User login
HM16 Takes a Look at Health IT, Post-Acute Care
Take a look at the HM16 program, and you get a snapshot of the most pressing topics in hospital medicine. Specifically, four new educational tracks are being rolled out at this year’s annual meeting, including a new track on the patient-doctor relationship, which is so crucial with today’s growing emphasis on patient satisfaction, and a track focused on perioperative medicine, an important area with a fast-moving frontier. Another new track covers post-acute care, a setting in which more and more hospitalists find themselves practicing. Then there’s the big daddy: health information technology (IT) for hospitalists.
Course Director Melissa Mattison, MD, SFHM, also points to a new twist in the way the conference will attempt to tackle the tough topic of work-life balance.
Read the full interview with Melissa Mattison, MD, SFHM.
Here’s a look at what’s new for HM16 attendees.
Health IT for Hospitalists
“There’s not a hospitalist in the country who’s not affected by IT and updates to their [electronic medical records (EMR)], new adoption of EMR technology, different vendors,” Dr. Mattison says. “We’re always searching for something to make our lives better and make the care that we provide more high quality.”
There will be sessions of a general nature, such as “There’s an App for That,” a review of mobile apps helpful to hospitalists. And there will be those for the more passionate technophiles, such as a session on clinical informatics and “Using IT to Help Drive the Shift from Volume to Value.”
“We’ve spent a lot of time trying to make sure there’s something for everyone,” says Kendall Rogers, MD, SFHM, chair of SHM’s IT Committee. “And even within each individual talk, we’ve tried to make sure that there is material that can be applicable from the frontline hospitalist to the CMIO of a hospital.”
Dr. Rogers says the committee has “really been pushing” to have its own track at the annual meeting.
Listen to more of our interview with Dr. Rogers.
“Health IT continues to be an area of great frustration and great promise,” he says. “I think most of the frustration that hospitalists have is because they realize the potential of health IT, and they see how far it is from the reality of what they’re working with every day.
“Hospitalists are well-suited for actively being involved in clinical informatics, but many of us would be far more effective in our roles with more formal education and training.”
Post-Acute Care
It’s estimated that as many as 35% of hospitalists work in the post-acute setting. The number very much surprised Dr. Mattison. When she heard of the figure, “[the committee] lobbied very hard to get a track for post-acute care.”
One session, “Building and Managing a PAC Practice,” will review setting up a staff, relevant regulations, billing, and collecting, and it should be of interest to both managers and physicians, says Sean Muldoon, MD, senior vice president and chief medical officer of the hospitalist division at Louisville, Ken.–based Kindred Healthcare and chair of SHM’s Post-Acute Care Task Force.
Another session, “Lost in Transitions,” will review information gaps and propose solutions “to the well-known voltage drop of information that can happen in transfer from the hospital to post-acute care.”
At Kindred, Dr. Muldoon says he has seen the benefits of hospitalist involvement in post-acute care.
“In many markets, we seek out and often are able to become a practice site for a large hospitalist medical group,” he says. “That’s really good for us, the patients, and, we think, the hospitalists because it allows the hospitalists to be exposed to the practice and benefits of post-acute care without having to make a full commitment to be a skilled-nursing physician or a long-term acute-care physician.”
It also makes transitions of care smoother and less disruptive, he says, “because a patient is simply transferred from one hospitalist in a group to another or often maintaining that same hospitalist in the post-acute-care setting.”
Dr. Muldoon says the new track is of value to any hospitalist, whether they actually work in post-acute care or not.
“A hospitalist would be hard-pressed to provide knowledgeable input into where a patient should receive post-acute care without a working knowledge of which patients should be directed to which post-acute-care setting,” he says.
Doctor-Patient Relationship
This topic was a pre-course last year, and organizers decided to make this a full track on the final day of the meeting schedule.
“It’s really about communication style,” Dr. Mattison says. “There’s one session called ‘The Language of Empathy and Engagement: Communication Essentials for Patient-Centered Care.’ There’s one on unconscious biases and our underlying assumptions and how it affects how we care for patients. [Another is focused] on improving the patient experience in the hospital.”
Co-Management/ Perioperative Medicine
“There are a lot of challenges around anticoagulation management, optimizing patients’ physical heath prior to the surgery, what things should we be doing, what medications should we be giving, what ones shouldn’t we be giving,” Dr. Mattison says. “It’s an evolving field that has, every year, new information.”
Hidden Gems
Dr. Mattison draws special attention to “Work-Life Balance: Is It Possible?” (Tuesday, March 8, 4:20–5:40 p.m.). This year, this problem—all too familiar to hospitalists—will be addressed in a panel discussion, which is a change from previous years.
“There’s been, year after year after year, a lot of discussion around, how can I make my job manageable if my boss isn’t listening to me or is not attuned to work-life balance? How can I navigate this process?” she says. “I’m hopeful that the panel discussion will provide people with some real examples and strategies for success.”
She also draws attention to the session “Perioperative Pitfalls: Overcoming Common Challenges in Managing Medical Problems in Surgical Patients” (Monday, March 7, 3:05–4:20 p.m.).
“There are some true leaders in perioperative management, and they’re going to come together and have a panel discussion,” she says. “It’ll be an opportunity to see some of the great minds think, if you will.” TH
Thomas R. Collins is a freelance writer in South Florida.
Take a look at the HM16 program, and you get a snapshot of the most pressing topics in hospital medicine. Specifically, four new educational tracks are being rolled out at this year’s annual meeting, including a new track on the patient-doctor relationship, which is so crucial with today’s growing emphasis on patient satisfaction, and a track focused on perioperative medicine, an important area with a fast-moving frontier. Another new track covers post-acute care, a setting in which more and more hospitalists find themselves practicing. Then there’s the big daddy: health information technology (IT) for hospitalists.
Course Director Melissa Mattison, MD, SFHM, also points to a new twist in the way the conference will attempt to tackle the tough topic of work-life balance.
Read the full interview with Melissa Mattison, MD, SFHM.
Here’s a look at what’s new for HM16 attendees.
Health IT for Hospitalists
“There’s not a hospitalist in the country who’s not affected by IT and updates to their [electronic medical records (EMR)], new adoption of EMR technology, different vendors,” Dr. Mattison says. “We’re always searching for something to make our lives better and make the care that we provide more high quality.”
There will be sessions of a general nature, such as “There’s an App for That,” a review of mobile apps helpful to hospitalists. And there will be those for the more passionate technophiles, such as a session on clinical informatics and “Using IT to Help Drive the Shift from Volume to Value.”
“We’ve spent a lot of time trying to make sure there’s something for everyone,” says Kendall Rogers, MD, SFHM, chair of SHM’s IT Committee. “And even within each individual talk, we’ve tried to make sure that there is material that can be applicable from the frontline hospitalist to the CMIO of a hospital.”
Dr. Rogers says the committee has “really been pushing” to have its own track at the annual meeting.
Listen to more of our interview with Dr. Rogers.
“Health IT continues to be an area of great frustration and great promise,” he says. “I think most of the frustration that hospitalists have is because they realize the potential of health IT, and they see how far it is from the reality of what they’re working with every day.
“Hospitalists are well-suited for actively being involved in clinical informatics, but many of us would be far more effective in our roles with more formal education and training.”
Post-Acute Care
It’s estimated that as many as 35% of hospitalists work in the post-acute setting. The number very much surprised Dr. Mattison. When she heard of the figure, “[the committee] lobbied very hard to get a track for post-acute care.”
One session, “Building and Managing a PAC Practice,” will review setting up a staff, relevant regulations, billing, and collecting, and it should be of interest to both managers and physicians, says Sean Muldoon, MD, senior vice president and chief medical officer of the hospitalist division at Louisville, Ken.–based Kindred Healthcare and chair of SHM’s Post-Acute Care Task Force.
Another session, “Lost in Transitions,” will review information gaps and propose solutions “to the well-known voltage drop of information that can happen in transfer from the hospital to post-acute care.”
At Kindred, Dr. Muldoon says he has seen the benefits of hospitalist involvement in post-acute care.
“In many markets, we seek out and often are able to become a practice site for a large hospitalist medical group,” he says. “That’s really good for us, the patients, and, we think, the hospitalists because it allows the hospitalists to be exposed to the practice and benefits of post-acute care without having to make a full commitment to be a skilled-nursing physician or a long-term acute-care physician.”
It also makes transitions of care smoother and less disruptive, he says, “because a patient is simply transferred from one hospitalist in a group to another or often maintaining that same hospitalist in the post-acute-care setting.”
Dr. Muldoon says the new track is of value to any hospitalist, whether they actually work in post-acute care or not.
“A hospitalist would be hard-pressed to provide knowledgeable input into where a patient should receive post-acute care without a working knowledge of which patients should be directed to which post-acute-care setting,” he says.
Doctor-Patient Relationship
This topic was a pre-course last year, and organizers decided to make this a full track on the final day of the meeting schedule.
“It’s really about communication style,” Dr. Mattison says. “There’s one session called ‘The Language of Empathy and Engagement: Communication Essentials for Patient-Centered Care.’ There’s one on unconscious biases and our underlying assumptions and how it affects how we care for patients. [Another is focused] on improving the patient experience in the hospital.”
Co-Management/ Perioperative Medicine
“There are a lot of challenges around anticoagulation management, optimizing patients’ physical heath prior to the surgery, what things should we be doing, what medications should we be giving, what ones shouldn’t we be giving,” Dr. Mattison says. “It’s an evolving field that has, every year, new information.”
Hidden Gems
Dr. Mattison draws special attention to “Work-Life Balance: Is It Possible?” (Tuesday, March 8, 4:20–5:40 p.m.). This year, this problem—all too familiar to hospitalists—will be addressed in a panel discussion, which is a change from previous years.
“There’s been, year after year after year, a lot of discussion around, how can I make my job manageable if my boss isn’t listening to me or is not attuned to work-life balance? How can I navigate this process?” she says. “I’m hopeful that the panel discussion will provide people with some real examples and strategies for success.”
She also draws attention to the session “Perioperative Pitfalls: Overcoming Common Challenges in Managing Medical Problems in Surgical Patients” (Monday, March 7, 3:05–4:20 p.m.).
“There are some true leaders in perioperative management, and they’re going to come together and have a panel discussion,” she says. “It’ll be an opportunity to see some of the great minds think, if you will.” TH
Thomas R. Collins is a freelance writer in South Florida.
Take a look at the HM16 program, and you get a snapshot of the most pressing topics in hospital medicine. Specifically, four new educational tracks are being rolled out at this year’s annual meeting, including a new track on the patient-doctor relationship, which is so crucial with today’s growing emphasis on patient satisfaction, and a track focused on perioperative medicine, an important area with a fast-moving frontier. Another new track covers post-acute care, a setting in which more and more hospitalists find themselves practicing. Then there’s the big daddy: health information technology (IT) for hospitalists.
Course Director Melissa Mattison, MD, SFHM, also points to a new twist in the way the conference will attempt to tackle the tough topic of work-life balance.
Read the full interview with Melissa Mattison, MD, SFHM.
Here’s a look at what’s new for HM16 attendees.
Health IT for Hospitalists
“There’s not a hospitalist in the country who’s not affected by IT and updates to their [electronic medical records (EMR)], new adoption of EMR technology, different vendors,” Dr. Mattison says. “We’re always searching for something to make our lives better and make the care that we provide more high quality.”
There will be sessions of a general nature, such as “There’s an App for That,” a review of mobile apps helpful to hospitalists. And there will be those for the more passionate technophiles, such as a session on clinical informatics and “Using IT to Help Drive the Shift from Volume to Value.”
“We’ve spent a lot of time trying to make sure there’s something for everyone,” says Kendall Rogers, MD, SFHM, chair of SHM’s IT Committee. “And even within each individual talk, we’ve tried to make sure that there is material that can be applicable from the frontline hospitalist to the CMIO of a hospital.”
Dr. Rogers says the committee has “really been pushing” to have its own track at the annual meeting.
Listen to more of our interview with Dr. Rogers.
“Health IT continues to be an area of great frustration and great promise,” he says. “I think most of the frustration that hospitalists have is because they realize the potential of health IT, and they see how far it is from the reality of what they’re working with every day.
“Hospitalists are well-suited for actively being involved in clinical informatics, but many of us would be far more effective in our roles with more formal education and training.”
Post-Acute Care
It’s estimated that as many as 35% of hospitalists work in the post-acute setting. The number very much surprised Dr. Mattison. When she heard of the figure, “[the committee] lobbied very hard to get a track for post-acute care.”
