criteria were used to establish the diagnosis of PJI. IL-6 had sensitivity of 87% and specificity of 90%, with +LR of 8.45 and –LR of 0.15 in predicting PJI. Synovial fluid IL-6 had strong associations with frozen section histology and growth of P acnes. Frangiamore and colleagues10 recommended an ideal IL-6 cutoff of 359.1 pg/mL and reported that, though not as accurate as AD, synovial fluid IL-6 levels can help predict positive cultures in patients who undergo revision TSA.

Lenski and Scherer11 conducted another retrospective clinical study of the diagnostic value of IL-6 in PJI.

Table 2.
Revision total joint arthroplasty (TJA) was performed for aseptic loosening (38 patients) or PJI (31 patients) based on criteria modeled after MSIS criteria. All joints were aspirated for synovial fluid IL-6, synovial fluid lactate dehydrogenase, synovial fluid glucose, synovial fluid lactate, synovial fluid WBCs, and serum CRP. IL-6 had sensitivity of 90.9%, specificity of 94.7%, +LR of 17.27, and –LR of 0.10. An optimal IL-6 cutoff value of 30,750 pg/mL was determined.

Randau and colleagues12 conducted a prospective clinical study of 120 patients who presented with painful THA or TKA and underwent revision for PJI, aseptic failure, or aseptic revision without signs of infection or loosening. Synovial fluid aspirate was collected before or during surgery.
Figure 3.
PJI was diagnosed with the modified MSIS criteria. IL-6 sensitivity and specificity depended on the cutoff value. A cutoff of >2100 pg/mL yielded sensitivity of 62.5% (95% CI, 43.69%-78.9%) and specificity of 85.71% (95% CI, 71.46%-94.57%), and a cutoff of >9000 pg/mL yielded sensitivity of 46.9% (95% CI, 29.09%-65.26%) and specificity of 97.62% (95% CI, 87.43%-99.94%). The authors concluded that synovial IL-6 is a more accurate marker than synovial WBC count.

Table 2 and Figure 3 provide a concise review of the findings of each study.

Leukocyte Esterase

LE strips are an inexpensive screening tool for PJI, according to some studies. In a prospective clinical study of 364 endoprosthetic joint (hip, knee, shoulder) interventions, Guenther and colleagues13 collected synovial fluid before surgery. Samples were tested with graded LE strips using PJI criteria set by the authors. Results were correlated with preoperative synovial fluid aspirations, serum CRP level, serum WBC count, and intraoperative histopathologic and microbiological findings. Whereas 293 (93.31%) of the 314 aseptic cases had negative test strip readings, 100% of the 50 infected cases were positive. LE had sensitivity of 100%, specificity of 96.5%, PPV of 82%, and NPV of 100%.

Wetters et al14 performed a prospective clinical study on 223 patients who underwent TKAs and THAs for suspected PJI based on having criteria defined by the authors of the study. Synovial fluid samples were collected either preoperatively or intraoperatively.

Table 3.
Using a synovial fluid WBC >3k WBC per microliter, the sensitivity, specificity, PPV, and NPV were 92.9%, 88.8%, 75%, and 97.2%, respectively. Using positive cultures or the presence of a draining sinus tract, the sensitivity, specificity, PPV, and NPV were 93.3%, 77%, 37.8%, and 98.7%, respectively. Of note, the most common organism found at the time of revision for infection was coagulase-negative Staphylococcus (6 out of 39).

Other authors have reported different findings that LE is an unreliable marker in PJI diagnosis. In one prospective clinical study of 85 patients who underwent primary or revision TSA, synovial fluid was collected during surgery.15 According to MSIS criteria, only 5 positive LE results predicted PJI among 21 primary and revision patients with positive cultures. Of the 7 revision patients who met the MSIS criteria for PJI, only 2 had a positive LE test. LE had sensitivity of 28.6%, specificity of 63.6%, PPV of 28.6%, and NPV of 87.5%. Six of the 7 revision patients grew P acnes. These results showed that LE was unreliable in detecting shoulder PJI.15

In another prospective clinical study, Tischler and colleagues16 enrolled 189 patients who underwent revision TKA or THA for aseptic failure or PJI as defined by the MSIS criteria. Synovial fluid was collected intraoperatively.
Figure 4.
Fifteen of the 52 patients with a MSIS defined PJI had positive cultures with the most common organism being coagulase-negative Staphylococcus (7). Two thresholds were used to consider a positive LE test. When using the first threshold that had a lower acceptance level for positivity, the sensitivity, specificity, PPV, and NPV were 79.2% (95% CI, 65.9%-89.2%), 80.8 (95% CI, 73.3%-87.1%), 61.8% (95% CI, 49.2%-73.3%), and 90.1% (95% CI, 84.3%-95.4%), respectively. When using the higher threshold, the sensitivity, specificity, PPV, and NPV were 66% (95% CI, 51.7%-78.5%), 97.1% (95% CI, 92.6%-99.2%), 89.7% (95% CI, 75.8%-97.1%), and 88% (95% CI, 81.7%-92.7%), respectively. Once again, these results were in line with LE not being a reliable marker in diagnosing PJI.

Table 3 and Figure 4 provide a concise review of the findings of each study.

 

 

Polymerase Chain Reaction

Studies have found that PCR analysis of synovial fluid is effective in detecting bacteria on the surface of implants removed during revision arthroplasties. Comparison of the 16S rRNA gene sequences of bacterial genomes showed a diverse range of bacterial species within biofilms on the surface of clinical and subclinical infections.17 These findings, along with those of other studies, suggest that PCR analysis of synovial fluid is useful in diagnosing PJI and identifying organisms and their sensitivities to antibiotics.

Gallo and colleagues18 performed a prospective clinical study on 115 patients who underwent revision TKAs or THAs. Synovial fluid was collected intraoperatively. PCR assays targeting the 16S rDNA were carried out on 101 patients. PJIs were classified based on criteria of the authors of this study, of which there were 42. The sensitivity, specificity, PPV, NPV, +LR, and -LR for PCR were 71.4% (95% CI, 61.5%-75.5%), 97% (95% CI, 91.7%-99.1%), 92.6% (95% CI, 79.8%-97.9%), 86.5% (95% CI, 81.8%-88.4%), 23.6 (95% CI, 5.9%-93.8%), and 0.29 (95% CI, 0.17%-0.49%), respectively. Of note the most common organism detected in 42 PJIs was coagulase-negative Staphylococcus.

Marin and colleagues19 conducted a prospective study of 122 patients who underwent arthroplasty for suspected infection or aseptic loosening as defined by the authors’ clinicohistopathologic criteria. Synovial fluid and biopsy specimens were collected during surgery, and 40 patients met the infection criteria. The authors concluded that 16S PCR is more specific and has better PPV than culture does as one positive 16S PCR resulted in a specificity and PPV of PJI of 96.3% and 91.7%, respectively. However, they noted that culture was more sensitive in diagnosing PJI.

Jacovides and colleagues20 conducted a prospective study on 82 patients undergoing primary TKA, revision TKA, and revision THA.

Table 4.
The synovial fluid aspirate was collected intraoperatively. PJI was diagnosed based on study specific criteria, which was a combination of clinical suspicion and standard laboratory tests (ESR, CRP, cell count and tissue culture). Using the study’s criteria, PJI was diagnosed in 23 samples, and 57 samples were diagnosed as uninfected. When 1 or more species were present, the PCR-Electrospray Ionization Mass Spectrometry (PCR-ESI/MS) yielded a sensitivity, specificity, PPV, and NPV value of 95.7%, 12.3%, 30.6%, and 87.5%, respectively.

The low PCR sensitivities reported in the literature were explained in a review by Hartley and Harris.21 They wrote that BR 16S rDNA and sequencing of PJI samples inherently have low sensitivity because of the contamination that can occur from the PCR reagents themselves or from sample mishandling. Techniques that address contaminant (extraneous DNA) removal, such as ultraviolet irradiation and DNase treatment, reduce Taq DNA polymerase activity, which reduces PCR sensitivity.
Figure 5.
The simplest way to avoid the effects of “low-level contaminants” is to decrease the number of PCR cycles, which also reduces sensitivity. However, loss of contaminants has resulted in increased specificities in studies that have used BR 16S rDNA PCR. The authors also stated that, when PCR incorporates cloning and sequencing, mass spectroscopic detection, or species-specific PCR, sensitivity is higher with increased contamination.

Table 4 and Figure 5 provide a concise review of the findings of each study.

Discussion

Although there is no gold standard for the diagnosis of PJIs, several clinical and laboratory criteria guidelines are currently used to help clinicians diagnose infections of prosthetic joints. However, despite standardization of diagnostic criteria, PJI continue to be a diagnostic challenge.

Table 5.
Diagnosing PJI has been difficult for several reasons, including lack of highly sensitive and specific clinical findings and laboratory tests, as well as difficulty in culturing organisms, particularly fastidious organisms. More effective diagnostic tools are needed to avoid failing to accurately detect infections which lead to poor outcomes in patients who undergo TJA. Moreover, PJIs with low-virulence organisms are especially troublesome, as they can present with normal serum inflammatory markers and negative synovial fluid analysis and cultures from joint aspiration.22

AD is a highly sensitive and specific synovial fluid biomarker in detecting common PJIs.

Table 6.
AD has a higher sensitivity and specificity for detecting PJI, as compared to synovial fluid cell count, culture, ESR, and CRP.15,16,19 Moreover, it has been shown that as many as 38% to 88% of patients diagnosed with aseptic loosening have PJIs with low-grade organisms,23,24 such as Coagulase-negative S acnes and P acnes. Several studies reviewed in this article have demonstrated that AD can detect infections with these low virulence organisms. Our systematic review supports the claim that AD can potentially be used as a screening tool for PJI with common, as well as difficult-to-detect, organisms.
Figure 6.
Our findings also support the claim that novel synovial fluid biomarkers have the potential to become of significant diagnostic use and help improve the ability to diagnose PJIs when combined with current laboratory and clinical diagnostic criteria.

In summary, 5 AD studies5-9 had sensitivity ranging from 63% to 100% and specificity ranging from 95% to 100%; 3 IL-6 studies10-12 had sensitivity ranging from 46.8% to 90.9% and specificity ranging from 85.7% to 97.6%; 4 LE studies13-16 had sensitivity ranging from 28.6% to 100% and specificity ranging from 63.6% to 96.5%; and 3 PCR studies18-20 had sensitivity ranging from 67.1% to 95.7% and specificity ranging from 12.3% to 97.8%. Sensitivity and specificity were consistently higher for AD than for IL-6, LE, and PCR, though there was significant overlap, heterogeneity, and variation across all the included studies.
Figure 7.
Moreover, the outlier study with the lowest sensitivity for AD (63%) was in patients undergoing TSA, where P acnes infection is more common and has been reported to be more difficult to detect by standard diagnostic tools. Tables 5, 6 and Figures 6, 7 provide the data for each of these studies.

Although the overall incidence of PJI is low, infected revisions remain a substantial financial burden to hospitals, as annual costs of infected revisions is estimated to exceed $1.62 billion by 2020.25 The usefulness of novel biomarkers and PCR in diagnosing PJI can be found in their ability to diagnose infections and facilitate appropriate early treatment. Several of these tests are readily available commercially and have the potential to be cost-effective diagnostic tools. The price to perform an AD test from Synovasure TM (Zimmer Biomet) ranges from $93 to $143. LE also provides an economic option for diagnosing PJI, as LE strips are commercially available for the cost of about 25 cents. PCR has also become an economic option, as costs can average $15.50 per sample extraction or PCR assay and $42.50 per amplicon sequence as reported in a study by Vandercam and colleagues.26 Future studies are needed to determine a diagnostic algorithm which incorporates these novel synovial markers to improve diagnostic accuracy of PJI in the most cost effective manner.

The current literature supports that AD can potentially be used to screen for PJI. Our findings suggest novel synovial fluid biomarkers may become of significant diagnostic use when combined with current laboratory and clinical diagnostic criteria. We recommend use of AD in cases in which pain, stiffness, and poor TJA outcome cannot be explained by errors in surgical technique, and infection is suspected despite MSIS criteria not being met.

The studies reviewed in this manuscript were limited in that none presented level I evidence (12 had level II evidence, and 3 had level III evidence), and there was significant heterogeneity (some studies used their own diagnostic standard, and others used the MSIS criteria). Larger scale prospective studies comparing serum ESR/CRP level and synovial fluid analysis to novel synovial markers are needed.

Am J Orthop. 2017;46(4):190-198. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

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3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

References

1. Maradit Kremers H, Larson DR, Crowson CS, et al. Prevalence of total hip and knee replacement in the United States. J Bone Joint Surg Am. 2015;97(17):1386-1397.

2. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785.

3. Sharkey PF, Lichstein PM, Shen C, Tokarski AT, Parvizi J. Why are total knee arthroplasties failing today—has anything changed after 10 years? J Arthroplasty. 2014;29(9):1774-1778.

4. Butler-Wu SM, Burns EM, Pottinger PS, et al. Optimization of periprosthetic culture for diagnosis of Propionibacterium acnes prosthetic joint infection. J Clin Microbiol. 2011;49(7):2490-2495.

5. Frangiamore SJ, Saleh A, Grosso MJ, et al. α-Defensin as a predictor of periprosthetic shoulder infection. J Shoulder Elbow Surg. 2015;24(7):1021-1027.

6. Deirmengian C, Kardos K, Kilmartin P, Cameron A, Schiller K, Parvizi J. Combined measurement of synovial fluid α-defensin and C-reactive protein levels: highly accurate for diagnosing periprosthetic joint infection. J Bone Joint Surg Am. 2014;96(17):1439-1445.

7. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009.

8. Deirmengian C, Kardos K, Kilmartin P, et al. The alpha-defensin test for periprosthetic joint infection outperforms the leukocyte esterase test strip. Clin Orthop Relat Res. 2015;473(1):198-203.

9. Frangiamore SJ, Gajewski ND, Saleh A, Farias-Kovac M, Barsoum WK, Higuera CA. α-Defensin accuracy to diagnose periprosthetic joint infection—best available test? J Arthroplasty. 2016;31(2):456-460.

10. Frangiamore SJ, Saleh A, Kovac MF, et al. Synovial fluid interleukin-6 as a predictor of periprosthetic shoulder infection. J Bone Joint Surg Am. 2015;97(1):63-70.

11. Lenski M, Scherer MA. Synovial IL-6 as inflammatory marker in periprosthetic joint infections. J Arthroplasty. 2014;29(6):1105-1109.

12. Randau TM, Friedrich MJ, Wimmer MD, et al. Interleukin-6 in serum and in synovial fluid enhances the differentiation between periprosthetic joint infection and aseptic loosening. PLoS One. 2014;9(2):e89045.

13. Guenther D, Kokenge T, Jacobs O, et al. Excluding infections in arthroplasty using leucocyte esterase test. Int Orthop. 2014;38(11):2385-2390.

14. Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty. 2012;27(8 suppl):8-11.

15. Nelson GN, Paxton ES, Narzikul A, Williams G, Lazarus MD, Abboud JA. Leukocyte esterase in the diagnosis of shoulder periprosthetic joint infection. J Shoulder Elbow Surg. 2015;24(9):1421-1426.

16. Tischler EH, Cavanaugh PK, Parvizi J. Leukocyte esterase strip test: matched for Musculoskeletal Infection Society criteria. J Bone Joint Surg Am. 2014;96(22):1917-1920.

17. Dempsey KE, Riggio MP, Lennon A, et al. Identification of bacteria on the surface of clinically infected and non-infected prosthetic hip joints removed during revision arthroplasties by 16S rRNA gene sequencing and by microbiological culture. Arthritis Res Ther. 2007;9(3):R46.

18. Gallo J, Kolar M, Dendis M, et al. Culture and PCR analysis of joint fluid in the diagnosis of prosthetic joint infection. New Microbiol. 2008;31(1):97-104.

19. Marin M, Garcia-Lechuz JM, Alonso P, et al. Role of universal 16S rRNA gene PCR and sequencing in diagnosis of prosthetic joint infection. J Clin Microbiol. 2012;50(3):583-589.

20. Jacovides CL, Kreft R, Adeli B, Hozack B, Ehrlich GD, Parvizi J. Successful identification of pathogens by polymerase chain reaction (PCR)-based electron spray ionization time-of-flight mass spectrometry (ESI-TOF-MS) in culture-negative periprosthetic joint infection. J Bone Joint Surg Am. 2012;94(24):2247-2254.

21. Hartley JC, Harris KA. Molecular techniques for diagnosing prosthetic joint infections. J Antimicrob Chemother. 2014;69(suppl 1):i21-i24.

22. Zappe B, Graf S, Ochsner PE, Zimmerli W, Sendi P. Propionibacterium spp. in prosthetic joint infections: a diagnostic challenge. Arch Orthop Trauma Surg. 2008;128(10):1039-1046.

23. Rasouli MR, Harandi AA, Adeli B, Purtill JJ, Parvizi J. Revision total knee arthroplasty: infection should be ruled out in all cases. J Arthroplasty. 2012;27(6):1239-1243.e1-e2.

24. Hunt RW, Bond MJ, Pater GD. Psychological responses to cancer: a case for cancer support groups. Community Health Stud. 1990;14(1):35-38.

25. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty. 2008;23(7):984-991.

26. Vandercam B, Jeumont S, Cornu O, et al. Amplification-based DNA analysis in the diagnosis of prosthetic joint infection. J Mol Diagn. 2008;10(6):537-543.

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Traumatic Anterior Shoulder Instability: The US Military Experience

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Traumatic Anterior Shoulder Instability: The US Military Experience

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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Bone Stress Injuries in the Military: Diagnosis, Management, and Prevention

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Bone Stress Injuries in the Military: Diagnosis, Management, and Prevention

Take-Home Points

  • Stress injuries, specifically of the lower extremity, are very common in new military trainees.
  • Stress injury can range from benign periosteal reaction to displaced fracture.
  • Stress injury should be treated on a case-by-case basis, depending on the severity of injury, the location of the injury, and the likelihood of healing with nonoperative management.
  • Modifiable risk factors such as nutritional status, training regiment, and even footwear should be investigated to determine potential causes of injury.
  • Prevention is a crucial part of the treatment of these injuries, and early intervention such as careful pre-enrollment physicals and vitamin supplementation can be essential in lowering injury rates.

Bone stress injuries, which are common in military recruits, present in weight-bearing (WB) areas as indolent pain caused by repetitive stress and microtrauma. They were first reported in the metatarsals of Prussian soldiers in 1855.1 Today, stress injuries are increasingly common. One study estimated they account for 10% of patients seen by sports medicine practitioners.2 This injury most commonly affects military members, endurance athletes, and dancers.3-5 Specifically, the incidence of stress fractures in military members has been reported to range from 0.8% to 6.9% for men and from 3.4% to 21.0% for women.4 Because of repetitive vigorous lower extremity loading, stress fractures typically occur in the pelvis, femoral neck, tibial shaft, and metatarsals. Delayed diagnosis and the subsequent duration of treatment required for adequate healing can result in significant morbidity. In a 2009 to 2012 study of US military members, Waterman and colleagues6 found an incidence rate of 5.69 stress fractures per 1000 person-years. Fractures most frequently involved the tibia/fibula (2.26/1000), followed by the metatarsals (0.92/1000) and the femoral neck (0.49/1000).6 In addition, these injuries were most commonly encountered in new recruits, who were less accustomed to the high-volume, high-intensity training required during basic training.4,7 Enlisted junior service members have been reported to account for 77.5% of all stress fractures.6 Age under 20 years or over 40 years and white race have also been found to be risk factors for stress injury.6

The pathogenesis of stress injury is controversial. Stanitski and colleagues8 theorized that multiple submaximal mechanical insults create cumulative stress greater than bone capacity, eventually leading to fracture. Johnson9 conducted a biopsy study and postulated that an accelerated remodeling phase was responsible, whereas Friedenberg10 argued that stress injuries are a form of reduced healing, not an attempt to increase healing, caused by the absence of callous formation in the disease process.

Various other nonmodifiable and modifiable risk factors predispose military service members to stress injury. Nonmodifiable risk factors include sex, bone geometry, limb alignment, race, age, and anatomy. Lower extremity movement biomechanics resulting from dynamic limb alignment during activity may be important. Cameron and colleagues11 examined 1843 patients and found that those with knees in >5° of valgus or >5° of external rotation had higher injury rates. Although variables such as sex and limb alignment cannot be changed, proper identification of modifiable risk factors can assist with injury prevention, and nonmodifiable risk factors can help clinicians and researchers target injury prevention interventions to patients at highest risk.

Metabolic, hormonal, and nutritional status is crucial to overall bone health. Multiple studies have found that low body mass index (BMI) is a significant risk factor for stress fracture.7,12,13 Although low BMI is a concern, patients with abnormally high BMI may also be at increased risk for bone stress injury. In a recently released consensus statement on relative energy deficiency in sport (RED-S), the International Olympic Committee addressed the complex interplay of impairments in physiologic function—including metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health—caused by relative energy deficiency.14 The committee stated that the cause of this syndrome is energy deficiency relative to the balance between dietary energy intake and energy expenditure required for health and activities of daily living, growth, and sporting activities. This finding reveals that conditions such as stress injury often may represent a much broader systemic deficit that may be influenced by a patient’s overall physiologic imbalance.

