Orthopedics

A fluorescent probe may make it easier to diagnose and monitor osteoarthritis, according to a study published in the February issue of Arthritis & Rheumatology. Researchers found that a fluorescent probe tracked the development of osteoarthritis in male mice, brightening as the disease progressed. Their study is the first to demonstrate that near-infared fluorescence can be used to detect osteoarthritis changes over time.

“Patients are frequently in pain by the time osteoarthritis is diagnosed. The imaging tests most frequently used, x-rays, do not indicate the level of pain or allow us to directly see the amount of cartilage loss, which is a challenge for physicians and patients,” said lead author Averi A. Leahy, BA, an MD/PhD student in the medical scientist training program at Tufts University School of Medicine (TUSM) and the Sackler School of Graduate Biomedical Sciences at Tufts in Boston.

For this study, the right knees of 54 mice were affected by injury-induced osteoarthritis and served as the experimental group. The healthy left knees of the mice served as the control group.

Over a 2-month period, the researchers took images of each knee every 2 weeks to determine if the fluorescent probe emitted a signal. The signal became brighter in the injured right knee, at every examined time point, through the early to moderate stages of osteoarthritis. The probe emitted a lower signal in the healthy left knee, and did not increase significantly over time.

According to the researchers, the fluorescent probe made it easy to see the activities that lead to cartilage breakdown in the initial and moderate stages of osteoarthritis, which is necessary for early detection and adequate monitoring of the disease.

Senior author Li Zeng, PhD, an Associate Professor in the Department of Integrative Physiology and Pathobiology at TUSM and member of the cellular, molecular, and developmental biology program faculty at the Sackler School reported that the next step is to monitor the fluorescent probe over a longer period of time to determine whether the same results are produced during the late stages of osteoarthritis.

A fluorescent probe may make it easier to diagnose and monitor osteoarthritis, according to a study published in the February issue of Arthritis & Rheumatology. Researchers found that a fluorescent probe tracked the development of osteoarthritis in male mice, brightening as the disease progressed. Their study is the first to demonstrate that near-infared fluorescence can be used to detect osteoarthritis changes over time.

“Patients are frequently in pain by the time osteoarthritis is diagnosed. The imaging tests most frequently used, x-rays, do not indicate the level of pain or allow us to directly see the amount of cartilage loss, which is a challenge for physicians and patients,” said lead author Averi A. Leahy, BA, an MD/PhD student in the medical scientist training program at Tufts University School of Medicine (TUSM) and the Sackler School of Graduate Biomedical Sciences at Tufts in Boston.

For this study, the right knees of 54 mice were affected by injury-induced osteoarthritis and served as the experimental group. The healthy left knees of the mice served as the control group.

Over a 2-month period, the researchers took images of each knee every 2 weeks to determine if the fluorescent probe emitted a signal. The signal became brighter in the injured right knee, at every examined time point, through the early to moderate stages of osteoarthritis. The probe emitted a lower signal in the healthy left knee, and did not increase significantly over time.

According to the researchers, the fluorescent probe made it easy to see the activities that lead to cartilage breakdown in the initial and moderate stages of osteoarthritis, which is necessary for early detection and adequate monitoring of the disease.

Senior author Li Zeng, PhD, an Associate Professor in the Department of Integrative Physiology and Pathobiology at TUSM and member of the cellular, molecular, and developmental biology program faculty at the Sackler School reported that the next step is to monitor the fluorescent probe over a longer period of time to determine whether the same results are produced during the late stages of osteoarthritis.

A fluorescent probe may make it easier to diagnose and monitor osteoarthritis, according to a study published in the February issue of Arthritis & Rheumatology. Researchers found that a fluorescent probe tracked the development of osteoarthritis in male mice, brightening as the disease progressed. Their study is the first to demonstrate that near-infared fluorescence can be used to detect osteoarthritis changes over time.

“Patients are frequently in pain by the time osteoarthritis is diagnosed. The imaging tests most frequently used, x-rays, do not indicate the level of pain or allow us to directly see the amount of cartilage loss, which is a challenge for physicians and patients,” said lead author Averi A. Leahy, BA, an MD/PhD student in the medical scientist training program at Tufts University School of Medicine (TUSM) and the Sackler School of Graduate Biomedical Sciences at Tufts in Boston.

For this study, the right knees of 54 mice were affected by injury-induced osteoarthritis and served as the experimental group. The healthy left knees of the mice served as the control group.

Over a 2-month period, the researchers took images of each knee every 2 weeks to determine if the fluorescent probe emitted a signal. The signal became brighter in the injured right knee, at every examined time point, through the early to moderate stages of osteoarthritis. The probe emitted a lower signal in the healthy left knee, and did not increase significantly over time.

According to the researchers, the fluorescent probe made it easy to see the activities that lead to cartilage breakdown in the initial and moderate stages of osteoarthritis, which is necessary for early detection and adequate monitoring of the disease.

Senior author Li Zeng, PhD, an Associate Professor in the Department of Integrative Physiology and Pathobiology at TUSM and member of the cellular, molecular, and developmental biology program faculty at the Sackler School reported that the next step is to monitor the fluorescent probe over a longer period of time to determine whether the same results are produced during the late stages of osteoarthritis.

New research reveals the physical and psychosocial factors that significantly increase the risk of low back pain onset. The trial results, which were published online ahead of print February 9 in Arthritis Care & Research, show that being engaged in manual tasks involving awkward positions will increase the risk of low back pain by 8 times. People who are distracted during activities or fatigued also significantly increase their risk of acute low back pain.

“Understanding which risk factors contribute to back pain and controlling exposure to these risks is an important first step in prevention,” said Manuela Ferreira, PhD, Associate Professor at the George Institute for Global Health and Sydney Medical School at the University of Sydney in New South Wales, Australia. “Our study is the first to examine brief exposure to a range of modifiable triggers for an acute episode of low back pain.”

For this case-crossover study, Dr. Ferreira and colleagues recruited 999 participants from 300 primary care clinics in Sydney, Australia, who had an acute low back pain episode between October 2011 and November 2012. Participants were asked to report exposure to 12 physical or psychosocial factors in the 96 hours prior to the onset of back pain.

The study found that:

• The risk of a new episode of low back pain significantly increased due to a range of triggers, from an odds ratio of 2.7 for moderate to vigorous physical activity to 25.0 for distraction during an activity.

• Back pain risk was highest between 7:00 am and at noontime.

• Age moderated the effect of exposure to heavy loads, with an odds ratio for individuals age 20, 40, or 60 at 13.6, 6.0, and 2.7, respectively.

“Understanding which modifiable risk factors lead to low back pain is an important step toward controlling a condition that affects so many worldwide,” said Dr. Ferreira. “Our findings enhance knowledge of low back pain triggers and will assist the development of new prevention programs that can reduce suffering from this potentially disabling condition.”

New research reveals the physical and psychosocial factors that significantly increase the risk of low back pain onset. The trial results, which were published online ahead of print February 9 in Arthritis Care & Research, show that being engaged in manual tasks involving awkward positions will increase the risk of low back pain by 8 times. People who are distracted during activities or fatigued also significantly increase their risk of acute low back pain.

“Understanding which risk factors contribute to back pain and controlling exposure to these risks is an important first step in prevention,” said Manuela Ferreira, PhD, Associate Professor at the George Institute for Global Health and Sydney Medical School at the University of Sydney in New South Wales, Australia. “Our study is the first to examine brief exposure to a range of modifiable triggers for an acute episode of low back pain.”

For this case-crossover study, Dr. Ferreira and colleagues recruited 999 participants from 300 primary care clinics in Sydney, Australia, who had an acute low back pain episode between October 2011 and November 2012. Participants were asked to report exposure to 12 physical or psychosocial factors in the 96 hours prior to the onset of back pain.

The study found that:

• The risk of a new episode of low back pain significantly increased due to a range of triggers, from an odds ratio of 2.7 for moderate to vigorous physical activity to 25.0 for distraction during an activity.

• Back pain risk was highest between 7:00 am and at noontime.

• Age moderated the effect of exposure to heavy loads, with an odds ratio for individuals age 20, 40, or 60 at 13.6, 6.0, and 2.7, respectively.

“Understanding which modifiable risk factors lead to low back pain is an important step toward controlling a condition that affects so many worldwide,” said Dr. Ferreira. “Our findings enhance knowledge of low back pain triggers and will assist the development of new prevention programs that can reduce suffering from this potentially disabling condition.”

New research reveals the physical and psychosocial factors that significantly increase the risk of low back pain onset. The trial results, which were published online ahead of print February 9 in Arthritis Care & Research, show that being engaged in manual tasks involving awkward positions will increase the risk of low back pain by 8 times. People who are distracted during activities or fatigued also significantly increase their risk of acute low back pain.

“Understanding which risk factors contribute to back pain and controlling exposure to these risks is an important first step in prevention,” said Manuela Ferreira, PhD, Associate Professor at the George Institute for Global Health and Sydney Medical School at the University of Sydney in New South Wales, Australia. “Our study is the first to examine brief exposure to a range of modifiable triggers for an acute episode of low back pain.”

For this case-crossover study, Dr. Ferreira and colleagues recruited 999 participants from 300 primary care clinics in Sydney, Australia, who had an acute low back pain episode between October 2011 and November 2012. Participants were asked to report exposure to 12 physical or psychosocial factors in the 96 hours prior to the onset of back pain.

The study found that:

• The risk of a new episode of low back pain significantly increased due to a range of triggers, from an odds ratio of 2.7 for moderate to vigorous physical activity to 25.0 for distraction during an activity.

• Back pain risk was highest between 7:00 am and at noontime.

• Age moderated the effect of exposure to heavy loads, with an odds ratio for individuals age 20, 40, or 60 at 13.6, 6.0, and 2.7, respectively.

“Understanding which modifiable risk factors lead to low back pain is an important step toward controlling a condition that affects so many worldwide,” said Dr. Ferreira. “Our findings enhance knowledge of low back pain triggers and will assist the development of new prevention programs that can reduce suffering from this potentially disabling condition.”

People who have had a knee reconstruction following trauma may be susceptible to osteoarthritis sooner than currently thought, according to new MRI findings at 1 year after anterior cruciate ligament reconstruction.

Almost a third of people studied had some evidence of early osteoarthritis (OA) at that early time point, challenging “existing dogma that degenerative joint disease does not become apparent for years post-ACLR,” reported Dr. Kay Crossley of the University of Queensland in Brisbane, Australia (Arthritis Rheumatol. 2015 Feb. 18 [doi:10.1002/art.39005]).

However, as they did not have access to preoperative images, they could not rule out that some OA features may have been preexisting and not related to knee trauma, they said.

“This is a sample that was taken after the injury and after the reconstruction, so they truly don’t know that what they’re finding is as a result of even the injury, surgery, or the meniscal damage or meniscal resection they had done at the time,” Dr. David J. Hunter, a leading OA expert from Sydney (Australia) University, said when asked to comment on the study’s findings.

“It may well be that these were people that had some underlying structural damage,” he added.

The researchers noted that radiographic knee OA was thought to be as high as 50%-90% a decade after anterior cruciate ligament reconstruction (ACLR). The issue is particularly important because ACL injuries typically occur in younger adults who are then prone to developing knee OA before they reach 40 years, they said.

“Early detection of knee OA after ACLR may permit early intervention such as load management, which is likely to be more effective prior to the development of advanced disease,” they wrote.

Their study included 111 patients aged 18-50 years who had undergone single-bundle hamstring-tendon autograft ACLR 1 year earlier.

MRI scans of their knees were compared with 20 uninjured asymptomatic matched controls. The researchers used the MRI Osteoarthritis Knee Score (MOAKS) to score specific OA features because the more recent Anterior Cruciate Ligament Osteoarthritis Score (ACLOAS) had not been published at the time of their study.

Results showed that 34 (31%) patients had MRI-defined knee OA following an ACLR a year earlier.

MRI-OA features were most frequently found in the patellofemoral compartment, particularly the medial femoral trochlea, a potentially underrecognized site of knee pathology following reconstruction, the researchers said.

Pathology in the patellofemoral joint included not only “early” features of OA, such as bone marrow lesions and partial-thickness cartilage loss, but also frank osteophytes on MRI, they noted.

None of the uninjured control knees had MRI-defined patellofemoral or tibiofemoral OA.

The authors acknowledged that a lack of access to preoperative knee images limited the conclusions they could reach in their study, but they noted that MRI-OA features were rarely seen in the small sample of uninjured matched control knees.

“Combined with the observation that six times as many reconstructed knees had radiographic osteophytes than uninjured contralateral knees, these findings suggest that knee trauma and/or reconstruction was strongly implicated in the development of OA features,” they wrote.

Another limitation that the authors acknowledged was that the MRI definition of OA was relatively new and was likely to be refined as the understanding of OA pathology evolved.

Dr. Hunter, who was the lead investigator involved in developing the MOAKS, agreed that the definition needed more validity and testing.

“This is the third study that uses that definition, and I do think that long-term clinical implications of what MRI definition means is unknown,” he said. “The challenge that we have is that we do kick up a lot of abnormalities, and we don’t truly know what the long-term clinical implications of those abnormalities are at this point.”

“There are a lot of problems with the way this study has been done, but I do think it is really helpful that it highlights how important injury is with regards to predisposing to early OA.”

“It’s something that a lot of people don’t really highlight or pay attention to,” he said.

The study was partly funded by the Queensland Orthopaedic Physiotherapy Network, a University of Melbourne Research Collaboration grant, and University of British Columbia’s Centre for Hip Health and Mobility via the Society for Mobility and Health. One study author is president of Boston Imaging Core Lab, LLC, and is a consultant to Merck Serono, Sanofi-Aventis, Genzyme and TissueGene. No other authors declared conflicts of interest.

People who have had a knee reconstruction following trauma may be susceptible to osteoarthritis sooner than currently thought, according to new MRI findings at 1 year after anterior cruciate ligament reconstruction.

Almost a third of people studied had some evidence of early osteoarthritis (OA) at that early time point, challenging “existing dogma that degenerative joint disease does not become apparent for years post-ACLR,” reported Dr. Kay Crossley of the University of Queensland in Brisbane, Australia (Arthritis Rheumatol. 2015 Feb. 18 [doi:10.1002/art.39005]).

However, as they did not have access to preoperative images, they could not rule out that some OA features may have been preexisting and not related to knee trauma, they said.

“This is a sample that was taken after the injury and after the reconstruction, so they truly don’t know that what they’re finding is as a result of even the injury, surgery, or the meniscal damage or meniscal resection they had done at the time,” Dr. David J. Hunter, a leading OA expert from Sydney (Australia) University, said when asked to comment on the study’s findings.

“It may well be that these were people that had some underlying structural damage,” he added.

The researchers noted that radiographic knee OA was thought to be as high as 50%-90% a decade after anterior cruciate ligament reconstruction (ACLR). The issue is particularly important because ACL injuries typically occur in younger adults who are then prone to developing knee OA before they reach 40 years, they said.

“Early detection of knee OA after ACLR may permit early intervention such as load management, which is likely to be more effective prior to the development of advanced disease,” they wrote.

Their study included 111 patients aged 18-50 years who had undergone single-bundle hamstring-tendon autograft ACLR 1 year earlier.

MRI scans of their knees were compared with 20 uninjured asymptomatic matched controls. The researchers used the MRI Osteoarthritis Knee Score (MOAKS) to score specific OA features because the more recent Anterior Cruciate Ligament Osteoarthritis Score (ACLOAS) had not been published at the time of their study.