One session, “Building and Managing a PAC Practice,” will review setting up a staff, relevant regulations, billing, and collecting, and it should be of interest to both managers and physicians, says Sean Muldoon, MD, senior vice president and chief medical officer of the hospitalist division at Louisville, Ken.–based Kindred Healthcare and chair of SHM’s Post-Acute Care Task Force.
Another session, “Lost in Transitions,” will review information gaps and propose solutions “to the well-known voltage drop of information that can happen in transfer from the hospital to post-acute care.”
At Kindred, Dr. Muldoon says he has seen the benefits of hospitalist involvement in post-acute care.
“In many markets, we seek out and often are able to become a practice site for a large hospitalist medical group,” he says. “That’s really good for us, the patients, and, we think, the hospitalists because it allows the hospitalists to be exposed to the practice and benefits of post-acute care without having to make a full commitment to be a skilled-nursing physician or a long-term acute-care physician.”
It also makes transitions of care smoother and less disruptive, he says, “because a patient is simply transferred from one hospitalist in a group to another or often maintaining that same hospitalist in the post-acute-care setting.”
Dr. Muldoon says the new track is of value to any hospitalist, whether they actually work in post-acute care or not.
“A hospitalist would be hard-pressed to provide knowledgeable input into where a patient should receive post-acute care without a working knowledge of which patients should be directed to which post-acute-care setting,” he says.
Doctor-Patient Relationship
This topic was a pre-course last year, and organizers decided to make this a full track on the final day of the meeting schedule.
“It’s really about communication style,” Dr. Mattison says. “There’s one session called ‘The Language of Empathy and Engagement: Communication Essentials for Patient-Centered Care.’ There’s one on unconscious biases and our underlying assumptions and how it affects how we care for patients. [Another is focused] on improving the patient experience in the hospital.”
Co-Management/ Perioperative Medicine
“There are a lot of challenges around anticoagulation management, optimizing patients’ physical heath prior to the surgery, what things should we be doing, what medications should we be giving, what ones shouldn’t we be giving,” Dr. Mattison says. “It’s an evolving field that has, every year, new information.”
Hidden Gems
Dr. Mattison draws special attention to “Work-Life Balance: Is It Possible?” (Tuesday, March 8, 4:20–5:40 p.m.). This year, this problem—all too familiar to hospitalists—will be addressed in a panel discussion, which is a change from previous years.
“There’s been, year after year after year, a lot of discussion around, how can I make my job manageable if my boss isn’t listening to me or is not attuned to work-life balance? How can I navigate this process?” she says. “I’m hopeful that the panel discussion will provide people with some real examples and strategies for success.”
She also draws attention to the session “Perioperative Pitfalls: Overcoming Common Challenges in Managing Medical Problems in Surgical Patients” (Monday, March 7, 3:05–4:20 p.m.).
“There are some true leaders in perioperative management, and they’re going to come together and have a panel discussion,” she says. “It’ll be an opportunity to see some of the great minds think, if you will.” TH
Thomas R. Collins is a freelance writer in South Florida.
FDA approves maintenance therapy for CLL
Photo courtesy of GSK
The US Food and Drug Administration (FDA) has approved the use of ofatumumab (Arzerra) as maintenance therapy for patients with chronic lymphocytic leukemia (CLL).
The drug can now be given for an extended period to patients who are in complete or partial response after receiving at least 2 lines of therapy for recurrent or progressive CLL.
Ofatumumab is also FDA-approved as a single agent to treat CLL that is refractory to fludarabine and alemtuzumab.
And the drug is approved for use in combination with chlorambucil to treat previously untreated patients with CLL for whom fludarabine-based therapy is considered inappropriate.
The FDA granted the new approval for ofatumumab based on an interim analysis of the PROLONG study. The results suggested that ofatumumab maintenance can improve progression-free survival (PFS) in CLL patients when compared to observation.
Ofatumumab is marketed as Arzerra under a collaboration agreement between Genmab and Novartis. For more details on ofatumumab, see the full prescribing information.
PROLONG trial
The PROLONG trial was designed to compare ofatumumab maintenance to no further treatment in patients with a complete or partial response after second- or third-line treatment for CLL. Interim results of the study were presented at ASH 2014.
These results—in 474 patients—suggested that ofatumumab can significantly improve PFS. The median PFS was about 29 months in patients who received ofatumumab and about 15 months for patients who did not receive maintenance therapy (P<0.0001).
There was no significant difference in the median overall survival, which was not reached in either treatment arm.
The researchers said there were no unexpected safety findings. The most common adverse events (≥10%) were infusion reactions, neutropenia, and upper respiratory tract infection. 
Photo courtesy of GSK
The US Food and Drug Administration (FDA) has approved the use of ofatumumab (Arzerra) as maintenance therapy for patients with chronic lymphocytic leukemia (CLL).
The drug can now be given for an extended period to patients who are in complete or partial response after receiving at least 2 lines of therapy for recurrent or progressive CLL.
Ofatumumab is also FDA-approved as a single agent to treat CLL that is refractory to fludarabine and alemtuzumab.
And the drug is approved for use in combination with chlorambucil to treat previously untreated patients with CLL for whom fludarabine-based therapy is considered inappropriate.
The FDA granted the new approval for ofatumumab based on an interim analysis of the PROLONG study. The results suggested that ofatumumab maintenance can improve progression-free survival (PFS) in CLL patients when compared to observation.
Ofatumumab is marketed as Arzerra under a collaboration agreement between Genmab and Novartis. For more details on ofatumumab, see the full prescribing information.
PROLONG trial
The PROLONG trial was designed to compare ofatumumab maintenance to no further treatment in patients with a complete or partial response after second- or third-line treatment for CLL. Interim results of the study were presented at ASH 2014.
These results—in 474 patients—suggested that ofatumumab can significantly improve PFS. The median PFS was about 29 months in patients who received ofatumumab and about 15 months for patients who did not receive maintenance therapy (P<0.0001).
There was no significant difference in the median overall survival, which was not reached in either treatment arm.
The researchers said there were no unexpected safety findings. The most common adverse events (≥10%) were infusion reactions, neutropenia, and upper respiratory tract infection.
Photo courtesy of GSK
The US Food and Drug Administration (FDA) has approved the use of ofatumumab (Arzerra) as maintenance therapy for patients with chronic lymphocytic leukemia (CLL).
The drug can now be given for an extended period to patients who are in complete or partial response after receiving at least 2 lines of therapy for recurrent or progressive CLL.
Ofatumumab is also FDA-approved as a single agent to treat CLL that is refractory to fludarabine and alemtuzumab.
And the drug is approved for use in combination with chlorambucil to treat previously untreated patients with CLL for whom fludarabine-based therapy is considered inappropriate.
The FDA granted the new approval for ofatumumab based on an interim analysis of the PROLONG study. The results suggested that ofatumumab maintenance can improve progression-free survival (PFS) in CLL patients when compared to observation.
Ofatumumab is marketed as Arzerra under a collaboration agreement between Genmab and Novartis. For more details on ofatumumab, see the full prescribing information.
PROLONG trial
The PROLONG trial was designed to compare ofatumumab maintenance to no further treatment in patients with a complete or partial response after second- or third-line treatment for CLL. Interim results of the study were presented at ASH 2014.
These results—in 474 patients—suggested that ofatumumab can significantly improve PFS. The median PFS was about 29 months in patients who received ofatumumab and about 15 months for patients who did not receive maintenance therapy (P<0.0001).
There was no significant difference in the median overall survival, which was not reached in either treatment arm.
The researchers said there were no unexpected safety findings. The most common adverse events (≥10%) were infusion reactions, neutropenia, and upper respiratory tract infection.
FDA approves generic drug for hemophilia
The US Food and Drug Administration (FDA) has approved a generic version of tranexamic acid for short-term control of bleeding in patients with hemophilia.
The drug, tranexamic acid injection (100 mg/mL) 1000 mg/10 mL single-dose vial, is a product of Aurobindo Pharma Limited.
The drug has been deemed bioequivalent and therapeutically equivalent to Cyklokapron® injection, 100 mg/mL, a product of Pharmacia and Upjohn Company.
Aurobindo Pharma Limited said the generic drug should be launched in the US by the end of March.
The US Food and Drug Administration (FDA) has approved a generic version of tranexamic acid for short-term control of bleeding in patients with hemophilia.
The drug, tranexamic acid injection (100 mg/mL) 1000 mg/10 mL single-dose vial, is a product of Aurobindo Pharma Limited.
The drug has been deemed bioequivalent and therapeutically equivalent to Cyklokapron® injection, 100 mg/mL, a product of Pharmacia and Upjohn Company.
Aurobindo Pharma Limited said the generic drug should be launched in the US by the end of March.
The US Food and Drug Administration (FDA) has approved a generic version of tranexamic acid for short-term control of bleeding in patients with hemophilia.
The drug, tranexamic acid injection (100 mg/mL) 1000 mg/10 mL single-dose vial, is a product of Aurobindo Pharma Limited.
The drug has been deemed bioequivalent and therapeutically equivalent to Cyklokapron® injection, 100 mg/mL, a product of Pharmacia and Upjohn Company.
Aurobindo Pharma Limited said the generic drug should be launched in the US by the end of March.
Research helps explain how RBCs move
Scientists say they have determined how red blood cells (RBCs) move, showing that RBCs can be moved by external forces and actively “wriggle” on their own.
Linking physical principles and biological reality, the team found that fast molecules in the vicinity of RBCs make the cell membranes wriggle, but the cells themselves also become active when they have enough reaction time.
The group recounted these findings in Nature Physics.
Previously, scientists had only shown that RBCs’ constant wriggling was caused by external forces. But biological considerations suggested that internal forces might also be responsible for the RBCs’ membranes changing shape.
“So we started with the following question, ‘As blood cells are living cells, why shouldn’t internal forces inside the cell also have an impact on the membrane?’” said study author Timo Betz, PhD, of Münster University in Münster, Germany.
“For biologists, this is all clear, but these forces were just never a part of any physical equation.”
Dr Betz and his colleagues wanted to find out more about the mechanics of blood cells and gain a detailed understanding of the forces that move and shape cells.
The team said it is important to learn about RBCs’ properties and their internal forces because they are unusually soft and elastic and must change their shape to pass through blood vessels. It is precisely because RBCs are normally so soft that, in previous studies, physicists measured large thermal fluctuations at the outer membrane of the cells.
These natural movements of molecules are defined by the ambient temperature. In other words, the cell membrane moves because molecules in the vicinity jog it. Under the microscope, this makes the RBCs appear to be wriggling.
Although this explains why RBCs move, it does not address the question of possible internal forces being a contributing factor.
So Dr Betz and his colleagues used optical tweezers to take a close look at the fluctuations of RBCs. The team stretched RBCs in a petri dish and analyzed the behavior of the cells.
The result was that, if the RBCs had enough reaction time, they became active themselves and were able to counteract the force of the optical tweezers. If they did not have this time, they were at the mercy of their environment, and only temperature-related forces were measured.
“By comparing both sets of measurements, we can exactly define how fast the cells become active themselves and what force they generate in order to change shape,” Dr Betz explained.
He and his colleagues have a theory as to which forces inside RBCs cause the cell membrane to change shape.
“Transport proteins could generate such forces in the membrane by moving ions from one side of the membrane to the other,” said study author Gerhard Gompper, PhD, of the Jülich Institute of Complex Systems in Jülich, Germany.
“Now, it’s up to the biologists, because we physicists only have a rough idea about which proteins might be the drivers for this movement,” Dr Betz added. “On the other hand, we can predict exactly how fast and how strong they are.”
Scientists say they have determined how red blood cells (RBCs) move, showing that RBCs can be moved by external forces and actively “wriggle” on their own.
Linking physical principles and biological reality, the team found that fast molecules in the vicinity of RBCs make the cell membranes wriggle, but the cells themselves also become active when they have enough reaction time.
The group recounted these findings in Nature Physics.
Previously, scientists had only shown that RBCs’ constant wriggling was caused by external forces. But biological considerations suggested that internal forces might also be responsible for the RBCs’ membranes changing shape.
“So we started with the following question, ‘As blood cells are living cells, why shouldn’t internal forces inside the cell also have an impact on the membrane?’” said study author Timo Betz, PhD, of Münster University in Münster, Germany.
“For biologists, this is all clear, but these forces were just never a part of any physical equation.”
Dr Betz and his colleagues wanted to find out more about the mechanics of blood cells and gain a detailed understanding of the forces that move and shape cells.
The team said it is important to learn about RBCs’ properties and their internal forces because they are unusually soft and elastic and must change their shape to pass through blood vessels. It is precisely because RBCs are normally so soft that, in previous studies, physicists measured large thermal fluctuations at the outer membrane of the cells.