Diagnosis

History and Physical Examination

The onset of stress reaction typically is insidious, with the classic presentation being a new military recruit who is experiencing a sudden increase in pain during physical activity.15 Pain typically is initially present only during activity, and is relieved with rest, but with disease progression this evolves to pain at rest. It is crucial that the physician elicit the patient’s history of training and physical activity. Hsu and colleagues7 reported increased prevalence of overweight civilian recruits, indicating an increase in the number of new recruits having limited experience with the repetitive physical activity encountered in basic training. Stress injury should be suspected in the setting of worsening, indolent lower extremity pain that has been present for several days, especially in the higher-risk patient populations mentioned. Diet should be assessed, with specific attention given to the intake of fruits, vegetables, and foods high in vitamin D and calcium and, most important, the energy balance between intake and output.16 Special attention should also be given to female patients, who may experience the female athlete triad, a spectrum of low energy availability, menstrual dysfunction, and impaired bone turnover (high amount of resorption relative to formation). A key part of the RED-S consensus statement14 alerted healthcare providers that metabolic derangements do not solely affect female patients. These types of patients sustain a major insult to the homeostatic balance of the hormones that sustain adequate bone health. Beck and colleagues17 found that women with disrupted menstrual cycles are 2 to 4 times more likely to sustain a stress fracture than women without disrupted menstrual cycles, making this abnormality an important part of the history.

Examination should begin with careful evaluation of limb alignment and specific attention given to varus or valgus alignment of the knees.11 The feet should also be inspected, as pes planus or cavus foot may increase the risk of stress fracture.18 Identification of the area of maximal tenderness is important. The area in question may also be erythematous or warm secondary to the inflammatory response associated with attempted fracture healing. In chronic fractures in superficial areas such as the metatarsals, callus may be palpable. Although there are few specific tests for stress injury, pain may be reproducible with deep palpation and WB.

Figure 1.
If a femoral fracture is suspected, the fulcrum test can be performed by applying downward pressure on the patient’s knee while levering the thigh over the examiner’s opposite arm or thigh (Figure 1).19 Patients with sacral stress fractures may have pain when standing or hopping on the affected side (positive flamingo test).20

Laboratory Testing

When a pathology is thought to have a nutritional or metabolic cause, particularly in a low-weight or underweight patient, a laboratory workup should be obtained. Specific laboratory tests that all patients should undergo are 25-hydroxyvitamin D3, complete blood cell count, and basic chemistry panel, including calcium and thyroid-stimulating hormone levels. Although not necessary for diagnosis, phosphate, parathyroid hormone, albumin, and prealbumin should also be considered. Females should undergo testing of follicle stimulating hormone, luteinizing hormone, estradiol, and testosterone and have a urine pregnancy test. In patients with signs of excessive cortisone, a dexamethasone suppression test can be administered.21 In males, low testosterone is a documented risk factor for stress injury.22

Imaging

Given their low cost and availability, plain radiographs typically are used for initial examination of a suspected stress injury. However, they often lack sensitivity, particularly in the early stages of stress fracture development (Figure 2).

Figure 2.
Although a fracture line or callus formation is present occasionally, findings may be subtler. Images should be inspected for blunting of cortical bone and periosteal reaction, which should be correlated with the site of maximal tenderness.11 When there is high clinical suspicion based on history and physical examination, but radiographs are negative, magnetic resonance imaging (MRI) or bone scan can be useful.23 MRI is the most accurate imaging modality, with sensitivity ranging from 86% to 100% and specificity as high as 100%.2,24,25 On MRI, stress fractures typically are seen as bright areas of increased edema. Arendt and Griffiths24 proposed an MRI-based grading system for stress fractures, with grades 1 and 2 representing low-grade injuries, and 3 and 4 representing high grade. Computed tomography (CT) also has a role in diagnosis and may be better than MRI in imaging stress fractures in the pelvis and sacrum.2 In a study involving tibial stress fractures, Gaeta and colleagues26 found MRI was 88% sensitive and 100% specific and had a positive predictive value of 100%, and CT was 42% sensitive and 100% specific and had a positive predictive value of 100%. They concluded MRI was superior to CT in the diagnosis of tibial stress fractures.

Management

Management of bone stress injury depends on many factors, including symptom duration, fracture location and severity, and risk of progression or nonunion (Table).13

Table.
Patients thought to have an underlying metabolic or nutritional derangement should be treated accordingly. Injuries with a low risk of nonunion or further displacement typically can be managed with a period of modified physical activity or reduced or non-WB (NWB) ambulation; higher risk injuries may require operative intervention.5

 

 

Pelvis

Pelvic stress fractures are rare and represent only 1.6% to 7.1% of all stress fractures.13,27,28 Given the low frequency, physicians must have a high index of suspicion to make the correct diagnosis. These fractures typically occur in marathon runners and other patients who present with persistent pain and a history of high levels of activity. As pelvic stress fractures typically involve the superior or inferior pubic rami, or sacrum, and are at low risk for nonunion,13 most are managed with nonoperative treatment and activity modification for 8 to 12 weeks.27

Femur

Femoral stress fractures are also relatively uncommon, accounting for about 10% of all stress fractures. Depending on their location, these fractures can be at high risk for progression, nonunion, and significant morbidity.29 Especially concerning are femoral neck stress fractures, which can involve either the tension side (lateral cortex) or the compression side (medial cortex) of the bone. Suspicion of a femoral neck stress fracture should prompt immediate NWB.5 Early recognition of these injuries is crucial because once displacement occurs, their complication and morbidity rates become high.13 Patients with compression-side fractures should undergo NWB treatment for 4 to 6 weeks and then slow progression to WB activity. Most return to light-impact activity by 3 to 4 months. By contrast, tension-side fractures are less likely to heal without operative intervention.11 All tension-side fractures (and any compression-side fractures >50% of the width of the femoral neck) should be treated with percutaneous placement of cannulated screws (Figure 3).

Figure 3.
Displaced fractures should be addressed urgently with open reduction and internal fixation to avoid avascular necrosis and other long-term sequelae.5 Results of operative treatment of femoral neck fractures in active individuals have been mixed. Neubauer and colleagues30 examined 48 runners who underwent surgical fixation for these injuries. Preinjury activity levels were resumed by a higher percentage of low-performance runners (72%, 23/32) than low-performance runners (31%, 5/16). Reporting on femoral neck stress fracture outcomes in Royal Marine recruits, Evans and colleagues31 found that, after operative intervention, all fractures united by 11 months on average. However, union in 50% of fractures took more than 1 year, revealing the difficulty in managing these injuries as well as the lengthy resulting disability.

Stress fractures of the femoral shaft are less common than those of the femoral neck and represent as little as 3% of all stress fractures.32 However, femoral shaft stress fractures are more common in military populations. In French military recruits, Niva and colleagues33 found an 18% incidence. Similar to femoral neck fractures, femoral shaft fractures typically are diagnosed with advanced imaging, though the fulcrum test and pain on WB can aid in the diagnosis.19 These injuries are often managed nonoperatively with NWB for a period. Weishaar and colleagues34 described US military cadets treated with progressive rehabilitation who returned to full activity within 12 weeks. Displaced femoral shaft fractures associated with bone stress injury are even less common, and should be managed operatively. Salminen and colleagues35 found an incidence of 1.5 fractures per 100,000 years of military service. Over a 20-year period, they surgically treated 10 of these fractures. Average time from intramedullary nailing to union was 3.5 months.

Tibia

The tibia is one of the more common locations for stress injury and fracture. In a prospective study with members of the military, Giladi and colleagues36 found that 71% of stress fractures were tibia fractures. In addition, a large study of 320 athletes with stress fractures found 49.1% in the tibia.37 Fractures typically are diaphyseal and transverse, usually occurring along the posteromedial cortex, where the bone experiences maximal compressive forces (Figure 4).5,13

Figure 4.
Fractures on the anterior cortex—thought to result from tensile forces applied by the large posterior musculature of the gastrocnemius during repetitive activity38—are more concerning.
Figure 5.
Compared with fractures on the compression side, fractures of the anterior tibial cortex are at higher risk for nonunion (reported nonunion rate, 4.6%).39 Radiographs of anterior tibial cortex fractures may show the “dreaded black line” (Figure 5).

Compression-side fractures often heal with nonoperative management, though healing may take several months. Swenson and colleagues40 studied the effects of pneumatic bracing on conservative management and return to play in athletes with tibial stress fractures. Patients with bracing returned to light activity within 7 days and full activity within 21 days, whereas those without bracing returned to light activity within 21 days and full activity within 77 days. Pulsed electromagnetic therapy is of controversial benefit in the management of these injuries. Rettig and colleagues41 conducted a prospective randomized trial in the treatment of US Navy midshipmen and found no reduction in healing time in those who underwent electromagnetic therapy. Stress fractures with displacement and fractures that have failed nonoperative treatment should undergo surgery. Reamed intramedullary nailing is the gold standard of operative management of these injuries.5 Varner and colleagues42 reported the outcomes of treating 11 tibial stress fractures with intramedullary nailing after nonoperative management (4 months minimum) had failed. With surgery, the union rate was 100%, and patients returned to full activity by a mean of 4 months.

Metatarsals

Stress fractures were first discovered by Briethaupt1 in the painful swollen feet of Prussian army members in 1855 and were initially named march fractures. Waterman and colleagues6 reported that metatarsal stress fractures accounted for 16% of all stress fractures in the US military between 2009 and 2012. The second metatarsal neck is the most common location for stress fractures, followed by the third and fourth metatarsals, with the fifth metatarsal being the least common.5 The second metatarsal is thought to sustain these injuries more often than the other metatarsals because of its relative lack of immobility. Donahue and Sharkey43 found that the dorsal aspect of the second metatarsal experiences twice the amount of strain experienced by the fifth metatarsal during gait, and that peak strain in the second metatarsal was further increased by simulated muscle fatigue. The risk of stress fracture can be additionally increased with use of minimalist footwear, as shown by Giuliani and colleagues,44 particularly in the absence of a progressive transition in gait and training volume with a change toward minimalist footwear. In patients with a suspected or confirmed fracture of the second, third, or fourth metatarsal, treatment typically is NWB and immobilization for at least 4 weeks.5 Fifth metatarsal stress injuries (Figure 2) typically are treated differently because of their higher risk of nonunion. Patients with a fifth metatarsal stress fracture complain of lateral midfoot pain with running and jumping. For those who present with this fracture early, acceptable treatment consists of 6 weeks of casting and NWB.5 In cases of failed nonoperative therapy, or presentation with radiographic evidence of nonunion, treatment should be intramedullary screw fixation, with bone graft supplementation based on surgeon preference. DeLee and colleagues45 reported on the results of 10 athletes with fifth metatarsal stress fractures treated with intramedullary screw fixation without bone grafting. All 10 experienced fracture union, at a mean of 7.5 weeks, and returned to sport within 8.5 weeks. One complication with this procedure is pain at the screw insertion site, but this can be successfully managed with footwear modification.45

Prevention

Proper identification of patients at high risk for stress injuries has the potential of reducing the incidence of these injuries. Lappe and colleagues46 prospectively examined female army recruits before and after 8 weeks of basic training and found that those who developed a stress fracture were more likely to have a smoking history, to drink more than 10 alcoholic beverages a week, to have a history of corticosteroid or depot medroxyprogesterone use, and to have lower body weight. In addition, the authors found that a history of prolonged exercise before enrollment was protective against fracture. This finding identifies the importance of having new recruits undergo risk factor screening, which could result in adjusting training regimens to try to reduce injury. The RED-S consensus statement14 offers a comprehensive description of the physiologic factors that can contribute to such injury. Similar to proper risk factor identification, implementation of proper exercise progression programs is a simple, modifiable method of limiting stress injuries. For new recruits or athletes who are resuming activity, injury can be effectively prevented by adjusting the frequency, duration, and intensity of training and the training loads used.47

Vitamin D and calcium supplementation is a simple intervention that can be helpful in injury prevention, and its use has very little downside. A double-blind study found a 20% lower incidence of stress fracture in female navy recruits who took 2000 mg of calcium and 800 IU of vitamin D as daily supplemention.48 Of importance, a meta-analysis of more than 65,000 patients found vitamin D supplementation was effective in reducing fracture risk only when combined with calcium, irrespective of age, sex, or prior fracture.49 In female patients with the female athlete triad, psychological counseling and nutritional consultation are essential in bone health maintenance and long-term prevention.50 Other therapies have been evaluated as well. Use of bisphosphonates is controversial for both treatment and prevention of stress fractures. In a randomized, double-blind study of the potential prophylactic effects of risedronate in 324 new infantry recruits, Milgrom and colleagues51 found no statistically significant differences in tibial, femoral, metatarsal, or total stress fracture incidence between the treatment and placebo groups. Therefore, bisphosphonates are seldom recommended as prevention or in primary management of stress fracture.

In addition to nutritional and pharmacologic therapy, activity modification may have a role in injury prevention. Gait retraining has been identified as a potential intervention for reducing stress fractures in patients with poor biomechanics.47 Crowell and Davis52 investigated the effect of gait retraining on the forces operating in the tibia in runners. After 1 month of gait retraining, tibial acceleration while running decreased by 50%, vertical force loading rate by 30%, and peak vertical force impact by 20%. Such studies indicate the importance of proper mechanics during repetitive activity, especially in patients not as accustomed to the rigorous training methods used with new military recruits. However, whether these reduced loads translate into reduced risk of stress fracture remains unclear. In addition, biomechanical shoe orthoses may lower the stress fracture risk in military recruits by reducing peak tibial strain.53 Warden and colleagues54 found a mechanical loading program was effective in enchaining the structural properties of bone in rats, leading the authors to hypothesize that a similar program aimed at modifying bone structure in humans could help prevent stress fracture. Although there have been no studies of such a strategy in humans, pretraining may be an area for future research, especially for military recruits.

Conclusion

Compared with the general population, members of the military (new recruits in particular) are at increased risk for bone stress injuries. Most of these injuries occur during basic training, when recruits significantly increase their repetitive physical activity. Although the exact pathophysiology of stress injury is debated, nutritional and metabolic abnormalities are contributors. The indolent nature of these injuries, and their high rate of false-negative plain radiographs, may result in a significant delay in diagnosis in the absence of advanced imaging studies. Although a majority of injuries heal with nonoperative management and NWB, several patterns, especially those on the tension side of the bone, are at high risk for progression to fracture and nonunion. These include lateral femoral cortex stress injuries and anterior tibial cortex fractures. There should be a low threshold for operative management in the setting of delayed union or failed nonoperative therapy. Of equal importance to orthopedic management of these injuries is the management of underlying systemic deficits, which may have subjected the patient to injury in the first place. Supplementation with vitamin D and calcium can be an important prophylaxis against stress injury. In addition, military recruits and athletes with underlying metabolic or hormonal deficiencies should receive proper attention with a focus on balancing energy intake and energy expenditure. Stress injury leading to fracture—increasingly common in military populations—often requires a multimodal approach for treatment and subsequent prevention.

Am J Orthop. 2017;46(4):176-183. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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45. DeLee JC, Evans JP, Julian J. Stress fracture of the fifth metatarsal. Am J Sports Med. 1983;11(5):349-353.

46. Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on stress fractures in female army recruits. Osteoporos Int. 2001;12(1):35-42.

47. Friedl KE, Evans RK, Moran DS. Stress fracture and military medical readiness: bridging basic and applied research. Med Sci Sports Exerc. 2008;40(11 suppl):S609-S622.

48. Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin D supplementation decreases incidence of stress fractures in female navy recruits. J Bone Miner Res. 2008;23(5):741-749.

49. DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major vitamin D fracture trials in US and Europe. BMJ. 2010;340:b5463.

50. Duckham RL, Peirce N, Meyer C, Summers GD, Cameron N, Brooke-Wavell K. Risk factors for stress fracture in female endurance athletes: a cross-sectional study. BMJ Open. 2012;2(6).

51. Milgrom C, Finestone A, Novack V, et al. The effect of prophylactic treatment with risedronate on stress fracture incidence among infantry recruits. Bone. 2004;35(2):418-424.

52. Crowell HP, Davis IS. Gait retraining to reduce lower extremity loading in runners. Clin Biomech. 2011;26(1):78-83.

53. Ekenman I, Milgrom C, Finestone A, et al. The role of biomechanical shoe orthoses in tibial stress fracture prevention. Am J Sports Med. 2002;30(6):866-870.

54. Warden SJ, Hurst JA, Sanders MS, Turner CH, Burr DB, Li J. Bone adaptation to a mechanical loading program significantly increases skeletal fatigue resistance. J Bone Miner Res. 2005;20(5):809-816.

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Take-Home Points

  • Stress injuries, specifically of the lower extremity, are very common in new military trainees.
  • Stress injury can range from benign periosteal reaction to displaced fracture.
  • Stress injury should be treated on a case-by-case basis, depending on the severity of injury, the location of the injury, and the likelihood of healing with nonoperative management.
  • Modifiable risk factors such as nutritional status, training regiment, and even footwear should be investigated to determine potential causes of injury.
  • Prevention is a crucial part of the treatment of these injuries, and early intervention such as careful pre-enrollment physicals and vitamin supplementation can be essential in lowering injury rates.

Bone stress injuries, which are common in military recruits, present in weight-bearing (WB) areas as indolent pain caused by repetitive stress and microtrauma. They were first reported in the metatarsals of Prussian soldiers in 1855.1 Today, stress injuries are increasingly common. One study estimated they account for 10% of patients seen by sports medicine practitioners.2 This injury most commonly affects military members, endurance athletes, and dancers.3-5 Specifically, the incidence of stress fractures in military members has been reported to range from 0.8% to 6.9% for men and from 3.4% to 21.0% for women.4 Because of repetitive vigorous lower extremity loading, stress fractures typically occur in the pelvis, femoral neck, tibial shaft, and metatarsals. Delayed diagnosis and the subsequent duration of treatment required for adequate healing can result in significant morbidity. In a 2009 to 2012 study of US military members, Waterman and colleagues6 found an incidence rate of 5.69 stress fractures per 1000 person-years. Fractures most frequently involved the tibia/fibula (2.26/1000), followed by the metatarsals (0.92/1000) and the femoral neck (0.49/1000).6 In addition, these injuries were most commonly encountered in new recruits, who were less accustomed to the high-volume, high-intensity training required during basic training.4,7 Enlisted junior service members have been reported to account for 77.5% of all stress fractures.6 Age under 20 years or over 40 years and white race have also been found to be risk factors for stress injury.6

The pathogenesis of stress injury is controversial. Stanitski and colleagues8 theorized that multiple submaximal mechanical insults create cumulative stress greater than bone capacity, eventually leading to fracture. Johnson9 conducted a biopsy study and postulated that an accelerated remodeling phase was responsible, whereas Friedenberg10 argued that stress injuries are a form of reduced healing, not an attempt to increase healing, caused by the absence of callous formation in the disease process.

Various other nonmodifiable and modifiable risk factors predispose military service members to stress injury. Nonmodifiable risk factors include sex, bone geometry, limb alignment, race, age, and anatomy. Lower extremity movement biomechanics resulting from dynamic limb alignment during activity may be important. Cameron and colleagues11 examined 1843 patients and found that those with knees in >5° of valgus or >5° of external rotation had higher injury rates. Although variables such as sex and limb alignment cannot be changed, proper identification of modifiable risk factors can assist with injury prevention, and nonmodifiable risk factors can help clinicians and researchers target injury prevention interventions to patients at highest risk.

Metabolic, hormonal, and nutritional status is crucial to overall bone health. Multiple studies have found that low body mass index (BMI) is a significant risk factor for stress fracture.7,12,13 Although low BMI is a concern, patients with abnormally high BMI may also be at increased risk for bone stress injury. In a recently released consensus statement on relative energy deficiency in sport (RED-S), the International Olympic Committee addressed the complex interplay of impairments in physiologic function—including metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health—caused by relative energy deficiency.14 The committee stated that the cause of this syndrome is energy deficiency relative to the balance between dietary energy intake and energy expenditure required for health and activities of daily living, growth, and sporting activities. This finding reveals that conditions such as stress injury often may represent a much broader systemic deficit that may be influenced by a patient’s overall physiologic imbalance.

Diagnosis

History and Physical Examination

The onset of stress reaction typically is insidious, with the classic presentation being a new military recruit who is experiencing a sudden increase in pain during physical activity.15 Pain typically is initially present only during activity, and is relieved with rest, but with disease progression this evolves to pain at rest. It is crucial that the physician elicit the patient’s history of training and physical activity. Hsu and colleagues7 reported increased prevalence of overweight civilian recruits, indicating an increase in the number of new recruits having limited experience with the repetitive physical activity encountered in basic training. Stress injury should be suspected in the setting of worsening, indolent lower extremity pain that has been present for several days, especially in the higher-risk patient populations mentioned. Diet should be assessed, with specific attention given to the intake of fruits, vegetables, and foods high in vitamin D and calcium and, most important, the energy balance between intake and output.16 Special attention should also be given to female patients, who may experience the female athlete triad, a spectrum of low energy availability, menstrual dysfunction, and impaired bone turnover (high amount of resorption relative to formation). A key part of the RED-S consensus statement14 alerted healthcare providers that metabolic derangements do not solely affect female patients. These types of patients sustain a major insult to the homeostatic balance of the hormones that sustain adequate bone health. Beck and colleagues17 found that women with disrupted menstrual cycles are 2 to 4 times more likely to sustain a stress fracture than women without disrupted menstrual cycles, making this abnormality an important part of the history.

Examination should begin with careful evaluation of limb alignment and specific attention given to varus or valgus alignment of the knees.11 The feet should also be inspected, as pes planus or cavus foot may increase the risk of stress fracture.18 Identification of the area of maximal tenderness is important. The area in question may also be erythematous or warm secondary to the inflammatory response associated with attempted fracture healing. In chronic fractures in superficial areas such as the metatarsals, callus may be palpable. Although there are few specific tests for stress injury, pain may be reproducible with deep palpation and WB.