Results showed that 34 (31%) patients had MRI-defined knee OA following an ACLR a year earlier.

MRI-OA features were most frequently found in the patellofemoral compartment, particularly the medial femoral trochlea, a potentially underrecognized site of knee pathology following reconstruction, the researchers said.

Pathology in the patellofemoral joint included not only “early” features of OA, such as bone marrow lesions and partial-thickness cartilage loss, but also frank osteophytes on MRI, they noted.

None of the uninjured control knees had MRI-defined patellofemoral or tibiofemoral OA.

The authors acknowledged that a lack of access to preoperative knee images limited the conclusions they could reach in their study, but they noted that MRI-OA features were rarely seen in the small sample of uninjured matched control knees.

“Combined with the observation that six times as many reconstructed knees had radiographic osteophytes than uninjured contralateral knees, these findings suggest that knee trauma and/or reconstruction was strongly implicated in the development of OA features,” they wrote.

Another limitation that the authors acknowledged was that the MRI definition of OA was relatively new and was likely to be refined as the understanding of OA pathology evolved.

Dr. Hunter, who was the lead investigator involved in developing the MOAKS, agreed that the definition needed more validity and testing.

“This is the third study that uses that definition, and I do think that long-term clinical implications of what MRI definition means is unknown,” he said. “The challenge that we have is that we do kick up a lot of abnormalities, and we don’t truly know what the long-term clinical implications of those abnormalities are at this point.”

“There are a lot of problems with the way this study has been done, but I do think it is really helpful that it highlights how important injury is with regards to predisposing to early OA.”

“It’s something that a lot of people don’t really highlight or pay attention to,” he said.

The study was partly funded by the Queensland Orthopaedic Physiotherapy Network, a University of Melbourne Research Collaboration grant, and University of British Columbia’s Centre for Hip Health and Mobility via the Society for Mobility and Health. One study author is president of Boston Imaging Core Lab, LLC, and is a consultant to Merck Serono, Sanofi-Aventis, Genzyme and TissueGene. No other authors declared conflicts of interest.

People who have had a knee reconstruction following trauma may be susceptible to osteoarthritis sooner than currently thought, according to new MRI findings at 1 year after anterior cruciate ligament reconstruction.

Almost a third of people studied had some evidence of early osteoarthritis (OA) at that early time point, challenging “existing dogma that degenerative joint disease does not become apparent for years post-ACLR,” reported Dr. Kay Crossley of the University of Queensland in Brisbane, Australia (Arthritis Rheumatol. 2015 Feb. 18 [doi:10.1002/art.39005]).

However, as they did not have access to preoperative images, they could not rule out that some OA features may have been preexisting and not related to knee trauma, they said.

“This is a sample that was taken after the injury and after the reconstruction, so they truly don’t know that what they’re finding is as a result of even the injury, surgery, or the meniscal damage or meniscal resection they had done at the time,” Dr. David J. Hunter, a leading OA expert from Sydney (Australia) University, said when asked to comment on the study’s findings.

“It may well be that these were people that had some underlying structural damage,” he added.

The researchers noted that radiographic knee OA was thought to be as high as 50%-90% a decade after anterior cruciate ligament reconstruction (ACLR). The issue is particularly important because ACL injuries typically occur in younger adults who are then prone to developing knee OA before they reach 40 years, they said.

“Early detection of knee OA after ACLR may permit early intervention such as load management, which is likely to be more effective prior to the development of advanced disease,” they wrote.

Their study included 111 patients aged 18-50 years who had undergone single-bundle hamstring-tendon autograft ACLR 1 year earlier.

MRI scans of their knees were compared with 20 uninjured asymptomatic matched controls. The researchers used the MRI Osteoarthritis Knee Score (MOAKS) to score specific OA features because the more recent Anterior Cruciate Ligament Osteoarthritis Score (ACLOAS) had not been published at the time of their study.

Results showed that 34 (31%) patients had MRI-defined knee OA following an ACLR a year earlier.

MRI-OA features were most frequently found in the patellofemoral compartment, particularly the medial femoral trochlea, a potentially underrecognized site of knee pathology following reconstruction, the researchers said.

Pathology in the patellofemoral joint included not only “early” features of OA, such as bone marrow lesions and partial-thickness cartilage loss, but also frank osteophytes on MRI, they noted.

None of the uninjured control knees had MRI-defined patellofemoral or tibiofemoral OA.

The authors acknowledged that a lack of access to preoperative knee images limited the conclusions they could reach in their study, but they noted that MRI-OA features were rarely seen in the small sample of uninjured matched control knees.

“Combined with the observation that six times as many reconstructed knees had radiographic osteophytes than uninjured contralateral knees, these findings suggest that knee trauma and/or reconstruction was strongly implicated in the development of OA features,” they wrote.

Another limitation that the authors acknowledged was that the MRI definition of OA was relatively new and was likely to be refined as the understanding of OA pathology evolved.

Dr. Hunter, who was the lead investigator involved in developing the MOAKS, agreed that the definition needed more validity and testing.

“This is the third study that uses that definition, and I do think that long-term clinical implications of what MRI definition means is unknown,” he said. “The challenge that we have is that we do kick up a lot of abnormalities, and we don’t truly know what the long-term clinical implications of those abnormalities are at this point.”

“There are a lot of problems with the way this study has been done, but I do think it is really helpful that it highlights how important injury is with regards to predisposing to early OA.”

“It’s something that a lot of people don’t really highlight or pay attention to,” he said.

The study was partly funded by the Queensland Orthopaedic Physiotherapy Network, a University of Melbourne Research Collaboration grant, and University of British Columbia’s Centre for Hip Health and Mobility via the Society for Mobility and Health. One study author is president of Boston Imaging Core Lab, LLC, and is a consultant to Merck Serono, Sanofi-Aventis, Genzyme and TissueGene. No other authors declared conflicts of interest.

SNOWMASS, COLO. – A novel approach to repairing anterior cruciate ligament injuries – and perhaps thereby avoiding a downstream tidal wave of knee osteoarthritis – is creating major buzz in sports medicine circles.

“You’ll probably hear much more about this bioenhanced repair, with the expectation of achieving strength equal to that of ACL reconstruction and perhaps preventing the development of osteoarthritis 15 years down the road,” Dr. M. Timothy Hresko predicted at the Winter Rheumatology Symposium sponsored by the American College of Rheumatology.

He cited research led by his colleague Dr. Martha M. Murray of Boston Children’s Hospital, which has resulted in development of a surgical technique combining a tissue-engineered composite scaffold with a suture repair of the torn ACL in what Dr. Murray has termed a bioenhanced repair.

Her work, to date preclinical, has garnered major awards from both the American Orthopaedic Society for Sports Medicine and the American Academy of Orthopaedic Surgeons. The Food and Drug Administration recently granted approval for the first clinical safety studies, to begin this year.

There is a major unmet need for better methods of repairing ACL injuries. They’re common, with an estimated 550,000 cases per year. The peak incidence occurs in 15- to 19-year-old female athletes. And the current gold standard therapy consisting of ACL reconstruction using an allograft or hamstring graft has a disturbingly high failure rate, both early and late. The graft failure rate is up to 20% in the first 2 years, climbing to 50% at 10 years.

“We just have to do better,” conceded Dr. Hresko, an orthopedic surgeon at Harvard Medical School, Boston, and Boston Children’s Hospital.

“One of the interesting and unfortunate facts,” he continued, “is that roughly 80% of people who have an ACL injury, with or without reconstruction, are still going to have osteoarthritis 14 years after the injury. So, if this is your 15-year-old daughter who plays basketball, she’ll only be 30 and will already have degenerative arthritis of the knee at what should still be a very active period of life.”

The bioenhanced repair now under study uses an extracellular matrix-based scaffold, which is loaded with a few milliliters of the patient’s own platelet-enriched plasma. The scaffold is applied between the torn ligament ends in order to stimulate collagen production and promote ligament healing. The suture repair of the ligament entails much less trauma than does standard reconstructive surgery.

In large-animal studies, the bioenhanced repair resulted in the same yield load, stiffness, and other desirable biomechanical properties at 1 year as with major reconstructive surgery. However, while premature posttraumatic osteoarthritis occurred in 80% of the knees treated with standard ACL reconstruction, there was no evidence of such damage 1 year following bioenhanced repair. Nor have adverse reactions to the scaffold been noted in the porcine model.

Dr. Hresko reported serving as a consultant to Depuy Spine.

bjancin@frontlinemedcom.com

SNOWMASS, COLO. – A novel approach to repairing anterior cruciate ligament injuries – and perhaps thereby avoiding a downstream tidal wave of knee osteoarthritis – is creating major buzz in sports medicine circles.

“You’ll probably hear much more about this bioenhanced repair, with the expectation of achieving strength equal to that of ACL reconstruction and perhaps preventing the development of osteoarthritis 15 years down the road,” Dr. M. Timothy Hresko predicted at the Winter Rheumatology Symposium sponsored by the American College of Rheumatology.

He cited research led by his colleague Dr. Martha M. Murray of Boston Children’s Hospital, which has resulted in development of a surgical technique combining a tissue-engineered composite scaffold with a suture repair of the torn ACL in what Dr. Murray has termed a bioenhanced repair.

Her work, to date preclinical, has garnered major awards from both the American Orthopaedic Society for Sports Medicine and the American Academy of Orthopaedic Surgeons. The Food and Drug Administration recently granted approval for the first clinical safety studies, to begin this year.

There is a major unmet need for better methods of repairing ACL injuries. They’re common, with an estimated 550,000 cases per year. The peak incidence occurs in 15- to 19-year-old female athletes. And the current gold standard therapy consisting of ACL reconstruction using an allograft or hamstring graft has a disturbingly high failure rate, both early and late. The graft failure rate is up to 20% in the first 2 years, climbing to 50% at 10 years.

“We just have to do better,” conceded Dr. Hresko, an orthopedic surgeon at Harvard Medical School, Boston, and Boston Children’s Hospital.

“One of the interesting and unfortunate facts,” he continued, “is that roughly 80% of people who have an ACL injury, with or without reconstruction, are still going to have osteoarthritis 14 years after the injury. So, if this is your 15-year-old daughter who plays basketball, she’ll only be 30 and will already have degenerative arthritis of the knee at what should still be a very active period of life.”

The bioenhanced repair now under study uses an extracellular matrix-based scaffold, which is loaded with a few milliliters of the patient’s own platelet-enriched plasma. The scaffold is applied between the torn ligament ends in order to stimulate collagen production and promote ligament healing. The suture repair of the ligament entails much less trauma than does standard reconstructive surgery.

In large-animal studies, the bioenhanced repair resulted in the same yield load, stiffness, and other desirable biomechanical properties at 1 year as with major reconstructive surgery. However, while premature posttraumatic osteoarthritis occurred in 80% of the knees treated with standard ACL reconstruction, there was no evidence of such damage 1 year following bioenhanced repair. Nor have adverse reactions to the scaffold been noted in the porcine model.

Dr. Hresko reported serving as a consultant to Depuy Spine.

bjancin@frontlinemedcom.com

SNOWMASS, COLO. – A novel approach to repairing anterior cruciate ligament injuries – and perhaps thereby avoiding a downstream tidal wave of knee osteoarthritis – is creating major buzz in sports medicine circles.

“You’ll probably hear much more about this bioenhanced repair, with the expectation of achieving strength equal to that of ACL reconstruction and perhaps preventing the development of osteoarthritis 15 years down the road,” Dr. M. Timothy Hresko predicted at the Winter Rheumatology Symposium sponsored by the American College of Rheumatology.

He cited research led by his colleague Dr. Martha M. Murray of Boston Children’s Hospital, which has resulted in development of a surgical technique combining a tissue-engineered composite scaffold with a suture repair of the torn ACL in what Dr. Murray has termed a bioenhanced repair.

Her work, to date preclinical, has garnered major awards from both the American Orthopaedic Society for Sports Medicine and the American Academy of Orthopaedic Surgeons. The Food and Drug Administration recently granted approval for the first clinical safety studies, to begin this year.

There is a major unmet need for better methods of repairing ACL injuries. They’re common, with an estimated 550,000 cases per year. The peak incidence occurs in 15- to 19-year-old female athletes. And the current gold standard therapy consisting of ACL reconstruction using an allograft or hamstring graft has a disturbingly high failure rate, both early and late. The graft failure rate is up to 20% in the first 2 years, climbing to 50% at 10 years.

“We just have to do better,” conceded Dr. Hresko, an orthopedic surgeon at Harvard Medical School, Boston, and Boston Children’s Hospital.

“One of the interesting and unfortunate facts,” he continued, “is that roughly 80% of people who have an ACL injury, with or without reconstruction, are still going to have osteoarthritis 14 years after the injury. So, if this is your 15-year-old daughter who plays basketball, she’ll only be 30 and will already have degenerative arthritis of the knee at what should still be a very active period of life.”

The bioenhanced repair now under study uses an extracellular matrix-based scaffold, which is loaded with a few milliliters of the patient’s own platelet-enriched plasma. The scaffold is applied between the torn ligament ends in order to stimulate collagen production and promote ligament healing. The suture repair of the ligament entails much less trauma than does standard reconstructive surgery.

In large-animal studies, the bioenhanced repair resulted in the same yield load, stiffness, and other desirable biomechanical properties at 1 year as with major reconstructive surgery. However, while premature posttraumatic osteoarthritis occurred in 80% of the knees treated with standard ACL reconstruction, there was no evidence of such damage 1 year following bioenhanced repair. Nor have adverse reactions to the scaffold been noted in the porcine model.

Dr. Hresko reported serving as a consultant to Depuy Spine.

bjancin@frontlinemedcom.com

Stenosing tenosynovitis, or trigger finger, is a pathology commonly referred to the plastic and hand surgery service of the North Florida/South Georgia Veterans Health System (NFSGVHS). Patients usually present to their primary care provider with symptoms of the finger being temporarily locked or stuck in the flexed position. This can be a painful problem due to the size mismatch between the flexor tendon and the pulley under which it glides.

Patients are typically referred to surgery after failing ≥ 1 attempt at nonoperative management. The surgery is relatively quick and straightforward; however, postoperative complications can lead to an unexpected costly and lengthy recovery. The objective of this study was to identify potential risk factors that can predispose patients to postoperative complications so that those risk factors may be better anticipated and modified, if possible.

Methods

A retrospective chart review of trigger finger release surgery was performed on-site at the Malcom Randall VAMC in Gainesville, Florida, from January 2005 to December 2010 to identify risk factors associated with postoperative complications. The study was approved by both the NFSGVHS Internal Review Board and the University of Florida Institutional Review Board. Patients who underwent surgery exclusively for ≥ 1 trigger fingers by the plastic surgery service were included in the study.

The surgery involves making an incision over the affected A1 pulley in the hand (Figure 1) and sharply releasing it (Figure 2) under direct vision. Potential risk factors for postoperative complications were recorded. These risk factors included smoking status, diabetic status, type of incision, and number of digits released during the surgical procedure.

Results

Ninety-eight digits (on 81 hands) were identified as meeting inclusion criteria. Surgeries were performed using a longitudinal (43), transverse (48), oblique (5), or Brunner (2) incision. There were 10 complications: cellulitis (3), pyogenic flexor tenosynovitis (3), scar adhesion (1), delayed healing (2), and incomplete release (1). The overall complication rate was 10.2%. The authors compared risk factors with complications, using the chi square test and a determining of P < .05.