These natural movements of molecules are defined by the ambient temperature. In other words, the cell membrane moves because molecules in the vicinity jog it. Under the microscope, this makes the RBCs appear to be wriggling.
Although this explains why RBCs move, it does not address the question of possible internal forces being a contributing factor.
So Dr Betz and his colleagues used optical tweezers to take a close look at the fluctuations of RBCs. The team stretched RBCs in a petri dish and analyzed the behavior of the cells.
The result was that, if the RBCs had enough reaction time, they became active themselves and were able to counteract the force of the optical tweezers. If they did not have this time, they were at the mercy of their environment, and only temperature-related forces were measured.
“By comparing both sets of measurements, we can exactly define how fast the cells become active themselves and what force they generate in order to change shape,” Dr Betz explained.
He and his colleagues have a theory as to which forces inside RBCs cause the cell membrane to change shape.
“Transport proteins could generate such forces in the membrane by moving ions from one side of the membrane to the other,” said study author Gerhard Gompper, PhD, of the Jülich Institute of Complex Systems in Jülich, Germany.
“Now, it’s up to the biologists, because we physicists only have a rough idea about which proteins might be the drivers for this movement,” Dr Betz added. “On the other hand, we can predict exactly how fast and how strong they are.”
Scientists say they have determined how red blood cells (RBCs) move, showing that RBCs can be moved by external forces and actively “wriggle” on their own.
Linking physical principles and biological reality, the team found that fast molecules in the vicinity of RBCs make the cell membranes wriggle, but the cells themselves also become active when they have enough reaction time.
The group recounted these findings in Nature Physics.
Previously, scientists had only shown that RBCs’ constant wriggling was caused by external forces. But biological considerations suggested that internal forces might also be responsible for the RBCs’ membranes changing shape.
“So we started with the following question, ‘As blood cells are living cells, why shouldn’t internal forces inside the cell also have an impact on the membrane?’” said study author Timo Betz, PhD, of Münster University in Münster, Germany.
“For biologists, this is all clear, but these forces were just never a part of any physical equation.”
Dr Betz and his colleagues wanted to find out more about the mechanics of blood cells and gain a detailed understanding of the forces that move and shape cells.
The team said it is important to learn about RBCs’ properties and their internal forces because they are unusually soft and elastic and must change their shape to pass through blood vessels. It is precisely because RBCs are normally so soft that, in previous studies, physicists measured large thermal fluctuations at the outer membrane of the cells.
These natural movements of molecules are defined by the ambient temperature. In other words, the cell membrane moves because molecules in the vicinity jog it. Under the microscope, this makes the RBCs appear to be wriggling.
Although this explains why RBCs move, it does not address the question of possible internal forces being a contributing factor.
So Dr Betz and his colleagues used optical tweezers to take a close look at the fluctuations of RBCs. The team stretched RBCs in a petri dish and analyzed the behavior of the cells.
The result was that, if the RBCs had enough reaction time, they became active themselves and were able to counteract the force of the optical tweezers. If they did not have this time, they were at the mercy of their environment, and only temperature-related forces were measured.
“By comparing both sets of measurements, we can exactly define how fast the cells become active themselves and what force they generate in order to change shape,” Dr Betz explained.
He and his colleagues have a theory as to which forces inside RBCs cause the cell membrane to change shape.
“Transport proteins could generate such forces in the membrane by moving ions from one side of the membrane to the other,” said study author Gerhard Gompper, PhD, of the Jülich Institute of Complex Systems in Jülich, Germany.
“Now, it’s up to the biologists, because we physicists only have a rough idea about which proteins might be the drivers for this movement,” Dr Betz added. “On the other hand, we can predict exactly how fast and how strong they are.”
Drug approved to treat ALL in EU
The European Commission has granted marketing authorization for pegaspargase (Oncaspar) to be used as part of combination antineoplastic therapy for pediatric and adult patients with acute lymphoblastic leukemia (ALL).
The approval means the drug can be marketed for this indication in the 28 member countries of the European Union (EU), as well as Iceland, Liechtenstein, and Norway.
Pegaspargase was already approved for use in Argentina, Belarus, Germany, Kazakhstan, Poland, Russia, Ukraine, and the US.
“Oncaspar has been used as an integral component of the treatment regimen for pediatric and adult patients with ALL for many years, in Europe and worldwide,” said Martin Schrappe, of Schleswig-Holstein University Hospital in Kiel, Germany.
“Today’s marketing authorization will ensure that more patients across the EU will benefit from access to Oncaspar as part of a standard of care regimen.”
The drug is being developed by Baxalta Incorporated.
First-line ALL
Researchers have evaluated the safety and effectiveness of pegaspargase in a study of 118 pediatric patients (ages 1 to 9) with newly diagnosed ALL. The patients were randomized 1:1 to pegaspargase or native E coli L-asparaginase, both as part of combination therapy.
Asparagine depletion (magnitude and duration) was similar between the 2 treatment arms. Event-free survival rates were also similar (about 80% in both arms), but the study was not designed to evaluate differences in event-free survival.
Grade 3/4 adverse events occurring in the pegaspargase and native E coli L-asparaginase arms, respectively, were abnormal liver tests (5% and 8%), elevated transaminases (3% and 7%), hyperbilirubinemia (2% and 2%), hyperglycemia (5% and 3%), central nervous system thrombosis (3% and 3%), coagulopathy (2% and 5%), pancreatitis (2% and 2%), and clinical allergic reactions to asparaginase (2% and 0%).
Previously treated ALL
Researchers have evaluated the effectiveness of pegaspargase in 4 open-label studies of patients with a history of prior clinical allergic reaction to asparaginase. The studies enrolled a total of 42 patients with multiply relapsed acute leukemia (39 with ALL).
Patients received pegaspargase as a single agent or as part of multi-agent chemotherapy. The re-induction response rate was 50%—36% complete responses and 14% partial responses. Three responses occurred in patients who received single-agent pegaspargase.
Adverse event information on pegaspargase in relapsed ALL has been compiled from 5 clinical trials. The studies enrolled a total of 174 patients with relapsed ALL who received pegaspargase as a single agent or as part of combination therapy.
Sixty-two of the patients had prior hypersensitivity reactions to asparaginase, and 112 did not. Allergic reactions to pegaspargase occurred in 32% of previously hypersensitive patients and 10% of non-hypersensitive patients.
The most common adverse events observed in patients who received pegaspargase were clinical allergic reactions, elevated transaminases, hyperbilirubinemia, and coagulopathies.
The most common serious adverse events due to pegaspargase were thrombosis (4%), hyperglycemia requiring insulin therapy (3%), and pancreatitis (1%).
For more details on these trials and pegaspargase in general, see the product information.
The European Commission has granted marketing authorization for pegaspargase (Oncaspar) to be used as part of combination antineoplastic therapy for pediatric and adult patients with acute lymphoblastic leukemia (ALL).
The approval means the drug can be marketed for this indication in the 28 member countries of the European Union (EU), as well as Iceland, Liechtenstein, and Norway.
Pegaspargase was already approved for use in Argentina, Belarus, Germany, Kazakhstan, Poland, Russia, Ukraine, and the US.
“Oncaspar has been used as an integral component of the treatment regimen for pediatric and adult patients with ALL for many years, in Europe and worldwide,” said Martin Schrappe, of Schleswig-Holstein University Hospital in Kiel, Germany.
“Today’s marketing authorization will ensure that more patients across the EU will benefit from access to Oncaspar as part of a standard of care regimen.”
The drug is being developed by Baxalta Incorporated.
First-line ALL
Researchers have evaluated the safety and effectiveness of pegaspargase in a study of 118 pediatric patients (ages 1 to 9) with newly diagnosed ALL. The patients were randomized 1:1 to pegaspargase or native E coli L-asparaginase, both as part of combination therapy.
Asparagine depletion (magnitude and duration) was similar between the 2 treatment arms. Event-free survival rates were also similar (about 80% in both arms), but the study was not designed to evaluate differences in event-free survival.
Grade 3/4 adverse events occurring in the pegaspargase and native E coli L-asparaginase arms, respectively, were abnormal liver tests (5% and 8%), elevated transaminases (3% and 7%), hyperbilirubinemia (2% and 2%), hyperglycemia (5% and 3%), central nervous system thrombosis (3% and 3%), coagulopathy (2% and 5%), pancreatitis (2% and 2%), and clinical allergic reactions to asparaginase (2% and 0%).
Previously treated ALL
Researchers have evaluated the effectiveness of pegaspargase in 4 open-label studies of patients with a history of prior clinical allergic reaction to asparaginase. The studies enrolled a total of 42 patients with multiply relapsed acute leukemia (39 with ALL).
Patients received pegaspargase as a single agent or as part of multi-agent chemotherapy. The re-induction response rate was 50%—36% complete responses and 14% partial responses. Three responses occurred in patients who received single-agent pegaspargase.
Adverse event information on pegaspargase in relapsed ALL has been compiled from 5 clinical trials. The studies enrolled a total of 174 patients with relapsed ALL who received pegaspargase as a single agent or as part of combination therapy.
Sixty-two of the patients had prior hypersensitivity reactions to asparaginase, and 112 did not. Allergic reactions to pegaspargase occurred in 32% of previously hypersensitive patients and 10% of non-hypersensitive patients.
The most common adverse events observed in patients who received pegaspargase were clinical allergic reactions, elevated transaminases, hyperbilirubinemia, and coagulopathies.
The most common serious adverse events due to pegaspargase were thrombosis (4%), hyperglycemia requiring insulin therapy (3%), and pancreatitis (1%).
For more details on these trials and pegaspargase in general, see the product information.
The European Commission has granted marketing authorization for pegaspargase (Oncaspar) to be used as part of combination antineoplastic therapy for pediatric and adult patients with acute lymphoblastic leukemia (ALL).
The approval means the drug can be marketed for this indication in the 28 member countries of the European Union (EU), as well as Iceland, Liechtenstein, and Norway.
Pegaspargase was already approved for use in Argentina, Belarus, Germany, Kazakhstan, Poland, Russia, Ukraine, and the US.
“Oncaspar has been used as an integral component of the treatment regimen for pediatric and adult patients with ALL for many years, in Europe and worldwide,” said Martin Schrappe, of Schleswig-Holstein University Hospital in Kiel, Germany.
“Today’s marketing authorization will ensure that more patients across the EU will benefit from access to Oncaspar as part of a standard of care regimen.”
The drug is being developed by Baxalta Incorporated.
First-line ALL
Researchers have evaluated the safety and effectiveness of pegaspargase in a study of 118 pediatric patients (ages 1 to 9) with newly diagnosed ALL. The patients were randomized 1:1 to pegaspargase or native E coli L-asparaginase, both as part of combination therapy.
Asparagine depletion (magnitude and duration) was similar between the 2 treatment arms. Event-free survival rates were also similar (about 80% in both arms), but the study was not designed to evaluate differences in event-free survival.
Grade 3/4 adverse events occurring in the pegaspargase and native E coli L-asparaginase arms, respectively, were abnormal liver tests (5% and 8%), elevated transaminases (3% and 7%), hyperbilirubinemia (2% and 2%), hyperglycemia (5% and 3%), central nervous system thrombosis (3% and 3%), coagulopathy (2% and 5%), pancreatitis (2% and 2%), and clinical allergic reactions to asparaginase (2% and 0%).
Previously treated ALL
Researchers have evaluated the effectiveness of pegaspargase in 4 open-label studies of patients with a history of prior clinical allergic reaction to asparaginase. The studies enrolled a total of 42 patients with multiply relapsed acute leukemia (39 with ALL).
Patients received pegaspargase as a single agent or as part of multi-agent chemotherapy. The re-induction response rate was 50%—36% complete responses and 14% partial responses. Three responses occurred in patients who received single-agent pegaspargase.
Adverse event information on pegaspargase in relapsed ALL has been compiled from 5 clinical trials. The studies enrolled a total of 174 patients with relapsed ALL who received pegaspargase as a single agent or as part of combination therapy.
Sixty-two of the patients had prior hypersensitivity reactions to asparaginase, and 112 did not. Allergic reactions to pegaspargase occurred in 32% of previously hypersensitive patients and 10% of non-hypersensitive patients.
The most common adverse events observed in patients who received pegaspargase were clinical allergic reactions, elevated transaminases, hyperbilirubinemia, and coagulopathies.
The most common serious adverse events due to pegaspargase were thrombosis (4%), hyperglycemia requiring insulin therapy (3%), and pancreatitis (1%).
For more details on these trials and pegaspargase in general, see the product information.