Figure 1.
If a femoral fracture is suspected, the fulcrum test can be performed by applying downward pressure on the patient’s knee while levering the thigh over the examiner’s opposite arm or thigh (Figure 1).19 Patients with sacral stress fractures may have pain when standing or hopping on the affected side (positive flamingo test).20

Laboratory Testing

When a pathology is thought to have a nutritional or metabolic cause, particularly in a low-weight or underweight patient, a laboratory workup should be obtained. Specific laboratory tests that all patients should undergo are 25-hydroxyvitamin D3, complete blood cell count, and basic chemistry panel, including calcium and thyroid-stimulating hormone levels. Although not necessary for diagnosis, phosphate, parathyroid hormone, albumin, and prealbumin should also be considered. Females should undergo testing of follicle stimulating hormone, luteinizing hormone, estradiol, and testosterone and have a urine pregnancy test. In patients with signs of excessive cortisone, a dexamethasone suppression test can be administered.21 In males, low testosterone is a documented risk factor for stress injury.22

Imaging

Given their low cost and availability, plain radiographs typically are used for initial examination of a suspected stress injury. However, they often lack sensitivity, particularly in the early stages of stress fracture development (Figure 2).

Figure 2.
Although a fracture line or callus formation is present occasionally, findings may be subtler. Images should be inspected for blunting of cortical bone and periosteal reaction, which should be correlated with the site of maximal tenderness.11 When there is high clinical suspicion based on history and physical examination, but radiographs are negative, magnetic resonance imaging (MRI) or bone scan can be useful.23 MRI is the most accurate imaging modality, with sensitivity ranging from 86% to 100% and specificity as high as 100%.2,24,25 On MRI, stress fractures typically are seen as bright areas of increased edema. Arendt and Griffiths24 proposed an MRI-based grading system for stress fractures, with grades 1 and 2 representing low-grade injuries, and 3 and 4 representing high grade. Computed tomography (CT) also has a role in diagnosis and may be better than MRI in imaging stress fractures in the pelvis and sacrum.2 In a study involving tibial stress fractures, Gaeta and colleagues26 found MRI was 88% sensitive and 100% specific and had a positive predictive value of 100%, and CT was 42% sensitive and 100% specific and had a positive predictive value of 100%. They concluded MRI was superior to CT in the diagnosis of tibial stress fractures.

Management

Management of bone stress injury depends on many factors, including symptom duration, fracture location and severity, and risk of progression or nonunion (Table).13

Table.
Patients thought to have an underlying metabolic or nutritional derangement should be treated accordingly. Injuries with a low risk of nonunion or further displacement typically can be managed with a period of modified physical activity or reduced or non-WB (NWB) ambulation; higher risk injuries may require operative intervention.5

 

 

Pelvis

Pelvic stress fractures are rare and represent only 1.6% to 7.1% of all stress fractures.13,27,28 Given the low frequency, physicians must have a high index of suspicion to make the correct diagnosis. These fractures typically occur in marathon runners and other patients who present with persistent pain and a history of high levels of activity. As pelvic stress fractures typically involve the superior or inferior pubic rami, or sacrum, and are at low risk for nonunion,13 most are managed with nonoperative treatment and activity modification for 8 to 12 weeks.27

Femur

Femoral stress fractures are also relatively uncommon, accounting for about 10% of all stress fractures. Depending on their location, these fractures can be at high risk for progression, nonunion, and significant morbidity.29 Especially concerning are femoral neck stress fractures, which can involve either the tension side (lateral cortex) or the compression side (medial cortex) of the bone. Suspicion of a femoral neck stress fracture should prompt immediate NWB.5 Early recognition of these injuries is crucial because once displacement occurs, their complication and morbidity rates become high.13 Patients with compression-side fractures should undergo NWB treatment for 4 to 6 weeks and then slow progression to WB activity. Most return to light-impact activity by 3 to 4 months. By contrast, tension-side fractures are less likely to heal without operative intervention.11 All tension-side fractures (and any compression-side fractures >50% of the width of the femoral neck) should be treated with percutaneous placement of cannulated screws (Figure 3).

Figure 3.
Displaced fractures should be addressed urgently with open reduction and internal fixation to avoid avascular necrosis and other long-term sequelae.5 Results of operative treatment of femoral neck fractures in active individuals have been mixed. Neubauer and colleagues30 examined 48 runners who underwent surgical fixation for these injuries. Preinjury activity levels were resumed by a higher percentage of low-performance runners (72%, 23/32) than low-performance runners (31%, 5/16). Reporting on femoral neck stress fracture outcomes in Royal Marine recruits, Evans and colleagues31 found that, after operative intervention, all fractures united by 11 months on average. However, union in 50% of fractures took more than 1 year, revealing the difficulty in managing these injuries as well as the lengthy resulting disability.

Stress fractures of the femoral shaft are less common than those of the femoral neck and represent as little as 3% of all stress fractures.32 However, femoral shaft stress fractures are more common in military populations. In French military recruits, Niva and colleagues33 found an 18% incidence. Similar to femoral neck fractures, femoral shaft fractures typically are diagnosed with advanced imaging, though the fulcrum test and pain on WB can aid in the diagnosis.19 These injuries are often managed nonoperatively with NWB for a period. Weishaar and colleagues34 described US military cadets treated with progressive rehabilitation who returned to full activity within 12 weeks. Displaced femoral shaft fractures associated with bone stress injury are even less common, and should be managed operatively. Salminen and colleagues35 found an incidence of 1.5 fractures per 100,000 years of military service. Over a 20-year period, they surgically treated 10 of these fractures. Average time from intramedullary nailing to union was 3.5 months.

Tibia

The tibia is one of the more common locations for stress injury and fracture. In a prospective study with members of the military, Giladi and colleagues36 found that 71% of stress fractures were tibia fractures. In addition, a large study of 320 athletes with stress fractures found 49.1% in the tibia.37 Fractures typically are diaphyseal and transverse, usually occurring along the posteromedial cortex, where the bone experiences maximal compressive forces (Figure 4).5,13

Figure 4.
Fractures on the anterior cortex—thought to result from tensile forces applied by the large posterior musculature of the gastrocnemius during repetitive activity38—are more concerning.
Figure 5.
Compared with fractures on the compression side, fractures of the anterior tibial cortex are at higher risk for nonunion (reported nonunion rate, 4.6%).39 Radiographs of anterior tibial cortex fractures may show the “dreaded black line” (Figure 5).

Compression-side fractures often heal with nonoperative management, though healing may take several months. Swenson and colleagues40 studied the effects of pneumatic bracing on conservative management and return to play in athletes with tibial stress fractures. Patients with bracing returned to light activity within 7 days and full activity within 21 days, whereas those without bracing returned to light activity within 21 days and full activity within 77 days. Pulsed electromagnetic therapy is of controversial benefit in the management of these injuries. Rettig and colleagues41 conducted a prospective randomized trial in the treatment of US Navy midshipmen and found no reduction in healing time in those who underwent electromagnetic therapy. Stress fractures with displacement and fractures that have failed nonoperative treatment should undergo surgery. Reamed intramedullary nailing is the gold standard of operative management of these injuries.5 Varner and colleagues42 reported the outcomes of treating 11 tibial stress fractures with intramedullary nailing after nonoperative management (4 months minimum) had failed. With surgery, the union rate was 100%, and patients returned to full activity by a mean of 4 months.

Metatarsals

Stress fractures were first discovered by Briethaupt1 in the painful swollen feet of Prussian army members in 1855 and were initially named march fractures. Waterman and colleagues6 reported that metatarsal stress fractures accounted for 16% of all stress fractures in the US military between 2009 and 2012. The second metatarsal neck is the most common location for stress fractures, followed by the third and fourth metatarsals, with the fifth metatarsal being the least common.5 The second metatarsal is thought to sustain these injuries more often than the other metatarsals because of its relative lack of immobility. Donahue and Sharkey43 found that the dorsal aspect of the second metatarsal experiences twice the amount of strain experienced by the fifth metatarsal during gait, and that peak strain in the second metatarsal was further increased by simulated muscle fatigue. The risk of stress fracture can be additionally increased with use of minimalist footwear, as shown by Giuliani and colleagues,44 particularly in the absence of a progressive transition in gait and training volume with a change toward minimalist footwear. In patients with a suspected or confirmed fracture of the second, third, or fourth metatarsal, treatment typically is NWB and immobilization for at least 4 weeks.5 Fifth metatarsal stress injuries (Figure 2) typically are treated differently because of their higher risk of nonunion. Patients with a fifth metatarsal stress fracture complain of lateral midfoot pain with running and jumping. For those who present with this fracture early, acceptable treatment consists of 6 weeks of casting and NWB.5 In cases of failed nonoperative therapy, or presentation with radiographic evidence of nonunion, treatment should be intramedullary screw fixation, with bone graft supplementation based on surgeon preference. DeLee and colleagues45 reported on the results of 10 athletes with fifth metatarsal stress fractures treated with intramedullary screw fixation without bone grafting. All 10 experienced fracture union, at a mean of 7.5 weeks, and returned to sport within 8.5 weeks. One complication with this procedure is pain at the screw insertion site, but this can be successfully managed with footwear modification.45

Prevention

Proper identification of patients at high risk for stress injuries has the potential of reducing the incidence of these injuries. Lappe and colleagues46 prospectively examined female army recruits before and after 8 weeks of basic training and found that those who developed a stress fracture were more likely to have a smoking history, to drink more than 10 alcoholic beverages a week, to have a history of corticosteroid or depot medroxyprogesterone use, and to have lower body weight. In addition, the authors found that a history of prolonged exercise before enrollment was protective against fracture. This finding identifies the importance of having new recruits undergo risk factor screening, which could result in adjusting training regimens to try to reduce injury. The RED-S consensus statement14 offers a comprehensive description of the physiologic factors that can contribute to such injury. Similar to proper risk factor identification, implementation of proper exercise progression programs is a simple, modifiable method of limiting stress injuries. For new recruits or athletes who are resuming activity, injury can be effectively prevented by adjusting the frequency, duration, and intensity of training and the training loads used.47

Vitamin D and calcium supplementation is a simple intervention that can be helpful in injury prevention, and its use has very little downside. A double-blind study found a 20% lower incidence of stress fracture in female navy recruits who took 2000 mg of calcium and 800 IU of vitamin D as daily supplemention.48 Of importance, a meta-analysis of more than 65,000 patients found vitamin D supplementation was effective in reducing fracture risk only when combined with calcium, irrespective of age, sex, or prior fracture.49 In female patients with the female athlete triad, psychological counseling and nutritional consultation are essential in bone health maintenance and long-term prevention.50 Other therapies have been evaluated as well. Use of bisphosphonates is controversial for both treatment and prevention of stress fractures. In a randomized, double-blind study of the potential prophylactic effects of risedronate in 324 new infantry recruits, Milgrom and colleagues51 found no statistically significant differences in tibial, femoral, metatarsal, or total stress fracture incidence between the treatment and placebo groups. Therefore, bisphosphonates are seldom recommended as prevention or in primary management of stress fracture.

In addition to nutritional and pharmacologic therapy, activity modification may have a role in injury prevention. Gait retraining has been identified as a potential intervention for reducing stress fractures in patients with poor biomechanics.47 Crowell and Davis52 investigated the effect of gait retraining on the forces operating in the tibia in runners. After 1 month of gait retraining, tibial acceleration while running decreased by 50%, vertical force loading rate by 30%, and peak vertical force impact by 20%. Such studies indicate the importance of proper mechanics during repetitive activity, especially in patients not as accustomed to the rigorous training methods used with new military recruits. However, whether these reduced loads translate into reduced risk of stress fracture remains unclear. In addition, biomechanical shoe orthoses may lower the stress fracture risk in military recruits by reducing peak tibial strain.53 Warden and colleagues54 found a mechanical loading program was effective in enchaining the structural properties of bone in rats, leading the authors to hypothesize that a similar program aimed at modifying bone structure in humans could help prevent stress fracture. Although there have been no studies of such a strategy in humans, pretraining may be an area for future research, especially for military recruits.

Conclusion

Compared with the general population, members of the military (new recruits in particular) are at increased risk for bone stress injuries. Most of these injuries occur during basic training, when recruits significantly increase their repetitive physical activity. Although the exact pathophysiology of stress injury is debated, nutritional and metabolic abnormalities are contributors. The indolent nature of these injuries, and their high rate of false-negative plain radiographs, may result in a significant delay in diagnosis in the absence of advanced imaging studies. Although a majority of injuries heal with nonoperative management and NWB, several patterns, especially those on the tension side of the bone, are at high risk for progression to fracture and nonunion. These include lateral femoral cortex stress injuries and anterior tibial cortex fractures. There should be a low threshold for operative management in the setting of delayed union or failed nonoperative therapy. Of equal importance to orthopedic management of these injuries is the management of underlying systemic deficits, which may have subjected the patient to injury in the first place. Supplementation with vitamin D and calcium can be an important prophylaxis against stress injury. In addition, military recruits and athletes with underlying metabolic or hormonal deficiencies should receive proper attention with a focus on balancing energy intake and energy expenditure. Stress injury leading to fracture—increasingly common in military populations—often requires a multimodal approach for treatment and subsequent prevention.

Am J Orthop. 2017;46(4):176-183. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Stress injuries, specifically of the lower extremity, are very common in new military trainees.
  • Stress injury can range from benign periosteal reaction to displaced fracture.
  • Stress injury should be treated on a case-by-case basis, depending on the severity of injury, the location of the injury, and the likelihood of healing with nonoperative management.
  • Modifiable risk factors such as nutritional status, training regiment, and even footwear should be investigated to determine potential causes of injury.
  • Prevention is a crucial part of the treatment of these injuries, and early intervention such as careful pre-enrollment physicals and vitamin supplementation can be essential in lowering injury rates.

Bone stress injuries, which are common in military recruits, present in weight-bearing (WB) areas as indolent pain caused by repetitive stress and microtrauma. They were first reported in the metatarsals of Prussian soldiers in 1855.1 Today, stress injuries are increasingly common. One study estimated they account for 10% of patients seen by sports medicine practitioners.2 This injury most commonly affects military members, endurance athletes, and dancers.3-5 Specifically, the incidence of stress fractures in military members has been reported to range from 0.8% to 6.9% for men and from 3.4% to 21.0% for women.4 Because of repetitive vigorous lower extremity loading, stress fractures typically occur in the pelvis, femoral neck, tibial shaft, and metatarsals. Delayed diagnosis and the subsequent duration of treatment required for adequate healing can result in significant morbidity. In a 2009 to 2012 study of US military members, Waterman and colleagues6 found an incidence rate of 5.69 stress fractures per 1000 person-years. Fractures most frequently involved the tibia/fibula (2.26/1000), followed by the metatarsals (0.92/1000) and the femoral neck (0.49/1000).6 In addition, these injuries were most commonly encountered in new recruits, who were less accustomed to the high-volume, high-intensity training required during basic training.4,7 Enlisted junior service members have been reported to account for 77.5% of all stress fractures.6 Age under 20 years or over 40 years and white race have also been found to be risk factors for stress injury.6

The pathogenesis of stress injury is controversial. Stanitski and colleagues8 theorized that multiple submaximal mechanical insults create cumulative stress greater than bone capacity, eventually leading to fracture. Johnson9 conducted a biopsy study and postulated that an accelerated remodeling phase was responsible, whereas Friedenberg10 argued that stress injuries are a form of reduced healing, not an attempt to increase healing, caused by the absence of callous formation in the disease process.

Various other nonmodifiable and modifiable risk factors predispose military service members to stress injury. Nonmodifiable risk factors include sex, bone geometry, limb alignment, race, age, and anatomy. Lower extremity movement biomechanics resulting from dynamic limb alignment during activity may be important. Cameron and colleagues11 examined 1843 patients and found that those with knees in >5° of valgus or >5° of external rotation had higher injury rates. Although variables such as sex and limb alignment cannot be changed, proper identification of modifiable risk factors can assist with injury prevention, and nonmodifiable risk factors can help clinicians and researchers target injury prevention interventions to patients at highest risk.

Metabolic, hormonal, and nutritional status is crucial to overall bone health. Multiple studies have found that low body mass index (BMI) is a significant risk factor for stress fracture.7,12,13 Although low BMI is a concern, patients with abnormally high BMI may also be at increased risk for bone stress injury. In a recently released consensus statement on relative energy deficiency in sport (RED-S), the International Olympic Committee addressed the complex interplay of impairments in physiologic function—including metabolic rate, menstrual function, bone health, immunity, protein synthesis, and cardiovascular health—caused by relative energy deficiency.14 The committee stated that the cause of this syndrome is energy deficiency relative to the balance between dietary energy intake and energy expenditure required for health and activities of daily living, growth, and sporting activities. This finding reveals that conditions such as stress injury often may represent a much broader systemic deficit that may be influenced by a patient’s overall physiologic imbalance.

Diagnosis

History and Physical Examination

The onset of stress reaction typically is insidious, with the classic presentation being a new military recruit who is experiencing a sudden increase in pain during physical activity.15 Pain typically is initially present only during activity, and is relieved with rest, but with disease progression this evolves to pain at rest. It is crucial that the physician elicit the patient’s history of training and physical activity. Hsu and colleagues7 reported increased prevalence of overweight civilian recruits, indicating an increase in the number of new recruits having limited experience with the repetitive physical activity encountered in basic training. Stress injury should be suspected in the setting of worsening, indolent lower extremity pain that has been present for several days, especially in the higher-risk patient populations mentioned. Diet should be assessed, with specific attention given to the intake of fruits, vegetables, and foods high in vitamin D and calcium and, most important, the energy balance between intake and output.16 Special attention should also be given to female patients, who may experience the female athlete triad, a spectrum of low energy availability, menstrual dysfunction, and impaired bone turnover (high amount of resorption relative to formation). A key part of the RED-S consensus statement14 alerted healthcare providers that metabolic derangements do not solely affect female patients. These types of patients sustain a major insult to the homeostatic balance of the hormones that sustain adequate bone health. Beck and colleagues17 found that women with disrupted menstrual cycles are 2 to 4 times more likely to sustain a stress fracture than women without disrupted menstrual cycles, making this abnormality an important part of the history.

Examination should begin with careful evaluation of limb alignment and specific attention given to varus or valgus alignment of the knees.11 The feet should also be inspected, as pes planus or cavus foot may increase the risk of stress fracture.18 Identification of the area of maximal tenderness is important. The area in question may also be erythematous or warm secondary to the inflammatory response associated with attempted fracture healing. In chronic fractures in superficial areas such as the metatarsals, callus may be palpable. Although there are few specific tests for stress injury, pain may be reproducible with deep palpation and WB.

Figure 1.
If a femoral fracture is suspected, the fulcrum test can be performed by applying downward pressure on the patient’s knee while levering the thigh over the examiner’s opposite arm or thigh (Figure 1).19 Patients with sacral stress fractures may have pain when standing or hopping on the affected side (positive flamingo test).20

Laboratory Testing

When a pathology is thought to have a nutritional or metabolic cause, particularly in a low-weight or underweight patient, a laboratory workup should be obtained. Specific laboratory tests that all patients should undergo are 25-hydroxyvitamin D3, complete blood cell count, and basic chemistry panel, including calcium and thyroid-stimulating hormone levels. Although not necessary for diagnosis, phosphate, parathyroid hormone, albumin, and prealbumin should also be considered. Females should undergo testing of follicle stimulating hormone, luteinizing hormone, estradiol, and testosterone and have a urine pregnancy test. In patients with signs of excessive cortisone, a dexamethasone suppression test can be administered.21 In males, low testosterone is a documented risk factor for stress injury.22

Imaging

Given their low cost and availability, plain radiographs typically are used for initial examination of a suspected stress injury. However, they often lack sensitivity, particularly in the early stages of stress fracture development (Figure 2).

Figure 2.
Although a fracture line or callus formation is present occasionally, findings may be subtler. Images should be inspected for blunting of cortical bone and periosteal reaction, which should be correlated with the site of maximal tenderness.11 When there is high clinical suspicion based on history and physical examination, but radiographs are negative, magnetic resonance imaging (MRI) or bone scan can be useful.23 MRI is the most accurate imaging modality, with sensitivity ranging from 86% to 100% and specificity as high as 100%.2,24,25 On MRI, stress fractures typically are seen as bright areas of increased edema. Arendt and Griffiths24 proposed an MRI-based grading system for stress fractures, with grades 1 and 2 representing low-grade injuries, and 3 and 4 representing high grade. Computed tomography (CT) also has a role in diagnosis and may be better than MRI in imaging stress fractures in the pelvis and sacrum.2 In a study involving tibial stress fractures, Gaeta and colleagues26 found MRI was 88% sensitive and 100% specific and had a positive predictive value of 100%, and CT was 42% sensitive and 100% specific and had a positive predictive value of 100%. They concluded MRI was superior to CT in the diagnosis of tibial stress fractures.