Related: Making the Case for Minimally Invasive Surgery

There was no link found between overall postoperative complications and diabetic status, incision type, or smoking status. There was a statistically significant link between diabetic patients and the incidence of postoperative infection (P = .002) and between 2 digits operated on during the same surgery and postoperative infection (P = .027)

Discussion

The routine practice of the NFSGVHS hand clinic is to offer a steroid injection as the initial treatment for trigger finger. Health care providers (HCPs) allow no more than 3 injections to the same digit to avoid the rare but potentially serious complication of a tendon rupture.¹ Due to the large NFSGVHS catchment area, wait time for elective trigger finger surgery is several months. This 3-injection plan has been well received by patients and referring providers due to these wait times. However, a recent article by Kerrigan and Stanwix concluded that the most cost-efficient treatment strategy is 2 steroid injections before surgery.²

More often than not, trigger finger release is a short, outpatient surgery with a quick recovery. To minimize the risk of stiffness and scar adhesions, the NFSGVHS practice is to refer all postoperative hand cases for ≥ 1 hand therapy appointment on the same day as their first postoperative visit.

Cost Estimates

When complications occur, they can be costly to patients due to both time spent away from home and work and additional expenses. When the current procedural terminology (CPT) codes are run through the VistA integrated billing system, based on the VHA Chief Business Office Reasonable Charges, a complication can more than double the charges associated with A1 pulley surgery.

A flexor sheath incision and drainage (I+D) (CPT 26020) charges $8,935.35 (facility charge, $6,911.95 plus professional fee, $2,023.40), compared with open trigger finger release (CPT 26055) at $8,365.66 (facility charge, $6,911.95 plus professional fee, $1,453.71). According to a conversation with the finance service officer at NFSGVHS (2/11/2014), the anesthesia bill ($490.56/15 min), anticipated level 3 emergency department visits (facility charge, $889.22 plus professional fee $493.40), and inpatient stays (daily floor bed $786.19) can make an infectious complication costly.

Trigger finger can also be released percutaneously. This is a reasonable option that avoids the operating room, but NFSGVHS surgeons prefer the open surgery due to concerns for tendon and nerve injury that can result from a blind sweep of the needle.^3,4 

Related: Prevention of Venous Thromboembolism After Total Joint Replacement

Existing studies found complications for trigger finger release ranging from 1% to 31%.^5,6 Wound complications and joint stiffness are known complications.^5-7 In this study, 60% of the complications were infections, and 80% of the complications were wound complications. Six of 8 patients with wound-healing complications received perioperative antibiotics. Three patients returned to the operating room for an I+D of the flexor sheath. The results showed a statistically significant link between > 1 digit treated at the same surgery and postoperative complications (P = .027). A PubMed search revealed no existing hand literature with this association.

Risk Factors

Diabetes, tobacco use, type of incision, and number of digits treated were assessed as risk factors for complications after trigger finger surgery. Nicotine is widely accepted as increasing the risk for wound complications.⁸ Almost 20% of the U.S. population smokes, compared with 22% of the VA population and 32% of active-duty military personnel.⁹ One in 4 veterans has been diagnosed with diabetes, a well-known predisposing factor in delayed wound healing and infection.^10,11 No prior studies were found comparing type of incision or multiple digits treated as complications risk factors.

There is also a well-known association between trigger finger and diabetes. Chronic hyperglycemia results in the accumulation of collagen within tendon sheaths due to impairment of collagen breakdown. Patients with diabetes tend to present with multiple digit involvement and respond less favorably to steroid injections compared with patients without diabetes.¹² Wound healing is also impaired in patients with diabetes. All 6 wound infections in this study were in patients with diabetes. Proposed etiologies for wound-healing complications include pathologic angiogenesis, impaired fibroblast proliferation and migration, impaired circulation, decreased oxygenation, and a defective immune response to the injured site.¹³

Trigger finger may develop in multiple digits. Once surgery has been planned for 1 digit, patients may request surgery on another digit on the same hand that has not had an attempt at nonoperative intervention. The NFSGVHS plastic surgeons have raised the threshold to offer multiple surgical procedures on the same hand at the same operative visit to minimize recovery time and number of visits, particularly when patients are travelling long distances. This may be less convenient; however, the overall cost to the patient and the health care system in the event of a complication is significant. Plastic surgery providers also run an alcohol prep pad over the incision site to prevent inoculation of the flexor sheath during suture removal.

Current recommendations to ameliorate the postoperative risks to the patient and costs to the system include endorsing a more conservative approach to treating trigger finger than was previously practiced at NFSGVHS. The known, less favorable response of patients with diabetes to steroid injections plus their elevated risk of postoperative infection create a catch-22 for the treatment plan. Given the low risk of a single steroid injection to the flexor sheath, this procedure is still recommended as a first-line treatment.

Related: Experience Tells in Hip Arthroplasty

During the 5-year study there was a lower threshold for surgical management and for treatment of multiple digits during the same surgery than the one currently practiced, with an overall consensus of the hospital’s HCPs. The authors recommend that all patients start with a steroid injection before committing to surgery. Patients with diabetes are informed that the injection will cause a temporary rise in their blood glucose.¹⁴ If they are resistant to the injection, high-dose oral nonsteroidal anti-inflammatory drugs and/or proximal interphalangeal joint splinting is ordered.

Verification of A_1C values showing better chronic management of blood sugar is a procedure HCPs from the NFSGVHS will begin to follow. Preoperative A_1C values between 6.5% and 8% in patients known to have diabetes has been recommended.¹⁵ A_1C values > 7% have been found to be an independent risk factor for stenosing tenosynovitis.¹⁶ The total number of trigger finger surgeries may drop with the benefit of improved utilization of resources.

Conclusion

The authors found a statistically significant association between postoperative infection and 2 patient populations: patients with diabetes (P = .002) and patients having > 1 digit released during the same surgery (P = .027). This outcome suggests using caution when offering A1 pulley release in select patient populations.

Acknowledgement
Justine Pierson, BS, research coordinator at University of Florida, for statistical analysis. Funding is through salary.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Stenosing tenosynovitis, or trigger finger, is a pathology commonly referred to the plastic and hand surgery service of the North Florida/South Georgia Veterans Health System (NFSGVHS). Patients usually present to their primary care provider with symptoms of the finger being temporarily locked or stuck in the flexed position. This can be a painful problem due to the size mismatch between the flexor tendon and the pulley under which it glides.

Patients are typically referred to surgery after failing ≥ 1 attempt at nonoperative management. The surgery is relatively quick and straightforward; however, postoperative complications can lead to an unexpected costly and lengthy recovery. The objective of this study was to identify potential risk factors that can predispose patients to postoperative complications so that those risk factors may be better anticipated and modified, if possible.

Methods

A retrospective chart review of trigger finger release surgery was performed on-site at the Malcom Randall VAMC in Gainesville, Florida, from January 2005 to December 2010 to identify risk factors associated with postoperative complications. The study was approved by both the NFSGVHS Internal Review Board and the University of Florida Institutional Review Board. Patients who underwent surgery exclusively for ≥ 1 trigger fingers by the plastic surgery service were included in the study.

The surgery involves making an incision over the affected A1 pulley in the hand (Figure 1) and sharply releasing it (Figure 2) under direct vision. Potential risk factors for postoperative complications were recorded. These risk factors included smoking status, diabetic status, type of incision, and number of digits released during the surgical procedure.

Results

Ninety-eight digits (on 81 hands) were identified as meeting inclusion criteria. Surgeries were performed using a longitudinal (43), transverse (48), oblique (5), or Brunner (2) incision. There were 10 complications: cellulitis (3), pyogenic flexor tenosynovitis (3), scar adhesion (1), delayed healing (2), and incomplete release (1). The overall complication rate was 10.2%. The authors compared risk factors with complications, using the chi square test and a determining of P < .05.

Related: Making the Case for Minimally Invasive Surgery

There was no link found between overall postoperative complications and diabetic status, incision type, or smoking status. There was a statistically significant link between diabetic patients and the incidence of postoperative infection (P = .002) and between 2 digits operated on during the same surgery and postoperative infection (P = .027)

Discussion

The routine practice of the NFSGVHS hand clinic is to offer a steroid injection as the initial treatment for trigger finger. Health care providers (HCPs) allow no more than 3 injections to the same digit to avoid the rare but potentially serious complication of a tendon rupture.¹ Due to the large NFSGVHS catchment area, wait time for elective trigger finger surgery is several months. This 3-injection plan has been well received by patients and referring providers due to these wait times. However, a recent article by Kerrigan and Stanwix concluded that the most cost-efficient treatment strategy is 2 steroid injections before surgery.²

More often than not, trigger finger release is a short, outpatient surgery with a quick recovery. To minimize the risk of stiffness and scar adhesions, the NFSGVHS practice is to refer all postoperative hand cases for ≥ 1 hand therapy appointment on the same day as their first postoperative visit.

Cost Estimates

When complications occur, they can be costly to patients due to both time spent away from home and work and additional expenses. When the current procedural terminology (CPT) codes are run through the VistA integrated billing system, based on the VHA Chief Business Office Reasonable Charges, a complication can more than double the charges associated with A1 pulley surgery.

A flexor sheath incision and drainage (I+D) (CPT 26020) charges $8,935.35 (facility charge, $6,911.95 plus professional fee, $2,023.40), compared with open trigger finger release (CPT 26055) at $8,365.66 (facility charge, $6,911.95 plus professional fee, $1,453.71). According to a conversation with the finance service officer at NFSGVHS (2/11/2014), the anesthesia bill ($490.56/15 min), anticipated level 3 emergency department visits (facility charge, $889.22 plus professional fee $493.40), and inpatient stays (daily floor bed $786.19) can make an infectious complication costly.

Trigger finger can also be released percutaneously. This is a reasonable option that avoids the operating room, but NFSGVHS surgeons prefer the open surgery due to concerns for tendon and nerve injury that can result from a blind sweep of the needle.^3,4 

Related: Prevention of Venous Thromboembolism After Total Joint Replacement

Existing studies found complications for trigger finger release ranging from 1% to 31%.^5,6 Wound complications and joint stiffness are known complications.^5-7 In this study, 60% of the complications were infections, and 80% of the complications were wound complications. Six of 8 patients with wound-healing complications received perioperative antibiotics. Three patients returned to the operating room for an I+D of the flexor sheath. The results showed a statistically significant link between > 1 digit treated at the same surgery and postoperative complications (P = .027). A PubMed search revealed no existing hand literature with this association.

Risk Factors

Diabetes, tobacco use, type of incision, and number of digits treated were assessed as risk factors for complications after trigger finger surgery. Nicotine is widely accepted as increasing the risk for wound complications.⁸ Almost 20% of the U.S. population smokes, compared with 22% of the VA population and 32% of active-duty military personnel.⁹ One in 4 veterans has been diagnosed with diabetes, a well-known predisposing factor in delayed wound healing and infection.^10,11 No prior studies were found comparing type of incision or multiple digits treated as complications risk factors.

There is also a well-known association between trigger finger and diabetes. Chronic hyperglycemia results in the accumulation of collagen within tendon sheaths due to impairment of collagen breakdown. Patients with diabetes tend to present with multiple digit involvement and respond less favorably to steroid injections compared with patients without diabetes.¹² Wound healing is also impaired in patients with diabetes. All 6 wound infections in this study were in patients with diabetes. Proposed etiologies for wound-healing complications include pathologic angiogenesis, impaired fibroblast proliferation and migration, impaired circulation, decreased oxygenation, and a defective immune response to the injured site.¹³

Trigger finger may develop in multiple digits. Once surgery has been planned for 1 digit, patients may request surgery on another digit on the same hand that has not had an attempt at nonoperative intervention. The NFSGVHS plastic surgeons have raised the threshold to offer multiple surgical procedures on the same hand at the same operative visit to minimize recovery time and number of visits, particularly when patients are travelling long distances. This may be less convenient; however, the overall cost to the patient and the health care system in the event of a complication is significant. Plastic surgery providers also run an alcohol prep pad over the incision site to prevent inoculation of the flexor sheath during suture removal.

Current recommendations to ameliorate the postoperative risks to the patient and costs to the system include endorsing a more conservative approach to treating trigger finger than was previously practiced at NFSGVHS. The known, less favorable response of patients with diabetes to steroid injections plus their elevated risk of postoperative infection create a catch-22 for the treatment plan. Given the low risk of a single steroid injection to the flexor sheath, this procedure is still recommended as a first-line treatment.

Related: Experience Tells in Hip Arthroplasty

During the 5-year study there was a lower threshold for surgical management and for treatment of multiple digits during the same surgery than the one currently practiced, with an overall consensus of the hospital’s HCPs. The authors recommend that all patients start with a steroid injection before committing to surgery. Patients with diabetes are informed that the injection will cause a temporary rise in their blood glucose.¹⁴ If they are resistant to the injection, high-dose oral nonsteroidal anti-inflammatory drugs and/or proximal interphalangeal joint splinting is ordered.

Verification of A_1C values showing better chronic management of blood sugar is a procedure HCPs from the NFSGVHS will begin to follow. Preoperative A_1C values between 6.5% and 8% in patients known to have diabetes has been recommended.¹⁵ A_1C values > 7% have been found to be an independent risk factor for stenosing tenosynovitis.¹⁶ The total number of trigger finger surgeries may drop with the benefit of improved utilization of resources.

Conclusion

The authors found a statistically significant association between postoperative infection and 2 patient populations: patients with diabetes (P = .002) and patients having > 1 digit released during the same surgery (P = .027). This outcome suggests using caution when offering A1 pulley release in select patient populations.

Acknowledgement
Justine Pierson, BS, research coordinator at University of Florida, for statistical analysis. Funding is through salary.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Stenosing tenosynovitis, or trigger finger, is a pathology commonly referred to the plastic and hand surgery service of the North Florida/South Georgia Veterans Health System (NFSGVHS). Patients usually present to their primary care provider with symptoms of the finger being temporarily locked or stuck in the flexed position. This can be a painful problem due to the size mismatch between the flexor tendon and the pulley under which it glides.

Patients are typically referred to surgery after failing ≥ 1 attempt at nonoperative management. The surgery is relatively quick and straightforward; however, postoperative complications can lead to an unexpected costly and lengthy recovery. The objective of this study was to identify potential risk factors that can predispose patients to postoperative complications so that those risk factors may be better anticipated and modified, if possible.

Methods

A retrospective chart review of trigger finger release surgery was performed on-site at the Malcom Randall VAMC in Gainesville, Florida, from January 2005 to December 2010 to identify risk factors associated with postoperative complications. The study was approved by both the NFSGVHS Internal Review Board and the University of Florida Institutional Review Board. Patients who underwent surgery exclusively for ≥ 1 trigger fingers by the plastic surgery service were included in the study.

The surgery involves making an incision over the affected A1 pulley in the hand (Figure 1) and sharply releasing it (Figure 2) under direct vision. Potential risk factors for postoperative complications were recorded. These risk factors included smoking status, diabetic status, type of incision, and number of digits released during the surgical procedure.

Results

Ninety-eight digits (on 81 hands) were identified as meeting inclusion criteria. Surgeries were performed using a longitudinal (43), transverse (48), oblique (5), or Brunner (2) incision. There were 10 complications: cellulitis (3), pyogenic flexor tenosynovitis (3), scar adhesion (1), delayed healing (2), and incomplete release (1). The overall complication rate was 10.2%. The authors compared risk factors with complications, using the chi square test and a determining of P < .05.