Ofatumumab approved for extended treatment of CLL patients in complete or partial response
Ofatumumab has been approved for extended treatment of patients who are in complete or partial response after at least two lines of therapy for recurrent or progressive chronic lymphocytic leukemia (CLL), the U.S. Food and Drug Administration announced on Jan. 19.
Ofatumumab (Arzerra Injection, Novartis Pharmaceuticals) was previously approved for treatment-naive patients with CLL for whom fludarabine-based therapy was considered inappropriate and for patients with CLL refractory to fludarabine and alemtuzumab.
Approval of the new indication was based on the results of a randomized, open-label trial that found improved progression-free survival with ofatumumab as compared with observation in patients whose disease had a complete or partial response after at least two lines of prior therapy, the FDA said in a press release.
In the study, 238 patients were randomized to ofatumumab and 236 to observation. Patients in the ofatumumab arm had received a range of two to five prior therapies. The median progression-free survival was significantly longer with ofatumumab at 29.4 months (95% confidence interval, 26.2-34.2) than with observation at 15.2 months (95% CI, 11.8-18.8).
Of patients treated with ofatumumab, 33% reported serious adverse reactions. The most common were pneumonia, pyrexia, and neutropenia (including febrile neutropenia).
The recommended dose and schedule for ofatumumab therapy is 300 mg by intravenous infusion on day 1 followed by 1,000 mg on day 8, and then 7 weeks later, and then every 8 weeks thereafter for up to a maximum of 2 years.
Full prescribing information is available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/125326s062lbl.pdf.
Ofatumumab has been approved for extended treatment of patients who are in complete or partial response after at least two lines of therapy for recurrent or progressive chronic lymphocytic leukemia (CLL), the U.S. Food and Drug Administration announced on Jan. 19.
Ofatumumab (Arzerra Injection, Novartis Pharmaceuticals) was previously approved for treatment-naive patients with CLL for whom fludarabine-based therapy was considered inappropriate and for patients with CLL refractory to fludarabine and alemtuzumab.
Approval of the new indication was based on the results of a randomized, open-label trial that found improved progression-free survival with ofatumumab as compared with observation in patients whose disease had a complete or partial response after at least two lines of prior therapy, the FDA said in a press release.
In the study, 238 patients were randomized to ofatumumab and 236 to observation. Patients in the ofatumumab arm had received a range of two to five prior therapies. The median progression-free survival was significantly longer with ofatumumab at 29.4 months (95% confidence interval, 26.2-34.2) than with observation at 15.2 months (95% CI, 11.8-18.8).
Of patients treated with ofatumumab, 33% reported serious adverse reactions. The most common were pneumonia, pyrexia, and neutropenia (including febrile neutropenia).
The recommended dose and schedule for ofatumumab therapy is 300 mg by intravenous infusion on day 1 followed by 1,000 mg on day 8, and then 7 weeks later, and then every 8 weeks thereafter for up to a maximum of 2 years.
Full prescribing information is available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/125326s062lbl.pdf.
Ofatumumab has been approved for extended treatment of patients who are in complete or partial response after at least two lines of therapy for recurrent or progressive chronic lymphocytic leukemia (CLL), the U.S. Food and Drug Administration announced on Jan. 19.
Ofatumumab (Arzerra Injection, Novartis Pharmaceuticals) was previously approved for treatment-naive patients with CLL for whom fludarabine-based therapy was considered inappropriate and for patients with CLL refractory to fludarabine and alemtuzumab.
Approval of the new indication was based on the results of a randomized, open-label trial that found improved progression-free survival with ofatumumab as compared with observation in patients whose disease had a complete or partial response after at least two lines of prior therapy, the FDA said in a press release.
In the study, 238 patients were randomized to ofatumumab and 236 to observation. Patients in the ofatumumab arm had received a range of two to five prior therapies. The median progression-free survival was significantly longer with ofatumumab at 29.4 months (95% confidence interval, 26.2-34.2) than with observation at 15.2 months (95% CI, 11.8-18.8).
Of patients treated with ofatumumab, 33% reported serious adverse reactions. The most common were pneumonia, pyrexia, and neutropenia (including febrile neutropenia).
The recommended dose and schedule for ofatumumab therapy is 300 mg by intravenous infusion on day 1 followed by 1,000 mg on day 8, and then 7 weeks later, and then every 8 weeks thereafter for up to a maximum of 2 years.
Full prescribing information is available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/125326s062lbl.pdf.
Pretreatment hydroquinone for nonablative laser resurfacing of acne scars?
Pretreatment of skin prior to nonablative or ablative laser resurfacing is common practice, particularly in darker skin types. Treatment regimens include using hydroquinone 4% (and other hydroquinone-containing combinations) once to twice daily for 1-2 weeks prior to the laser procedure. The rationale makes sense. Quieting melanin production by inhibiting tyrosinase would seem to decrease the incidence of postinflammatory hyperpigmentation after laser resurfacing procedures. But is this common practice effective?
For ablative CO2 resurfacing in 100 patients Fitzpatrick Skin Types (FST) I-III, there was no significant difference in the incidence of hyperpigmentation in those randomized to be pretreated with either hydroquinone, glycolic acid, tretinoin, or to no treatment.1 The thought was that the follicular melanocytes involved in re-epithelialization were not affected by the pretreatment. This is the only published laser resurfacing today to date examining various pretreatment protocols with hyperpigmentation as a primary study outcome. From this study, it seems as though pretreatment before laser resurfacing is not helpful, but what about for nonablative resurfacing in darker skin types (FST IV-VI)?
In darker skin types (FST IV-VI), the risk of postinflammatory hyperpigmentation (PIH) is inherently higher and the incidence after laser resurfacing is greater. While the incidence of PIH is lower with nonablative fractional resurfacing, compared with ablative resurfacing, PIH can still occur whether pretreatment hydroquinone is used or not.2,3,4 To date, there are no published studies looking at the incidence of PIH when comparing pretreatment antipigment agents versus no pretreatment for laser resurfacing for acne scars in darker skin types. A split-face study comparing pretreatment on one side and no pretreatment on the other could help delineate whether this practice is evidence based.
For nonablative fractional laser resurfacing of acne scars, lower densities in darker skin types are recommended and may help reduce PIH risk. There is no statistically significant difference in improvement of acne scars in using low versus high densities using the same fluences. However, some studies note that higher densities clinically resulted in a mild improvement of acne scars over lower densities (not statistically significant); thus, if lower densities are used, it is possible that more treatments may be needed.4,5
Vigorous sun protection before and after treatment is prudent, with sun avoidance and physical sunscreens reducing the risk of PIH in darker skin from irritant or allergic contact dermatitis, compared with chemical sunscreens. If PIH occurs, it is often self limited (up to 1-2 months). Sun protection and posttreatment regimens of hydroquinone (or other lightening agent) aid in hastening improvement.
If the patient is undergoing nonablative laser resurfacing to treat pigmentation, such as melasma, then hydroquinone pre- and postlaser is appropriate. In my opinion, laser treatment of melasma should not be first line because of safety and efficacy concerns. However, in these cases, hydroquinone prior to laser has shown benefit.6 In addition, hydroquinone after nonablative fractional resurfacing may enhance penetration of the topical and improve efficacy.
In summary, the evidence shows that pretreatment with antipigment agents is not warranted in skin types I-III for ablative laser resurfacing. Pretreatment with antipigment agents for nonablative laser resurfacing for melasma (which should not be considered a first line treatment for melasma) is warranted. However, at this time, it is not clear whether pretreatment with antipigments for nonablative laser resurfacing for acne scars in darker skin types is useful. Lower densities should be used and if PIH does occur, it is usually self limited, and posttreatment hydroquinone or other antipigment agents may be useful.
References
1. Dermatol Surg. 1999 Jan;25(1):15-7.
2. Dermatol Surg. 2010 May;36(5):602-9.
3. Br J Dermatol. 2012 Jun;166(6):1160-9.
4.Lasers Surg Med. 2007 Jun;39(5):381-5.
5. Lasers Surg Med. 2007 Apr;39(4):311-4.
6. Dermatol Surg. 2010 Jun;36(6):909-18.
Dr. Wesley and Dr. Talakoub are co-contributors to the monthly Aesthetic Dermatology column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.
Pretreatment of skin prior to nonablative or ablative laser resurfacing is common practice, particularly in darker skin types. Treatment regimens include using hydroquinone 4% (and other hydroquinone-containing combinations) once to twice daily for 1-2 weeks prior to the laser procedure. The rationale makes sense. Quieting melanin production by inhibiting tyrosinase would seem to decrease the incidence of postinflammatory hyperpigmentation after laser resurfacing procedures. But is this common practice effective?
For ablative CO2 resurfacing in 100 patients Fitzpatrick Skin Types (FST) I-III, there was no significant difference in the incidence of hyperpigmentation in those randomized to be pretreated with either hydroquinone, glycolic acid, tretinoin, or to no treatment.1 The thought was that the follicular melanocytes involved in re-epithelialization were not affected by the pretreatment. This is the only published laser resurfacing today to date examining various pretreatment protocols with hyperpigmentation as a primary study outcome. From this study, it seems as though pretreatment before laser resurfacing is not helpful, but what about for nonablative resurfacing in darker skin types (FST IV-VI)?
In darker skin types (FST IV-VI), the risk of postinflammatory hyperpigmentation (PIH) is inherently higher and the incidence after laser resurfacing is greater. While the incidence of PIH is lower with nonablative fractional resurfacing, compared with ablative resurfacing, PIH can still occur whether pretreatment hydroquinone is used or not.2,3,4 To date, there are no published studies looking at the incidence of PIH when comparing pretreatment antipigment agents versus no pretreatment for laser resurfacing for acne scars in darker skin types. A split-face study comparing pretreatment on one side and no pretreatment on the other could help delineate whether this practice is evidence based.
For nonablative fractional laser resurfacing of acne scars, lower densities in darker skin types are recommended and may help reduce PIH risk. There is no statistically significant difference in improvement of acne scars in using low versus high densities using the same fluences. However, some studies note that higher densities clinically resulted in a mild improvement of acne scars over lower densities (not statistically significant); thus, if lower densities are used, it is possible that more treatments may be needed.4,5
Vigorous sun protection before and after treatment is prudent, with sun avoidance and physical sunscreens reducing the risk of PIH in darker skin from irritant or allergic contact dermatitis, compared with chemical sunscreens. If PIH occurs, it is often self limited (up to 1-2 months). Sun protection and posttreatment regimens of hydroquinone (or other lightening agent) aid in hastening improvement.
If the patient is undergoing nonablative laser resurfacing to treat pigmentation, such as melasma, then hydroquinone pre- and postlaser is appropriate. In my opinion, laser treatment of melasma should not be first line because of safety and efficacy concerns. However, in these cases, hydroquinone prior to laser has shown benefit.6 In addition, hydroquinone after nonablative fractional resurfacing may enhance penetration of the topical and improve efficacy.
In summary, the evidence shows that pretreatment with antipigment agents is not warranted in skin types I-III for ablative laser resurfacing. Pretreatment with antipigment agents for nonablative laser resurfacing for melasma (which should not be considered a first line treatment for melasma) is warranted. However, at this time, it is not clear whether pretreatment with antipigments for nonablative laser resurfacing for acne scars in darker skin types is useful. Lower densities should be used and if PIH does occur, it is usually self limited, and posttreatment hydroquinone or other antipigment agents may be useful.
References
1. Dermatol Surg. 1999 Jan;25(1):15-7.
2. Dermatol Surg. 2010 May;36(5):602-9.
3. Br J Dermatol. 2012 Jun;166(6):1160-9.
4.Lasers Surg Med. 2007 Jun;39(5):381-5.
5. Lasers Surg Med. 2007 Apr;39(4):311-4.
6. Dermatol Surg. 2010 Jun;36(6):909-18.
Dr. Wesley and Dr. Talakoub are co-contributors to the monthly Aesthetic Dermatology column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.
Pretreatment of skin prior to nonablative or ablative laser resurfacing is common practice, particularly in darker skin types. Treatment regimens include using hydroquinone 4% (and other hydroquinone-containing combinations) once to twice daily for 1-2 weeks prior to the laser procedure. The rationale makes sense. Quieting melanin production by inhibiting tyrosinase would seem to decrease the incidence of postinflammatory hyperpigmentation after laser resurfacing procedures. But is this common practice effective?
For ablative CO2 resurfacing in 100 patients Fitzpatrick Skin Types (FST) I-III, there was no significant difference in the incidence of hyperpigmentation in those randomized to be pretreated with either hydroquinone, glycolic acid, tretinoin, or to no treatment.1 The thought was that the follicular melanocytes involved in re-epithelialization were not affected by the pretreatment. This is the only published laser resurfacing today to date examining various pretreatment protocols with hyperpigmentation as a primary study outcome. From this study, it seems as though pretreatment before laser resurfacing is not helpful, but what about for nonablative resurfacing in darker skin types (FST IV-VI)?