Management

Management of bone stress injury depends on many factors, including symptom duration, fracture location and severity, and risk of progression or nonunion (Table).13

Table.
Patients thought to have an underlying metabolic or nutritional derangement should be treated accordingly. Injuries with a low risk of nonunion or further displacement typically can be managed with a period of modified physical activity or reduced or non-WB (NWB) ambulation; higher risk injuries may require operative intervention.5

 

 

Pelvis

Pelvic stress fractures are rare and represent only 1.6% to 7.1% of all stress fractures.13,27,28 Given the low frequency, physicians must have a high index of suspicion to make the correct diagnosis. These fractures typically occur in marathon runners and other patients who present with persistent pain and a history of high levels of activity. As pelvic stress fractures typically involve the superior or inferior pubic rami, or sacrum, and are at low risk for nonunion,13 most are managed with nonoperative treatment and activity modification for 8 to 12 weeks.27

Femur

Femoral stress fractures are also relatively uncommon, accounting for about 10% of all stress fractures. Depending on their location, these fractures can be at high risk for progression, nonunion, and significant morbidity.29 Especially concerning are femoral neck stress fractures, which can involve either the tension side (lateral cortex) or the compression side (medial cortex) of the bone. Suspicion of a femoral neck stress fracture should prompt immediate NWB.5 Early recognition of these injuries is crucial because once displacement occurs, their complication and morbidity rates become high.13 Patients with compression-side fractures should undergo NWB treatment for 4 to 6 weeks and then slow progression to WB activity. Most return to light-impact activity by 3 to 4 months. By contrast, tension-side fractures are less likely to heal without operative intervention.11 All tension-side fractures (and any compression-side fractures >50% of the width of the femoral neck) should be treated with percutaneous placement of cannulated screws (Figure 3).

Figure 3.
Displaced fractures should be addressed urgently with open reduction and internal fixation to avoid avascular necrosis and other long-term sequelae.5 Results of operative treatment of femoral neck fractures in active individuals have been mixed. Neubauer and colleagues30 examined 48 runners who underwent surgical fixation for these injuries. Preinjury activity levels were resumed by a higher percentage of low-performance runners (72%, 23/32) than low-performance runners (31%, 5/16). Reporting on femoral neck stress fracture outcomes in Royal Marine recruits, Evans and colleagues31 found that, after operative intervention, all fractures united by 11 months on average. However, union in 50% of fractures took more than 1 year, revealing the difficulty in managing these injuries as well as the lengthy resulting disability.

Stress fractures of the femoral shaft are less common than those of the femoral neck and represent as little as 3% of all stress fractures.32 However, femoral shaft stress fractures are more common in military populations. In French military recruits, Niva and colleagues33 found an 18% incidence. Similar to femoral neck fractures, femoral shaft fractures typically are diagnosed with advanced imaging, though the fulcrum test and pain on WB can aid in the diagnosis.19 These injuries are often managed nonoperatively with NWB for a period. Weishaar and colleagues34 described US military cadets treated with progressive rehabilitation who returned to full activity within 12 weeks. Displaced femoral shaft fractures associated with bone stress injury are even less common, and should be managed operatively. Salminen and colleagues35 found an incidence of 1.5 fractures per 100,000 years of military service. Over a 20-year period, they surgically treated 10 of these fractures. Average time from intramedullary nailing to union was 3.5 months.

Tibia

The tibia is one of the more common locations for stress injury and fracture. In a prospective study with members of the military, Giladi and colleagues36 found that 71% of stress fractures were tibia fractures. In addition, a large study of 320 athletes with stress fractures found 49.1% in the tibia.37 Fractures typically are diaphyseal and transverse, usually occurring along the posteromedial cortex, where the bone experiences maximal compressive forces (Figure 4).5,13

Figure 4.
Fractures on the anterior cortex—thought to result from tensile forces applied by the large posterior musculature of the gastrocnemius during repetitive activity38—are more concerning.
Figure 5.
Compared with fractures on the compression side, fractures of the anterior tibial cortex are at higher risk for nonunion (reported nonunion rate, 4.6%).39 Radiographs of anterior tibial cortex fractures may show the “dreaded black line” (Figure 5).

Compression-side fractures often heal with nonoperative management, though healing may take several months. Swenson and colleagues40 studied the effects of pneumatic bracing on conservative management and return to play in athletes with tibial stress fractures. Patients with bracing returned to light activity within 7 days and full activity within 21 days, whereas those without bracing returned to light activity within 21 days and full activity within 77 days. Pulsed electromagnetic therapy is of controversial benefit in the management of these injuries. Rettig and colleagues41 conducted a prospective randomized trial in the treatment of US Navy midshipmen and found no reduction in healing time in those who underwent electromagnetic therapy. Stress fractures with displacement and fractures that have failed nonoperative treatment should undergo surgery. Reamed intramedullary nailing is the gold standard of operative management of these injuries.5 Varner and colleagues42 reported the outcomes of treating 11 tibial stress fractures with intramedullary nailing after nonoperative management (4 months minimum) had failed. With surgery, the union rate was 100%, and patients returned to full activity by a mean of 4 months.

Metatarsals

Stress fractures were first discovered by Briethaupt1 in the painful swollen feet of Prussian army members in 1855 and were initially named march fractures. Waterman and colleagues6 reported that metatarsal stress fractures accounted for 16% of all stress fractures in the US military between 2009 and 2012. The second metatarsal neck is the most common location for stress fractures, followed by the third and fourth metatarsals, with the fifth metatarsal being the least common.5 The second metatarsal is thought to sustain these injuries more often than the other metatarsals because of its relative lack of immobility. Donahue and Sharkey43 found that the dorsal aspect of the second metatarsal experiences twice the amount of strain experienced by the fifth metatarsal during gait, and that peak strain in the second metatarsal was further increased by simulated muscle fatigue. The risk of stress fracture can be additionally increased with use of minimalist footwear, as shown by Giuliani and colleagues,44 particularly in the absence of a progressive transition in gait and training volume with a change toward minimalist footwear. In patients with a suspected or confirmed fracture of the second, third, or fourth metatarsal, treatment typically is NWB and immobilization for at least 4 weeks.5 Fifth metatarsal stress injuries (Figure 2) typically are treated differently because of their higher risk of nonunion. Patients with a fifth metatarsal stress fracture complain of lateral midfoot pain with running and jumping. For those who present with this fracture early, acceptable treatment consists of 6 weeks of casting and NWB.5 In cases of failed nonoperative therapy, or presentation with radiographic evidence of nonunion, treatment should be intramedullary screw fixation, with bone graft supplementation based on surgeon preference. DeLee and colleagues45 reported on the results of 10 athletes with fifth metatarsal stress fractures treated with intramedullary screw fixation without bone grafting. All 10 experienced fracture union, at a mean of 7.5 weeks, and returned to sport within 8.5 weeks. One complication with this procedure is pain at the screw insertion site, but this can be successfully managed with footwear modification.45

Prevention

Proper identification of patients at high risk for stress injuries has the potential of reducing the incidence of these injuries. Lappe and colleagues46 prospectively examined female army recruits before and after 8 weeks of basic training and found that those who developed a stress fracture were more likely to have a smoking history, to drink more than 10 alcoholic beverages a week, to have a history of corticosteroid or depot medroxyprogesterone use, and to have lower body weight. In addition, the authors found that a history of prolonged exercise before enrollment was protective against fracture. This finding identifies the importance of having new recruits undergo risk factor screening, which could result in adjusting training regimens to try to reduce injury. The RED-S consensus statement14 offers a comprehensive description of the physiologic factors that can contribute to such injury. Similar to proper risk factor identification, implementation of proper exercise progression programs is a simple, modifiable method of limiting stress injuries. For new recruits or athletes who are resuming activity, injury can be effectively prevented by adjusting the frequency, duration, and intensity of training and the training loads used.47

Vitamin D and calcium supplementation is a simple intervention that can be helpful in injury prevention, and its use has very little downside. A double-blind study found a 20% lower incidence of stress fracture in female navy recruits who took 2000 mg of calcium and 800 IU of vitamin D as daily supplemention.48 Of importance, a meta-analysis of more than 65,000 patients found vitamin D supplementation was effective in reducing fracture risk only when combined with calcium, irrespective of age, sex, or prior fracture.49 In female patients with the female athlete triad, psychological counseling and nutritional consultation are essential in bone health maintenance and long-term prevention.50 Other therapies have been evaluated as well. Use of bisphosphonates is controversial for both treatment and prevention of stress fractures. In a randomized, double-blind study of the potential prophylactic effects of risedronate in 324 new infantry recruits, Milgrom and colleagues51 found no statistically significant differences in tibial, femoral, metatarsal, or total stress fracture incidence between the treatment and placebo groups. Therefore, bisphosphonates are seldom recommended as prevention or in primary management of stress fracture.

In addition to nutritional and pharmacologic therapy, activity modification may have a role in injury prevention. Gait retraining has been identified as a potential intervention for reducing stress fractures in patients with poor biomechanics.47 Crowell and Davis52 investigated the effect of gait retraining on the forces operating in the tibia in runners. After 1 month of gait retraining, tibial acceleration while running decreased by 50%, vertical force loading rate by 30%, and peak vertical force impact by 20%. Such studies indicate the importance of proper mechanics during repetitive activity, especially in patients not as accustomed to the rigorous training methods used with new military recruits. However, whether these reduced loads translate into reduced risk of stress fracture remains unclear. In addition, biomechanical shoe orthoses may lower the stress fracture risk in military recruits by reducing peak tibial strain.53 Warden and colleagues54 found a mechanical loading program was effective in enchaining the structural properties of bone in rats, leading the authors to hypothesize that a similar program aimed at modifying bone structure in humans could help prevent stress fracture. Although there have been no studies of such a strategy in humans, pretraining may be an area for future research, especially for military recruits.

Conclusion

Compared with the general population, members of the military (new recruits in particular) are at increased risk for bone stress injuries. Most of these injuries occur during basic training, when recruits significantly increase their repetitive physical activity. Although the exact pathophysiology of stress injury is debated, nutritional and metabolic abnormalities are contributors. The indolent nature of these injuries, and their high rate of false-negative plain radiographs, may result in a significant delay in diagnosis in the absence of advanced imaging studies. Although a majority of injuries heal with nonoperative management and NWB, several patterns, especially those on the tension side of the bone, are at high risk for progression to fracture and nonunion. These include lateral femoral cortex stress injuries and anterior tibial cortex fractures. There should be a low threshold for operative management in the setting of delayed union or failed nonoperative therapy. Of equal importance to orthopedic management of these injuries is the management of underlying systemic deficits, which may have subjected the patient to injury in the first place. Supplementation with vitamin D and calcium can be an important prophylaxis against stress injury. In addition, military recruits and athletes with underlying metabolic or hormonal deficiencies should receive proper attention with a focus on balancing energy intake and energy expenditure. Stress injury leading to fracture—increasingly common in military populations—often requires a multimodal approach for treatment and subsequent prevention.

Am J Orthop. 2017;46(4):176-183. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Briethaupt MD. Zur Pathologie des menschlichen Fusses [To the pathology of the human foot]. Med Zeitung. 1855;24:169-177.

2. Berger FH, de Jonge MC, Maas M. Stress fractures in the lower extremity. Eur J Radiol. 2007;62(1):16-26.

3. Almeida SA, Williams KM, Shaffer RA, Brodine SK. Epidemiological patterns of musculoskeletal injuries and physical training. Med Sci Sports Exerc. 1999;31(8):1176-1182.

4. Jones BH, Thacker SB, Gilchrist J, Kimsey CD, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev. 2002;24(2):228-247.

5. Jacobs JM, Cameron KL, Bojescul JA. Lower extremity stress fractures in the military. Clin Sports Med. 2014;33(4):591-613.

6. Waterman BR, Gun B, Bader JO, Orr JD, Belmont PJ. Epidemiology of lower extremity stress fractures in the United States military. Mil Med. 2016;181(10):1308-1313.

7. Hsu LL, Nevin RL, Tobler SK, Rubertone MV. Trends in overweight and obesity among 18-year-old applicants to the United States military, 1993–2006. J Adolesc Health. 2007;41(6):610-612.

8. Stanitski CL, McMaster JH, Scranton PE. On the nature of stress fractures. Am J Sports Med. 1978;6(6):391-396.

9. Johnson LC. Histogenesis of stress fractures [annual lecture]. Washington, DC: Armed Forces Institute of Pathology; 1963.

10. Friedenberg ZB. Fatigue fractures of the tibia. Clin Orthop Relat Res. 1971;(76):111-115.

11. Cameron KL, Peck KY, Owens BD, et al. Biomechanical risk factors for lower extremity stress fracture. Orthop J Sports Med. 2013;1(4 suppl).

12. Knapik J, Montain S, McGraw S, Grier T, Ely M, Jones B. Stress fracture risk factors in basic combat training. Int J Sports Med. 2012;33(11):940-946.

13. Behrens SB, Deren ME, Matson A, Fadale PD, Monchik KO. Stress fractures of the pelvis and legs in athletes. Sports Health. 2013;5(2):165-174.

14. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the female athlete triad—relative energy deficiency in sport (RED-S). Br J Sports Med. 2014;48(7):491-497.

15. Maitra RS, Johnson DL. Stress fractures. Clinical history and physical examination. Clin Sports Med. 1997;16(2):259-274.

16. Nieves JW, Melsop K, Curtis M, et al. Nutritional factors that influence change in bone density and stress fracture risk among young female cross-country runners. PM R. 2010;2(8):740-750.

17. Beck BR, Matheson GO, Bergman G, et al. Do capacitively coupled electric fields accelerate tibial stress fracture healing? Am J Sports Med. 2008;36(3):545-553.

18. Simkin A, Leichter I, Giladi M, Stein M, Milgrom C. Combined effect of foot arch structure and an orthotic device on stress fractures. Foot Ankle. 1989;10(1):25-29.

19. Johnson AW, Weiss CB, Wheeler DL. Stress fractures of the femoral shaft in athletes—more common than expected: a new clinical test. Am J Sports Med. 1994;22(2):248-256.

20. Clement D, Ammann W, Taunton J, et al. Exercise-induced stress injuries to the femur. Int J Sports Med. 1993;14(6):347-352.

21. Wood PJ, Barth JH, Freedman DB, Perry L, Sheridan B. Evidence for the low dose dexamethasone suppression test to screen for Cushing’s syndrome—recommendations for a protocol for biochemistry laboratories. Ann Clin Biochem. 1997;34(pt 3):222-229.

22. Bennell K, Matheson G, Meeuwisse W, Brukner P. Risk factors for stress fractures. Sports Med. 1999;28(2):91-122.

23. Prather JL, Nusynowitz ML, Snowdy HA, Hughes AD, McCartney WH, Bagg RJ. Scintigraphic findings in stress fractures. J Bone Joint Surg Am. 1977;59(7):869-874.

24. Arendt EA, Griffiths HJ. The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes. Clin Sports Med. 1997;16(2):291-306.

25. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and treatment. J Am Acad Orthop Surg. 2000;8(6):344-353.

26. Gaeta M, Minutoli F, Scribano E, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology. 2005;235(2):553-561.

27. Matheson GO, Clement DB, Mckenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Stress fractures in athletes. Am J Sports Med. 1987;15(1):46-58.

28. Iwamoto J, Takeda T. Stress fractures in athletes: review of 196 cases. J Orthop Sci. 2003;8(3):273-278.

29. Noakes TD, Smith JA, Lindenberg G, Wills CE. Pelvic stress fractures in long distance runners. Am J Sports Med. 1985;13(2):120-123.

30. Neubauer T, Brand J, Lidder S, Krawany M. Stress fractures of the femoral neck in runners: a review. Res Sports Med. 2016;24(3):283-297.

31. Evans JT, Guyver PM, Kassam AM, Hubble MJW. Displaced femoral neck stress fractures in Royal Marine recruits—management and results of operative treatment. J R Nav Med Serv. 2012;98(2):3-5.

32. Orava S. Stress fractures. Br J Sports Med. 1980;14(1):40-44.

 

 

33. Niva MH, Kiuru MJ, Haataja R, Pihlajamäki HK. Fatigue injuries of the femur. J Bone Joint Surg Br. 2005;87(10):1385-1390.

34. Weishaar MD, McMillian DJ, Moore JH. Identification and management of 2 femoral shaft stress injuries. J Orthop Sports Phys Ther. 2005;35(10):665-673.

35. Salminen ST, Pihlajamäki HK, Visuri TI, Böstman OM. Displaced fatigue fractures of the femoral shaft. Clin Orthop Relat Res. 2003;(409):250-259.

36. Giladi M, Ahronson Z, Stein M, Danon YL, Milgrom C. Unusual distribution and onset of stress fractures in soldiers. Clin Orthop Relat Res. 1985;(192):142-146.

37. Matheson GO, Clement DB, Mckenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Stress fractures in athletes. Am J Sports Med. 1987;15(1):46-58.

38. Green NE, Rogers RA, Lipscomb AB. Nonunions of stress fractures of the tibia. Am J Sports Med. 1985;13(3):171-176.

39. Orava S, Hulkko A. Stress fracture of the mid-tibial shaft. Acta Orthop Scand. 1984;55(1):35-37.

40. Swenson EJ Jr, DeHaven KE, Sebastianelli WJ, Hanks G, Kalenak A, Lynch JM. The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med. 1997;25(3):322-328.

41. Rettig AC, Shelbourne KD, McCarroll JR, Bisesi M, Watts J. The natural history and treatment of delayed union stress fractures of the anterior cortex of the tibia. Am J Sports Med. 1988;16(3):250-255.

42. Varner KE, Younas SA, Lintner DM, Marymont JV. Chronic anterior midtibial stress fractures in athletes treated with reamed intramedullary nailing. Am J Sports Med. 2005;33(7):1071-1076.

43. Donahue SW, Sharkey NA. Strains in the metatarsals during the stance phase of gait: implications for stress fractures. J Bone Joint Surg Am. 1999;81(9):1236-1244.

44. Giuliani J, Masini B, Alitz C, Owens BD. Barefoot-simulating footwear associated with metatarsal stress injury in 2 runners. Orthopedics. 2011;34(7):e320-e323.

45. DeLee JC, Evans JP, Julian J. Stress fracture of the fifth metatarsal. Am J Sports Med. 1983;11(5):349-353.

46. Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on stress fractures in female army recruits. Osteoporos Int. 2001;12(1):35-42.

47. Friedl KE, Evans RK, Moran DS. Stress fracture and military medical readiness: bridging basic and applied research. Med Sci Sports Exerc. 2008;40(11 suppl):S609-S622.

48. Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin D supplementation decreases incidence of stress fractures in female navy recruits. J Bone Miner Res. 2008;23(5):741-749.

49. DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major vitamin D fracture trials in US and Europe. BMJ. 2010;340:b5463.

50. Duckham RL, Peirce N, Meyer C, Summers GD, Cameron N, Brooke-Wavell K. Risk factors for stress fracture in female endurance athletes: a cross-sectional study. BMJ Open. 2012;2(6).

51. Milgrom C, Finestone A, Novack V, et al. The effect of prophylactic treatment with risedronate on stress fracture incidence among infantry recruits. Bone. 2004;35(2):418-424.

52. Crowell HP, Davis IS. Gait retraining to reduce lower extremity loading in runners. Clin Biomech. 2011;26(1):78-83.

53. Ekenman I, Milgrom C, Finestone A, et al. The role of biomechanical shoe orthoses in tibial stress fracture prevention. Am J Sports Med. 2002;30(6):866-870.

54. Warden SJ, Hurst JA, Sanders MS, Turner CH, Burr DB, Li J. Bone adaptation to a mechanical loading program significantly increases skeletal fatigue resistance. J Bone Miner Res. 2005;20(5):809-816.

References

1. Briethaupt MD. Zur Pathologie des menschlichen Fusses [To the pathology of the human foot]. Med Zeitung. 1855;24:169-177.

2. Berger FH, de Jonge MC, Maas M. Stress fractures in the lower extremity. Eur J Radiol. 2007;62(1):16-26.

3. Almeida SA, Williams KM, Shaffer RA, Brodine SK. Epidemiological patterns of musculoskeletal injuries and physical training. Med Sci Sports Exerc. 1999;31(8):1176-1182.

4. Jones BH, Thacker SB, Gilchrist J, Kimsey CD, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev. 2002;24(2):228-247.

5. Jacobs JM, Cameron KL, Bojescul JA. Lower extremity stress fractures in the military. Clin Sports Med. 2014;33(4):591-613.

6. Waterman BR, Gun B, Bader JO, Orr JD, Belmont PJ. Epidemiology of lower extremity stress fractures in the United States military. Mil Med. 2016;181(10):1308-1313.

7. Hsu LL, Nevin RL, Tobler SK, Rubertone MV. Trends in overweight and obesity among 18-year-old applicants to the United States military, 1993–2006. J Adolesc Health. 2007;41(6):610-612.

8. Stanitski CL, McMaster JH, Scranton PE. On the nature of stress fractures. Am J Sports Med. 1978;6(6):391-396.

9. Johnson LC. Histogenesis of stress fractures [annual lecture]. Washington, DC: Armed Forces Institute of Pathology; 1963.

10. Friedenberg ZB. Fatigue fractures of the tibia. Clin Orthop Relat Res. 1971;(76):111-115.

11. Cameron KL, Peck KY, Owens BD, et al. Biomechanical risk factors for lower extremity stress fracture. Orthop J Sports Med. 2013;1(4 suppl).

12. Knapik J, Montain S, McGraw S, Grier T, Ely M, Jones B. Stress fracture risk factors in basic combat training. Int J Sports Med. 2012;33(11):940-946.

13. Behrens SB, Deren ME, Matson A, Fadale PD, Monchik KO. Stress fractures of the pelvis and legs in athletes. Sports Health. 2013;5(2):165-174.

14. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the female athlete triad—relative energy deficiency in sport (RED-S). Br J Sports Med. 2014;48(7):491-497.

15. Maitra RS, Johnson DL. Stress fractures. Clinical history and physical examination. Clin Sports Med. 1997;16(2):259-274.

16. Nieves JW, Melsop K, Curtis M, et al. Nutritional factors that influence change in bone density and stress fracture risk among young female cross-country runners. PM R. 2010;2(8):740-750.