Related: Making the Case for Minimally Invasive Surgery

There was no link found between overall postoperative complications and diabetic status, incision type, or smoking status. There was a statistically significant link between diabetic patients and the incidence of postoperative infection (P = .002) and between 2 digits operated on during the same surgery and postoperative infection (P = .027)

Discussion

The routine practice of the NFSGVHS hand clinic is to offer a steroid injection as the initial treatment for trigger finger. Health care providers (HCPs) allow no more than 3 injections to the same digit to avoid the rare but potentially serious complication of a tendon rupture.¹ Due to the large NFSGVHS catchment area, wait time for elective trigger finger surgery is several months. This 3-injection plan has been well received by patients and referring providers due to these wait times. However, a recent article by Kerrigan and Stanwix concluded that the most cost-efficient treatment strategy is 2 steroid injections before surgery.²

More often than not, trigger finger release is a short, outpatient surgery with a quick recovery. To minimize the risk of stiffness and scar adhesions, the NFSGVHS practice is to refer all postoperative hand cases for ≥ 1 hand therapy appointment on the same day as their first postoperative visit.

Cost Estimates

When complications occur, they can be costly to patients due to both time spent away from home and work and additional expenses. When the current procedural terminology (CPT) codes are run through the VistA integrated billing system, based on the VHA Chief Business Office Reasonable Charges, a complication can more than double the charges associated with A1 pulley surgery.

A flexor sheath incision and drainage (I+D) (CPT 26020) charges $8,935.35 (facility charge, $6,911.95 plus professional fee, $2,023.40), compared with open trigger finger release (CPT 26055) at $8,365.66 (facility charge, $6,911.95 plus professional fee, $1,453.71). According to a conversation with the finance service officer at NFSGVHS (2/11/2014), the anesthesia bill ($490.56/15 min), anticipated level 3 emergency department visits (facility charge, $889.22 plus professional fee $493.40), and inpatient stays (daily floor bed $786.19) can make an infectious complication costly.

Trigger finger can also be released percutaneously. This is a reasonable option that avoids the operating room, but NFSGVHS surgeons prefer the open surgery due to concerns for tendon and nerve injury that can result from a blind sweep of the needle.^3,4 

Related: Prevention of Venous Thromboembolism After Total Joint Replacement

Existing studies found complications for trigger finger release ranging from 1% to 31%.^5,6 Wound complications and joint stiffness are known complications.^5-7 In this study, 60% of the complications were infections, and 80% of the complications were wound complications. Six of 8 patients with wound-healing complications received perioperative antibiotics. Three patients returned to the operating room for an I+D of the flexor sheath. The results showed a statistically significant link between > 1 digit treated at the same surgery and postoperative complications (P = .027). A PubMed search revealed no existing hand literature with this association.

Risk Factors

Diabetes, tobacco use, type of incision, and number of digits treated were assessed as risk factors for complications after trigger finger surgery. Nicotine is widely accepted as increasing the risk for wound complications.⁸ Almost 20% of the U.S. population smokes, compared with 22% of the VA population and 32% of active-duty military personnel.⁹ One in 4 veterans has been diagnosed with diabetes, a well-known predisposing factor in delayed wound healing and infection.^10,11 No prior studies were found comparing type of incision or multiple digits treated as complications risk factors.

There is also a well-known association between trigger finger and diabetes. Chronic hyperglycemia results in the accumulation of collagen within tendon sheaths due to impairment of collagen breakdown. Patients with diabetes tend to present with multiple digit involvement and respond less favorably to steroid injections compared with patients without diabetes.¹² Wound healing is also impaired in patients with diabetes. All 6 wound infections in this study were in patients with diabetes. Proposed etiologies for wound-healing complications include pathologic angiogenesis, impaired fibroblast proliferation and migration, impaired circulation, decreased oxygenation, and a defective immune response to the injured site.¹³

Trigger finger may develop in multiple digits. Once surgery has been planned for 1 digit, patients may request surgery on another digit on the same hand that has not had an attempt at nonoperative intervention. The NFSGVHS plastic surgeons have raised the threshold to offer multiple surgical procedures on the same hand at the same operative visit to minimize recovery time and number of visits, particularly when patients are travelling long distances. This may be less convenient; however, the overall cost to the patient and the health care system in the event of a complication is significant. Plastic surgery providers also run an alcohol prep pad over the incision site to prevent inoculation of the flexor sheath during suture removal.

Current recommendations to ameliorate the postoperative risks to the patient and costs to the system include endorsing a more conservative approach to treating trigger finger than was previously practiced at NFSGVHS. The known, less favorable response of patients with diabetes to steroid injections plus their elevated risk of postoperative infection create a catch-22 for the treatment plan. Given the low risk of a single steroid injection to the flexor sheath, this procedure is still recommended as a first-line treatment.

Related: Experience Tells in Hip Arthroplasty

During the 5-year study there was a lower threshold for surgical management and for treatment of multiple digits during the same surgery than the one currently practiced, with an overall consensus of the hospital’s HCPs. The authors recommend that all patients start with a steroid injection before committing to surgery. Patients with diabetes are informed that the injection will cause a temporary rise in their blood glucose.¹⁴ If they are resistant to the injection, high-dose oral nonsteroidal anti-inflammatory drugs and/or proximal interphalangeal joint splinting is ordered.

Verification of A_1C values showing better chronic management of blood sugar is a procedure HCPs from the NFSGVHS will begin to follow. Preoperative A_1C values between 6.5% and 8% in patients known to have diabetes has been recommended.¹⁵ A_1C values > 7% have been found to be an independent risk factor for stenosing tenosynovitis.¹⁶ The total number of trigger finger surgeries may drop with the benefit of improved utilization of resources.

Conclusion

The authors found a statistically significant association between postoperative infection and 2 patient populations: patients with diabetes (P = .002) and patients having > 1 digit released during the same surgery (P = .027). This outcome suggests using caution when offering A1 pulley release in select patient populations.

Acknowledgement
Justine Pierson, BS, research coordinator at University of Florida, for statistical analysis. Funding is through salary.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Compared with monoarticular arthritis, polyarticular arthritis may yield an initially narrower differential diagnosis that focuses on systemic inflammatory conditions, such as rheumatoid arthritis (RA). Approximately 15% to 30% of septic arthritis is polyarticular, of which about 45% is associated with underlying RA.^1,2 Regardless of the number of joints involved, septic (infectious) arthritis is a valid consideration given the morbidity and mortality.

In a retrospective study in the United Kingdom (UK) between 1982 and 1991, the morbidity and mortality of septic arthritis was 31.6% and 11.5%, respectively, and 16% of the study population had RA.³ A review of the literature by Dubost and colleagues found that polyarticular septic arthritis (PASA) has a mortality of 31% to 42% compared with 4% to 8% for monoarticular septic arthritis, and RA was present in 67% of the PASA fatalities.¹

Related: The Golden Era of Treatment in Rheumatology

Rheumatoid arthritis and its treatment predispose patients to septic arthritis. Septic arthritis in the UK general population is 0.42 per 100 patient-years for patients with RA on antitumor necrosis factor therapy.^3,4 In a retrospective study in the U.S., the incidence of septic arthritis was 0.40 per 100 patient-years for patients with RA compared with 0.02 per 100 patient-years for patients without RA.⁵

Other complications of RA include infectious tenosynovitis and tendon rupture. The incidence and prevalence of infectious tenosynovitis and tendon rupture in RA are not firmly established in the literature.

We present a patient with RA and psoriasis who responded initially to acute management for RA but subsequently was diagnosed with culture-negative polyarticular arthritis and infectious tenosynovitis associated with beta hemolytic group G Streptococcus (GGS), a part of Streptococcus milleri (S. milleri). During surgery, he was also found to have bilateral extensor pollicus longus (EPL) tendon rupture. Given the possible morbidity, the authors believe this patient may be of interest to the medical community.

Case Presentation

A 69-year-old African American male presented with 3 to 4 days of swelling and pain of bilateral wrists, bilateral hands, and the left ankle with subjective, but resolved, fevers and chills. His medical history was significant for seropositive erosive RA, psoriasis, hypertension, hyperlipidemia, alcohol abuse, chronic tobacco use, osteoporosis, and glaucoma. He did not have diabetes, reported no IV drug abuse, and except for the immunosuppressive effects of his medications, was not otherwise immunocompromised.

For 2 years in the outpatient setting, the rheumatology clinic had been managing the patient’s rheumatoid factor (RF) positive and anti-cyclic citrullinated peptide (CCP) antibody positive erosive RA with etanercept 25 mg subcutaneously twice a week. The RA affected his hands, wrists, shoulders, and ankles bilaterally but was successfully controlled. The dermatology clinic was managing the patient’s psoriasis with calcipotriene cream 0.005% twice a week and clobetasol ointment 0.05% twice a week. Psoriatic plaques were noted on bilateral elbows, bilateral dorsal hands, and bilateral dorsal feet.

Initial Evaluation

At evaluation, the patient’s vital signs revealed a temperature of 36.3°C (97.3°F), pulse of 102 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 99% on room air, and blood pressure of 102/70 mm Hg. He was found to have edema, tenderness, and erythema of the wrists bilaterally and left metacarpophalangeal joints (MCPs) and edematous right MCPs and left medial ankle.

The patient had been nonadherent with etanercept for 5 monthsand restarted taking the medication only 2 weeks before presentation. He had noticed worsening arthritis for at least 1 month. His last RA flare was approximately 1 year before presentation. Additional symptoms included 4 days of nausea, nonbloody and nonbilious emesis, left lower quadrant pain, and diarrhea without melena or hematochezia.

Initial laboratory studies found 3.2 k/μL white blood cells (WBCs) with a differential of 11.9% lymphocytes, 4.2% monocytes, 83.3% neutrophils, 0.5% eosinophils, and 0.1% basophils; 165 k/μL platelets; 96 mm/h erythrocyte sedimentation rate (ESR); and 45 mg/dL C-reactive protein. The patient was diagnosed with viral gastroenteritis and RA flare and was admitted for inpatient management secondary to limited ability to care for himself.

Related: Infliximab-Induced Complications

The patient was started on prednisone 40 mg orally once a day (for 5 days) for empiric treatment of an RA flare and continued on etanercept. The inpatient rheumatology service was consulted. Further evaluation later that day found involvement of the proximal interphalangeal joints and elbows and tenderness of the tendons of the dorsal hand bilaterally. Over the next 2 days, the patient remained afebrile and WBCs were within normal limits. Edema, erythema, and tenderness of the involved joints somewhat improved, but tenderness along the tendons of the dorsal hand worsened, which concerned the managing teams for infectious tenosynovitis.

By day 4, the patient was afebrile and had a leukocytosis of 12.9 k/μLwith neutrophils 86.7%, but improvement of erythema, pain, and range of motion of involved joints and no tenderness to palpation of tendons was noted. The inpatient orthopedic surgery service evaluated the patient and did not find sufficient evidence necessitating surgical intervention.

Worsening Condition

On day 6, arthrocentesis of the left wrist was performed secondary to worsening of erythema and edema. The patient experienced new edema of the left shoulder and leukocytosis continued to trend upward (15.7 k/μL on day 6). Purulent aspirate (1.5 mL) was obtained from the fluctuance and tenosynovium of the left wrist. Empiric vancomycin 1 g IV twice daily and ceftriaxone 2 g IV daily were started and continued for 3 days. By this point in his hospital course, the patient had received 1 dose of etanercept. Prednisone and etanercept were previously discontinued because of the discovered infection. Blood cultures were drawn and had no growth (Table). Gastroenterology studies were limited to stool cultures and did not include colonoscopy. Leukocytosis began trending down.

On day 8, antibiotics were tailored to penicillin G 4 million units IV every 4 hours following growth of GGS from the sample of the left wrist. Subsequently, synovial fluid (3 mL) from the left shoulder was obtained following initiation of antibiotic therapy and had no growth. Magnetic resonance imaging (MRI) found tenosynovitis of the left ankle and right wrist.

On day 9, transthoracic echocardiography was performed and found no evidence of infectious endocarditis. Later that night, the patient was taken to surgery for incision and drainage/debridement of bilateral wrists and left ankle, synovectomy of right wrist, and aspiration of right shoulder. Findings included abscess in the left wrist and inflammatory synovitis and bilateral EPL tendon rupture consistent with RA. Pus from the left ankle had few gram-positive cocci in chains with no growth, and the specimens from both wrists grew GGS. Aspirate from the left ankle was an opaque yellow fluid with 14,900/mm³ WBC, 30,000/mm³ red blood cells (RBC), 97% neutrophils, 1% macrophages, 2% lymphocytes, and 0% monocytes. Aspirate from the right shoulder was an opaque bloody fluid with 10,100/mm³ WBC, 40,000/mm³ RBC, 95% neutrophils, 2% macrophages, 1% lymphocytes, and 1% monocytes. On day 10, sulfasalazine 500 mg twice a day was initiated for RA.

Following surgery and continued antibiotics, the patient’s leukocytosis resolved, and improvement was seen in all joints with decreased edema, erythema, and pain and increased range of motion. Postoperative recovery was complicated by ileus, urinary retention, and fungal (Candida albicans) urinary tract infection, all of which resolved without significant complications. The inpatient rheumatology service restarted prednisone at a lower dose of 20 mg. The patient became afebrile and sufficiently stable for transfer to a lower level of care with continued physical therapy and IV antibiotics for another 3 weeks.

Discussion

The patient had 2 underlying systemic inflammatory conditions: RA and psoriasis. The underlying chronic arthritis was likely caused by RA, not psoriatic arthritis (PsA). The patient met the 2010 American College of Rheumatology criteria but failed to meet the classification criteria for PsA.^6,7 However, the clinical features of RA and PsA overlap. Rheumatoid factor and CCP can be positive laboratory findings in both RA and PsA.^8-14 Tenosynovitis is found in about half of RA patients and PsA patients (P > .05).¹⁵ In its evaluation of the patient, the inpatient rheumatology service suspected that the patient may have had RA with components of PsA.

Rheumatoid arthritis complicates the diagnosis of septic arthritis. In a study by Nolla and colleagues, a mean of 7.3 days (range 3 to 18 days) elapsed before a diagnosis of septic arthritis was made in 10 patients with RA on corticosteroids.² Consideration of risk factors such as increasing age, male sex, tobacco use, extra-articular manifestations of RA, positive RF, rheumatoid nodules, poor functional capacity, high ESR, leukopenia, comorbidities (chronic lung disease, alcoholism, organic brain disease, and diabetes), and the use of corticosteroids may expedite the diagnosis of infections in patients with RA.¹⁶ In this case, the patient had some of these risk factors: age, male sex, alcoholism, chronic tobacco use, positive RF, high ESR, and leukopenia (at presentation).

Related: Trend Toward Concomitant Supplements and Medications

The history of medication nonadherence of etanercept with progressively worsening arthritis and early clinical improvement (reduction in erythema, edema, and pain and temporary loss of signs of tenosynovitis on examination) while on prednisone suggested that the patient had a RA flare. The prednisone likely alleviated the inflammatory process but created an immunosuppressed state that allowed GGS to invade and possibly disseminate. Alternately, the patient may have been infected before presentation. The lack of a definitive time line for his case prevented the authors from forming conclusions about a possible causal relationship between the infection and medications. The subjective fevers before admission were nonspecific and could have been caused by RA, presumed gastroenteritis, or other undiagnosed infectious processes. The observed leukocytosis may have been initially corticosteroid-induced.¹⁷

Septic Arthritis

The suspicion of septic arthritis and infectious tenosynovitis substantially increased on day 6 with worsening symptoms, involvement of additional joints, and spiking fevers. Group G Streptococcus was obtained from the aspirate of the left wrist and from the surgical specimens from the bilateral wrists. The clinical presentation, MRI imaging studies, and surgical and nonsurgical specimens supported a diagnosis of GGS tenosynovitis. However, there was no clear evidence (ie, positive culture with identified organism) of septic arthritis, likely secondary to early septic arthritis and initiation of antibiotics before joint aspirations. The aspirate from the left ankle was yellow and opaque, but the culture was negative.