In darker skin types (FST IV-VI), the risk of postinflammatory hyperpigmentation (PIH) is inherently higher and the incidence after laser resurfacing is greater. While the incidence of PIH is lower with nonablative fractional resurfacing, compared with ablative resurfacing, PIH can still occur whether pretreatment hydroquinone is used or not.2,3,4 To date, there are no published studies looking at the incidence of PIH when comparing pretreatment antipigment agents versus no pretreatment for laser resurfacing for acne scars in darker skin types. A split-face study comparing pretreatment on one side and no pretreatment on the other could help delineate whether this practice is evidence based.
For nonablative fractional laser resurfacing of acne scars, lower densities in darker skin types are recommended and may help reduce PIH risk. There is no statistically significant difference in improvement of acne scars in using low versus high densities using the same fluences. However, some studies note that higher densities clinically resulted in a mild improvement of acne scars over lower densities (not statistically significant); thus, if lower densities are used, it is possible that more treatments may be needed.4,5
Vigorous sun protection before and after treatment is prudent, with sun avoidance and physical sunscreens reducing the risk of PIH in darker skin from irritant or allergic contact dermatitis, compared with chemical sunscreens. If PIH occurs, it is often self limited (up to 1-2 months). Sun protection and posttreatment regimens of hydroquinone (or other lightening agent) aid in hastening improvement.
If the patient is undergoing nonablative laser resurfacing to treat pigmentation, such as melasma, then hydroquinone pre- and postlaser is appropriate. In my opinion, laser treatment of melasma should not be first line because of safety and efficacy concerns. However, in these cases, hydroquinone prior to laser has shown benefit.6 In addition, hydroquinone after nonablative fractional resurfacing may enhance penetration of the topical and improve efficacy.
In summary, the evidence shows that pretreatment with antipigment agents is not warranted in skin types I-III for ablative laser resurfacing. Pretreatment with antipigment agents for nonablative laser resurfacing for melasma (which should not be considered a first line treatment for melasma) is warranted. However, at this time, it is not clear whether pretreatment with antipigments for nonablative laser resurfacing for acne scars in darker skin types is useful. Lower densities should be used and if PIH does occur, it is usually self limited, and posttreatment hydroquinone or other antipigment agents may be useful.
References
1. Dermatol Surg. 1999 Jan;25(1):15-7.
2. Dermatol Surg. 2010 May;36(5):602-9.
3. Br J Dermatol. 2012 Jun;166(6):1160-9.
4.Lasers Surg Med. 2007 Jun;39(5):381-5.
5. Lasers Surg Med. 2007 Apr;39(4):311-4.
6. Dermatol Surg. 2010 Jun;36(6):909-18.
Dr. Wesley and Dr. Talakoub are co-contributors to the monthly Aesthetic Dermatology column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley.
Minimum 5-Year Results With Duracon Press-Fit Metal-Backed Patellae
The metal-backed patella was originally designed to address the shortcomings of cemented, all-polyethylene patellae: deformation, aseptic loosening, stress fractures of polyethylene, and possible thermal damage from bone cement.1-3 Several long-term studies have found very good outcomes with use of all-polyethylene patellae.4-6 However, complications of using an all-polyethylene patella reportedly accounted for up to half of all knee revisions, and during revision surgery patellar bone stock was often found to have been compromised.7
The intention behind the design of press-fit metal-backed patellae was to address the shortcomings of all-polyethylene patellae by eliminating the need for bone cement and providing stiffness that would help resist polyethylene deformation while decreasing implant–bone interface stresses.8 However, early design iterations of metal-backed patellae demonstrated short-term failures—most commonly, local polyethylene wear damaging the locking mechanism and subsequent dissociation or fracture from the metal baseplate; polyethylene delamination from the metal baseplate; and failure of interface fixation.9,10 On the other hand, good fixation with bony ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9,11-13 Overall, however, negative outcomes reported for metal-backed patellae led many surgeons to abandon these components and return to using cemented all-polyethylene patellae.
Negative outcomes of earlier metal-backed patellae designs have overshadowed reports of positive outcomes achieved with careful attention paid to component design, patellar tracking, and surgical technique.2,3,14 Subsequent design improvements (eg, a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15 The advantages of using a metal-backed patella (eg, uniform load sharing, decreased polyethylene deformation, potential for biological fixation) may be unjustly outweighed by the fear of patellar component failure.3
Our 30-plus years of experience with metal-backed patellar components reflect the evolving effect of component design on outcome. Much as reported elsewhere, we found earlier component failures were caused by poor locking mechanisms, thin polyethylene, poor tracking, and minimal femur contact. Over the past decade, however, our outcomes with Duracon metal-backed patellae (Stryker) have been encouraging. We think these positive outcomes, seen over minimum 5-year follow-up, are largely attributable to the thicker polyethylene and improved articular conformity of this component relative to earlier designs. We have also found it helpful to adhere to certain criteria when implanting metal-backed patellae, and we think adhering to these criteria, along with improved component design, indicates use of press-fit metal-backed patellae. In this article, we report our failure incidence with use of this device at minimum 5-year follow-up.
Materials and Methods
In this single-center study, we performed clinical and independent radiographic reviews of 88 primary press-fit metal-backed patellae with minimum 5-year follow-up. All components were the same design (Duracon metal-backed patella) from the same manufacturer (Stryker).
This study, which began in September 2003, was reviewed and approved by the Western Institutional Review Board (WIRB). Either the investigator (Dr. Hedley) or the clinical study coordinator gave study candidates a full explanation of the study and answered any questions. Patients who still wanted to participate in the study signed WIRB consent forms after their index surgery but before minimum 5-year follow-up.
Device Description
This Duracon patella has a porous-coated cobalt-chromium metal back intended for press-fit fixation, 3 cobalt-chromium porous-coated pegs, and a preassembled polyethylene anterior surface (Figure 1). Four sizes are available to fit the peripheral shape of the resected patella.
This patella has 3 styles: symmetric, asymmetric, and conversion. In this study, we used only the asymmetric and conversion styles. The design of each style incorporates medial/lateral facets intended to conform to the convex intercondylar radii of the femoral component, thereby allowing the patella to ride deeply in the recessed patellofemoral groove. The asymmetric patella is a resurfacing component with a generous polyethylene thickness (4.6 mm at its thinnest) and a larger lateral facet for more bone coverage. The asymmetric patella naturally medializes component placement. The articulating surface of the conversion patella is identical to that of the asymmetric patella. However, the conversion patella allows for exchange of the polyethylene portion of the implant without revising a stable, well-fixed metal baseplate.
Patient Selection
Candidates were recruited from a group of metal-backed patella patients within Dr. Hedley’s medical practice. All candidates had undergone primary total knee arthroplasty and received a Duracon press-fit metal-backed patella. All recruited patients had undergone primary knee arthroplasty at least 5 years before clinical and radiographic evaluation. Patients were included in the study if they had a diagnosis of noninflammatory degenerative joint disease (eg, osteoarthritis, traumatic arthritis, avascular necrosis). Patients with body mass index higher than 40 were excluded from the study.
Surgical Technique
The patella is everted completely or as much as feasible. Debridement is done circumferentially around the patella. Adherent fat and pseudomeniscus are stripped back until the surgeon sees the entry point of the quadriceps tendon fibers above and the patella tendon fibers below. The cut is then made at this level to remove as much bone as needed to restore the normal height of the patella with the implant in place. The cut is usually made by hand—without guides but with the patella stabilized with a towel clip above and below to prevent any movement during the action.
The desired cut must be absolutely planar, and this should be checked by placing the edge of the blade across the interface. Repeated passes with the saw blade are needed if the cut is not 100% planar. Once the cut is made, the patella is sized with the patella sizers and drill guide. After the appropriate size is selected, the patella is drilled with a bit that is slightly undersized from the size of the pegs (1/32 inch smaller than the bit supplied by the manufacturer).
Once the patella is prepared, the rest of the knee arthroplasty is performed. The patella is press-fit as the last component to be inserted.
Radiologic Review
Radiographic analysis was performed by an independent reviewer according to the current Knee Society total knee arthroplasty roentgenographic evaluation and scoring system (Figure 2).16 The reviewer was an orthopedist specializing in hip and knee surgery. Radiographs the reviewer deemed questionable were shown to another independent hip and knee surgeon for validation. In all cases, the second reviewer confirmed the first reviewer’s initial recorded observations.
KSS (Knee Society Scale), WOMAC (Western Ontario and McMaster Universities Arthritis Index), and SF-36 (36-Item Short Form Health Survey) were also used to evaluate effectiveness in this protocol.
Survivorship Calculations
Kaplan-Meier survivorship was determined for all metal-backed patellae. For survival analysis, only knees with radiographic data were included (74 knees). Mean follow-up was 75.8 months (range, 60-105 months).
Seventy-four patients (88 knees) met the study criteria (Table). At minimum 5-year follow-up, complete data were acquired for 59 patients (72 knees). Of the total group, 14 knees did not have radiographic data. Those knees were categorized as lost to follow-up and were excluded from the survivorship analysis. The status of patients enrolled in the study at minimum 5-year follow-up is shown in the Table.
Mann-Whitney U test (nonparametric t test) was used to compare WOMAC and SF-36 scores between the “complete” and the “WOMAC and SF-36 only” data groups.
Statistical Analysis
Kaplan-Meier survivorship probabilities (asymmetric method) were calculated using SAS Version 9.2 (SAS Institute); 95% pointwise confidence limits were used.
The Mann-Whitney U test is a nonparametric analogue to the independent-samples t test. It was used here to compare WOMAC and SF-36 scores of patients with “complete” data with scores of patients with “WOMAC and SF-36 only” data. In either group, for patients who had primary bilateral knee arthroplasty, mean WOMAC and SF-36 scores were used.
Comparisons were made between the unilateral and bilateral knee arthroplasty groups. There were no differences in age, height, or weight (Mann-Whitney U test) or in sex, primary diagnosis, or number of patients lost to follow-up (Fisher exact test). Fisher exact test (vs χ2 test) was used for the contingency table analysis because of small cell sizes (eg, ≤10 females in ‘‘both knees” group), suggesting the unilateral and bilateral patients did not differ in demographics.
For all patient-reported questionnaires, bilateral patients were given the opportunity to note any differences between their knee arthroplasties, but none of these patients made any special notations. We interpreted this to mean that all survey responses from bilateral patients were applicable to both knee arthroplasties.
Results
Seventy-four patients (88 knees) were enrolled in the study: 31 women (41.2%) and 43 men (58.1%). At time of surgery, mean age was 59.7 years (range, 40-86 years), and mean body mass index was 30.6 (range, 19.1-39.6). Eighty-three knees were diagnosed with osteoarthritis, and 5 knees were diagnosed with posttraumatic arthritis. Mean time to follow-up was 74.8 months (range, 60-105 months). Fourteen knees (14 patients) were considered lost to follow-up. However, 8 patients (8 knees) were contacted by telephone about the status of their knee(s), and all 8 completed and returned the minimum 5-year follow-up WOMAC and SF-36 forms; they did not return for their minimum 5-year clinical or radiographic evaluations.
Asymmetric patellae were used in 24 knees, conversion patellae in 64 knees (88 knees total). Forty-nine months after surgery, 1 patella was revised for loosening at its interface with the bone. The 51-year-old active female patient’s asymmetric patella was revised to a conversion patella. The decision to implant another metal-backed device was based on its high density; proper intrusion of acrylic cement would have been questionable. Some early wear was observed on the tibial insert, which was replaced. Sixty-eight months after the revision, the patient was asymptomatic, with a KSS Pain score of 96 and a KSS Function score of 100 (Figure 3). Another revision, for tibial insert exchange only, was performed 48 months after surgery. During this revision, the patella was evaluated and found to be well fixed and functioning normally.
Survivorship of the Duracon metal-backed patella at minimum 5-year follow-up was estimated to be 93.95%, with bounds of 73.61% and 98.74%.
Radiographic analysis revealed no radiolucencies larger than 1 mm (Figure 4). Seventeen 1-mm radiolucencies were recorded: 6 (35.3%) in zone 1, 2 (11.8%) in zone 2, and 9 (52.9%) in zone 4. Twelve (70.6%) of the 17 radiolucencies were in the left knee. Nine radiolucencies were in women and 8 in men. Most (55.6%) of the women’s radiolucencies were in zone 1, and most (75.0%) of the men’s were in zone 4. There were no loose beads other than in the case that was later revised.