17. Beck BR, Matheson GO, Bergman G, et al. Do capacitively coupled electric fields accelerate tibial stress fracture healing? Am J Sports Med. 2008;36(3):545-553.

18. Simkin A, Leichter I, Giladi M, Stein M, Milgrom C. Combined effect of foot arch structure and an orthotic device on stress fractures. Foot Ankle. 1989;10(1):25-29.

19. Johnson AW, Weiss CB, Wheeler DL. Stress fractures of the femoral shaft in athletes—more common than expected: a new clinical test. Am J Sports Med. 1994;22(2):248-256.

20. Clement D, Ammann W, Taunton J, et al. Exercise-induced stress injuries to the femur. Int J Sports Med. 1993;14(6):347-352.

21. Wood PJ, Barth JH, Freedman DB, Perry L, Sheridan B. Evidence for the low dose dexamethasone suppression test to screen for Cushing’s syndrome—recommendations for a protocol for biochemistry laboratories. Ann Clin Biochem. 1997;34(pt 3):222-229.

22. Bennell K, Matheson G, Meeuwisse W, Brukner P. Risk factors for stress fractures. Sports Med. 1999;28(2):91-122.

23. Prather JL, Nusynowitz ML, Snowdy HA, Hughes AD, McCartney WH, Bagg RJ. Scintigraphic findings in stress fractures. J Bone Joint Surg Am. 1977;59(7):869-874.

24. Arendt EA, Griffiths HJ. The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes. Clin Sports Med. 1997;16(2):291-306.

25. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and treatment. J Am Acad Orthop Surg. 2000;8(6):344-353.

26. Gaeta M, Minutoli F, Scribano E, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology. 2005;235(2):553-561.

27. Matheson GO, Clement DB, Mckenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Stress fractures in athletes. Am J Sports Med. 1987;15(1):46-58.

28. Iwamoto J, Takeda T. Stress fractures in athletes: review of 196 cases. J Orthop Sci. 2003;8(3):273-278.

29. Noakes TD, Smith JA, Lindenberg G, Wills CE. Pelvic stress fractures in long distance runners. Am J Sports Med. 1985;13(2):120-123.

30. Neubauer T, Brand J, Lidder S, Krawany M. Stress fractures of the femoral neck in runners: a review. Res Sports Med. 2016;24(3):283-297.

31. Evans JT, Guyver PM, Kassam AM, Hubble MJW. Displaced femoral neck stress fractures in Royal Marine recruits—management and results of operative treatment. J R Nav Med Serv. 2012;98(2):3-5.

32. Orava S. Stress fractures. Br J Sports Med. 1980;14(1):40-44.

 

 

33. Niva MH, Kiuru MJ, Haataja R, Pihlajamäki HK. Fatigue injuries of the femur. J Bone Joint Surg Br. 2005;87(10):1385-1390.

34. Weishaar MD, McMillian DJ, Moore JH. Identification and management of 2 femoral shaft stress injuries. J Orthop Sports Phys Ther. 2005;35(10):665-673.

35. Salminen ST, Pihlajamäki HK, Visuri TI, Böstman OM. Displaced fatigue fractures of the femoral shaft. Clin Orthop Relat Res. 2003;(409):250-259.

36. Giladi M, Ahronson Z, Stein M, Danon YL, Milgrom C. Unusual distribution and onset of stress fractures in soldiers. Clin Orthop Relat Res. 1985;(192):142-146.

37. Matheson GO, Clement DB, Mckenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Stress fractures in athletes. Am J Sports Med. 1987;15(1):46-58.

38. Green NE, Rogers RA, Lipscomb AB. Nonunions of stress fractures of the tibia. Am J Sports Med. 1985;13(3):171-176.

39. Orava S, Hulkko A. Stress fracture of the mid-tibial shaft. Acta Orthop Scand. 1984;55(1):35-37.

40. Swenson EJ Jr, DeHaven KE, Sebastianelli WJ, Hanks G, Kalenak A, Lynch JM. The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med. 1997;25(3):322-328.

41. Rettig AC, Shelbourne KD, McCarroll JR, Bisesi M, Watts J. The natural history and treatment of delayed union stress fractures of the anterior cortex of the tibia. Am J Sports Med. 1988;16(3):250-255.

42. Varner KE, Younas SA, Lintner DM, Marymont JV. Chronic anterior midtibial stress fractures in athletes treated with reamed intramedullary nailing. Am J Sports Med. 2005;33(7):1071-1076.

43. Donahue SW, Sharkey NA. Strains in the metatarsals during the stance phase of gait: implications for stress fractures. J Bone Joint Surg Am. 1999;81(9):1236-1244.

44. Giuliani J, Masini B, Alitz C, Owens BD. Barefoot-simulating footwear associated with metatarsal stress injury in 2 runners. Orthopedics. 2011;34(7):e320-e323.

45. DeLee JC, Evans JP, Julian J. Stress fracture of the fifth metatarsal. Am J Sports Med. 1983;11(5):349-353.

46. Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on stress fractures in female army recruits. Osteoporos Int. 2001;12(1):35-42.

47. Friedl KE, Evans RK, Moran DS. Stress fracture and military medical readiness: bridging basic and applied research. Med Sci Sports Exerc. 2008;40(11 suppl):S609-S622.

48. Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin D supplementation decreases incidence of stress fractures in female navy recruits. J Bone Miner Res. 2008;23(5):741-749.

49. DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major vitamin D fracture trials in US and Europe. BMJ. 2010;340:b5463.

50. Duckham RL, Peirce N, Meyer C, Summers GD, Cameron N, Brooke-Wavell K. Risk factors for stress fracture in female endurance athletes: a cross-sectional study. BMJ Open. 2012;2(6).

51. Milgrom C, Finestone A, Novack V, et al. The effect of prophylactic treatment with risedronate on stress fracture incidence among infantry recruits. Bone. 2004;35(2):418-424.

52. Crowell HP, Davis IS. Gait retraining to reduce lower extremity loading in runners. Clin Biomech. 2011;26(1):78-83.

53. Ekenman I, Milgrom C, Finestone A, et al. The role of biomechanical shoe orthoses in tibial stress fracture prevention. Am J Sports Med. 2002;30(6):866-870.

54. Warden SJ, Hurst JA, Sanders MS, Turner CH, Burr DB, Li J. Bone adaptation to a mechanical loading program significantly increases skeletal fatigue resistance. J Bone Miner Res. 2005;20(5):809-816.

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In Memoriam

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In Memoriam

 

Warren R. Kadrmas, MD, COL, MC, USAF

November 6, 1969-May 8, 2014

Matthew T. Provencher, MD, CAPT, MC, USNR, and John M. Tokish, MD

A Selfless Leader and Former Head of Air Force Orthopedics

In 2014, we tragically lost a true friend, outstanding clinician, great family man, and incredible human being. As one of the preeminent sports orthopedists in the military, Dr. Kadrmas was beloved by all and heralded for his many selfless contributions to military musculoskeletal medicine and injury prevention. He was known for his humble nature and steadfast integrity, and served as an exemplary role model whom we all aspired to emulate. We all remember our time with Warren fondly, and he left us all with lasting memories to cherish and countless stories sure to regale.

Warren Kadrmas was born in 1969 in Vermillion, South Dakota and grew up in Sheridan, Wyoming. Dr. Kadrmas graduated with distinction from both the US Air Force Academy in 1992 and Duke University School of Medicine in 1996. He then went on to complete his residency in 2003 at the Hospital for Special Surgery (HSS) in New York City and was recognized with the Jean C. McDaniel Outstanding Resident Award. He began his Air Force orthopedic career at Wilford Hall Ambulatory Surgical Center on the grounds of Lackland Air Force Base in San Antonio, Texas as part of the 59th Medical Wing. Warren was deployed and served as 1 of 5 people on the mobile-field surgical team assigned to the 379th Expeditionary Medical Group. Subsequently, he returned to HSS, where he excelled in sports medicine and shoulder service subspecialty training.

After his fellowship, Warren returned to San Antonio to continue his work as a top military sports surgeon, serving as a mentor, educator, and leader for all of Air Force orthopedics. During this time he served several tours overseas, becoming an invaluable member of the 332nd Expeditionary Medical Group operating out of the Air Force Theater Hospital at Balad Air Base, Iraq. Warren served as the Program Director of the Orthopedic Residency Program at Wilford Hall Ambulatory Surgical Center. He held the position of Head of Orthopedics for the Air Force as Orthopedic Surgery Consultant to the Air Force Surgeon General for 5 years, a role that entailed coordinating all orthopedic assets for the Global War on Terror for the Air Force. Selfless to a fault, he would never ask anything of anyone that he had not done himself. He completed 6 deployments away from family, loved ones, and work in San Antonio.

A true innovator and visionary, Warren was a pioneer in the integration of high-caliber hip arthroscopy, as well as cutting-edge shoulder and knee care for our active-duty military personnel. He was a prominent member of the American Orthopaedic Society for Sports Medicine (AOSSM) and Arthroscopy Association of North America, and was in line to be the incoming President of the Society of Military Orthopaedic Surgeons, after having previously served as the society’s 2nd Vice President. He was selected for and was scheduled to participate in the AOSSM Traveling Fellowship touring Asia just prior to his untimely accident.

One of Warren’s favorite quotes was on the topic of leading from behind. Nelson Mandela said, “It is better to lead from behind and to put others in front, especially when you celebrate victory when nice things occur. You take the front line when there is danger. Then people will appreciate your leadership.” Warren was the embodiment of this quote. He led from the front, and by example, in times of danger to inspire those he led. But he also honed the skill of leading from behind, with quiet self-sacrifice, to celebrate the success of those he led. His tireless dedication was prominent in all the facets of his life, whether as a father, son, brother, surgeon, educator, mentor, or friend. We miss him dearly, and try to embody his spirit by living our lives through what he taught us all.

 

Brian Allgood, MD, COL

1960-2007

Dean Taylor, MD

An Exemplary Selfless Leader in Orthopedics and Medicine

When people ask me what effective, ethical healthcare leadership looks like, I think of Brian Allgood. Brian was the epitome of leadership. He led quietly, by example and selflessly–always putting the interests of patients and those on his team ahead of his own.

Brian was a 1982 graduate of the United States Military Academy at West Point, and received a Doctor of Medicine degree from the University of Oklahoma. He completed his orthopedic training at Brooke Army Medical Center in San Antonio. I first met Brian in 1994 when he was practicing as an orthopedic surgeon at Womack Army Medical Center at Ft. Bragg, North Carolina, where he also served at the Division Surgeon for the 82nd Airborne Division. At the time, I was extremely impressed with Brian’s outstanding orthopedic skills, and his unwavering commitment to leadership in orthopedics, military medicine, and medicine.

Brian’s role as the 82nd Airborne Division Surgeon was on the leadership track in Army medicine, a track that many of us who enjoyed and were good at patient care shunned because it was structured to limit the amount of time an administrative leader could spend in patient care. Brian was certainly a skilled orthopedic surgeon who loved caring for patients; however, he was courageous enough to put his responsibility to military medicine and the medical profession ahead of his own clinical interests. He realized that he could provide exceptional leadership that would benefit many instead of only those in his sphere of care. And what an exceptional leader he was!

From 2002 to 2004, I saw firsthand Brian’s extraordinary leadership when he served as the hospital commander of Keller Army Community Hospital at West Point. He was the best hospital commander I worked with during my 11 years at West Point. I saw the sacrifices he made for the rest of us. He gave up something he loved–orthopedic surgery–so that he could effectively lead our hospital. While we operated, he occasionally would look longingly through the operating room (OR) windows. When we saw him, we would invite him to scrub in, much to his delight. He would also show up in other services’ ORs and the hospital’s clinics, staying connected to patients and patient care. This patient-centeredness contributed significantly to the beloved leader he was.

Brian’s final assignment was in 2006 as the Command Surgeon of Multi-National Forces, the highest-ranking medical officer in Iraq. On January 20, 2007, Brian Allgood—on the verge of promotion to brigadier general and on the fast track to Surgeon General of the Army—was killed along with 11 other American service members when their helicopter was shot down.

In his life, Brian was an exemplary leader. After his death, he lives on in our memories as an example to which we should all aspire–an ethical, selfless leader who cared for all patients, always striving to do the right thing.

 

 

 

LCpl Benjamin Whetstone Schmidt

1987-2011

David R. Schmidt, MD

A Fallen Hero’s Legacy

On September 11, 2011, LCpl Benjamin Whetstone Schmidt posted on his Facebook page, “I guess you can use today as a reason for us to be here in Afghanistan. Just know I am fighting for myself, but most of all for my friends and family who read this. Everyone, it’s an honor to be your ambassador.”

Benjamin was a Marine Scout Sniper on his second tour to Afghanistan, this time voluntarily. Not one member of his platoon had combat experience. He felt called to lead, to be with his boys. During his first deployment to Afghanistan he was awarded the Navy/USMC Achievement Medal with Valor for his action in combat.

Less than a month later, on October 6, 2011, he was killed while on patrol in Helmand Province. Even now, 6 years after his death, his comrades continue to hail his virtues as a leader, a friend, a patriot, and an inspiration. He was also a fine athlete and a courageous, energetic young man with bold plans for his future.

Other than his family, few knew what Benjamin would inspire in his death. He left $200,000 of his life insurance to establish a scholarship in the History Department at his beloved Texas Christian University (TCU). With a matching gift from his father, orthopedic surgeon David R. Schmidt, MD, and stepmom Teresa, the scholarship provides annual funding for a graduate student. Asked why he chose to support graduate students, Benjamin replied with his signature humor and wisdom, “I wouldn’t invest in a freshman like myself.” Benjamin had spent 2 years at TCU prior to enlisting in the Marine Corps, and intended to return to TCU to complete his undergraduate and graduate degrees.

Certainly not many young men at age 24 years, prior to going to war, have the foresight to envision and implement a legacy bigger than themselves, with the promise of influencing generations into the future. For his actions, Benjamin was a finalist for a Congressional Medal of Honor Society “Citizen Service Before Self” award.

David and Teresa Schmidt subsequently raised $1 million dollars to endow the LCpl Benjamin W. Schmidt Professor of War, Conflict and Society. It is truly inspirational to know that a young man’s selfless vision and his friends’ and family’s support could produce such a lasting legacy.

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Warren R. Kadrmas, MD, COL, MC, USAF

November 6, 1969-May 8, 2014

Matthew T. Provencher, MD, CAPT, MC, USNR, and John M. Tokish, MD

A Selfless Leader and Former Head of Air Force Orthopedics

In 2014, we tragically lost a true friend, outstanding clinician, great family man, and incredible human being. As one of the preeminent sports orthopedists in the military, Dr. Kadrmas was beloved by all and heralded for his many selfless contributions to military musculoskeletal medicine and injury prevention. He was known for his humble nature and steadfast integrity, and served as an exemplary role model whom we all aspired to emulate. We all remember our time with Warren fondly, and he left us all with lasting memories to cherish and countless stories sure to regale.

Warren Kadrmas was born in 1969 in Vermillion, South Dakota and grew up in Sheridan, Wyoming. Dr. Kadrmas graduated with distinction from both the US Air Force Academy in 1992 and Duke University School of Medicine in 1996. He then went on to complete his residency in 2003 at the Hospital for Special Surgery (HSS) in New York City and was recognized with the Jean C. McDaniel Outstanding Resident Award. He began his Air Force orthopedic career at Wilford Hall Ambulatory Surgical Center on the grounds of Lackland Air Force Base in San Antonio, Texas as part of the 59th Medical Wing. Warren was deployed and served as 1 of 5 people on the mobile-field surgical team assigned to the 379th Expeditionary Medical Group. Subsequently, he returned to HSS, where he excelled in sports medicine and shoulder service subspecialty training.

After his fellowship, Warren returned to San Antonio to continue his work as a top military sports surgeon, serving as a mentor, educator, and leader for all of Air Force orthopedics. During this time he served several tours overseas, becoming an invaluable member of the 332nd Expeditionary Medical Group operating out of the Air Force Theater Hospital at Balad Air Base, Iraq. Warren served as the Program Director of the Orthopedic Residency Program at Wilford Hall Ambulatory Surgical Center. He held the position of Head of Orthopedics for the Air Force as Orthopedic Surgery Consultant to the Air Force Surgeon General for 5 years, a role that entailed coordinating all orthopedic assets for the Global War on Terror for the Air Force. Selfless to a fault, he would never ask anything of anyone that he had not done himself. He completed 6 deployments away from family, loved ones, and work in San Antonio.

A true innovator and visionary, Warren was a pioneer in the integration of high-caliber hip arthroscopy, as well as cutting-edge shoulder and knee care for our active-duty military personnel. He was a prominent member of the American Orthopaedic Society for Sports Medicine (AOSSM) and Arthroscopy Association of North America, and was in line to be the incoming President of the Society of Military Orthopaedic Surgeons, after having previously served as the society’s 2nd Vice President. He was selected for and was scheduled to participate in the AOSSM Traveling Fellowship touring Asia just prior to his untimely accident.

One of Warren’s favorite quotes was on the topic of leading from behind. Nelson Mandela said, “It is better to lead from behind and to put others in front, especially when you celebrate victory when nice things occur. You take the front line when there is danger. Then people will appreciate your leadership.” Warren was the embodiment of this quote. He led from the front, and by example, in times of danger to inspire those he led. But he also honed the skill of leading from behind, with quiet self-sacrifice, to celebrate the success of those he led. His tireless dedication was prominent in all the facets of his life, whether as a father, son, brother, surgeon, educator, mentor, or friend. We miss him dearly, and try to embody his spirit by living our lives through what he taught us all.

 

Brian Allgood, MD, COL

1960-2007

Dean Taylor, MD

An Exemplary Selfless Leader in Orthopedics and Medicine

When people ask me what effective, ethical healthcare leadership looks like, I think of Brian Allgood. Brian was the epitome of leadership. He led quietly, by example and selflessly–always putting the interests of patients and those on his team ahead of his own.

Brian was a 1982 graduate of the United States Military Academy at West Point, and received a Doctor of Medicine degree from the University of Oklahoma. He completed his orthopedic training at Brooke Army Medical Center in San Antonio. I first met Brian in 1994 when he was practicing as an orthopedic surgeon at Womack Army Medical Center at Ft. Bragg, North Carolina, where he also served at the Division Surgeon for the 82nd Airborne Division. At the time, I was extremely impressed with Brian’s outstanding orthopedic skills, and his unwavering commitment to leadership in orthopedics, military medicine, and medicine.

Brian’s role as the 82nd Airborne Division Surgeon was on the leadership track in Army medicine, a track that many of us who enjoyed and were good at patient care shunned because it was structured to limit the amount of time an administrative leader could spend in patient care. Brian was certainly a skilled orthopedic surgeon who loved caring for patients; however, he was courageous enough to put his responsibility to military medicine and the medical profession ahead of his own clinical interests. He realized that he could provide exceptional leadership that would benefit many instead of only those in his sphere of care. And what an exceptional leader he was!

From 2002 to 2004, I saw firsthand Brian’s extraordinary leadership when he served as the hospital commander of Keller Army Community Hospital at West Point. He was the best hospital commander I worked with during my 11 years at West Point. I saw the sacrifices he made for the rest of us. He gave up something he loved–orthopedic surgery–so that he could effectively lead our hospital. While we operated, he occasionally would look longingly through the operating room (OR) windows. When we saw him, we would invite him to scrub in, much to his delight. He would also show up in other services’ ORs and the hospital’s clinics, staying connected to patients and patient care. This patient-centeredness contributed significantly to the beloved leader he was.

Brian’s final assignment was in 2006 as the Command Surgeon of Multi-National Forces, the highest-ranking medical officer in Iraq. On January 20, 2007, Brian Allgood—on the verge of promotion to brigadier general and on the fast track to Surgeon General of the Army—was killed along with 11 other American service members when their helicopter was shot down.

In his life, Brian was an exemplary leader. After his death, he lives on in our memories as an example to which we should all aspire–an ethical, selfless leader who cared for all patients, always striving to do the right thing.

 

 

 

LCpl Benjamin Whetstone Schmidt

1987-2011

David R. Schmidt, MD

A Fallen Hero’s Legacy

On September 11, 2011, LCpl Benjamin Whetstone Schmidt posted on his Facebook page, “I guess you can use today as a reason for us to be here in Afghanistan. Just know I am fighting for myself, but most of all for my friends and family who read this. Everyone, it’s an honor to be your ambassador.”

Benjamin was a Marine Scout Sniper on his second tour to Afghanistan, this time voluntarily. Not one member of his platoon had combat experience. He felt called to lead, to be with his boys. During his first deployment to Afghanistan he was awarded the Navy/USMC Achievement Medal with Valor for his action in combat.

Less than a month later, on October 6, 2011, he was killed while on patrol in Helmand Province. Even now, 6 years after his death, his comrades continue to hail his virtues as a leader, a friend, a patriot, and an inspiration. He was also a fine athlete and a courageous, energetic young man with bold plans for his future.

Other than his family, few knew what Benjamin would inspire in his death. He left $200,000 of his life insurance to establish a scholarship in the History Department at his beloved Texas Christian University (TCU). With a matching gift from his father, orthopedic surgeon David R. Schmidt, MD, and stepmom Teresa, the scholarship provides annual funding for a graduate student. Asked why he chose to support graduate students, Benjamin replied with his signature humor and wisdom, “I wouldn’t invest in a freshman like myself.” Benjamin had spent 2 years at TCU prior to enlisting in the Marine Corps, and intended to return to TCU to complete his undergraduate and graduate degrees.