The pathogenic organism in the patient was GGS. Group G Streptococcus is normal flora of the oral cavity, gastrointestinal (GI) tract, upper respiratory tract, genital tract, and skin, which were all possible sources of seeding.¹⁸ Streptococcal species account for about 20% of septic arthritis, and GGS arthritis accounts for 4% to 19% of streptococcal arthritis.^19-22 From a review of the literature, 2 cases of GGS tenosynovitis have been published.^23,24 However, in an ultrasound study and MRI study, 49% and 43%, respectively, of patients with RA had tenosynovitis of the tendons of the hands.^15,25

GGS Demographics

About three-quarters (71%) of patients with GGS arthritis are male.¹⁹ The analysis of the literature by Bronze and colleagues found that chronic joint disease and alcoholism are present in 34% and 14% of patients with GGS arthritis, respectively. One-quarter (23% from Dubost and colleagues) to one-third (32% from Schattner and colleagues) of patients with GGS arthritis have RA.^19,26

Fever is present in less than half (43%) of patients with GGS arthritis.¹⁹ Positive synovial fluid is expected in 90% of patients.¹⁹ Leukocytosis and elevated ESR need not be present.^27,28 The arthritis is polyarticular in one-quarter of patients (24% from Bronze and colleagues and 26% from Dubost and colleagues).^19,26

Positive blood cultures can be expected in one-fourth (26%) of patients with GGS arthritis.¹⁹ The patient’s blood cultures were negative. Blood cultures drawn before initiation of antibiotics yielded no growth, so if the spread was hematogenous, the bacteremia was transient or intermittent. Before and after initiation of antibiotics, specimens from the shoulders did not grow colonies, whereas specimens from the wrists did. If the shoulders were truly infected, these findings and the notably later involvement of the shoulders suggest that the shoulders may have been seeded later in the hospital course.

Trenkner and colleagues proposed that GI abnormalities provide a portal of entry for GGS, which is under the umbrella of S. milleri.²⁹S. milleri is associated with abscess formation, usually of the GI tract.^30-32 In the study patient, the possible gastroenteritis may have provided such a portal of entry and subsequent seeding to the joints, and an abscess was found in the left wrist.

Tendon Rupture

Additionally, bilateral EPL tendon rupture likely occurred as a consequence of the inflammatory process from RA and infectious tenosynovitis in the patient. According to Zheng and colleagues, tenosynovitis is an inflammatory process of the synovial tendon sheath that may result in degeneration and rupture of the tendons and may contribute to bone erosions, development of joint deformities, and loss of functional capacity.³³ In a histologic study of a ruptured EPL tendon from a patient with RA, Harris observed a chronic inflammatory cellular reaction.³⁴ Harris also described a male with RA with unconfirmed bilateral EPL rupture.³⁴ Björkman and colleague identified previous injury, RA, and local or systemic steroids as important etiologic factors for EPL tendon rupture.³⁵

As in the case of this patient, the utilization of both medical and surgical therapy is not uncommon for treating GGS infection. Antibiotic therapy typically consists of penicillin (74%).²⁶ Surgical intervention is necessary in 16% to 37% of patients.^19,26 This patient required both penicillin and incision and drainage/debridement before significant clinical improvement was noted. Prognosis of GGS arthritis is favorable with 5% mortality.²⁶

Conclusion

Septic arthritis and infectious tenosynovitis are readily treatable with low mortality if promptly identified. Identification can be masked by other medical conditions, such as RA and psoriasis, and their associated immunosuppressive treatment. Bilateral EPL tendon rupture may be a complication of RA, particularly with an underlying septic arthritis and infectious tenosynovitis.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Compared with monoarticular arthritis, polyarticular arthritis may yield an initially narrower differential diagnosis that focuses on systemic inflammatory conditions, such as rheumatoid arthritis (RA). Approximately 15% to 30% of septic arthritis is polyarticular, of which about 45% is associated with underlying RA.^1,2 Regardless of the number of joints involved, septic (infectious) arthritis is a valid consideration given the morbidity and mortality.

In a retrospective study in the United Kingdom (UK) between 1982 and 1991, the morbidity and mortality of septic arthritis was 31.6% and 11.5%, respectively, and 16% of the study population had RA.³ A review of the literature by Dubost and colleagues found that polyarticular septic arthritis (PASA) has a mortality of 31% to 42% compared with 4% to 8% for monoarticular septic arthritis, and RA was present in 67% of the PASA fatalities.¹

Related: The Golden Era of Treatment in Rheumatology

Rheumatoid arthritis and its treatment predispose patients to septic arthritis. Septic arthritis in the UK general population is 0.42 per 100 patient-years for patients with RA on antitumor necrosis factor therapy.^3,4 In a retrospective study in the U.S., the incidence of septic arthritis was 0.40 per 100 patient-years for patients with RA compared with 0.02 per 100 patient-years for patients without RA.⁵

Other complications of RA include infectious tenosynovitis and tendon rupture. The incidence and prevalence of infectious tenosynovitis and tendon rupture in RA are not firmly established in the literature.

We present a patient with RA and psoriasis who responded initially to acute management for RA but subsequently was diagnosed with culture-negative polyarticular arthritis and infectious tenosynovitis associated with beta hemolytic group G Streptococcus (GGS), a part of Streptococcus milleri (S. milleri). During surgery, he was also found to have bilateral extensor pollicus longus (EPL) tendon rupture. Given the possible morbidity, the authors believe this patient may be of interest to the medical community.

Case Presentation

A 69-year-old African American male presented with 3 to 4 days of swelling and pain of bilateral wrists, bilateral hands, and the left ankle with subjective, but resolved, fevers and chills. His medical history was significant for seropositive erosive RA, psoriasis, hypertension, hyperlipidemia, alcohol abuse, chronic tobacco use, osteoporosis, and glaucoma. He did not have diabetes, reported no IV drug abuse, and except for the immunosuppressive effects of his medications, was not otherwise immunocompromised.

For 2 years in the outpatient setting, the rheumatology clinic had been managing the patient’s rheumatoid factor (RF) positive and anti-cyclic citrullinated peptide (CCP) antibody positive erosive RA with etanercept 25 mg subcutaneously twice a week. The RA affected his hands, wrists, shoulders, and ankles bilaterally but was successfully controlled. The dermatology clinic was managing the patient’s psoriasis with calcipotriene cream 0.005% twice a week and clobetasol ointment 0.05% twice a week. Psoriatic plaques were noted on bilateral elbows, bilateral dorsal hands, and bilateral dorsal feet.

Initial Evaluation

At evaluation, the patient’s vital signs revealed a temperature of 36.3°C (97.3°F), pulse of 102 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 99% on room air, and blood pressure of 102/70 mm Hg. He was found to have edema, tenderness, and erythema of the wrists bilaterally and left metacarpophalangeal joints (MCPs) and edematous right MCPs and left medial ankle.

The patient had been nonadherent with etanercept for 5 monthsand restarted taking the medication only 2 weeks before presentation. He had noticed worsening arthritis for at least 1 month. His last RA flare was approximately 1 year before presentation. Additional symptoms included 4 days of nausea, nonbloody and nonbilious emesis, left lower quadrant pain, and diarrhea without melena or hematochezia.

Initial laboratory studies found 3.2 k/μL white blood cells (WBCs) with a differential of 11.9% lymphocytes, 4.2% monocytes, 83.3% neutrophils, 0.5% eosinophils, and 0.1% basophils; 165 k/μL platelets; 96 mm/h erythrocyte sedimentation rate (ESR); and 45 mg/dL C-reactive protein. The patient was diagnosed with viral gastroenteritis and RA flare and was admitted for inpatient management secondary to limited ability to care for himself.

Related: Infliximab-Induced Complications

The patient was started on prednisone 40 mg orally once a day (for 5 days) for empiric treatment of an RA flare and continued on etanercept. The inpatient rheumatology service was consulted. Further evaluation later that day found involvement of the proximal interphalangeal joints and elbows and tenderness of the tendons of the dorsal hand bilaterally. Over the next 2 days, the patient remained afebrile and WBCs were within normal limits. Edema, erythema, and tenderness of the involved joints somewhat improved, but tenderness along the tendons of the dorsal hand worsened, which concerned the managing teams for infectious tenosynovitis.

By day 4, the patient was afebrile and had a leukocytosis of 12.9 k/μLwith neutrophils 86.7%, but improvement of erythema, pain, and range of motion of involved joints and no tenderness to palpation of tendons was noted. The inpatient orthopedic surgery service evaluated the patient and did not find sufficient evidence necessitating surgical intervention.

Worsening Condition

On day 6, arthrocentesis of the left wrist was performed secondary to worsening of erythema and edema. The patient experienced new edema of the left shoulder and leukocytosis continued to trend upward (15.7 k/μL on day 6). Purulent aspirate (1.5 mL) was obtained from the fluctuance and tenosynovium of the left wrist. Empiric vancomycin 1 g IV twice daily and ceftriaxone 2 g IV daily were started and continued for 3 days. By this point in his hospital course, the patient had received 1 dose of etanercept. Prednisone and etanercept were previously discontinued because of the discovered infection. Blood cultures were drawn and had no growth (Table). Gastroenterology studies were limited to stool cultures and did not include colonoscopy. Leukocytosis began trending down.

On day 8, antibiotics were tailored to penicillin G 4 million units IV every 4 hours following growth of GGS from the sample of the left wrist. Subsequently, synovial fluid (3 mL) from the left shoulder was obtained following initiation of antibiotic therapy and had no growth. Magnetic resonance imaging (MRI) found tenosynovitis of the left ankle and right wrist.

On day 9, transthoracic echocardiography was performed and found no evidence of infectious endocarditis. Later that night, the patient was taken to surgery for incision and drainage/debridement of bilateral wrists and left ankle, synovectomy of right wrist, and aspiration of right shoulder. Findings included abscess in the left wrist and inflammatory synovitis and bilateral EPL tendon rupture consistent with RA. Pus from the left ankle had few gram-positive cocci in chains with no growth, and the specimens from both wrists grew GGS. Aspirate from the left ankle was an opaque yellow fluid with 14,900/mm³ WBC, 30,000/mm³ red blood cells (RBC), 97% neutrophils, 1% macrophages, 2% lymphocytes, and 0% monocytes. Aspirate from the right shoulder was an opaque bloody fluid with 10,100/mm³ WBC, 40,000/mm³ RBC, 95% neutrophils, 2% macrophages, 1% lymphocytes, and 1% monocytes. On day 10, sulfasalazine 500 mg twice a day was initiated for RA.

Following surgery and continued antibiotics, the patient’s leukocytosis resolved, and improvement was seen in all joints with decreased edema, erythema, and pain and increased range of motion. Postoperative recovery was complicated by ileus, urinary retention, and fungal (Candida albicans) urinary tract infection, all of which resolved without significant complications. The inpatient rheumatology service restarted prednisone at a lower dose of 20 mg. The patient became afebrile and sufficiently stable for transfer to a lower level of care with continued physical therapy and IV antibiotics for another 3 weeks.

Discussion

The patient had 2 underlying systemic inflammatory conditions: RA and psoriasis. The underlying chronic arthritis was likely caused by RA, not psoriatic arthritis (PsA). The patient met the 2010 American College of Rheumatology criteria but failed to meet the classification criteria for PsA.^6,7 However, the clinical features of RA and PsA overlap. Rheumatoid factor and CCP can be positive laboratory findings in both RA and PsA.^8-14 Tenosynovitis is found in about half of RA patients and PsA patients (P > .05).¹⁵ In its evaluation of the patient, the inpatient rheumatology service suspected that the patient may have had RA with components of PsA.

Rheumatoid arthritis complicates the diagnosis of septic arthritis. In a study by Nolla and colleagues, a mean of 7.3 days (range 3 to 18 days) elapsed before a diagnosis of septic arthritis was made in 10 patients with RA on corticosteroids.² Consideration of risk factors such as increasing age, male sex, tobacco use, extra-articular manifestations of RA, positive RF, rheumatoid nodules, poor functional capacity, high ESR, leukopenia, comorbidities (chronic lung disease, alcoholism, organic brain disease, and diabetes), and the use of corticosteroids may expedite the diagnosis of infections in patients with RA.¹⁶ In this case, the patient had some of these risk factors: age, male sex, alcoholism, chronic tobacco use, positive RF, high ESR, and leukopenia (at presentation).

Related: Trend Toward Concomitant Supplements and Medications

The history of medication nonadherence of etanercept with progressively worsening arthritis and early clinical improvement (reduction in erythema, edema, and pain and temporary loss of signs of tenosynovitis on examination) while on prednisone suggested that the patient had a RA flare. The prednisone likely alleviated the inflammatory process but created an immunosuppressed state that allowed GGS to invade and possibly disseminate. Alternately, the patient may have been infected before presentation. The lack of a definitive time line for his case prevented the authors from forming conclusions about a possible causal relationship between the infection and medications. The subjective fevers before admission were nonspecific and could have been caused by RA, presumed gastroenteritis, or other undiagnosed infectious processes. The observed leukocytosis may have been initially corticosteroid-induced.¹⁷

Septic Arthritis

The suspicion of septic arthritis and infectious tenosynovitis substantially increased on day 6 with worsening symptoms, involvement of additional joints, and spiking fevers. Group G Streptococcus was obtained from the aspirate of the left wrist and from the surgical specimens from the bilateral wrists. The clinical presentation, MRI imaging studies, and surgical and nonsurgical specimens supported a diagnosis of GGS tenosynovitis. However, there was no clear evidence (ie, positive culture with identified organism) of septic arthritis, likely secondary to early septic arthritis and initiation of antibiotics before joint aspirations. The aspirate from the left ankle was yellow and opaque, but the culture was negative.

The pathogenic organism in the patient was GGS. Group G Streptococcus is normal flora of the oral cavity, gastrointestinal (GI) tract, upper respiratory tract, genital tract, and skin, which were all possible sources of seeding.¹⁸ Streptococcal species account for about 20% of septic arthritis, and GGS arthritis accounts for 4% to 19% of streptococcal arthritis.^19-22 From a review of the literature, 2 cases of GGS tenosynovitis have been published.^23,24 However, in an ultrasound study and MRI study, 49% and 43%, respectively, of patients with RA had tenosynovitis of the tendons of the hands.^15,25

GGS Demographics

About three-quarters (71%) of patients with GGS arthritis are male.¹⁹ The analysis of the literature by Bronze and colleagues found that chronic joint disease and alcoholism are present in 34% and 14% of patients with GGS arthritis, respectively. One-quarter (23% from Dubost and colleagues) to one-third (32% from Schattner and colleagues) of patients with GGS arthritis have RA.^19,26

Fever is present in less than half (43%) of patients with GGS arthritis.¹⁹ Positive synovial fluid is expected in 90% of patients.¹⁹ Leukocytosis and elevated ESR need not be present.^27,28 The arthritis is polyarticular in one-quarter of patients (24% from Bronze and colleagues and 26% from Dubost and colleagues).^19,26

Positive blood cultures can be expected in one-fourth (26%) of patients with GGS arthritis.¹⁹ The patient’s blood cultures were negative. Blood cultures drawn before initiation of antibiotics yielded no growth, so if the spread was hematogenous, the bacteremia was transient or intermittent. Before and after initiation of antibiotics, specimens from the shoulders did not grow colonies, whereas specimens from the wrists did. If the shoulders were truly infected, these findings and the notably later involvement of the shoulders suggest that the shoulders may have been seeded later in the hospital course.