KSS, WOMAC, and SF-36 scores and radiographic reviews were used to evaluate effectiveness in accordance with the protocol. At minimum 5-year follow-up, mean KSS Pain score was 94.10 (range, 55-100), and mean KSS Function score was 92.67 (range, 60-100). Mean WOMAC score was 2.21 (range, 0-19.70), mean SF-36 Physical score was 83.65 (range, 30.70-100), and mean SF-36 Mental score was 89.41 (range, 1.4-100).
The preceding calculations do not include WOMAC and SF-36 data for the 8 patients (8 knees) who were counted as lost to follow-up but who submitted minimum 5-year follow-up data. We compared these 8 patients with the 60 patients (74 knees) who had complete WOMAC and SF-36 data at the end of the study in order to determine whether there were any statistically significant differences between the 2 groups’ mean scores. No statistically significant differences were detected in any WOMAC or SF-36 category (α = 0.05).
Discussion
Metal-backed patellar components were originally designed to address the shortcomings (eg, fracture, deformation, aseptic loosening) of cemented all-polyethylene patellae.1-3 It was thought that the stiffness of the metal could help resist polyethylene deformation and that the press-fit interface with bone might eliminate issues related to bone cement.8 However, short-term failures were reported with early metal-backed designs.9,10 At the same time, good fixation with bone ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9-12,17 Further, reports of poor outcomes with some metal-backed patella designs overshadowed reports of positive outcomes.2,3 In all reports (of both poor and positive outcomes), component design, patellar tracking, and surgical technique were cited as contributing to implant success.2,3,14,17,18 Subsequent design improvements (eg, use of a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15
Our early results are similar to those reported in the literature, and we observed markedly better outcomes that we think resulted from component design improvements. Over the past decade, this has been particularly true with our use of the Duracon metal-backed patella, which has thicker polyethylene, better articular conformity, and a third stabilizing peg, all of which were previously noted as contributing to a successful metal-backed patellar component.2,12,14,15,19 In our study, all 72 knees radiographically evaluated and independently reviewed at minimum 5-year follow-up had well-fixed press-fit metal-backed patellae. Seventeen patellae had 1-mm radiolucencies; the other 59 had no radiolucencies in any zone around the patella–bone interface.
One of the most important aspects of removing a metal-backed patellar component from a patella is that the remaining bone stock is often far superior to the stock available after revision of a cemented patella. Careful removal should leave an excellent bony bed for reimplantation.
We think that surgeons should adhere to certain indications and contraindications when implanting metal-backed patellae and that doing so can contribute to successful outcomes. Type of bone stock available should be considered, as successful biological fixation relies on a good blood supply. A dense (or thin) patella in which intrusion of acrylic cement is improbable or impossible may favor use of a metal-backed patella. Cement is not an adhesive but a grout, so successful cementation requires intrusion of cement into the interstices of the cancellous bone. As adequate intrusion of cement into dense bone is not possible, cementation may not be the best option. Some patellae have failed because of peg “shear-off,”9 likely caused not by failure of peg strength but by failure of cement fixation at the nonpeg interface.20,21 Polyethylene pegs fail when used as the sole method of fixation (they were never designed for that). In addition, we think younger patients are often indicated for a metal-backed patella because, over the long term, loosening of a cemented patella (and the accompanying stress shielding and osteolysis) may cause severe patellar bone destruction. Last, we have found that abnormally high or small patellae are not good candidates for cement fixation because they tend to work themselves loose riding on and off the superior flange. These types of patellae appear to have a much sturdier and longer lasting interface than cement, once biological fixation has occurred.
In summary, we think the indications for a metal-backed implant are a patella that is dense or sclerotic; a patella that is thin, abnormally high, or small; and a younger patient. In addition, a metal-backed implant is not indicated for soft, osteoporotic bone.
This study had a few limitations. Fourteen knees (14 patients), or 15.9% of all knees in the study, were categorized as lost to follow-up. Comparing the WOMAC and SF-36 scores of 8 patients (8 knees) who completed minimum 5-year follow-up but were not clinically evaluated with the scores of patients who had complete data, we found no statistically significant differences in any category. However, 5-year follow-up clinical data were available for those 8 patients. Nevertheless, 74 knees were available for radiologic evaluation, and during telephone interviews all 8 patients indicated they had their original implant(s) and were asymptomatic.
Our experience with the Duracon metal-backed patella has been encouraging. In the study reported here, there were no failures caused by dissociation of plastic. We think that, because the porous coating is under almost constant compression, biological fixation is likely in most instances, as observed in our minimum 5-year radiologic results. Given our minimum 5-year follow-up results with uncemented metal-backed patellae, we think their use may be a viable alternative to use of all-polyethylene patellae.
1. Firestone TP, Teeny SM, Krackow KA, Hungerford DS. The clinical and roentgenographic results of cementless porous-coated patellar fixation. Clin Orthop Relat Res. 1991;273:184-189.
2. Laskin RS, Bucknell A. The use of metal-backed patellar prostheses in total knee arthroplasty. Clin Orthop Relat Res. 1990;260:52-55.
3. Evanich CJ, Tkach TK, von Glinski S, Camargo MP, Hofmann AA. 6- to 10-year experience using countersunk metal-backed patellas. J Arthroplasty. 1997;12(2):149-154.
4. Schwartz AJ, Della Vale CJ, Rosenberg AG, Jacobs JJ, Berger RA, Galante JO. Cruciate-retaining TKA using a third-generation system with a four-pegged tibial component: a minimum 10-year followup note. Clin Orthop Relat Res. 2010;468(8):2160-2167.
5. Bisschop R, Brouwer RW, Van Raay JJ. Total knee arthroplasty in younger patients: a 13-year follow-up study. Orthopedics. 2010;33(12):876-880.
6. Dixon MC, Brown RR, Parsch D, Scott RD. Modular fixed-bearing total knee arthroplasty with retention of the posterior cruciate ligament. A study of patients followed for a minimum of fifteen years. J Bone Joint Surg Am. 2005;87(3):598-603.
7. Brick GW, Scott RD. The patellofemoral component of total knee arthroplasty. Clin Orthop Relat Res. 1988;231)163-178.
8. Garcia RM, Kraay MJ, Goldberg VM. Isolated all-polyethylene patellar revisions for metal-backed patellar failure. Clin Orthop Relat Res. 2008;466(11):2784-2789.
9. Rosenberg AG, Andriacchi TP, Barden R, Galante JO. Patellar component failure in cementless total knee arthroplasty. Clin Orthop Relat Res. 1988;(236):106-114.
10. Stulberg SD, Stulberg BN, Hamati Y, Tsao A. Failure mechanisms of metal-backed patellar components. Clin Orthop Relat Res. 1988;236:88-105.
11. Sundfeldt M, Johansson CB, Regner L, Albrektsson T, Carlsson LV. Long-term results of a cementless knee prosthesis with a metal-backed patellar component: clinical and radiological follow-up with histology from retrieved components. J Long Term Eff Med Implants. 2003;13(4):341-354.
12. Kraay MJ, Darr OJ, Salata MJ, Goldberg VM. Outcome of metal-backed cementless patellar components: the effect of implant design. Clin Orthop Relat Res. 2001;392:239-244.
13. Jensen LN, Lund B, Gotfredsen K. Bone growth into a revised porous-coated patellar implant. Acta Orthop Scand. 1990;61(3):213-216.
14. Hsu HP, Walker PS. Wear and deformation of patellar components in total knee arthroplasty. Clin Orthop Relat Res. 1989;246:260-265.
15. Jordan LR, Sorrells RB, Jordan LC, Olivo JL. The long-term results of a metal-backed mobile bearing patella. Clin Orthop Relat Res. 2005;436:111-118.
16. Ewald FC. The Knee Society total knee arthroplasty roentgenographic evaluation and scoring system. Clin Orthop Relat Res. 1989;248:9-12.
17. Bayley JC, Scott RD, Ewald FC, Holmes GB Jr. Failure of the metal-backed patellar component after total knee replacement. J Bone Joint Surg Am. 1988;70(5):668-674.
18. Lombardi AV Jr, Engh GA, Volz RG, Albrigo JL, Brainard BJ. Fracture/dissociation of the polyethylene in metal-backed patellar components in total knee arthroplasty. J Bone Joint Surg Am. 1988;70(5):675-679.
19. Moreland JR. Mechanisms of failure in total knee arthroplasty. Clin Orthop Relat Res. 1988;226:49-64.
20. Francke EI, Lachiewicz PF. Failure of a cemented all-polyethylene patellar component of a press-fit condylar total knee arthroplasty. J Arthroplasty. 2000;15(2):234-237.
21. Stulberg BN, Wright TM, Stoller AP, Mimnaugh KL, Mason JJ. Bilateral patellar component shear failure of highly cross-linked polyethylene components: report of a case and laboratory analysis of failure mechanisms. J Arthroplasty. 2012;27(5):789-796.
The metal-backed patella was originally designed to address the shortcomings of cemented, all-polyethylene patellae: deformation, aseptic loosening, stress fractures of polyethylene, and possible thermal damage from bone cement.1-3 Several long-term studies have found very good outcomes with use of all-polyethylene patellae.4-6 However, complications of using an all-polyethylene patella reportedly accounted for up to half of all knee revisions, and during revision surgery patellar bone stock was often found to have been compromised.7
The intention behind the design of press-fit metal-backed patellae was to address the shortcomings of all-polyethylene patellae by eliminating the need for bone cement and providing stiffness that would help resist polyethylene deformation while decreasing implant–bone interface stresses.8 However, early design iterations of metal-backed patellae demonstrated short-term failures—most commonly, local polyethylene wear damaging the locking mechanism and subsequent dissociation or fracture from the metal baseplate; polyethylene delamination from the metal baseplate; and failure of interface fixation.9,10 On the other hand, good fixation with bony ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9,11-13 Overall, however, negative outcomes reported for metal-backed patellae led many surgeons to abandon these components and return to using cemented all-polyethylene patellae.
Negative outcomes of earlier metal-backed patellae designs have overshadowed reports of positive outcomes achieved with careful attention paid to component design, patellar tracking, and surgical technique.2,3,14 Subsequent design improvements (eg, a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15 The advantages of using a metal-backed patella (eg, uniform load sharing, decreased polyethylene deformation, potential for biological fixation) may be unjustly outweighed by the fear of patellar component failure.3
Our 30-plus years of experience with metal-backed patellar components reflect the evolving effect of component design on outcome. Much as reported elsewhere, we found earlier component failures were caused by poor locking mechanisms, thin polyethylene, poor tracking, and minimal femur contact. Over the past decade, however, our outcomes with Duracon metal-backed patellae (Stryker) have been encouraging. We think these positive outcomes, seen over minimum 5-year follow-up, are largely attributable to the thicker polyethylene and improved articular conformity of this component relative to earlier designs. We have also found it helpful to adhere to certain criteria when implanting metal-backed patellae, and we think adhering to these criteria, along with improved component design, indicates use of press-fit metal-backed patellae. In this article, we report our failure incidence with use of this device at minimum 5-year follow-up.
Materials and Methods
In this single-center study, we performed clinical and independent radiographic reviews of 88 primary press-fit metal-backed patellae with minimum 5-year follow-up. All components were the same design (Duracon metal-backed patella) from the same manufacturer (Stryker).
This study, which began in September 2003, was reviewed and approved by the Western Institutional Review Board (WIRB). Either the investigator (Dr. Hedley) or the clinical study coordinator gave study candidates a full explanation of the study and answered any questions. Patients who still wanted to participate in the study signed WIRB consent forms after their index surgery but before minimum 5-year follow-up.
Device Description
This Duracon patella has a porous-coated cobalt-chromium metal back intended for press-fit fixation, 3 cobalt-chromium porous-coated pegs, and a preassembled polyethylene anterior surface (Figure 1). Four sizes are available to fit the peripheral shape of the resected patella.
This patella has 3 styles: symmetric, asymmetric, and conversion. In this study, we used only the asymmetric and conversion styles. The design of each style incorporates medial/lateral facets intended to conform to the convex intercondylar radii of the femoral component, thereby allowing the patella to ride deeply in the recessed patellofemoral groove. The asymmetric patella is a resurfacing component with a generous polyethylene thickness (4.6 mm at its thinnest) and a larger lateral facet for more bone coverage. The asymmetric patella naturally medializes component placement. The articulating surface of the conversion patella is identical to that of the asymmetric patella. However, the conversion patella allows for exchange of the polyethylene portion of the implant without revising a stable, well-fixed metal baseplate.