Certainly not many young men at age 24 years, prior to going to war, have the foresight to envision and implement a legacy bigger than themselves, with the promise of influencing generations into the future. For his actions, Benjamin was a finalist for a Congressional Medal of Honor Society “Citizen Service Before Self” award.

David and Teresa Schmidt subsequently raised $1 million dollars to endow the LCpl Benjamin W. Schmidt Professor of War, Conflict and Society. It is truly inspirational to know that a young man’s selfless vision and his friends’ and family’s support could produce such a lasting legacy.

 

Warren R. Kadrmas, MD, COL, MC, USAF

November 6, 1969-May 8, 2014

Matthew T. Provencher, MD, CAPT, MC, USNR, and John M. Tokish, MD

A Selfless Leader and Former Head of Air Force Orthopedics

In 2014, we tragically lost a true friend, outstanding clinician, great family man, and incredible human being. As one of the preeminent sports orthopedists in the military, Dr. Kadrmas was beloved by all and heralded for his many selfless contributions to military musculoskeletal medicine and injury prevention. He was known for his humble nature and steadfast integrity, and served as an exemplary role model whom we all aspired to emulate. We all remember our time with Warren fondly, and he left us all with lasting memories to cherish and countless stories sure to regale.

Warren Kadrmas was born in 1969 in Vermillion, South Dakota and grew up in Sheridan, Wyoming. Dr. Kadrmas graduated with distinction from both the US Air Force Academy in 1992 and Duke University School of Medicine in 1996. He then went on to complete his residency in 2003 at the Hospital for Special Surgery (HSS) in New York City and was recognized with the Jean C. McDaniel Outstanding Resident Award. He began his Air Force orthopedic career at Wilford Hall Ambulatory Surgical Center on the grounds of Lackland Air Force Base in San Antonio, Texas as part of the 59th Medical Wing. Warren was deployed and served as 1 of 5 people on the mobile-field surgical team assigned to the 379th Expeditionary Medical Group. Subsequently, he returned to HSS, where he excelled in sports medicine and shoulder service subspecialty training.

After his fellowship, Warren returned to San Antonio to continue his work as a top military sports surgeon, serving as a mentor, educator, and leader for all of Air Force orthopedics. During this time he served several tours overseas, becoming an invaluable member of the 332nd Expeditionary Medical Group operating out of the Air Force Theater Hospital at Balad Air Base, Iraq. Warren served as the Program Director of the Orthopedic Residency Program at Wilford Hall Ambulatory Surgical Center. He held the position of Head of Orthopedics for the Air Force as Orthopedic Surgery Consultant to the Air Force Surgeon General for 5 years, a role that entailed coordinating all orthopedic assets for the Global War on Terror for the Air Force. Selfless to a fault, he would never ask anything of anyone that he had not done himself. He completed 6 deployments away from family, loved ones, and work in San Antonio.

A true innovator and visionary, Warren was a pioneer in the integration of high-caliber hip arthroscopy, as well as cutting-edge shoulder and knee care for our active-duty military personnel. He was a prominent member of the American Orthopaedic Society for Sports Medicine (AOSSM) and Arthroscopy Association of North America, and was in line to be the incoming President of the Society of Military Orthopaedic Surgeons, after having previously served as the society’s 2nd Vice President. He was selected for and was scheduled to participate in the AOSSM Traveling Fellowship touring Asia just prior to his untimely accident.

One of Warren’s favorite quotes was on the topic of leading from behind. Nelson Mandela said, “It is better to lead from behind and to put others in front, especially when you celebrate victory when nice things occur. You take the front line when there is danger. Then people will appreciate your leadership.” Warren was the embodiment of this quote. He led from the front, and by example, in times of danger to inspire those he led. But he also honed the skill of leading from behind, with quiet self-sacrifice, to celebrate the success of those he led. His tireless dedication was prominent in all the facets of his life, whether as a father, son, brother, surgeon, educator, mentor, or friend. We miss him dearly, and try to embody his spirit by living our lives through what he taught us all.

 

Brian Allgood, MD, COL

1960-2007

Dean Taylor, MD

An Exemplary Selfless Leader in Orthopedics and Medicine

When people ask me what effective, ethical healthcare leadership looks like, I think of Brian Allgood. Brian was the epitome of leadership. He led quietly, by example and selflessly–always putting the interests of patients and those on his team ahead of his own.

Brian was a 1982 graduate of the United States Military Academy at West Point, and received a Doctor of Medicine degree from the University of Oklahoma. He completed his orthopedic training at Brooke Army Medical Center in San Antonio. I first met Brian in 1994 when he was practicing as an orthopedic surgeon at Womack Army Medical Center at Ft. Bragg, North Carolina, where he also served at the Division Surgeon for the 82nd Airborne Division. At the time, I was extremely impressed with Brian’s outstanding orthopedic skills, and his unwavering commitment to leadership in orthopedics, military medicine, and medicine.

Brian’s role as the 82nd Airborne Division Surgeon was on the leadership track in Army medicine, a track that many of us who enjoyed and were good at patient care shunned because it was structured to limit the amount of time an administrative leader could spend in patient care. Brian was certainly a skilled orthopedic surgeon who loved caring for patients; however, he was courageous enough to put his responsibility to military medicine and the medical profession ahead of his own clinical interests. He realized that he could provide exceptional leadership that would benefit many instead of only those in his sphere of care. And what an exceptional leader he was!

From 2002 to 2004, I saw firsthand Brian’s extraordinary leadership when he served as the hospital commander of Keller Army Community Hospital at West Point. He was the best hospital commander I worked with during my 11 years at West Point. I saw the sacrifices he made for the rest of us. He gave up something he loved–orthopedic surgery–so that he could effectively lead our hospital. While we operated, he occasionally would look longingly through the operating room (OR) windows. When we saw him, we would invite him to scrub in, much to his delight. He would also show up in other services’ ORs and the hospital’s clinics, staying connected to patients and patient care. This patient-centeredness contributed significantly to the beloved leader he was.

Brian’s final assignment was in 2006 as the Command Surgeon of Multi-National Forces, the highest-ranking medical officer in Iraq. On January 20, 2007, Brian Allgood—on the verge of promotion to brigadier general and on the fast track to Surgeon General of the Army—was killed along with 11 other American service members when their helicopter was shot down.

In his life, Brian was an exemplary leader. After his death, he lives on in our memories as an example to which we should all aspire–an ethical, selfless leader who cared for all patients, always striving to do the right thing.

 

 

 

LCpl Benjamin Whetstone Schmidt

1987-2011

David R. Schmidt, MD

A Fallen Hero’s Legacy

On September 11, 2011, LCpl Benjamin Whetstone Schmidt posted on his Facebook page, “I guess you can use today as a reason for us to be here in Afghanistan. Just know I am fighting for myself, but most of all for my friends and family who read this. Everyone, it’s an honor to be your ambassador.”

Benjamin was a Marine Scout Sniper on his second tour to Afghanistan, this time voluntarily. Not one member of his platoon had combat experience. He felt called to lead, to be with his boys. During his first deployment to Afghanistan he was awarded the Navy/USMC Achievement Medal with Valor for his action in combat.

Less than a month later, on October 6, 2011, he was killed while on patrol in Helmand Province. Even now, 6 years after his death, his comrades continue to hail his virtues as a leader, a friend, a patriot, and an inspiration. He was also a fine athlete and a courageous, energetic young man with bold plans for his future.

Other than his family, few knew what Benjamin would inspire in his death. He left $200,000 of his life insurance to establish a scholarship in the History Department at his beloved Texas Christian University (TCU). With a matching gift from his father, orthopedic surgeon David R. Schmidt, MD, and stepmom Teresa, the scholarship provides annual funding for a graduate student. Asked why he chose to support graduate students, Benjamin replied with his signature humor and wisdom, “I wouldn’t invest in a freshman like myself.” Benjamin had spent 2 years at TCU prior to enlisting in the Marine Corps, and intended to return to TCU to complete his undergraduate and graduate degrees.

Certainly not many young men at age 24 years, prior to going to war, have the foresight to envision and implement a legacy bigger than themselves, with the promise of influencing generations into the future. For his actions, Benjamin was a finalist for a Congressional Medal of Honor Society “Citizen Service Before Self” award.

David and Teresa Schmidt subsequently raised $1 million dollars to endow the LCpl Benjamin W. Schmidt Professor of War, Conflict and Society. It is truly inspirational to know that a young man’s selfless vision and his friends’ and family’s support could produce such a lasting legacy.

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Applying Military Strategy to Complex Knee Reconstruction: Tips for Planning and Executing Advanced Surgery

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Applying Military Strategy to Complex Knee Reconstruction: Tips for Planning and Executing Advanced Surgery

Take-Home Points

  • Thorough preoperative planning is imperative and inclusive of history, physical examination, radiographs, and MRI and potentially CT scan.
  • Plan carefully for needed graft sources (autografts and allografts).
  • Rehabilitation starts preoperatively and a detailed individualized plan is often warranted.
  • Indicated ligamentous repair or augmented repair with reconstruction is more likely to succeed when performed within 2 weeks of injury.
  • Complex combined knee restoration surgery can be safely performed in an outpatient setting.

Complex combined knee restoration surgery can be safely performed in an outpatient setting. The term complex knee restoration is used to describe management of knee injuries that are more involved—that is, there is damage to the menisci, cartilage, ligaments, and bones. Management entails not only determining the best treatment options but navigating the more complex logistics of making sure all necessary grafts (fresh and frozen allografts and autografts), implants, and instrumentation are readily available as these cases come to fruition.

The military healthcare paradigm often involves the added logistics of transporting the service member to the correct military treatment facility at the correct time and ensuring the patient’s work-up is complete before he or she arrives for the complex knee restoration. Such cases require significant rehabilitation and time away from family and work, so anything that reduces the morbidity of the surgical undertaking and the overall “morbidity footprint” of time away and that helps the patient return to normal function are value-added and worthy of our attention and diligence in developing an efficient system for managing complex cases.

The globally integrated military healthcare system that is in place has matured over the past decades to allow for the significant majority of the necessary preoperative work-up to be performed at a soldier’s current duty station, wherever in the world that may be, under the guidance of local healthcare providers with specific inputs from the knee restoration surgeon who eventually receives the patient for the planned surgical intervention.

Algorithm for Knee Restoration Planning

Alignment Issues

The first task is to confirm the realignment indication. Realignment may be performed with a proximal opening-wedge medial tibial osteotomy (OWMTO), a distal opening-wedge lateral femoral osteotomy (OWLFO), or a tibial tubercle osteotomy (TTO).1 Given the reproducible clinical improvement achieved and the robust nature of the fixation, these osteotomies are often the first surgical step in complex knee restorations.2 The final determination, made by the surgeon in consultation with the patient, is whether to perform the indicated osteotomy alone or in combination with the rest of the planned restoration surgery. In the vast majority of cases I have managed over the past 2 decades, I have performed the entire knee restoration in a single operation.3 Within the past 5 years, combining the procedures has become even more feasible with the important progress made in multimodal pain management and with the close collaboration of anesthesiologists.4

Meniscus and Cartilage Status

The integration status of meniscus and cartilage within the medial and lateral tibiofemoral compartments is crucial to the comprehensive restoration plan. In fact, the success of the restoration can be said to be dependent on the functional status and health of meniscus and cartilage—which either succeed together or fail apart.

Important covariables are age, prior surgical interventions, activity level expected or allowed after surgery, and size, location, and depth of cartilage injury.5 Whether a cartilage injury is monopolar or bipolar is determined with advanced imaging (magnetic resonance imaging [MRI], computed tomography [CT], weight-bearing radiography) along with analysis of a thorough history (including a review of prior operative reports and arthroscopic images) and a knee examination. Bipolar injuries that involve the condyle and juxtaposed plateau often bode poorly for good clinical outcomes—compared with unipolar lesions, which usually involve the condylar surfaces in isolation. The same thinking regarding the patellofemoral compartment is appropriate. Cartilage lesions that involve the juxtaposed surfaces of the patellar and trochlear groove do poorer than isolated lesions, which are more amenable to cartilage restoration options. The literature on potential cartilage restoration options for the patella and trochlea is expanding. I use the 3-dimensional cartilage restoration option of a fresh patellar osteochondral allograft (OCA) for high-grade cartilage lesions thought to be clinically significant. Other options, such as microfracture, cell-based cartilage restoration, and Osteochondral Autograft Transfer System (Arthrex) procedures (from the thinner condylar cartilage), have varied in their outcomes for patellar lesions. According to more recent literature and a review of my clinical results, fresh patellar OCAs are a good option for patellar lesions.6 Similarly, trochlear lesions can be managed with microfracture, cell-based therapies, or fresh OCAs, depending on surgeon preference.

Functional total or subtotal meniscectomies are often best managed with meniscal allograft transplantation (MAT). An intact or replaced medial or lateral meniscus works synergistically with any planned anterior cruciate ligament (ACL) reconstruction. Again, the adage that meniscus and cartilage succeed together or fail apart is appropriate when planning complex knee restoration. Signs of extrusion or joint-space narrowing and root avulsion or significant loss of meniscal tissue, visualized on MRI or on prior surgical images, often help substantiate a MAT plan. MAT has had the best long-term results when performed in compartments with cartilage damage limited to grade I and grade II changes, in stable knees, and in knees that can be concurrently stabilized.5 Technological advances have increased the value of MAT by limiting the morbidity of the operation and thus allowing for other surgery to be performed concomitantly and safely as part of comprehensive knee restoration. Over the past 20 years, I have arthroscopically performed MAT with bone plugs for medial and lateral procedures, and my results with active-duty soldiers have been promising, paralleling the clinic success reported in the literature.5 Alignment must be considered when performing MAT or cartilage restoration. If the addition of meniscal transplantation or cartilage restoration leaves the knee with residual malalignment of 6° or more, corrective osteotomy is performed.

My view and practice have been to plan for an unloading chondroprotective osteotomy. The goal is a balanced mechanical axis, whether achieved with mere joint-space restoration or with an osteotomy added.

Ligament Status

A comprehensive plan for establishing ligamentous stability is paramount to the overall clinical success of complex knee restorations. Meniscus and cartilage restoration efforts are wasted if clinically significant ligamentous laxity is not concomitantly treated with reconstruction surgery. Revision ACL surgery is by far the most commonly performed surgery in complex knee cases. Diligence in interpreting advanced MRI and physical examination findings is required to make sure there are no concomitant patholaxities in the medial, lateral, posterior, posteromedial, and posterolateral ligamentous complexes. Appropriate ligamentous reconstruction is warranted to maximize clinical results in complex knee restorations. Such cases more commonly require allograft tissue, as the availability of autograft tissue is the limiting issue with 2 or more ligament reconstructions. Military treatment facilities, in which comprehensive knee restorations are performed, have soft-tissue allografts on hand at all times. Having tissue readily available makes it less imperative to determine the most appropriate combined ligamentous reconstruction surgery before the patient arrives—a process that is often difficult. This situation is in contradistinction to the need for specific matched-for-size allograft frozen meniscus and fresh cartilage tissues, both of which require tissue-form procurement in advance of planned restoration surgery.

Rehabilitation Plan

The rehabilitation plan is driven by the part of the complex knee restoration that demands the most caution with respect to weight-bearing and range of motion (ROM) during the first 6 weeks after surgery. The most limiting restorative surgeries involve meniscus and cartilage. Recent clinical trial results support weight-bearing soon after tibial osteotomy performed in the absence of meniscus and cartilage restoration that would otherwise limit weight-bearing for 6 weeks.7 Therefore, most of these complex knee restorations are appropriately managed with a hinged brace locked in extension for toe-touch weight-bearing ambulation, with ROM usually limited to 0° to 90° during the first 6 weeks. Quadriceps rehabilitation with straight-leg raises and isometric contractions is prescribed with a focus on maintaining full extension as the default resting knee position until normalized resting quadriceps tone returns. Full weight-bearing and advancement to full flexion are routinely allowed by 6 weeks.

Case Report

A 41-year-old male service member who was overseas was referred to my clinic for high tibial osteotomy consideration and possible revision ACL reconstruction. His symptoms were medial pain, recurrent instability, and patellofemoral crepitance. Three years earlier, he underwent autograft transtibial ACL reconstruction with significant débridement of the medial meniscus. Before his trip to the United States, I asked that new MRI scans, full-length standing hip–knee–ankle bilateral alignment radiographs, and a 4-view weight-bearing knee series (including a posteroanterior Rosenberg view) be obtained and sent for my review (Figure 1).

Figure 1.
In retrospect, this request obviated the need for the patient to make a second overseas trip.

Review of the patient’s detailed preoperative imaging work-up and electronic medical record (available through the military’s healthcare system) made it clear that far more surgical intervention was needed than originally assumed. A significant full-thickness chondral lesion of the patella and a subtotal medial meniscectomy would necessitate patellar cartilage restoration and medial MAT in addition to the high tibial osteotomy and revision ACL reconstruction.

Had this patient been sent through the military medical evacuation system, he would have had to make 2 overseas trips—one trip for preoperative evaluation and advanced imaging, whereby he would have been placed on a match list and had to wait for a requested meniscal allograft and an appropriate graft for his patella, and the other trip for his complex surgery. Fortunately, the military’s integrated healthcare network with true 2-way communication and the collaborative use of integrated electronic medical records proved extremely valuable in making management of this complex knee restoration as efficient as possible. From the perspective of the soldier and his military unit, only 1 big overseas trip was needed; from the perspective of the military healthcare system, responsible use of healthcare personnel and monetary resources and well-planned complex knee restoration surgery saved a knee and allowed a soldier-athlete to rejoin the fields of friendly strife.

 

 


This patient had undergone functional complete medial meniscectomy and had significant medial compartment pain, varus alignment, and minimal medial joint-space narrowing (assumed grossly intact cartilage about plateau and condyle), plus patellofemoral pain and crepitance with a large high-grade posttraumatic patellar chondral lesion with normal patellofemoral alignment. He also had an isolated failed ACL graft from prior ACL reconstruction. The previous hardware placement was analyzed, and it was determined that the femoral interference screw could be left in place and that the tibial interference screw most likely would be removed. The mechanical axis determined from the bilateral long-leg standing images dictated a need for proximal OWMTO for correction up to 8° to allow the axis to cross the center of the knee. The 8° correction is the measured correction needed to move the axis from its pass through the medial compartment to a more balanced position across the middle of the knee.

The overall plan encompassed major concomitant corrective and restorative surgery: tibial osteotomy, medial MAT, revision ACL reconstruction, and fresh mega-patellar OCA. Once the frozen meniscus and eventually the fresh patella (both matched for size) were obtained, arrangements for the patient’s trip for the complex surgery were finalized.

Surgery was started with brief arthroscopic evaluation to confirm the overall appropriateness of the planned procedure and to determine if any other minor deficiencies would warrant operative intervention. Once confirmed, the restoration proceeded as planned. The OWMTO was performed with a PEEK (polyetheretherketone) wedge implant (iBalance; Arthrex) followed by arthroscopic preparation for medial MAT with removal of any meniscal remnants and placement of passing sutures (Figure 2A).
Figure 2.
The meniscus was delivered across the compartment through an enlarged medial portal. The posterior horn bone plug was secured in the retrosocket with sutures tied off to an anterior tibial cortical 2-hole button (Figure 2B). The body of the posterior third of the meniscus was secured to the posterior capsule by tying the 2 previously placed vertical sutures to each other over the intervening capsule. The anterior horn bone plug (10 mm in diameter × 7 mm thick) was then secured within a 10-mm socket drilled antegrade to a depth of 10 mm with a SwiveLock anchor (Arthrex) for interference bony fixation and recapitulation of the normal hoop stresses. Inside-out sutures were placed to secure the capsule to the meniscus and thereby prevent iatrogenic meniscal extrusion. A standard all-inside allograft revision ACL reconstruction was performed with an 11-mm FlipCutter and guide system (Arthrex) to make the femoral and tibial retrosockets.
Figure 3.
Passing sutures were used to deploy the ACL graft construct, which was fashioned into a quadruple-stranded GraftLink construct (Arthrex) from a 28-mm allograft peroneus longus tendon (Figure 3).

When the arthroscopic portion of the surgery was finished, a medial parapatellar arthrotomy was made to allow the patella to be inverted and complete fresh mega-patellar OCA placement (Figure 4).
Figure 4.
A drill guide system was used to prepare the host patella with the largest contained circular socket (35 mm) with a 1-mm to 2-mm cortical margin to a marginal bony depth and an 8- to 10-mm central bony depth.
Figure 5.
The donor patella was then prepared on the graft preparation guide to allow a mega-patellar osteochondral plug to be press-fit into the recipient socket after thorough pulse lavaging of the bony portion of the graft to negate as much of the marrow cellular elements as possible (Figure 5). After appropriate tracking was confirmed, the arthrotomy and skin incision were closed.

The knee was placed in a ROM brace locked in full extension. The patient was able to do straight-leg raises and calf pumps in the recovery room and was discharged home with a saphenous nerve block and an iPACK (Interspace between the Popliteal Artery and the Capsule of the posterior Knee) nerve block in place. Home-based therapy was started immediately. After the patient’s first postoperative visit, formal therapy (discussed earlier) was initiated (Figure 6).
Figure 6.
Toe-touch weight-bearing with the brace locked in extension and ROM limited to 0° to 90° were maintained until 6 weeks, when full weight-bearing and full ROM were allowed. The rehabilitation course was uneventful. The patient continued on active duty and completed his military service, retiring 3 years later with 20 years of service.