Trenkner and colleagues proposed that GI abnormalities provide a portal of entry for GGS, which is under the umbrella of S. milleri.²⁹S. milleri is associated with abscess formation, usually of the GI tract.^30-32 In the study patient, the possible gastroenteritis may have provided such a portal of entry and subsequent seeding to the joints, and an abscess was found in the left wrist.

Tendon Rupture

Additionally, bilateral EPL tendon rupture likely occurred as a consequence of the inflammatory process from RA and infectious tenosynovitis in the patient. According to Zheng and colleagues, tenosynovitis is an inflammatory process of the synovial tendon sheath that may result in degeneration and rupture of the tendons and may contribute to bone erosions, development of joint deformities, and loss of functional capacity.³³ In a histologic study of a ruptured EPL tendon from a patient with RA, Harris observed a chronic inflammatory cellular reaction.³⁴ Harris also described a male with RA with unconfirmed bilateral EPL rupture.³⁴ Björkman and colleague identified previous injury, RA, and local or systemic steroids as important etiologic factors for EPL tendon rupture.³⁵

As in the case of this patient, the utilization of both medical and surgical therapy is not uncommon for treating GGS infection. Antibiotic therapy typically consists of penicillin (74%).²⁶ Surgical intervention is necessary in 16% to 37% of patients.^19,26 This patient required both penicillin and incision and drainage/debridement before significant clinical improvement was noted. Prognosis of GGS arthritis is favorable with 5% mortality.²⁶

Conclusion

Septic arthritis and infectious tenosynovitis are readily treatable with low mortality if promptly identified. Identification can be masked by other medical conditions, such as RA and psoriasis, and their associated immunosuppressive treatment. Bilateral EPL tendon rupture may be a complication of RA, particularly with an underlying septic arthritis and infectious tenosynovitis.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Compared with monoarticular arthritis, polyarticular arthritis may yield an initially narrower differential diagnosis that focuses on systemic inflammatory conditions, such as rheumatoid arthritis (RA). Approximately 15% to 30% of septic arthritis is polyarticular, of which about 45% is associated with underlying RA.^1,2 Regardless of the number of joints involved, septic (infectious) arthritis is a valid consideration given the morbidity and mortality.

In a retrospective study in the United Kingdom (UK) between 1982 and 1991, the morbidity and mortality of septic arthritis was 31.6% and 11.5%, respectively, and 16% of the study population had RA.³ A review of the literature by Dubost and colleagues found that polyarticular septic arthritis (PASA) has a mortality of 31% to 42% compared with 4% to 8% for monoarticular septic arthritis, and RA was present in 67% of the PASA fatalities.¹

Related: The Golden Era of Treatment in Rheumatology

Rheumatoid arthritis and its treatment predispose patients to septic arthritis. Septic arthritis in the UK general population is 0.42 per 100 patient-years for patients with RA on antitumor necrosis factor therapy.^3,4 In a retrospective study in the U.S., the incidence of septic arthritis was 0.40 per 100 patient-years for patients with RA compared with 0.02 per 100 patient-years for patients without RA.⁵

Other complications of RA include infectious tenosynovitis and tendon rupture. The incidence and prevalence of infectious tenosynovitis and tendon rupture in RA are not firmly established in the literature.

We present a patient with RA and psoriasis who responded initially to acute management for RA but subsequently was diagnosed with culture-negative polyarticular arthritis and infectious tenosynovitis associated with beta hemolytic group G Streptococcus (GGS), a part of Streptococcus milleri (S. milleri). During surgery, he was also found to have bilateral extensor pollicus longus (EPL) tendon rupture. Given the possible morbidity, the authors believe this patient may be of interest to the medical community.

Case Presentation

A 69-year-old African American male presented with 3 to 4 days of swelling and pain of bilateral wrists, bilateral hands, and the left ankle with subjective, but resolved, fevers and chills. His medical history was significant for seropositive erosive RA, psoriasis, hypertension, hyperlipidemia, alcohol abuse, chronic tobacco use, osteoporosis, and glaucoma. He did not have diabetes, reported no IV drug abuse, and except for the immunosuppressive effects of his medications, was not otherwise immunocompromised.

For 2 years in the outpatient setting, the rheumatology clinic had been managing the patient’s rheumatoid factor (RF) positive and anti-cyclic citrullinated peptide (CCP) antibody positive erosive RA with etanercept 25 mg subcutaneously twice a week. The RA affected his hands, wrists, shoulders, and ankles bilaterally but was successfully controlled. The dermatology clinic was managing the patient’s psoriasis with calcipotriene cream 0.005% twice a week and clobetasol ointment 0.05% twice a week. Psoriatic plaques were noted on bilateral elbows, bilateral dorsal hands, and bilateral dorsal feet.

Initial Evaluation

At evaluation, the patient’s vital signs revealed a temperature of 36.3°C (97.3°F), pulse of 102 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 99% on room air, and blood pressure of 102/70 mm Hg. He was found to have edema, tenderness, and erythema of the wrists bilaterally and left metacarpophalangeal joints (MCPs) and edematous right MCPs and left medial ankle.

The patient had been nonadherent with etanercept for 5 monthsand restarted taking the medication only 2 weeks before presentation. He had noticed worsening arthritis for at least 1 month. His last RA flare was approximately 1 year before presentation. Additional symptoms included 4 days of nausea, nonbloody and nonbilious emesis, left lower quadrant pain, and diarrhea without melena or hematochezia.

Initial laboratory studies found 3.2 k/μL white blood cells (WBCs) with a differential of 11.9% lymphocytes, 4.2% monocytes, 83.3% neutrophils, 0.5% eosinophils, and 0.1% basophils; 165 k/μL platelets; 96 mm/h erythrocyte sedimentation rate (ESR); and 45 mg/dL C-reactive protein. The patient was diagnosed with viral gastroenteritis and RA flare and was admitted for inpatient management secondary to limited ability to care for himself.

Related: Infliximab-Induced Complications

The patient was started on prednisone 40 mg orally once a day (for 5 days) for empiric treatment of an RA flare and continued on etanercept. The inpatient rheumatology service was consulted. Further evaluation later that day found involvement of the proximal interphalangeal joints and elbows and tenderness of the tendons of the dorsal hand bilaterally. Over the next 2 days, the patient remained afebrile and WBCs were within normal limits. Edema, erythema, and tenderness of the involved joints somewhat improved, but tenderness along the tendons of the dorsal hand worsened, which concerned the managing teams for infectious tenosynovitis.

By day 4, the patient was afebrile and had a leukocytosis of 12.9 k/μLwith neutrophils 86.7%, but improvement of erythema, pain, and range of motion of involved joints and no tenderness to palpation of tendons was noted. The inpatient orthopedic surgery service evaluated the patient and did not find sufficient evidence necessitating surgical intervention.

Worsening Condition

On day 6, arthrocentesis of the left wrist was performed secondary to worsening of erythema and edema. The patient experienced new edema of the left shoulder and leukocytosis continued to trend upward (15.7 k/μL on day 6). Purulent aspirate (1.5 mL) was obtained from the fluctuance and tenosynovium of the left wrist. Empiric vancomycin 1 g IV twice daily and ceftriaxone 2 g IV daily were started and continued for 3 days. By this point in his hospital course, the patient had received 1 dose of etanercept. Prednisone and etanercept were previously discontinued because of the discovered infection. Blood cultures were drawn and had no growth (Table). Gastroenterology studies were limited to stool cultures and did not include colonoscopy. Leukocytosis began trending down.

On day 8, antibiotics were tailored to penicillin G 4 million units IV every 4 hours following growth of GGS from the sample of the left wrist. Subsequently, synovial fluid (3 mL) from the left shoulder was obtained following initiation of antibiotic therapy and had no growth. Magnetic resonance imaging (MRI) found tenosynovitis of the left ankle and right wrist.

On day 9, transthoracic echocardiography was performed and found no evidence of infectious endocarditis. Later that night, the patient was taken to surgery for incision and drainage/debridement of bilateral wrists and left ankle, synovectomy of right wrist, and aspiration of right shoulder. Findings included abscess in the left wrist and inflammatory synovitis and bilateral EPL tendon rupture consistent with RA. Pus from the left ankle had few gram-positive cocci in chains with no growth, and the specimens from both wrists grew GGS. Aspirate from the left ankle was an opaque yellow fluid with 14,900/mm³ WBC, 30,000/mm³ red blood cells (RBC), 97% neutrophils, 1% macrophages, 2% lymphocytes, and 0% monocytes. Aspirate from the right shoulder was an opaque bloody fluid with 10,100/mm³ WBC, 40,000/mm³ RBC, 95% neutrophils, 2% macrophages, 1% lymphocytes, and 1% monocytes. On day 10, sulfasalazine 500 mg twice a day was initiated for RA.

Following surgery and continued antibiotics, the patient’s leukocytosis resolved, and improvement was seen in all joints with decreased edema, erythema, and pain and increased range of motion. Postoperative recovery was complicated by ileus, urinary retention, and fungal (Candida albicans) urinary tract infection, all of which resolved without significant complications. The inpatient rheumatology service restarted prednisone at a lower dose of 20 mg. The patient became afebrile and sufficiently stable for transfer to a lower level of care with continued physical therapy and IV antibiotics for another 3 weeks.

Discussion

The patient had 2 underlying systemic inflammatory conditions: RA and psoriasis. The underlying chronic arthritis was likely caused by RA, not psoriatic arthritis (PsA). The patient met the 2010 American College of Rheumatology criteria but failed to meet the classification criteria for PsA.^6,7 However, the clinical features of RA and PsA overlap. Rheumatoid factor and CCP can be positive laboratory findings in both RA and PsA.^8-14 Tenosynovitis is found in about half of RA patients and PsA patients (P > .05).¹⁵ In its evaluation of the patient, the inpatient rheumatology service suspected that the patient may have had RA with components of PsA.

Rheumatoid arthritis complicates the diagnosis of septic arthritis. In a study by Nolla and colleagues, a mean of 7.3 days (range 3 to 18 days) elapsed before a diagnosis of septic arthritis was made in 10 patients with RA on corticosteroids.² Consideration of risk factors such as increasing age, male sex, tobacco use, extra-articular manifestations of RA, positive RF, rheumatoid nodules, poor functional capacity, high ESR, leukopenia, comorbidities (chronic lung disease, alcoholism, organic brain disease, and diabetes), and the use of corticosteroids may expedite the diagnosis of infections in patients with RA.¹⁶ In this case, the patient had some of these risk factors: age, male sex, alcoholism, chronic tobacco use, positive RF, high ESR, and leukopenia (at presentation).

Related: Trend Toward Concomitant Supplements and Medications

The history of medication nonadherence of etanercept with progressively worsening arthritis and early clinical improvement (reduction in erythema, edema, and pain and temporary loss of signs of tenosynovitis on examination) while on prednisone suggested that the patient had a RA flare. The prednisone likely alleviated the inflammatory process but created an immunosuppressed state that allowed GGS to invade and possibly disseminate. Alternately, the patient may have been infected before presentation. The lack of a definitive time line for his case prevented the authors from forming conclusions about a possible causal relationship between the infection and medications. The subjective fevers before admission were nonspecific and could have been caused by RA, presumed gastroenteritis, or other undiagnosed infectious processes. The observed leukocytosis may have been initially corticosteroid-induced.¹⁷

Septic Arthritis

The suspicion of septic arthritis and infectious tenosynovitis substantially increased on day 6 with worsening symptoms, involvement of additional joints, and spiking fevers. Group G Streptococcus was obtained from the aspirate of the left wrist and from the surgical specimens from the bilateral wrists. The clinical presentation, MRI imaging studies, and surgical and nonsurgical specimens supported a diagnosis of GGS tenosynovitis. However, there was no clear evidence (ie, positive culture with identified organism) of septic arthritis, likely secondary to early septic arthritis and initiation of antibiotics before joint aspirations. The aspirate from the left ankle was yellow and opaque, but the culture was negative.

The pathogenic organism in the patient was GGS. Group G Streptococcus is normal flora of the oral cavity, gastrointestinal (GI) tract, upper respiratory tract, genital tract, and skin, which were all possible sources of seeding.¹⁸ Streptococcal species account for about 20% of septic arthritis, and GGS arthritis accounts for 4% to 19% of streptococcal arthritis.^19-22 From a review of the literature, 2 cases of GGS tenosynovitis have been published.^23,24 However, in an ultrasound study and MRI study, 49% and 43%, respectively, of patients with RA had tenosynovitis of the tendons of the hands.^15,25

GGS Demographics

About three-quarters (71%) of patients with GGS arthritis are male.¹⁹ The analysis of the literature by Bronze and colleagues found that chronic joint disease and alcoholism are present in 34% and 14% of patients with GGS arthritis, respectively. One-quarter (23% from Dubost and colleagues) to one-third (32% from Schattner and colleagues) of patients with GGS arthritis have RA.^19,26

Fever is present in less than half (43%) of patients with GGS arthritis.¹⁹ Positive synovial fluid is expected in 90% of patients.¹⁹ Leukocytosis and elevated ESR need not be present.^27,28 The arthritis is polyarticular in one-quarter of patients (24% from Bronze and colleagues and 26% from Dubost and colleagues).^19,26

Positive blood cultures can be expected in one-fourth (26%) of patients with GGS arthritis.¹⁹ The patient’s blood cultures were negative. Blood cultures drawn before initiation of antibiotics yielded no growth, so if the spread was hematogenous, the bacteremia was transient or intermittent. Before and after initiation of antibiotics, specimens from the shoulders did not grow colonies, whereas specimens from the wrists did. If the shoulders were truly infected, these findings and the notably later involvement of the shoulders suggest that the shoulders may have been seeded later in the hospital course.

Trenkner and colleagues proposed that GI abnormalities provide a portal of entry for GGS, which is under the umbrella of S. milleri.²⁹S. milleri is associated with abscess formation, usually of the GI tract.^30-32 In the study patient, the possible gastroenteritis may have provided such a portal of entry and subsequent seeding to the joints, and an abscess was found in the left wrist.