Patient Selection
Candidates were recruited from a group of metal-backed patella patients within Dr. Hedley’s medical practice. All candidates had undergone primary total knee arthroplasty and received a Duracon press-fit metal-backed patella. All recruited patients had undergone primary knee arthroplasty at least 5 years before clinical and radiographic evaluation. Patients were included in the study if they had a diagnosis of noninflammatory degenerative joint disease (eg, osteoarthritis, traumatic arthritis, avascular necrosis). Patients with body mass index higher than 40 were excluded from the study.
Surgical Technique
The patella is everted completely or as much as feasible. Debridement is done circumferentially around the patella. Adherent fat and pseudomeniscus are stripped back until the surgeon sees the entry point of the quadriceps tendon fibers above and the patella tendon fibers below. The cut is then made at this level to remove as much bone as needed to restore the normal height of the patella with the implant in place. The cut is usually made by hand—without guides but with the patella stabilized with a towel clip above and below to prevent any movement during the action.
The desired cut must be absolutely planar, and this should be checked by placing the edge of the blade across the interface. Repeated passes with the saw blade are needed if the cut is not 100% planar. Once the cut is made, the patella is sized with the patella sizers and drill guide. After the appropriate size is selected, the patella is drilled with a bit that is slightly undersized from the size of the pegs (1/32 inch smaller than the bit supplied by the manufacturer).
Once the patella is prepared, the rest of the knee arthroplasty is performed. The patella is press-fit as the last component to be inserted.
Radiologic Review
Radiographic analysis was performed by an independent reviewer according to the current Knee Society total knee arthroplasty roentgenographic evaluation and scoring system (Figure 2).16 The reviewer was an orthopedist specializing in hip and knee surgery. Radiographs the reviewer deemed questionable were shown to another independent hip and knee surgeon for validation. In all cases, the second reviewer confirmed the first reviewer’s initial recorded observations.
KSS (Knee Society Scale), WOMAC (Western Ontario and McMaster Universities Arthritis Index), and SF-36 (36-Item Short Form Health Survey) were also used to evaluate effectiveness in this protocol.
Survivorship Calculations
Kaplan-Meier survivorship was determined for all metal-backed patellae. For survival analysis, only knees with radiographic data were included (74 knees). Mean follow-up was 75.8 months (range, 60-105 months).
Seventy-four patients (88 knees) met the study criteria (Table). At minimum 5-year follow-up, complete data were acquired for 59 patients (72 knees). Of the total group, 14 knees did not have radiographic data. Those knees were categorized as lost to follow-up and were excluded from the survivorship analysis. The status of patients enrolled in the study at minimum 5-year follow-up is shown in the Table.
Mann-Whitney U test (nonparametric t test) was used to compare WOMAC and SF-36 scores between the “complete” and the “WOMAC and SF-36 only” data groups.
Statistical Analysis
Kaplan-Meier survivorship probabilities (asymmetric method) were calculated using SAS Version 9.2 (SAS Institute); 95% pointwise confidence limits were used.
The Mann-Whitney U test is a nonparametric analogue to the independent-samples t test. It was used here to compare WOMAC and SF-36 scores of patients with “complete” data with scores of patients with “WOMAC and SF-36 only” data. In either group, for patients who had primary bilateral knee arthroplasty, mean WOMAC and SF-36 scores were used.
Comparisons were made between the unilateral and bilateral knee arthroplasty groups. There were no differences in age, height, or weight (Mann-Whitney U test) or in sex, primary diagnosis, or number of patients lost to follow-up (Fisher exact test). Fisher exact test (vs χ2 test) was used for the contingency table analysis because of small cell sizes (eg, ≤10 females in ‘‘both knees” group), suggesting the unilateral and bilateral patients did not differ in demographics.
For all patient-reported questionnaires, bilateral patients were given the opportunity to note any differences between their knee arthroplasties, but none of these patients made any special notations. We interpreted this to mean that all survey responses from bilateral patients were applicable to both knee arthroplasties.
Results
Seventy-four patients (88 knees) were enrolled in the study: 31 women (41.2%) and 43 men (58.1%). At time of surgery, mean age was 59.7 years (range, 40-86 years), and mean body mass index was 30.6 (range, 19.1-39.6). Eighty-three knees were diagnosed with osteoarthritis, and 5 knees were diagnosed with posttraumatic arthritis. Mean time to follow-up was 74.8 months (range, 60-105 months). Fourteen knees (14 patients) were considered lost to follow-up. However, 8 patients (8 knees) were contacted by telephone about the status of their knee(s), and all 8 completed and returned the minimum 5-year follow-up WOMAC and SF-36 forms; they did not return for their minimum 5-year clinical or radiographic evaluations.
Asymmetric patellae were used in 24 knees, conversion patellae in 64 knees (88 knees total). Forty-nine months after surgery, 1 patella was revised for loosening at its interface with the bone. The 51-year-old active female patient’s asymmetric patella was revised to a conversion patella. The decision to implant another metal-backed device was based on its high density; proper intrusion of acrylic cement would have been questionable. Some early wear was observed on the tibial insert, which was replaced. Sixty-eight months after the revision, the patient was asymptomatic, with a KSS Pain score of 96 and a KSS Function score of 100 (Figure 3). Another revision, for tibial insert exchange only, was performed 48 months after surgery. During this revision, the patella was evaluated and found to be well fixed and functioning normally.
Survivorship of the Duracon metal-backed patella at minimum 5-year follow-up was estimated to be 93.95%, with bounds of 73.61% and 98.74%.
Radiographic analysis revealed no radiolucencies larger than 1 mm (Figure 4). Seventeen 1-mm radiolucencies were recorded: 6 (35.3%) in zone 1, 2 (11.8%) in zone 2, and 9 (52.9%) in zone 4. Twelve (70.6%) of the 17 radiolucencies were in the left knee. Nine radiolucencies were in women and 8 in men. Most (55.6%) of the women’s radiolucencies were in zone 1, and most (75.0%) of the men’s were in zone 4. There were no loose beads other than in the case that was later revised.
KSS, WOMAC, and SF-36 scores and radiographic reviews were used to evaluate effectiveness in accordance with the protocol. At minimum 5-year follow-up, mean KSS Pain score was 94.10 (range, 55-100), and mean KSS Function score was 92.67 (range, 60-100). Mean WOMAC score was 2.21 (range, 0-19.70), mean SF-36 Physical score was 83.65 (range, 30.70-100), and mean SF-36 Mental score was 89.41 (range, 1.4-100).
The preceding calculations do not include WOMAC and SF-36 data for the 8 patients (8 knees) who were counted as lost to follow-up but who submitted minimum 5-year follow-up data. We compared these 8 patients with the 60 patients (74 knees) who had complete WOMAC and SF-36 data at the end of the study in order to determine whether there were any statistically significant differences between the 2 groups’ mean scores. No statistically significant differences were detected in any WOMAC or SF-36 category (α = 0.05).
Discussion
Metal-backed patellar components were originally designed to address the shortcomings (eg, fracture, deformation, aseptic loosening) of cemented all-polyethylene patellae.1-3 It was thought that the stiffness of the metal could help resist polyethylene deformation and that the press-fit interface with bone might eliminate issues related to bone cement.8 However, short-term failures were reported with early metal-backed designs.9,10 At the same time, good fixation with bone ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9-12,17 Further, reports of poor outcomes with some metal-backed patella designs overshadowed reports of positive outcomes.2,3 In all reports (of both poor and positive outcomes), component design, patellar tracking, and surgical technique were cited as contributing to implant success.2,3,14,17,18 Subsequent design improvements (eg, use of a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15
Our early results are similar to those reported in the literature, and we observed markedly better outcomes that we think resulted from component design improvements. Over the past decade, this has been particularly true with our use of the Duracon metal-backed patella, which has thicker polyethylene, better articular conformity, and a third stabilizing peg, all of which were previously noted as contributing to a successful metal-backed patellar component.2,12,14,15,19 In our study, all 72 knees radiographically evaluated and independently reviewed at minimum 5-year follow-up had well-fixed press-fit metal-backed patellae. Seventeen patellae had 1-mm radiolucencies; the other 59 had no radiolucencies in any zone around the patella–bone interface.
One of the most important aspects of removing a metal-backed patellar component from a patella is that the remaining bone stock is often far superior to the stock available after revision of a cemented patella. Careful removal should leave an excellent bony bed for reimplantation.
We think that surgeons should adhere to certain indications and contraindications when implanting metal-backed patellae and that doing so can contribute to successful outcomes. Type of bone stock available should be considered, as successful biological fixation relies on a good blood supply. A dense (or thin) patella in which intrusion of acrylic cement is improbable or impossible may favor use of a metal-backed patella. Cement is not an adhesive but a grout, so successful cementation requires intrusion of cement into the interstices of the cancellous bone. As adequate intrusion of cement into dense bone is not possible, cementation may not be the best option. Some patellae have failed because of peg “shear-off,”9 likely caused not by failure of peg strength but by failure of cement fixation at the nonpeg interface.20,21 Polyethylene pegs fail when used as the sole method of fixation (they were never designed for that). In addition, we think younger patients are often indicated for a metal-backed patella because, over the long term, loosening of a cemented patella (and the accompanying stress shielding and osteolysis) may cause severe patellar bone destruction. Last, we have found that abnormally high or small patellae are not good candidates for cement fixation because they tend to work themselves loose riding on and off the superior flange. These types of patellae appear to have a much sturdier and longer lasting interface than cement, once biological fixation has occurred.
In summary, we think the indications for a metal-backed implant are a patella that is dense or sclerotic; a patella that is thin, abnormally high, or small; and a younger patient. In addition, a metal-backed implant is not indicated for soft, osteoporotic bone.
This study had a few limitations. Fourteen knees (14 patients), or 15.9% of all knees in the study, were categorized as lost to follow-up. Comparing the WOMAC and SF-36 scores of 8 patients (8 knees) who completed minimum 5-year follow-up but were not clinically evaluated with the scores of patients who had complete data, we found no statistically significant differences in any category. However, 5-year follow-up clinical data were available for those 8 patients. Nevertheless, 74 knees were available for radiologic evaluation, and during telephone interviews all 8 patients indicated they had their original implant(s) and were asymptomatic.
Our experience with the Duracon metal-backed patella has been encouraging. In the study reported here, there were no failures caused by dissociation of plastic. We think that, because the porous coating is under almost constant compression, biological fixation is likely in most instances, as observed in our minimum 5-year radiologic results. Given our minimum 5-year follow-up results with uncemented metal-backed patellae, we think their use may be a viable alternative to use of all-polyethylene patellae.
The metal-backed patella was originally designed to address the shortcomings of cemented, all-polyethylene patellae: deformation, aseptic loosening, stress fractures of polyethylene, and possible thermal damage from bone cement.1-3 Several long-term studies have found very good outcomes with use of all-polyethylene patellae.4-6 However, complications of using an all-polyethylene patella reportedly accounted for up to half of all knee revisions, and during revision surgery patellar bone stock was often found to have been compromised.7
The intention behind the design of press-fit metal-backed patellae was to address the shortcomings of all-polyethylene patellae by eliminating the need for bone cement and providing stiffness that would help resist polyethylene deformation while decreasing implant–bone interface stresses.8 However, early design iterations of metal-backed patellae demonstrated short-term failures—most commonly, local polyethylene wear damaging the locking mechanism and subsequent dissociation or fracture from the metal baseplate; polyethylene delamination from the metal baseplate; and failure of interface fixation.9,10 On the other hand, good fixation with bony ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9,11-13 Overall, however, negative outcomes reported for metal-backed patellae led many surgeons to abandon these components and return to using cemented all-polyethylene patellae.
Negative outcomes of earlier metal-backed patellae designs have overshadowed reports of positive outcomes achieved with careful attention paid to component design, patellar tracking, and surgical technique.2,3,14 Subsequent design improvements (eg, a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15 The advantages of using a metal-backed patella (eg, uniform load sharing, decreased polyethylene deformation, potential for biological fixation) may be unjustly outweighed by the fear of patellar component failure.3
Our 30-plus years of experience with metal-backed patellar components reflect the evolving effect of component design on outcome. Much as reported elsewhere, we found earlier component failures were caused by poor locking mechanisms, thin polyethylene, poor tracking, and minimal femur contact. Over the past decade, however, our outcomes with Duracon metal-backed patellae (Stryker) have been encouraging. We think these positive outcomes, seen over minimum 5-year follow-up, are largely attributable to the thicker polyethylene and improved articular conformity of this component relative to earlier designs. We have also found it helpful to adhere to certain criteria when implanting metal-backed patellae, and we think adhering to these criteria, along with improved component design, indicates use of press-fit metal-backed patellae. In this article, we report our failure incidence with use of this device at minimum 5-year follow-up.