Discussion

All-inside GraftLink ACL reconstruction with cortical suspensory fixation appears well suited to combined medial and lateral MAT and/or cartilage restoration—whether it be large fresh OCA combined with medial MAT (as in this patient’s case) or another form of cartilage restoration. Arthroscopic MAT with anatomically fashioned and placed bone plugs minimizes the morbidity within the notch footprints and allows for discrete revision socket formation for both femoral and tibial ACL graft placement. In this case, preparation for the medial MAT and ACL sockets was followed by MAT/ACL construct implantation and secure fixation. The arthrotomy was thereby minimized and placed to allow for efficient mega-patellar OCA graft placement.

Over the past decade, I have performed similar concomitant procedures using the same surgical principles that allow for efficient and reproducible complex knee restoration (Figure 7).

Figure 7.
Common examples are multiligamentous reconstructions (ACL–posterior cruciate ligament–posterolateral corner, ACL–posterior cruciate ligament–medial collateral ligament, ACL–anterolateral ligament, and ACL–medial patellofemoral ligament) combined with concomitant meniscus and cartilage restoration and various osteotomies.

Although use of an algorithm for the management of complex knee restorations is not universally feasible, I offer guidelines for complex knee injuries:

  • At each decision point, determine whether the knee and the patient can withstand the planned surgical intervention.
  • After deciding to proceed with knee restoration, list the meniscus, cartilage, and ligament injuries that must be addressed.
  • Determine which repairs (meniscus, cartilage, ligament) are warranted. Repairs generally are best performed within a period of 7 to 14 days.
  • Determine which ligament injuries warrant reconstruction. Allograft tissue typically is used for multiligament reconstruction.
  • Rank-order the ligament reconstruction requirements. It is fine to proceed with all of the reconstructions if the case is moving smoothly, if there are no developing tourniquet-time issues, and if the soft-tissue envelope is responding as expected.
  • Consider autograft and/or allograft tissue needs for concomitant or staged meniscus and cartilage restoration options/requirements.


Am J Orthop. 2017;46(4):170-175, 202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Uquillas C, Rossy W, Nathasingh CK, Strauss E, Jazrawi L, Gonzalez-Lomas G. Osteotomies about the knee: AAOS exhibit selection. J Bone Joint Surg Am. 2014;96(24):e199.

2. Mehl J, Paul J, Feucht MJ, et al. ACL deficiency and varus osteoarthritis: high tibial osteotomy alone or combined with ACL reconstruction? Arch Orthop Trauma Surg. 2017;137(2):233-240.

3. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

4. Ferrari D, Lopes TJ, França PF, Azevedo FM, Pappas E. Outpatient versus inpatient anterior cruciate ligament reconstruction: a systematic review with meta-analysis. Knee. 2017;24(2):197-206.

5. Weber AE, Gitelis ME, McCarthy MA, Yanke AB, Cole BJ. Malalignment: a requirement for cartilage and organ restoration. Sports Med Arthrosc. 2016;24(2):e14-e22.

6. Prince MR, King AH, Stuart MJ, Dahm DL, Krych AJ. Treatment of patellofemoral cartilage lesions in the young, active patient. J Knee Surg. 2015;28(4):285-295.

7. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

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Take-Home Points

  • Thorough preoperative planning is imperative and inclusive of history, physical examination, radiographs, and MRI and potentially CT scan.
  • Plan carefully for needed graft sources (autografts and allografts).
  • Rehabilitation starts preoperatively and a detailed individualized plan is often warranted.
  • Indicated ligamentous repair or augmented repair with reconstruction is more likely to succeed when performed within 2 weeks of injury.
  • Complex combined knee restoration surgery can be safely performed in an outpatient setting.

Complex combined knee restoration surgery can be safely performed in an outpatient setting. The term complex knee restoration is used to describe management of knee injuries that are more involved—that is, there is damage to the menisci, cartilage, ligaments, and bones. Management entails not only determining the best treatment options but navigating the more complex logistics of making sure all necessary grafts (fresh and frozen allografts and autografts), implants, and instrumentation are readily available as these cases come to fruition.

The military healthcare paradigm often involves the added logistics of transporting the service member to the correct military treatment facility at the correct time and ensuring the patient’s work-up is complete before he or she arrives for the complex knee restoration. Such cases require significant rehabilitation and time away from family and work, so anything that reduces the morbidity of the surgical undertaking and the overall “morbidity footprint” of time away and that helps the patient return to normal function are value-added and worthy of our attention and diligence in developing an efficient system for managing complex cases.

The globally integrated military healthcare system that is in place has matured over the past decades to allow for the significant majority of the necessary preoperative work-up to be performed at a soldier’s current duty station, wherever in the world that may be, under the guidance of local healthcare providers with specific inputs from the knee restoration surgeon who eventually receives the patient for the planned surgical intervention.

Algorithm for Knee Restoration Planning

Alignment Issues

The first task is to confirm the realignment indication. Realignment may be performed with a proximal opening-wedge medial tibial osteotomy (OWMTO), a distal opening-wedge lateral femoral osteotomy (OWLFO), or a tibial tubercle osteotomy (TTO).1 Given the reproducible clinical improvement achieved and the robust nature of the fixation, these osteotomies are often the first surgical step in complex knee restorations.2 The final determination, made by the surgeon in consultation with the patient, is whether to perform the indicated osteotomy alone or in combination with the rest of the planned restoration surgery. In the vast majority of cases I have managed over the past 2 decades, I have performed the entire knee restoration in a single operation.3 Within the past 5 years, combining the procedures has become even more feasible with the important progress made in multimodal pain management and with the close collaboration of anesthesiologists.4

Meniscus and Cartilage Status

The integration status of meniscus and cartilage within the medial and lateral tibiofemoral compartments is crucial to the comprehensive restoration plan. In fact, the success of the restoration can be said to be dependent on the functional status and health of meniscus and cartilage—which either succeed together or fail apart.

Important covariables are age, prior surgical interventions, activity level expected or allowed after surgery, and size, location, and depth of cartilage injury.5 Whether a cartilage injury is monopolar or bipolar is determined with advanced imaging (magnetic resonance imaging [MRI], computed tomography [CT], weight-bearing radiography) along with analysis of a thorough history (including a review of prior operative reports and arthroscopic images) and a knee examination. Bipolar injuries that involve the condyle and juxtaposed plateau often bode poorly for good clinical outcomes—compared with unipolar lesions, which usually involve the condylar surfaces in isolation. The same thinking regarding the patellofemoral compartment is appropriate. Cartilage lesions that involve the juxtaposed surfaces of the patellar and trochlear groove do poorer than isolated lesions, which are more amenable to cartilage restoration options. The literature on potential cartilage restoration options for the patella and trochlea is expanding. I use the 3-dimensional cartilage restoration option of a fresh patellar osteochondral allograft (OCA) for high-grade cartilage lesions thought to be clinically significant. Other options, such as microfracture, cell-based cartilage restoration, and Osteochondral Autograft Transfer System (Arthrex) procedures (from the thinner condylar cartilage), have varied in their outcomes for patellar lesions. According to more recent literature and a review of my clinical results, fresh patellar OCAs are a good option for patellar lesions.6 Similarly, trochlear lesions can be managed with microfracture, cell-based therapies, or fresh OCAs, depending on surgeon preference.

Functional total or subtotal meniscectomies are often best managed with meniscal allograft transplantation (MAT). An intact or replaced medial or lateral meniscus works synergistically with any planned anterior cruciate ligament (ACL) reconstruction. Again, the adage that meniscus and cartilage succeed together or fail apart is appropriate when planning complex knee restoration. Signs of extrusion or joint-space narrowing and root avulsion or significant loss of meniscal tissue, visualized on MRI or on prior surgical images, often help substantiate a MAT plan. MAT has had the best long-term results when performed in compartments with cartilage damage limited to grade I and grade II changes, in stable knees, and in knees that can be concurrently stabilized.5 Technological advances have increased the value of MAT by limiting the morbidity of the operation and thus allowing for other surgery to be performed concomitantly and safely as part of comprehensive knee restoration. Over the past 20 years, I have arthroscopically performed MAT with bone plugs for medial and lateral procedures, and my results with active-duty soldiers have been promising, paralleling the clinic success reported in the literature.5 Alignment must be considered when performing MAT or cartilage restoration. If the addition of meniscal transplantation or cartilage restoration leaves the knee with residual malalignment of 6° or more, corrective osteotomy is performed.

My view and practice have been to plan for an unloading chondroprotective osteotomy. The goal is a balanced mechanical axis, whether achieved with mere joint-space restoration or with an osteotomy added.

Ligament Status

A comprehensive plan for establishing ligamentous stability is paramount to the overall clinical success of complex knee restorations. Meniscus and cartilage restoration efforts are wasted if clinically significant ligamentous laxity is not concomitantly treated with reconstruction surgery. Revision ACL surgery is by far the most commonly performed surgery in complex knee cases. Diligence in interpreting advanced MRI and physical examination findings is required to make sure there are no concomitant patholaxities in the medial, lateral, posterior, posteromedial, and posterolateral ligamentous complexes. Appropriate ligamentous reconstruction is warranted to maximize clinical results in complex knee restorations. Such cases more commonly require allograft tissue, as the availability of autograft tissue is the limiting issue with 2 or more ligament reconstructions. Military treatment facilities, in which comprehensive knee restorations are performed, have soft-tissue allografts on hand at all times. Having tissue readily available makes it less imperative to determine the most appropriate combined ligamentous reconstruction surgery before the patient arrives—a process that is often difficult. This situation is in contradistinction to the need for specific matched-for-size allograft frozen meniscus and fresh cartilage tissues, both of which require tissue-form procurement in advance of planned restoration surgery.

Rehabilitation Plan

The rehabilitation plan is driven by the part of the complex knee restoration that demands the most caution with respect to weight-bearing and range of motion (ROM) during the first 6 weeks after surgery. The most limiting restorative surgeries involve meniscus and cartilage. Recent clinical trial results support weight-bearing soon after tibial osteotomy performed in the absence of meniscus and cartilage restoration that would otherwise limit weight-bearing for 6 weeks.7 Therefore, most of these complex knee restorations are appropriately managed with a hinged brace locked in extension for toe-touch weight-bearing ambulation, with ROM usually limited to 0° to 90° during the first 6 weeks. Quadriceps rehabilitation with straight-leg raises and isometric contractions is prescribed with a focus on maintaining full extension as the default resting knee position until normalized resting quadriceps tone returns. Full weight-bearing and advancement to full flexion are routinely allowed by 6 weeks.

Case Report

A 41-year-old male service member who was overseas was referred to my clinic for high tibial osteotomy consideration and possible revision ACL reconstruction. His symptoms were medial pain, recurrent instability, and patellofemoral crepitance. Three years earlier, he underwent autograft transtibial ACL reconstruction with significant débridement of the medial meniscus. Before his trip to the United States, I asked that new MRI scans, full-length standing hip–knee–ankle bilateral alignment radiographs, and a 4-view weight-bearing knee series (including a posteroanterior Rosenberg view) be obtained and sent for my review (Figure 1).

Figure 1.
In retrospect, this request obviated the need for the patient to make a second overseas trip.

Review of the patient’s detailed preoperative imaging work-up and electronic medical record (available through the military’s healthcare system) made it clear that far more surgical intervention was needed than originally assumed. A significant full-thickness chondral lesion of the patella and a subtotal medial meniscectomy would necessitate patellar cartilage restoration and medial MAT in addition to the high tibial osteotomy and revision ACL reconstruction.

Had this patient been sent through the military medical evacuation system, he would have had to make 2 overseas trips—one trip for preoperative evaluation and advanced imaging, whereby he would have been placed on a match list and had to wait for a requested meniscal allograft and an appropriate graft for his patella, and the other trip for his complex surgery. Fortunately, the military’s integrated healthcare network with true 2-way communication and the collaborative use of integrated electronic medical records proved extremely valuable in making management of this complex knee restoration as efficient as possible. From the perspective of the soldier and his military unit, only 1 big overseas trip was needed; from the perspective of the military healthcare system, responsible use of healthcare personnel and monetary resources and well-planned complex knee restoration surgery saved a knee and allowed a soldier-athlete to rejoin the fields of friendly strife.

 

 


This patient had undergone functional complete medial meniscectomy and had significant medial compartment pain, varus alignment, and minimal medial joint-space narrowing (assumed grossly intact cartilage about plateau and condyle), plus patellofemoral pain and crepitance with a large high-grade posttraumatic patellar chondral lesion with normal patellofemoral alignment. He also had an isolated failed ACL graft from prior ACL reconstruction. The previous hardware placement was analyzed, and it was determined that the femoral interference screw could be left in place and that the tibial interference screw most likely would be removed. The mechanical axis determined from the bilateral long-leg standing images dictated a need for proximal OWMTO for correction up to 8° to allow the axis to cross the center of the knee. The 8° correction is the measured correction needed to move the axis from its pass through the medial compartment to a more balanced position across the middle of the knee.

The overall plan encompassed major concomitant corrective and restorative surgery: tibial osteotomy, medial MAT, revision ACL reconstruction, and fresh mega-patellar OCA. Once the frozen meniscus and eventually the fresh patella (both matched for size) were obtained, arrangements for the patient’s trip for the complex surgery were finalized.

Surgery was started with brief arthroscopic evaluation to confirm the overall appropriateness of the planned procedure and to determine if any other minor deficiencies would warrant operative intervention. Once confirmed, the restoration proceeded as planned. The OWMTO was performed with a PEEK (polyetheretherketone) wedge implant (iBalance; Arthrex) followed by arthroscopic preparation for medial MAT with removal of any meniscal remnants and placement of passing sutures (Figure 2A).
Figure 2.
The meniscus was delivered across the compartment through an enlarged medial portal. The posterior horn bone plug was secured in the retrosocket with sutures tied off to an anterior tibial cortical 2-hole button (Figure 2B). The body of the posterior third of the meniscus was secured to the posterior capsule by tying the 2 previously placed vertical sutures to each other over the intervening capsule. The anterior horn bone plug (10 mm in diameter × 7 mm thick) was then secured within a 10-mm socket drilled antegrade to a depth of 10 mm with a SwiveLock anchor (Arthrex) for interference bony fixation and recapitulation of the normal hoop stresses. Inside-out sutures were placed to secure the capsule to the meniscus and thereby prevent iatrogenic meniscal extrusion. A standard all-inside allograft revision ACL reconstruction was performed with an 11-mm FlipCutter and guide system (Arthrex) to make the femoral and tibial retrosockets.
Figure 3.
Passing sutures were used to deploy the ACL graft construct, which was fashioned into a quadruple-stranded GraftLink construct (Arthrex) from a 28-mm allograft peroneus longus tendon (Figure 3).

When the arthroscopic portion of the surgery was finished, a medial parapatellar arthrotomy was made to allow the patella to be inverted and complete fresh mega-patellar OCA placement (Figure 4).
Figure 4.
A drill guide system was used to prepare the host patella with the largest contained circular socket (35 mm) with a 1-mm to 2-mm cortical margin to a marginal bony depth and an 8- to 10-mm central bony depth.
Figure 5.
The donor patella was then prepared on the graft preparation guide to allow a mega-patellar osteochondral plug to be press-fit into the recipient socket after thorough pulse lavaging of the bony portion of the graft to negate as much of the marrow cellular elements as possible (Figure 5). After appropriate tracking was confirmed, the arthrotomy and skin incision were closed.

The knee was placed in a ROM brace locked in full extension. The patient was able to do straight-leg raises and calf pumps in the recovery room and was discharged home with a saphenous nerve block and an iPACK (Interspace between the Popliteal Artery and the Capsule of the posterior Knee) nerve block in place. Home-based therapy was started immediately. After the patient’s first postoperative visit, formal therapy (discussed earlier) was initiated (Figure 6).
Figure 6.
Toe-touch weight-bearing with the brace locked in extension and ROM limited to 0° to 90° were maintained until 6 weeks, when full weight-bearing and full ROM were allowed. The rehabilitation course was uneventful. The patient continued on active duty and completed his military service, retiring 3 years later with 20 years of service.

Discussion

All-inside GraftLink ACL reconstruction with cortical suspensory fixation appears well suited to combined medial and lateral MAT and/or cartilage restoration—whether it be large fresh OCA combined with medial MAT (as in this patient’s case) or another form of cartilage restoration. Arthroscopic MAT with anatomically fashioned and placed bone plugs minimizes the morbidity within the notch footprints and allows for discrete revision socket formation for both femoral and tibial ACL graft placement. In this case, preparation for the medial MAT and ACL sockets was followed by MAT/ACL construct implantation and secure fixation. The arthrotomy was thereby minimized and placed to allow for efficient mega-patellar OCA graft placement.

Over the past decade, I have performed similar concomitant procedures using the same surgical principles that allow for efficient and reproducible complex knee restoration (Figure 7).

Figure 7.
Common examples are multiligamentous reconstructions (ACL–posterior cruciate ligament–posterolateral corner, ACL–posterior cruciate ligament–medial collateral ligament, ACL–anterolateral ligament, and ACL–medial patellofemoral ligament) combined with concomitant meniscus and cartilage restoration and various osteotomies.

Although use of an algorithm for the management of complex knee restorations is not universally feasible, I offer guidelines for complex knee injuries:

  • At each decision point, determine whether the knee and the patient can withstand the planned surgical intervention.
  • After deciding to proceed with knee restoration, list the meniscus, cartilage, and ligament injuries that must be addressed.
  • Determine which repairs (meniscus, cartilage, ligament) are warranted. Repairs generally are best performed within a period of 7 to 14 days.
  • Determine which ligament injuries warrant reconstruction. Allograft tissue typically is used for multiligament reconstruction.
  • Rank-order the ligament reconstruction requirements. It is fine to proceed with all of the reconstructions if the case is moving smoothly, if there are no developing tourniquet-time issues, and if the soft-tissue envelope is responding as expected.
  • Consider autograft and/or allograft tissue needs for concomitant or staged meniscus and cartilage restoration options/requirements.


Am J Orthop. 2017;46(4):170-175, 202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Thorough preoperative planning is imperative and inclusive of history, physical examination, radiographs, and MRI and potentially CT scan.
  • Plan carefully for needed graft sources (autografts and allografts).
  • Rehabilitation starts preoperatively and a detailed individualized plan is often warranted.
  • Indicated ligamentous repair or augmented repair with reconstruction is more likely to succeed when performed within 2 weeks of injury.
  • Complex combined knee restoration surgery can be safely performed in an outpatient setting.

Complex combined knee restoration surgery can be safely performed in an outpatient setting. The term complex knee restoration is used to describe management of knee injuries that are more involved—that is, there is damage to the menisci, cartilage, ligaments, and bones. Management entails not only determining the best treatment options but navigating the more complex logistics of making sure all necessary grafts (fresh and frozen allografts and autografts), implants, and instrumentation are readily available as these cases come to fruition.

The military healthcare paradigm often involves the added logistics of transporting the service member to the correct military treatment facility at the correct time and ensuring the patient’s work-up is complete before he or she arrives for the complex knee restoration. Such cases require significant rehabilitation and time away from family and work, so anything that reduces the morbidity of the surgical undertaking and the overall “morbidity footprint” of time away and that helps the patient return to normal function are value-added and worthy of our attention and diligence in developing an efficient system for managing complex cases.

The globally integrated military healthcare system that is in place has matured over the past decades to allow for the significant majority of the necessary preoperative work-up to be performed at a soldier’s current duty station, wherever in the world that may be, under the guidance of local healthcare providers with specific inputs from the knee restoration surgeon who eventually receives the patient for the planned surgical intervention.

Algorithm for Knee Restoration Planning

Alignment Issues

The first task is to confirm the realignment indication. Realignment may be performed with a proximal opening-wedge medial tibial osteotomy (OWMTO), a distal opening-wedge lateral femoral osteotomy (OWLFO), or a tibial tubercle osteotomy (TTO).1 Given the reproducible clinical improvement achieved and the robust nature of the fixation, these osteotomies are often the first surgical step in complex knee restorations.2 The final determination, made by the surgeon in consultation with the patient, is whether to perform the indicated osteotomy alone or in combination with the rest of the planned restoration surgery. In the vast majority of cases I have managed over the past 2 decades, I have performed the entire knee restoration in a single operation.3 Within the past 5 years, combining the procedures has become even more feasible with the important progress made in multimodal pain management and with the close collaboration of anesthesiologists.4

Meniscus and Cartilage Status

The integration status of meniscus and cartilage within the medial and lateral tibiofemoral compartments is crucial to the comprehensive restoration plan. In fact, the success of the restoration can be said to be dependent on the functional status and health of meniscus and cartilage—which either succeed together or fail apart.

Important covariables are age, prior surgical interventions, activity level expected or allowed after surgery, and size, location, and depth of cartilage injury.5 Whether a cartilage injury is monopolar or bipolar is determined with advanced imaging (magnetic resonance imaging [MRI], computed tomography [CT], weight-bearing radiography) along with analysis of a thorough history (including a review of prior operative reports and arthroscopic images) and a knee examination. Bipolar injuries that involve the condyle and juxtaposed plateau often bode poorly for good clinical outcomes—compared with unipolar lesions, which usually involve the condylar surfaces in isolation. The same thinking regarding the patellofemoral compartment is appropriate. Cartilage lesions that involve the juxtaposed surfaces of the patellar and trochlear groove do poorer than isolated lesions, which are more amenable to cartilage restoration options. The literature on potential cartilage restoration options for the patella and trochlea is expanding. I use the 3-dimensional cartilage restoration option of a fresh patellar osteochondral allograft (OCA) for high-grade cartilage lesions thought to be clinically significant. Other options, such as microfracture, cell-based cartilage restoration, and Osteochondral Autograft Transfer System (Arthrex) procedures (from the thinner condylar cartilage), have varied in their outcomes for patellar lesions. According to more recent literature and a review of my clinical results, fresh patellar OCAs are a good option for patellar lesions.6 Similarly, trochlear lesions can be managed with microfracture, cell-based therapies, or fresh OCAs, depending on surgeon preference.