Tendon Rupture

Additionally, bilateral EPL tendon rupture likely occurred as a consequence of the inflammatory process from RA and infectious tenosynovitis in the patient. According to Zheng and colleagues, tenosynovitis is an inflammatory process of the synovial tendon sheath that may result in degeneration and rupture of the tendons and may contribute to bone erosions, development of joint deformities, and loss of functional capacity.³³ In a histologic study of a ruptured EPL tendon from a patient with RA, Harris observed a chronic inflammatory cellular reaction.³⁴ Harris also described a male with RA with unconfirmed bilateral EPL rupture.³⁴ Björkman and colleague identified previous injury, RA, and local or systemic steroids as important etiologic factors for EPL tendon rupture.³⁵

As in the case of this patient, the utilization of both medical and surgical therapy is not uncommon for treating GGS infection. Antibiotic therapy typically consists of penicillin (74%).²⁶ Surgical intervention is necessary in 16% to 37% of patients.^19,26 This patient required both penicillin and incision and drainage/debridement before significant clinical improvement was noted. Prognosis of GGS arthritis is favorable with 5% mortality.²⁶

Conclusion

Septic arthritis and infectious tenosynovitis are readily treatable with low mortality if promptly identified. Identification can be masked by other medical conditions, such as RA and psoriasis, and their associated immunosuppressive treatment. Bilateral EPL tendon rupture may be a complication of RA, particularly with an underlying septic arthritis and infectious tenosynovitis.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Several surgical options are available for treatment of supracondylar and intercondylar distal femur fractures, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 33. Preserving the osseous blood supply via indirect reduction techniques has been shown to increase union rates without the need for bone grafting.^1,2 The Less-Invasive Stabilization System (LISS) made by Synthes (Paoli, Pennsylvania) melds minimally invasive internal fixation with multiple fixed-angle distal screws. It allows for submuscular placement, percutaneous unicortical screws in the diaphysis, and preservation of the metaphyseal fracture soft-tissue envelope.³

Proper lateral placement of the plate on the femur proximally can be difficult. Kregor and colleagues³ noted that 6% of cases did not have ideal placement on the lateral shaft of the femur when the 13-hole LISS plate was used. They advocated making a small incision at the proximal end of the LISS plate to aid in proper lateral placement. Kolb and colleagues⁴ noted that 2 of 31 patients had a “cutting out” of the proximal screws on LISS plates with anterior placement on the femur that eventually required repeat surgery in order to heal. This malpositioned plate was present at the end of the operation. These authors also recommended a proximal incision to avoid the issue. Schütz and colleagues⁵ noted that there were 4 cases of implant loosening among 107 distal femur fractures treated with LISS plating and that the unicortical screws in the diaphysis had loosened. They suggested anterior placement of the plate as a possible reason for fixation failure.

Although several studies have noted proximal screw pull-out, and proximal anterior malposition in the sagittal plane of the LISS plate has been suggested as a possible cause, we found no studies comparing incorrect proximal positioning on the femoral shaft with correct lateral placement of the LISS plate. Therefore, we used a previously established biomechanical model to compare LISS plates proximally placed either too anterior or too posterior to the direct lateral position on the femoral shaft. The constructs were tested in axial, torsional, and cyclical axial modes to assess plastic and total deformation, stiffness, and fixation failure.

Materials and Methods

Using fourth-generation femoral synthetic composite bones (Sawbones; Pacific Research Laboratories, Vashon, Washington) and a 13-hole Synthes femoral LISS plate, we made 3 groups of 9 specimens each, for a total of 27 femurs. The number of specimens was based on a power assessment in a study by Khalafi and colleagues.⁸ Several studies have validated use of Sawbones instead of cadavers in biomechanical testing to prevent variability.^6-9 Proximal fixation was achieved with 5 unicortical screws (26 mm long) at screw holes 13, 11, 9, 7, and 4. All distal screw holes were filled for distal fixation with 75-mm-long screws to achieve bicortical fixation.

After application of the LISS plate, an AO/OTA 33-A3 fracture model was created in each specimen. A 1-cm gap was made 6 cm proximal to the intercondylar notch to create an unstable distal femur fracture pattern. In the method described by Zlowodzki and colleagues,¹⁰ an additional 3-cm cut was made diagonally in the medial cortex to prevent contact of the bone during mechanical testing.

Three different plate positions were used. The correct group was placed directly laterally proximally (Figure 1A). One incorrect group was plated with the proximal aspect of the plate 1 cm anterior (anterior group) (Figure 1B), and another incorrect group was plated with the proximal aspect of the plate 1 cm posterior (posterior group) (Figure 1C). Anterior or posterior plate placement resulted in some of the proximal screws having a more tangential placement, with fewer screws engaged compared with the properly placed plate.

The distal and proximal ends of each specimen were held to simulate the mechanical axis of the femur. This design was based on a model by Cordey and colleagues.¹¹ A materials testing system (MTS, Minneapolis, Minnesota) was used for mechanical testing of the model.

Based on the protocol of Khalafi and colleagues,⁸ the models were tested in axial, torsional, and cyclical axial modes (Figures 2, 3). Axial loading consisted of a preload of 100 N followed by a compressive loading rate of 100 mm per minute in a displacement control mode. Testing was considered completed when 1 of 3 events occurred: 500 N was reached, the medial fracture gap closed, or fixation was lost. Torsional loading involved a preload of 5 Nm and subsequent torqueing at 20° per minute up to 20 Nm or loss of fixation or screw pull-out.⁸ Cyclical axial loading was based on protocols described by Marti and colleagues² and Zlowodzki and colleagues.¹⁰ The initial load was 10 cycles of 300 N. Each subsequent load increment was increased by 100 N up to 1000 N, providing 10-second rest increments. This loading was conducted in a displacement control mode at 0.75 mm per second. Testing was aborted on fixation loss or complete closure of the medial fracture gap.

After testing was completed, statistically significant between-groups differences in plastic deformation and axial and torsional stiffness were determined by performing a Tukey-Kramer honestly significant difference test. Significance was set at P ≤ .05.

Results

During axial loading, there was no visual loss of fixation or change in displacement of the fracture gap for any group, and there was no screw cut-out or pull-out from the cortex during testing. In 1 plate in the posterior group, the most proximal screw made only loose contact with the cortex at only the distal portion of the screw. There was no significant difference (P = .9762) in stiffness in axial loading between the anterior group and the correct group. There was a significant (P = .0261) 16.4% increase in stiffness in the posterior group compared with the correct group (Table).

There was no screw cut-out, fixation failure, or change in displacement of the fracture gap for any group during torsional loading. There was a statistically significant (P = .0062) 12% increase in mean torsional stiffness in the anterior group compared with the correct group. There was no statistically significant difference (P = .1623) between the posterior group and the correct group (Table).

For cyclical axial testing, total deformation and plastic deformation were obtained by determining displacement under the initial 100 N load in the static/resting state. That number was then subtracted from maximum displacement, the peak value on the time-versus-displacement graph, to obtain the value for total deformation. Plastic deformation was calculated by subtracting initial displacement from final displacement in the static/resting state. The static/resting state is represented by the dips in displacement after each cycle on the time-versus-displacement graph (Figure 4).

There was a statistically significant (P = .0207) 14% increase in total deformation of the anteriorly positioned plate compared with the correctly positioned plate. There was no statistically significant difference in total deformation between the posteriorly placed plates and the correctly placed plates (Table).

There was no significant difference in plastic deformation between any of the groups in this study. There was no screw cut-out or fixation loss in any group to suggest a clinically relevant difference based on proximal placement of the LISS plate.

Discussion

In evaluating the stability of various constructs for fixation of distal femur fractures, the literature is consistent in reporting stiffness as the key factor. Stiffness is determined most often in terms of motion at the fracture site, as measured by displacement under axial and torsional loads.^2,8,10,13 The LISS plate, which acts essentially as an “internal fixator” with proximal unicortical fixed-angle locking screws, has been shown to be comparable to other established methods of fixation.^10,12 Zlowodzki and colleagues¹⁰ reported that the LISS plate had a higher load to failure when compared with angled blade plating and intramedullary nailing. Their study used fresh-frozen cadaver specimens from patients 70 years old or older. They concluded that, for distal femur fractures in osteoporotic bone, the LISS plate provided improved distal fixation.

In the present study, the posteriorly placed LISS plate outperformed the correctly placed plate in axial stiffness by 16.4%. However, there was no statistically significant difference in torsional stiffness and cyclical axial loading. This result is difficult to explain given that there was no screw cut-out or fixation loss for any of the constructs. Theoretically, with less proximal screw purchase in the posteriorly placed plate, the overall construct should be more susceptible to screw cut-out and fixation loss resulting in less axial stiffness overall.

Khalafi and colleagues⁸ created a distal femur fracture model using Sawbones with a 1-cm fracture gap. Using the 9-hole LISS plate for fixation, they tested this construct under axial, torsional, and cyclical axial loads. They tested 2 groups of 9 femurs. For group 1, the LISS plate was placed in the correct position on the distal femur, with the proximal end in the correct position on the femoral shaft. In group 2, the LISS plate was rotated 1 cm anteriorly. They found that axial stiffness (N/mm) was 21.5% greater in the correctly positioned plate. The anteriorly positioned group demonstrated 55% more irreversible or plastic deformation. The authors concluded that correct positioning of the femoral LISS plate provided improved mechanical stability.

Overall, our study results did not agree with those of Khalafi and colleagues⁸ in terms of the mechanical stability of a malpositioned LISS plate. Our construct showed a significant increase in torsional stiffness in the anteriorly placed plate. However, our construct also showed a significant increase in total deformation in cyclical axial loading in the anteriorly placed plate. There was no increased plastic deformation in either of the incorrectly placed groups in our study. The difference in results between studies can best be explained by the difference in plate lengths. We used a 13-hole plate, and Khalafi and colleagues⁸ used a 9-hole plate. Our theory is that the longer plate provided more resistance to relatively minor variations in plate position at the proximal end and thus resulted in less change in stiffness and stability around the fracture site.

Our model differed from that used in other biomechanical studies using Sawbones to simulate distal femur fractures in that it used the entire femur, including the proximal portion.^8,13 This setup theoretically resulted in a more anatomical weight distribution compared with other models, in which the proximal portion of the femur was potted in polymethylmethacrylate. This difference in weight distribution could explain the variation in our results compared with other biomechanical studies. In addition, with use of different boundary conditions, the distal femur had unconstrained distal motion similar to the native environment of the femur.

This study had several limitations. First is its relatively low power (9 femurs per group). Although groups of 9 specimens in 2 groups were used in the study by Khalafi and colleagues⁸, testing a larger number of femurs could potentially identify more subtle differences between the 3 groups in our study. Second, given that femoral LISS plates come in different lengths, this study could be expanded to include the other plate sizes, as plate length could potentially play a role in stability at the fracture site. Third, though this Sawbones model has consistently reproduced the stability characteristics of human bone without variation between specimens, an osteoporotic model could be explored, as the femoral LISS plate is often used in osteoporotic fractures.^7,14

Conclusion

Overall, our study results showed that 1-cm variations, anterior or posterior, had little effect on axial or torsional stiffness or plastic deformation under cyclical axial loading. Although these data can be promising for clinical application, the anterior placement of the LISS plate noted in failed fixation in other studies necessitates cautious interpretation of this study. Our use of a 13-hole (longer) plate, versus the 9-hole plate used in other studies, could explain the lack of variation between the 2 groups as well as the stability and tolerance of inappropriate placement. An osteoporotic model could help clinicians further discern the importance of accurate proximal placement of the femoral LISS plate.

Several surgical options are available for treatment of supracondylar and intercondylar distal femur fractures, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 33. Preserving the osseous blood supply via indirect reduction techniques has been shown to increase union rates without the need for bone grafting.^1,2 The Less-Invasive Stabilization System (LISS) made by Synthes (Paoli, Pennsylvania) melds minimally invasive internal fixation with multiple fixed-angle distal screws. It allows for submuscular placement, percutaneous unicortical screws in the diaphysis, and preservation of the metaphyseal fracture soft-tissue envelope.³

Proper lateral placement of the plate on the femur proximally can be difficult. Kregor and colleagues³ noted that 6% of cases did not have ideal placement on the lateral shaft of the femur when the 13-hole LISS plate was used. They advocated making a small incision at the proximal end of the LISS plate to aid in proper lateral placement. Kolb and colleagues⁴ noted that 2 of 31 patients had a “cutting out” of the proximal screws on LISS plates with anterior placement on the femur that eventually required repeat surgery in order to heal. This malpositioned plate was present at the end of the operation. These authors also recommended a proximal incision to avoid the issue. Schütz and colleagues⁵ noted that there were 4 cases of implant loosening among 107 distal femur fractures treated with LISS plating and that the unicortical screws in the diaphysis had loosened. They suggested anterior placement of the plate as a possible reason for fixation failure.

Although several studies have noted proximal screw pull-out, and proximal anterior malposition in the sagittal plane of the LISS plate has been suggested as a possible cause, we found no studies comparing incorrect proximal positioning on the femoral shaft with correct lateral placement of the LISS plate. Therefore, we used a previously established biomechanical model to compare LISS plates proximally placed either too anterior or too posterior to the direct lateral position on the femoral shaft. The constructs were tested in axial, torsional, and cyclical axial modes to assess plastic and total deformation, stiffness, and fixation failure.

Materials and Methods

Using fourth-generation femoral synthetic composite bones (Sawbones; Pacific Research Laboratories, Vashon, Washington) and a 13-hole Synthes femoral LISS plate, we made 3 groups of 9 specimens each, for a total of 27 femurs. The number of specimens was based on a power assessment in a study by Khalafi and colleagues.⁸ Several studies have validated use of Sawbones instead of cadavers in biomechanical testing to prevent variability.^6-9 Proximal fixation was achieved with 5 unicortical screws (26 mm long) at screw holes 13, 11, 9, 7, and 4. All distal screw holes were filled for distal fixation with 75-mm-long screws to achieve bicortical fixation.

After application of the LISS plate, an AO/OTA 33-A3 fracture model was created in each specimen. A 1-cm gap was made 6 cm proximal to the intercondylar notch to create an unstable distal femur fracture pattern. In the method described by Zlowodzki and colleagues,¹⁰ an additional 3-cm cut was made diagonally in the medial cortex to prevent contact of the bone during mechanical testing.

Three different plate positions were used. The correct group was placed directly laterally proximally (Figure 1A). One incorrect group was plated with the proximal aspect of the plate 1 cm anterior (anterior group) (Figure 1B), and another incorrect group was plated with the proximal aspect of the plate 1 cm posterior (posterior group) (Figure 1C). Anterior or posterior plate placement resulted in some of the proximal screws having a more tangential placement, with fewer screws engaged compared with the properly placed plate.

The distal and proximal ends of each specimen were held to simulate the mechanical axis of the femur. This design was based on a model by Cordey and colleagues.¹¹ A materials testing system (MTS, Minneapolis, Minnesota) was used for mechanical testing of the model.

Based on the protocol of Khalafi and colleagues,⁸ the models were tested in axial, torsional, and cyclical axial modes (Figures 2, 3). Axial loading consisted of a preload of 100 N followed by a compressive loading rate of 100 mm per minute in a displacement control mode. Testing was considered completed when 1 of 3 events occurred: 500 N was reached, the medial fracture gap closed, or fixation was lost. Torsional loading involved a preload of 5 Nm and subsequent torqueing at 20° per minute up to 20 Nm or loss of fixation or screw pull-out.⁸ Cyclical axial loading was based on protocols described by Marti and colleagues² and Zlowodzki and colleagues.¹⁰ The initial load was 10 cycles of 300 N. Each subsequent load increment was increased by 100 N up to 1000 N, providing 10-second rest increments. This loading was conducted in a displacement control mode at 0.75 mm per second. Testing was aborted on fixation loss or complete closure of the medial fracture gap.

After testing was completed, statistically significant between-groups differences in plastic deformation and axial and torsional stiffness were determined by performing a Tukey-Kramer honestly significant difference test. Significance was set at P ≤ .05.

Results

During axial loading, there was no visual loss of fixation or change in displacement of the fracture gap for any group, and there was no screw cut-out or pull-out from the cortex during testing. In 1 plate in the posterior group, the most proximal screw made only loose contact with the cortex at only the distal portion of the screw. There was no significant difference (P = .9762) in stiffness in axial loading between the anterior group and the correct group. There was a significant (P = .0261) 16.4% increase in stiffness in the posterior group compared with the correct group (Table).

There was no screw cut-out, fixation failure, or change in displacement of the fracture gap for any group during torsional loading. There was a statistically significant (P = .0062) 12% increase in mean torsional stiffness in the anterior group compared with the correct group. There was no statistically significant difference (P = .1623) between the posterior group and the correct group (Table).

For cyclical axial testing, total deformation and plastic deformation were obtained by determining displacement under the initial 100 N load in the static/resting state. That number was then subtracted from maximum displacement, the peak value on the time-versus-displacement graph, to obtain the value for total deformation. Plastic deformation was calculated by subtracting initial displacement from final displacement in the static/resting state. The static/resting state is represented by the dips in displacement after each cycle on the time-versus-displacement graph (Figure 4).

There was a statistically significant (P = .0207) 14% increase in total deformation of the anteriorly positioned plate compared with the correctly positioned plate. There was no statistically significant difference in total deformation between the posteriorly placed plates and the correctly placed plates (Table).

There was no significant difference in plastic deformation between any of the groups in this study. There was no screw cut-out or fixation loss in any group to suggest a clinically relevant difference based on proximal placement of the LISS plate.

Discussion

In evaluating the stability of various constructs for fixation of distal femur fractures, the literature is consistent in reporting stiffness as the key factor. Stiffness is determined most often in terms of motion at the fracture site, as measured by displacement under axial and torsional loads.^2,8,10,13 The LISS plate, which acts essentially as an “internal fixator” with proximal unicortical fixed-angle locking screws, has been shown to be comparable to other established methods of fixation.^10,12 Zlowodzki and colleagues¹⁰ reported that the LISS plate had a higher load to failure when compared with angled blade plating and intramedullary nailing. Their study used fresh-frozen cadaver specimens from patients 70 years old or older. They concluded that, for distal femur fractures in osteoporotic bone, the LISS plate provided improved distal fixation.

In the present study, the posteriorly placed LISS plate outperformed the correctly placed plate in axial stiffness by 16.4%. However, there was no statistically significant difference in torsional stiffness and cyclical axial loading. This result is difficult to explain given that there was no screw cut-out or fixation loss for any of the constructs. Theoretically, with less proximal screw purchase in the posteriorly placed plate, the overall construct should be more susceptible to screw cut-out and fixation loss resulting in less axial stiffness overall.

Khalafi and colleagues⁸ created a distal femur fracture model using Sawbones with a 1-cm fracture gap. Using the 9-hole LISS plate for fixation, they tested this construct under axial, torsional, and cyclical axial loads. They tested 2 groups of 9 femurs. For group 1, the LISS plate was placed in the correct position on the distal femur, with the proximal end in the correct position on the femoral shaft. In group 2, the LISS plate was rotated 1 cm anteriorly. They found that axial stiffness (N/mm) was 21.5% greater in the correctly positioned plate. The anteriorly positioned group demonstrated 55% more irreversible or plastic deformation. The authors concluded that correct positioning of the femoral LISS plate provided improved mechanical stability.

Overall, our study results did not agree with those of Khalafi and colleagues⁸ in terms of the mechanical stability of a malpositioned LISS plate. Our construct showed a significant increase in torsional stiffness in the anteriorly placed plate. However, our construct also showed a significant increase in total deformation in cyclical axial loading in the anteriorly placed plate. There was no increased plastic deformation in either of the incorrectly placed groups in our study. The difference in results between studies can best be explained by the difference in plate lengths. We used a 13-hole plate, and Khalafi and colleagues⁸ used a 9-hole plate. Our theory is that the longer plate provided more resistance to relatively minor variations in plate position at the proximal end and thus resulted in less change in stiffness and stability around the fracture site.

Our model differed from that used in other biomechanical studies using Sawbones to simulate distal femur fractures in that it used the entire femur, including the proximal portion.^8,13 This setup theoretically resulted in a more anatomical weight distribution compared with other models, in which the proximal portion of the femur was potted in polymethylmethacrylate. This difference in weight distribution could explain the variation in our results compared with other biomechanical studies. In addition, with use of different boundary conditions, the distal femur had unconstrained distal motion similar to the native environment of the femur.

This study had several limitations. First is its relatively low power (9 femurs per group). Although groups of 9 specimens in 2 groups were used in the study by Khalafi and colleagues⁸, testing a larger number of femurs could potentially identify more subtle differences between the 3 groups in our study. Second, given that femoral LISS plates come in different lengths, this study could be expanded to include the other plate sizes, as plate length could potentially play a role in stability at the fracture site. Third, though this Sawbones model has consistently reproduced the stability characteristics of human bone without variation between specimens, an osteoporotic model could be explored, as the femoral LISS plate is often used in osteoporotic fractures.^7,14

Conclusion

Overall, our study results showed that 1-cm variations, anterior or posterior, had little effect on axial or torsional stiffness or plastic deformation under cyclical axial loading. Although these data can be promising for clinical application, the anterior placement of the LISS plate noted in failed fixation in other studies necessitates cautious interpretation of this study. Our use of a 13-hole (longer) plate, versus the 9-hole plate used in other studies, could explain the lack of variation between the 2 groups as well as the stability and tolerance of inappropriate placement. An osteoporotic model could help clinicians further discern the importance of accurate proximal placement of the femoral LISS plate.

Several surgical options are available for treatment of supracondylar and intercondylar distal femur fractures, AO/OTA (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 33. Preserving the osseous blood supply via indirect reduction techniques has been shown to increase union rates without the need for bone grafting.^1,2 The Less-Invasive Stabilization System (LISS) made by Synthes (Paoli, Pennsylvania) melds minimally invasive internal fixation with multiple fixed-angle distal screws. It allows for submuscular placement, percutaneous unicortical screws in the diaphysis, and preservation of the metaphyseal fracture soft-tissue envelope.³

Proper lateral placement of the plate on the femur proximally can be difficult. Kregor and colleagues³ noted that 6% of cases did not have ideal placement on the lateral shaft of the femur when the 13-hole LISS plate was used. They advocated making a small incision at the proximal end of the LISS plate to aid in proper lateral placement. Kolb and colleagues⁴ noted that 2 of 31 patients had a “cutting out” of the proximal screws on LISS plates with anterior placement on the femur that eventually required repeat surgery in order to heal. This malpositioned plate was present at the end of the operation. These authors also recommended a proximal incision to avoid the issue. Schütz and colleagues⁵ noted that there were 4 cases of implant loosening among 107 distal femur fractures treated with LISS plating and that the unicortical screws in the diaphysis had loosened. They suggested anterior placement of the plate as a possible reason for fixation failure.

Although several studies have noted proximal screw pull-out, and proximal anterior malposition in the sagittal plane of the LISS plate has been suggested as a possible cause, we found no studies comparing incorrect proximal positioning on the femoral shaft with correct lateral placement of the LISS plate. Therefore, we used a previously established biomechanical model to compare LISS plates proximally placed either too anterior or too posterior to the direct lateral position on the femoral shaft. The constructs were tested in axial, torsional, and cyclical axial modes to assess plastic and total deformation, stiffness, and fixation failure.

Materials and Methods

Using fourth-generation femoral synthetic composite bones (Sawbones; Pacific Research Laboratories, Vashon, Washington) and a 13-hole Synthes femoral LISS plate, we made 3 groups of 9 specimens each, for a total of 27 femurs. The number of specimens was based on a power assessment in a study by Khalafi and colleagues.⁸ Several studies have validated use of Sawbones instead of cadavers in biomechanical testing to prevent variability.^6-9 Proximal fixation was achieved with 5 unicortical screws (26 mm long) at screw holes 13, 11, 9, 7, and 4. All distal screw holes were filled for distal fixation with 75-mm-long screws to achieve bicortical fixation.

After application of the LISS plate, an AO/OTA 33-A3 fracture model was created in each specimen. A 1-cm gap was made 6 cm proximal to the intercondylar notch to create an unstable distal femur fracture pattern. In the method described by Zlowodzki and colleagues,¹⁰ an additional 3-cm cut was made diagonally in the medial cortex to prevent contact of the bone during mechanical testing.

Three different plate positions were used. The correct group was placed directly laterally proximally (Figure 1A). One incorrect group was plated with the proximal aspect of the plate 1 cm anterior (anterior group) (Figure 1B), and another incorrect group was plated with the proximal aspect of the plate 1 cm posterior (posterior group) (Figure 1C). Anterior or posterior plate placement resulted in some of the proximal screws having a more tangential placement, with fewer screws engaged compared with the properly placed plate.

The distal and proximal ends of each specimen were held to simulate the mechanical axis of the femur. This design was based on a model by Cordey and colleagues.¹¹ A materials testing system (MTS, Minneapolis, Minnesota) was used for mechanical testing of the model.

Based on the protocol of Khalafi and colleagues,⁸ the models were tested in axial, torsional, and cyclical axial modes (Figures 2, 3). Axial loading consisted of a preload of 100 N followed by a compressive loading rate of 100 mm per minute in a displacement control mode. Testing was considered completed when 1 of 3 events occurred: 500 N was reached, the medial fracture gap closed, or fixation was lost. Torsional loading involved a preload of 5 Nm and subsequent torqueing at 20° per minute up to 20 Nm or loss of fixation or screw pull-out.⁸ Cyclical axial loading was based on protocols described by Marti and colleagues² and Zlowodzki and colleagues.¹⁰ The initial load was 10 cycles of 300 N. Each subsequent load increment was increased by 100 N up to 1000 N, providing 10-second rest increments. This loading was conducted in a displacement control mode at 0.75 mm per second. Testing was aborted on fixation loss or complete closure of the medial fracture gap.

After testing was completed, statistically significant between-groups differences in plastic deformation and axial and torsional stiffness were determined by performing a Tukey-Kramer honestly significant difference test. Significance was set at P ≤ .05.

Results

During axial loading, there was no visual loss of fixation or change in displacement of the fracture gap for any group, and there was no screw cut-out or pull-out from the cortex during testing. In 1 plate in the posterior group, the most proximal screw made only loose contact with the cortex at only the distal portion of the screw. There was no significant difference (P = .9762) in stiffness in axial loading between the anterior group and the correct group. There was a significant (P = .0261) 16.4% increase in stiffness in the posterior group compared with the correct group (Table).

There was no screw cut-out, fixation failure, or change in displacement of the fracture gap for any group during torsional loading. There was a statistically significant (P = .0062) 12% increase in mean torsional stiffness in the anterior group compared with the correct group. There was no statistically significant difference (P = .1623) between the posterior group and the correct group (Table).

For cyclical axial testing, total deformation and plastic deformation were obtained by determining displacement under the initial 100 N load in the static/resting state. That number was then subtracted from maximum displacement, the peak value on the time-versus-displacement graph, to obtain the value for total deformation. Plastic deformation was calculated by subtracting initial displacement from final displacement in the static/resting state. The static/resting state is represented by the dips in displacement after each cycle on the time-versus-displacement graph (Figure 4).

There was a statistically significant (P = .0207) 14% increase in total deformation of the anteriorly positioned plate compared with the correctly positioned plate. There was no statistically significant difference in total deformation between the posteriorly placed plates and the correctly placed plates (Table).

There was no significant difference in plastic deformation between any of the groups in this study. There was no screw cut-out or fixation loss in any group to suggest a clinically relevant difference based on proximal placement of the LISS plate.

Discussion

In evaluating the stability of various constructs for fixation of distal femur fractures, the literature is consistent in reporting stiffness as the key factor. Stiffness is determined most often in terms of motion at the fracture site, as measured by displacement under axial and torsional loads.^2,8,10,13 The LISS plate, which acts essentially as an “internal fixator” with proximal unicortical fixed-angle locking screws, has been shown to be comparable to other established methods of fixation.^10,12 Zlowodzki and colleagues¹⁰ reported that the LISS plate had a higher load to failure when compared with angled blade plating and intramedullary nailing. Their study used fresh-frozen cadaver specimens from patients 70 years old or older. They concluded that, for distal femur fractures in osteoporotic bone, the LISS plate provided improved distal fixation.

In the present study, the posteriorly placed LISS plate outperformed the correctly placed plate in axial stiffness by 16.4%. However, there was no statistically significant difference in torsional stiffness and cyclical axial loading. This result is difficult to explain given that there was no screw cut-out or fixation loss for any of the constructs. Theoretically, with less proximal screw purchase in the posteriorly placed plate, the overall construct should be more susceptible to screw cut-out and fixation loss resulting in less axial stiffness overall.

Khalafi and colleagues⁸ created a distal femur fracture model using Sawbones with a 1-cm fracture gap. Using the 9-hole LISS plate for fixation, they tested this construct under axial, torsional, and cyclical axial loads. They tested 2 groups of 9 femurs. For group 1, the LISS plate was placed in the correct position on the distal femur, with the proximal end in the correct position on the femoral shaft. In group 2, the LISS plate was rotated 1 cm anteriorly. They found that axial stiffness (N/mm) was 21.5% greater in the correctly positioned plate. The anteriorly positioned group demonstrated 55% more irreversible or plastic deformation. The authors concluded that correct positioning of the femoral LISS plate provided improved mechanical stability.

Overall, our study results did not agree with those of Khalafi and colleagues⁸ in terms of the mechanical stability of a malpositioned LISS plate. Our construct showed a significant increase in torsional stiffness in the anteriorly placed plate. However, our construct also showed a significant increase in total deformation in cyclical axial loading in the anteriorly placed plate. There was no increased plastic deformation in either of the incorrectly placed groups in our study. The difference in results between studies can best be explained by the difference in plate lengths. We used a 13-hole plate, and Khalafi and colleagues⁸ used a 9-hole plate. Our theory is that the longer plate provided more resistance to relatively minor variations in plate position at the proximal end and thus resulted in less change in stiffness and stability around the fracture site.

Our model differed from that used in other biomechanical studies using Sawbones to simulate distal femur fractures in that it used the entire femur, including the proximal portion.^8,13 This setup theoretically resulted in a more anatomical weight distribution compared with other models, in which the proximal portion of the femur was potted in polymethylmethacrylate. This difference in weight distribution could explain the variation in our results compared with other biomechanical studies. In addition, with use of different boundary conditions, the distal femur had unconstrained distal motion similar to the native environment of the femur.

This study had several limitations. First is its relatively low power (9 femurs per group). Although groups of 9 specimens in 2 groups were used in the study by Khalafi and colleagues⁸, testing a larger number of femurs could potentially identify more subtle differences between the 3 groups in our study. Second, given that femoral LISS plates come in different lengths, this study could be expanded to include the other plate sizes, as plate length could potentially play a role in stability at the fracture site. Third, though this Sawbones model has consistently reproduced the stability characteristics of human bone without variation between specimens, an osteoporotic model could be explored, as the femoral LISS plate is often used in osteoporotic fractures.^7,14

Conclusion

Overall, our study results showed that 1-cm variations, anterior or posterior, had little effect on axial or torsional stiffness or plastic deformation under cyclical axial loading. Although these data can be promising for clinical application, the anterior placement of the LISS plate noted in failed fixation in other studies necessitates cautious interpretation of this study. Our use of a 13-hole (longer) plate, versus the 9-hole plate used in other studies, could explain the lack of variation between the 2 groups as well as the stability and tolerance of inappropriate placement. An osteoporotic model could help clinicians further discern the importance of accurate proximal placement of the femoral LISS plate.