Functional total or subtotal meniscectomies are often best managed with meniscal allograft transplantation (MAT). An intact or replaced medial or lateral meniscus works synergistically with any planned anterior cruciate ligament (ACL) reconstruction. Again, the adage that meniscus and cartilage succeed together or fail apart is appropriate when planning complex knee restoration. Signs of extrusion or joint-space narrowing and root avulsion or significant loss of meniscal tissue, visualized on MRI or on prior surgical images, often help substantiate a MAT plan. MAT has had the best long-term results when performed in compartments with cartilage damage limited to grade I and grade II changes, in stable knees, and in knees that can be concurrently stabilized.5 Technological advances have increased the value of MAT by limiting the morbidity of the operation and thus allowing for other surgery to be performed concomitantly and safely as part of comprehensive knee restoration. Over the past 20 years, I have arthroscopically performed MAT with bone plugs for medial and lateral procedures, and my results with active-duty soldiers have been promising, paralleling the clinic success reported in the literature.5 Alignment must be considered when performing MAT or cartilage restoration. If the addition of meniscal transplantation or cartilage restoration leaves the knee with residual malalignment of 6° or more, corrective osteotomy is performed.

My view and practice have been to plan for an unloading chondroprotective osteotomy. The goal is a balanced mechanical axis, whether achieved with mere joint-space restoration or with an osteotomy added.

Ligament Status

A comprehensive plan for establishing ligamentous stability is paramount to the overall clinical success of complex knee restorations. Meniscus and cartilage restoration efforts are wasted if clinically significant ligamentous laxity is not concomitantly treated with reconstruction surgery. Revision ACL surgery is by far the most commonly performed surgery in complex knee cases. Diligence in interpreting advanced MRI and physical examination findings is required to make sure there are no concomitant patholaxities in the medial, lateral, posterior, posteromedial, and posterolateral ligamentous complexes. Appropriate ligamentous reconstruction is warranted to maximize clinical results in complex knee restorations. Such cases more commonly require allograft tissue, as the availability of autograft tissue is the limiting issue with 2 or more ligament reconstructions. Military treatment facilities, in which comprehensive knee restorations are performed, have soft-tissue allografts on hand at all times. Having tissue readily available makes it less imperative to determine the most appropriate combined ligamentous reconstruction surgery before the patient arrives—a process that is often difficult. This situation is in contradistinction to the need for specific matched-for-size allograft frozen meniscus and fresh cartilage tissues, both of which require tissue-form procurement in advance of planned restoration surgery.

Rehabilitation Plan

The rehabilitation plan is driven by the part of the complex knee restoration that demands the most caution with respect to weight-bearing and range of motion (ROM) during the first 6 weeks after surgery. The most limiting restorative surgeries involve meniscus and cartilage. Recent clinical trial results support weight-bearing soon after tibial osteotomy performed in the absence of meniscus and cartilage restoration that would otherwise limit weight-bearing for 6 weeks.7 Therefore, most of these complex knee restorations are appropriately managed with a hinged brace locked in extension for toe-touch weight-bearing ambulation, with ROM usually limited to 0° to 90° during the first 6 weeks. Quadriceps rehabilitation with straight-leg raises and isometric contractions is prescribed with a focus on maintaining full extension as the default resting knee position until normalized resting quadriceps tone returns. Full weight-bearing and advancement to full flexion are routinely allowed by 6 weeks.

Case Report

A 41-year-old male service member who was overseas was referred to my clinic for high tibial osteotomy consideration and possible revision ACL reconstruction. His symptoms were medial pain, recurrent instability, and patellofemoral crepitance. Three years earlier, he underwent autograft transtibial ACL reconstruction with significant débridement of the medial meniscus. Before his trip to the United States, I asked that new MRI scans, full-length standing hip–knee–ankle bilateral alignment radiographs, and a 4-view weight-bearing knee series (including a posteroanterior Rosenberg view) be obtained and sent for my review (Figure 1).

Figure 1.
In retrospect, this request obviated the need for the patient to make a second overseas trip.

Review of the patient’s detailed preoperative imaging work-up and electronic medical record (available through the military’s healthcare system) made it clear that far more surgical intervention was needed than originally assumed. A significant full-thickness chondral lesion of the patella and a subtotal medial meniscectomy would necessitate patellar cartilage restoration and medial MAT in addition to the high tibial osteotomy and revision ACL reconstruction.

Had this patient been sent through the military medical evacuation system, he would have had to make 2 overseas trips—one trip for preoperative evaluation and advanced imaging, whereby he would have been placed on a match list and had to wait for a requested meniscal allograft and an appropriate graft for his patella, and the other trip for his complex surgery. Fortunately, the military’s integrated healthcare network with true 2-way communication and the collaborative use of integrated electronic medical records proved extremely valuable in making management of this complex knee restoration as efficient as possible. From the perspective of the soldier and his military unit, only 1 big overseas trip was needed; from the perspective of the military healthcare system, responsible use of healthcare personnel and monetary resources and well-planned complex knee restoration surgery saved a knee and allowed a soldier-athlete to rejoin the fields of friendly strife.

 

 


This patient had undergone functional complete medial meniscectomy and had significant medial compartment pain, varus alignment, and minimal medial joint-space narrowing (assumed grossly intact cartilage about plateau and condyle), plus patellofemoral pain and crepitance with a large high-grade posttraumatic patellar chondral lesion with normal patellofemoral alignment. He also had an isolated failed ACL graft from prior ACL reconstruction. The previous hardware placement was analyzed, and it was determined that the femoral interference screw could be left in place and that the tibial interference screw most likely would be removed. The mechanical axis determined from the bilateral long-leg standing images dictated a need for proximal OWMTO for correction up to 8° to allow the axis to cross the center of the knee. The 8° correction is the measured correction needed to move the axis from its pass through the medial compartment to a more balanced position across the middle of the knee.

The overall plan encompassed major concomitant corrective and restorative surgery: tibial osteotomy, medial MAT, revision ACL reconstruction, and fresh mega-patellar OCA. Once the frozen meniscus and eventually the fresh patella (both matched for size) were obtained, arrangements for the patient’s trip for the complex surgery were finalized.

Surgery was started with brief arthroscopic evaluation to confirm the overall appropriateness of the planned procedure and to determine if any other minor deficiencies would warrant operative intervention. Once confirmed, the restoration proceeded as planned. The OWMTO was performed with a PEEK (polyetheretherketone) wedge implant (iBalance; Arthrex) followed by arthroscopic preparation for medial MAT with removal of any meniscal remnants and placement of passing sutures (Figure 2A).
Figure 2.
The meniscus was delivered across the compartment through an enlarged medial portal. The posterior horn bone plug was secured in the retrosocket with sutures tied off to an anterior tibial cortical 2-hole button (Figure 2B). The body of the posterior third of the meniscus was secured to the posterior capsule by tying the 2 previously placed vertical sutures to each other over the intervening capsule. The anterior horn bone plug (10 mm in diameter × 7 mm thick) was then secured within a 10-mm socket drilled antegrade to a depth of 10 mm with a SwiveLock anchor (Arthrex) for interference bony fixation and recapitulation of the normal hoop stresses. Inside-out sutures were placed to secure the capsule to the meniscus and thereby prevent iatrogenic meniscal extrusion. A standard all-inside allograft revision ACL reconstruction was performed with an 11-mm FlipCutter and guide system (Arthrex) to make the femoral and tibial retrosockets.
Figure 3.
Passing sutures were used to deploy the ACL graft construct, which was fashioned into a quadruple-stranded GraftLink construct (Arthrex) from a 28-mm allograft peroneus longus tendon (Figure 3).

When the arthroscopic portion of the surgery was finished, a medial parapatellar arthrotomy was made to allow the patella to be inverted and complete fresh mega-patellar OCA placement (Figure 4).
Figure 4.
A drill guide system was used to prepare the host patella with the largest contained circular socket (35 mm) with a 1-mm to 2-mm cortical margin to a marginal bony depth and an 8- to 10-mm central bony depth.
Figure 5.
The donor patella was then prepared on the graft preparation guide to allow a mega-patellar osteochondral plug to be press-fit into the recipient socket after thorough pulse lavaging of the bony portion of the graft to negate as much of the marrow cellular elements as possible (Figure 5). After appropriate tracking was confirmed, the arthrotomy and skin incision were closed.

The knee was placed in a ROM brace locked in full extension. The patient was able to do straight-leg raises and calf pumps in the recovery room and was discharged home with a saphenous nerve block and an iPACK (Interspace between the Popliteal Artery and the Capsule of the posterior Knee) nerve block in place. Home-based therapy was started immediately. After the patient’s first postoperative visit, formal therapy (discussed earlier) was initiated (Figure 6).
Figure 6.
Toe-touch weight-bearing with the brace locked in extension and ROM limited to 0° to 90° were maintained until 6 weeks, when full weight-bearing and full ROM were allowed. The rehabilitation course was uneventful. The patient continued on active duty and completed his military service, retiring 3 years later with 20 years of service.

Discussion

All-inside GraftLink ACL reconstruction with cortical suspensory fixation appears well suited to combined medial and lateral MAT and/or cartilage restoration—whether it be large fresh OCA combined with medial MAT (as in this patient’s case) or another form of cartilage restoration. Arthroscopic MAT with anatomically fashioned and placed bone plugs minimizes the morbidity within the notch footprints and allows for discrete revision socket formation for both femoral and tibial ACL graft placement. In this case, preparation for the medial MAT and ACL sockets was followed by MAT/ACL construct implantation and secure fixation. The arthrotomy was thereby minimized and placed to allow for efficient mega-patellar OCA graft placement.

Over the past decade, I have performed similar concomitant procedures using the same surgical principles that allow for efficient and reproducible complex knee restoration (Figure 7).

Figure 7.
Common examples are multiligamentous reconstructions (ACL–posterior cruciate ligament–posterolateral corner, ACL–posterior cruciate ligament–medial collateral ligament, ACL–anterolateral ligament, and ACL–medial patellofemoral ligament) combined with concomitant meniscus and cartilage restoration and various osteotomies.

Although use of an algorithm for the management of complex knee restorations is not universally feasible, I offer guidelines for complex knee injuries:

  • At each decision point, determine whether the knee and the patient can withstand the planned surgical intervention.
  • After deciding to proceed with knee restoration, list the meniscus, cartilage, and ligament injuries that must be addressed.
  • Determine which repairs (meniscus, cartilage, ligament) are warranted. Repairs generally are best performed within a period of 7 to 14 days.
  • Determine which ligament injuries warrant reconstruction. Allograft tissue typically is used for multiligament reconstruction.
  • Rank-order the ligament reconstruction requirements. It is fine to proceed with all of the reconstructions if the case is moving smoothly, if there are no developing tourniquet-time issues, and if the soft-tissue envelope is responding as expected.
  • Consider autograft and/or allograft tissue needs for concomitant or staged meniscus and cartilage restoration options/requirements.


Am J Orthop. 2017;46(4):170-175, 202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Uquillas C, Rossy W, Nathasingh CK, Strauss E, Jazrawi L, Gonzalez-Lomas G. Osteotomies about the knee: AAOS exhibit selection. J Bone Joint Surg Am. 2014;96(24):e199.

2. Mehl J, Paul J, Feucht MJ, et al. ACL deficiency and varus osteoarthritis: high tibial osteotomy alone or combined with ACL reconstruction? Arch Orthop Trauma Surg. 2017;137(2):233-240.

3. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

4. Ferrari D, Lopes TJ, França PF, Azevedo FM, Pappas E. Outpatient versus inpatient anterior cruciate ligament reconstruction: a systematic review with meta-analysis. Knee. 2017;24(2):197-206.

5. Weber AE, Gitelis ME, McCarthy MA, Yanke AB, Cole BJ. Malalignment: a requirement for cartilage and organ restoration. Sports Med Arthrosc. 2016;24(2):e14-e22.

6. Prince MR, King AH, Stuart MJ, Dahm DL, Krych AJ. Treatment of patellofemoral cartilage lesions in the young, active patient. J Knee Surg. 2015;28(4):285-295.

7. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

References

1. Uquillas C, Rossy W, Nathasingh CK, Strauss E, Jazrawi L, Gonzalez-Lomas G. Osteotomies about the knee: AAOS exhibit selection. J Bone Joint Surg Am. 2014;96(24):e199.

2. Mehl J, Paul J, Feucht MJ, et al. ACL deficiency and varus osteoarthritis: high tibial osteotomy alone or combined with ACL reconstruction? Arch Orthop Trauma Surg. 2017;137(2):233-240.

3. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

4. Ferrari D, Lopes TJ, França PF, Azevedo FM, Pappas E. Outpatient versus inpatient anterior cruciate ligament reconstruction: a systematic review with meta-analysis. Knee. 2017;24(2):197-206.

5. Weber AE, Gitelis ME, McCarthy MA, Yanke AB, Cole BJ. Malalignment: a requirement for cartilage and organ restoration. Sports Med Arthrosc. 2016;24(2):e14-e22.

6. Prince MR, King AH, Stuart MJ, Dahm DL, Krych AJ. Treatment of patellofemoral cartilage lesions in the young, active patient. J Knee Surg. 2015;28(4):285-295.

7. Scordino LE, DeBerardino TM. Surgical treatment of osteoarthritis in the middle-aged athlete: new horizons in high tibial osteotomies. Sports Med Arthrosc. 2013;21(1):47-51.

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Home of the Brave

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This Memorial Day, with all that is taking place in the world, it was hard not to think about the brave men and women who have sacrificed so much to preserve our freedom. They are away from their families, sometimes for years at a time, and they operate in the most dangerous places in the world. A safe return is not guaranteed. I am thankful for these intrepid men and women whose sacrifices and commitment to their country allow me to live comfortably at home with my family and practice orthopedic surgery.

A few years ago, my wife and I traveled to Normandy and visited the American cemetery. It was a moving experience that I will never forget. We then toured Pointe du Hoc, the elevated peninsula separating Omaha and Utah beach and the location of German gun emplacements covering both beaches. The bunkers, and even the craters from the bombs, are still there. Army Rangers were tasked with launching an amphibious assault on the beach and then scaling the 100-foot cliffs using grappling hooks, ropes, and ladders. Once at the top, they faced a heavily fortified German force that was dug in. Looking down at the beach and out over the ocean from above, I thought of the troops who landed there and the impossible task they faced. Despite the overwhelming odds stacked against them, the Rangers took Pointe du Hoc in 25 minutes and then repelled multiple counterattacks with their backs against the cliff. In my opinion, it’s one of the greatest testaments to the incredible determination and ability of our military personnel.

Speaking of incredible ability, AJO would like to recognize our military orthopedists. They are often deployed in combat zones and provide the best of care for our soldiers while working in the most stressful of conditions, and doing it all on a government salary. In their spare time, they’ve contributed so much to the orthopedic literature, authoring numerous landmark articles.

In this issue, AJO looks at classic military injuries: shoulder instability, stress fractures, and multi-ligamentous knee injuries. Provencher and colleagues authored a comprehensive review of instability with current guidelines for determining surgical approach. DeBerardino shows our readers how to take a military approach to multi-ligament and complex knee injuries, and Owens and colleagues provide a guide to the diagnosis and treatment of stress injuries to bone.

We also take a moment to recognize 3 members of our military orthopedic family whose lives were tragically cut short. Warren R. Kadrmas, Brian Allgood, and Benjamin Whetstone Schmidt’s memorials are included on the following pages. Benjamin Whetstone Schmidt, son of orthopedist David R. Schmidt from San Antonio, was a Marine Sniper killed in action in Afghanistan after volunteering for a second tour. After his death, the LCpl Benjamin Whetstone Schmidt Endowed Professorship in History was created at the Texas Christian University. Contributions can be made in his memory at www.heartofpurple.com.

As Independence Day is celebrated, AJO is pleased to present “Military Orthopedics” to honor our troops and the military doctors who support them. As you read this issue, take a moment to reflect on the freedoms you enjoy because America is truly the Home of the Brave.

Am J Orthop. 2017;46(4):166. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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This Memorial Day, with all that is taking place in the world, it was hard not to think about the brave men and women who have sacrificed so much to preserve our freedom. They are away from their families, sometimes for years at a time, and they operate in the most dangerous places in the world. A safe return is not guaranteed. I am thankful for these intrepid men and women whose sacrifices and commitment to their country allow me to live comfortably at home with my family and practice orthopedic surgery.

A few years ago, my wife and I traveled to Normandy and visited the American cemetery. It was a moving experience that I will never forget. We then toured Pointe du Hoc, the elevated peninsula separating Omaha and Utah beach and the location of German gun emplacements covering both beaches. The bunkers, and even the craters from the bombs, are still there. Army Rangers were tasked with launching an amphibious assault on the beach and then scaling the 100-foot cliffs using grappling hooks, ropes, and ladders. Once at the top, they faced a heavily fortified German force that was dug in. Looking down at the beach and out over the ocean from above, I thought of the troops who landed there and the impossible task they faced. Despite the overwhelming odds stacked against them, the Rangers took Pointe du Hoc in 25 minutes and then repelled multiple counterattacks with their backs against the cliff. In my opinion, it’s one of the greatest testaments to the incredible determination and ability of our military personnel.

Speaking of incredible ability, AJO would like to recognize our military orthopedists. They are often deployed in combat zones and provide the best of care for our soldiers while working in the most stressful of conditions, and doing it all on a government salary. In their spare time, they’ve contributed so much to the orthopedic literature, authoring numerous landmark articles.

In this issue, AJO looks at classic military injuries: shoulder instability, stress fractures, and multi-ligamentous knee injuries. Provencher and colleagues authored a comprehensive review of instability with current guidelines for determining surgical approach. DeBerardino shows our readers how to take a military approach to multi-ligament and complex knee injuries, and Owens and colleagues provide a guide to the diagnosis and treatment of stress injuries to bone.

We also take a moment to recognize 3 members of our military orthopedic family whose lives were tragically cut short. Warren R. Kadrmas, Brian Allgood, and Benjamin Whetstone Schmidt’s memorials are included on the following pages. Benjamin Whetstone Schmidt, son of orthopedist David R. Schmidt from San Antonio, was a Marine Sniper killed in action in Afghanistan after volunteering for a second tour. After his death, the LCpl Benjamin Whetstone Schmidt Endowed Professorship in History was created at the Texas Christian University. Contributions can be made in his memory at www.heartofpurple.com.

As Independence Day is celebrated, AJO is pleased to present “Military Orthopedics” to honor our troops and the military doctors who support them. As you read this issue, take a moment to reflect on the freedoms you enjoy because America is truly the Home of the Brave.

Am J Orthop. 2017;46(4):166. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

This Memorial Day, with all that is taking place in the world, it was hard not to think about the brave men and women who have sacrificed so much to preserve our freedom. They are away from their families, sometimes for years at a time, and they operate in the most dangerous places in the world. A safe return is not guaranteed. I am thankful for these intrepid men and women whose sacrifices and commitment to their country allow me to live comfortably at home with my family and practice orthopedic surgery.

A few years ago, my wife and I traveled to Normandy and visited the American cemetery. It was a moving experience that I will never forget. We then toured Pointe du Hoc, the elevated peninsula separating Omaha and Utah beach and the location of German gun emplacements covering both beaches. The bunkers, and even the craters from the bombs, are still there. Army Rangers were tasked with launching an amphibious assault on the beach and then scaling the 100-foot cliffs using grappling hooks, ropes, and ladders. Once at the top, they faced a heavily fortified German force that was dug in. Looking down at the beach and out over the ocean from above, I thought of the troops who landed there and the impossible task they faced. Despite the overwhelming odds stacked against them, the Rangers took Pointe du Hoc in 25 minutes and then repelled multiple counterattacks with their backs against the cliff. In my opinion, it’s one of the greatest testaments to the incredible determination and ability of our military personnel.

Speaking of incredible ability, AJO would like to recognize our military orthopedists. They are often deployed in combat zones and provide the best of care for our soldiers while working in the most stressful of conditions, and doing it all on a government salary. In their spare time, they’ve contributed so much to the orthopedic literature, authoring numerous landmark articles.

In this issue, AJO looks at classic military injuries: shoulder instability, stress fractures, and multi-ligamentous knee injuries. Provencher and colleagues authored a comprehensive review of instability with current guidelines for determining surgical approach. DeBerardino shows our readers how to take a military approach to multi-ligament and complex knee injuries, and Owens and colleagues provide a guide to the diagnosis and treatment of stress injuries to bone.

We also take a moment to recognize 3 members of our military orthopedic family whose lives were tragically cut short. Warren R. Kadrmas, Brian Allgood, and Benjamin Whetstone Schmidt’s memorials are included on the following pages. Benjamin Whetstone Schmidt, son of orthopedist David R. Schmidt from San Antonio, was a Marine Sniper killed in action in Afghanistan after volunteering for a second tour. After his death, the LCpl Benjamin Whetstone Schmidt Endowed Professorship in History was created at the Texas Christian University. Contributions can be made in his memory at www.heartofpurple.com.

As Independence Day is celebrated, AJO is pleased to present “Military Orthopedics” to honor our troops and the military doctors who support them. As you read this issue, take a moment to reflect on the freedoms you enjoy because America is truly the Home of the Brave.

Am J Orthop. 2017;46(4):166. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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