Materials and Methods
In this single-center study, we performed clinical and independent radiographic reviews of 88 primary press-fit metal-backed patellae with minimum 5-year follow-up. All components were the same design (Duracon metal-backed patella) from the same manufacturer (Stryker).
This study, which began in September 2003, was reviewed and approved by the Western Institutional Review Board (WIRB). Either the investigator (Dr. Hedley) or the clinical study coordinator gave study candidates a full explanation of the study and answered any questions. Patients who still wanted to participate in the study signed WIRB consent forms after their index surgery but before minimum 5-year follow-up.
Device Description
This Duracon patella has a porous-coated cobalt-chromium metal back intended for press-fit fixation, 3 cobalt-chromium porous-coated pegs, and a preassembled polyethylene anterior surface (Figure 1). Four sizes are available to fit the peripheral shape of the resected patella.
This patella has 3 styles: symmetric, asymmetric, and conversion. In this study, we used only the asymmetric and conversion styles. The design of each style incorporates medial/lateral facets intended to conform to the convex intercondylar radii of the femoral component, thereby allowing the patella to ride deeply in the recessed patellofemoral groove. The asymmetric patella is a resurfacing component with a generous polyethylene thickness (4.6 mm at its thinnest) and a larger lateral facet for more bone coverage. The asymmetric patella naturally medializes component placement. The articulating surface of the conversion patella is identical to that of the asymmetric patella. However, the conversion patella allows for exchange of the polyethylene portion of the implant without revising a stable, well-fixed metal baseplate.
Patient Selection
Candidates were recruited from a group of metal-backed patella patients within Dr. Hedley’s medical practice. All candidates had undergone primary total knee arthroplasty and received a Duracon press-fit metal-backed patella. All recruited patients had undergone primary knee arthroplasty at least 5 years before clinical and radiographic evaluation. Patients were included in the study if they had a diagnosis of noninflammatory degenerative joint disease (eg, osteoarthritis, traumatic arthritis, avascular necrosis). Patients with body mass index higher than 40 were excluded from the study.
Surgical Technique
The patella is everted completely or as much as feasible. Debridement is done circumferentially around the patella. Adherent fat and pseudomeniscus are stripped back until the surgeon sees the entry point of the quadriceps tendon fibers above and the patella tendon fibers below. The cut is then made at this level to remove as much bone as needed to restore the normal height of the patella with the implant in place. The cut is usually made by hand—without guides but with the patella stabilized with a towel clip above and below to prevent any movement during the action.
The desired cut must be absolutely planar, and this should be checked by placing the edge of the blade across the interface. Repeated passes with the saw blade are needed if the cut is not 100% planar. Once the cut is made, the patella is sized with the patella sizers and drill guide. After the appropriate size is selected, the patella is drilled with a bit that is slightly undersized from the size of the pegs (1/32 inch smaller than the bit supplied by the manufacturer).
Once the patella is prepared, the rest of the knee arthroplasty is performed. The patella is press-fit as the last component to be inserted.
Radiologic Review
Radiographic analysis was performed by an independent reviewer according to the current Knee Society total knee arthroplasty roentgenographic evaluation and scoring system (Figure 2).16 The reviewer was an orthopedist specializing in hip and knee surgery. Radiographs the reviewer deemed questionable were shown to another independent hip and knee surgeon for validation. In all cases, the second reviewer confirmed the first reviewer’s initial recorded observations.
KSS (Knee Society Scale), WOMAC (Western Ontario and McMaster Universities Arthritis Index), and SF-36 (36-Item Short Form Health Survey) were also used to evaluate effectiveness in this protocol.
Survivorship Calculations
Kaplan-Meier survivorship was determined for all metal-backed patellae. For survival analysis, only knees with radiographic data were included (74 knees). Mean follow-up was 75.8 months (range, 60-105 months).
Seventy-four patients (88 knees) met the study criteria (Table). At minimum 5-year follow-up, complete data were acquired for 59 patients (72 knees). Of the total group, 14 knees did not have radiographic data. Those knees were categorized as lost to follow-up and were excluded from the survivorship analysis. The status of patients enrolled in the study at minimum 5-year follow-up is shown in the Table.
Mann-Whitney U test (nonparametric t test) was used to compare WOMAC and SF-36 scores between the “complete” and the “WOMAC and SF-36 only” data groups.
Statistical Analysis
Kaplan-Meier survivorship probabilities (asymmetric method) were calculated using SAS Version 9.2 (SAS Institute); 95% pointwise confidence limits were used.
The Mann-Whitney U test is a nonparametric analogue to the independent-samples t test. It was used here to compare WOMAC and SF-36 scores of patients with “complete” data with scores of patients with “WOMAC and SF-36 only” data. In either group, for patients who had primary bilateral knee arthroplasty, mean WOMAC and SF-36 scores were used.
Comparisons were made between the unilateral and bilateral knee arthroplasty groups. There were no differences in age, height, or weight (Mann-Whitney U test) or in sex, primary diagnosis, or number of patients lost to follow-up (Fisher exact test). Fisher exact test (vs χ2 test) was used for the contingency table analysis because of small cell sizes (eg, ≤10 females in ‘‘both knees” group), suggesting the unilateral and bilateral patients did not differ in demographics.
For all patient-reported questionnaires, bilateral patients were given the opportunity to note any differences between their knee arthroplasties, but none of these patients made any special notations. We interpreted this to mean that all survey responses from bilateral patients were applicable to both knee arthroplasties.
Results
Seventy-four patients (88 knees) were enrolled in the study: 31 women (41.2%) and 43 men (58.1%). At time of surgery, mean age was 59.7 years (range, 40-86 years), and mean body mass index was 30.6 (range, 19.1-39.6). Eighty-three knees were diagnosed with osteoarthritis, and 5 knees were diagnosed with posttraumatic arthritis. Mean time to follow-up was 74.8 months (range, 60-105 months). Fourteen knees (14 patients) were considered lost to follow-up. However, 8 patients (8 knees) were contacted by telephone about the status of their knee(s), and all 8 completed and returned the minimum 5-year follow-up WOMAC and SF-36 forms; they did not return for their minimum 5-year clinical or radiographic evaluations.
Asymmetric patellae were used in 24 knees, conversion patellae in 64 knees (88 knees total). Forty-nine months after surgery, 1 patella was revised for loosening at its interface with the bone. The 51-year-old active female patient’s asymmetric patella was revised to a conversion patella. The decision to implant another metal-backed device was based on its high density; proper intrusion of acrylic cement would have been questionable. Some early wear was observed on the tibial insert, which was replaced. Sixty-eight months after the revision, the patient was asymptomatic, with a KSS Pain score of 96 and a KSS Function score of 100 (Figure 3). Another revision, for tibial insert exchange only, was performed 48 months after surgery. During this revision, the patella was evaluated and found to be well fixed and functioning normally.
Survivorship of the Duracon metal-backed patella at minimum 5-year follow-up was estimated to be 93.95%, with bounds of 73.61% and 98.74%.
Radiographic analysis revealed no radiolucencies larger than 1 mm (Figure 4). Seventeen 1-mm radiolucencies were recorded: 6 (35.3%) in zone 1, 2 (11.8%) in zone 2, and 9 (52.9%) in zone 4. Twelve (70.6%) of the 17 radiolucencies were in the left knee. Nine radiolucencies were in women and 8 in men. Most (55.6%) of the women’s radiolucencies were in zone 1, and most (75.0%) of the men’s were in zone 4. There were no loose beads other than in the case that was later revised.
KSS, WOMAC, and SF-36 scores and radiographic reviews were used to evaluate effectiveness in accordance with the protocol. At minimum 5-year follow-up, mean KSS Pain score was 94.10 (range, 55-100), and mean KSS Function score was 92.67 (range, 60-100). Mean WOMAC score was 2.21 (range, 0-19.70), mean SF-36 Physical score was 83.65 (range, 30.70-100), and mean SF-36 Mental score was 89.41 (range, 1.4-100).
The preceding calculations do not include WOMAC and SF-36 data for the 8 patients (8 knees) who were counted as lost to follow-up but who submitted minimum 5-year follow-up data. We compared these 8 patients with the 60 patients (74 knees) who had complete WOMAC and SF-36 data at the end of the study in order to determine whether there were any statistically significant differences between the 2 groups’ mean scores. No statistically significant differences were detected in any WOMAC or SF-36 category (α = 0.05).
Discussion
Metal-backed patellar components were originally designed to address the shortcomings (eg, fracture, deformation, aseptic loosening) of cemented all-polyethylene patellae.1-3 It was thought that the stiffness of the metal could help resist polyethylene deformation and that the press-fit interface with bone might eliminate issues related to bone cement.8 However, short-term failures were reported with early metal-backed designs.9,10 At the same time, good fixation with bone ingrowth was observed in both titanium and cobalt-chromium porous-coated patellae.1,3,9-12,17 Further, reports of poor outcomes with some metal-backed patella designs overshadowed reports of positive outcomes.2,3 In all reports (of both poor and positive outcomes), component design, patellar tracking, and surgical technique were cited as contributing to implant success.2,3,14,17,18 Subsequent design improvements (eg, use of a third stabilizing peg, thicker polyethylene, improved conformity) produced excellent outcomes.8,12,15
Our early results are similar to those reported in the literature, and we observed markedly better outcomes that we think resulted from component design improvements. Over the past decade, this has been particularly true with our use of the Duracon metal-backed patella, which has thicker polyethylene, better articular conformity, and a third stabilizing peg, all of which were previously noted as contributing to a successful metal-backed patellar component.2,12,14,15,19 In our study, all 72 knees radiographically evaluated and independently reviewed at minimum 5-year follow-up had well-fixed press-fit metal-backed patellae. Seventeen patellae had 1-mm radiolucencies; the other 59 had no radiolucencies in any zone around the patella–bone interface.
One of the most important aspects of removing a metal-backed patellar component from a patella is that the remaining bone stock is often far superior to the stock available after revision of a cemented patella. Careful removal should leave an excellent bony bed for reimplantation.
We think that surgeons should adhere to certain indications and contraindications when implanting metal-backed patellae and that doing so can contribute to successful outcomes. Type of bone stock available should be considered, as successful biological fixation relies on a good blood supply. A dense (or thin) patella in which intrusion of acrylic cement is improbable or impossible may favor use of a metal-backed patella. Cement is not an adhesive but a grout, so successful cementation requires intrusion of cement into the interstices of the cancellous bone. As adequate intrusion of cement into dense bone is not possible, cementation may not be the best option. Some patellae have failed because of peg “shear-off,”9 likely caused not by failure of peg strength but by failure of cement fixation at the nonpeg interface.20,21 Polyethylene pegs fail when used as the sole method of fixation (they were never designed for that). In addition, we think younger patients are often indicated for a metal-backed patella because, over the long term, loosening of a cemented patella (and the accompanying stress shielding and osteolysis) may cause severe patellar bone destruction. Last, we have found that abnormally high or small patellae are not good candidates for cement fixation because they tend to work themselves loose riding on and off the superior flange. These types of patellae appear to have a much sturdier and longer lasting interface than cement, once biological fixation has occurred.
In summary, we think the indications for a metal-backed implant are a patella that is dense or sclerotic; a patella that is thin, abnormally high, or small; and a younger patient. In addition, a metal-backed implant is not indicated for soft, osteoporotic bone.
This study had a few limitations. Fourteen knees (14 patients), or 15.9% of all knees in the study, were categorized as lost to follow-up. Comparing the WOMAC and SF-36 scores of 8 patients (8 knees) who completed minimum 5-year follow-up but were not clinically evaluated with the scores of patients who had complete data, we found no statistically significant differences in any category. However, 5-year follow-up clinical data were available for those 8 patients. Nevertheless, 74 knees were available for radiologic evaluation, and during telephone interviews all 8 patients indicated they had their original implant(s) and were asymptomatic.
Our experience with the Duracon metal-backed patella has been encouraging. In the study reported here, there were no failures caused by dissociation of plastic. We think that, because the porous coating is under almost constant compression, biological fixation is likely in most instances, as observed in our minimum 5-year radiologic results. Given our minimum 5-year follow-up results with uncemented metal-backed patellae, we think their use may be a viable alternative to use of all-polyethylene patellae.
1. Firestone TP, Teeny SM, Krackow KA, Hungerford DS. The clinical and roentgenographic results of cementless porous-coated patellar fixation. Clin Orthop Relat Res. 1991;273:184-189.
2. Laskin RS, Bucknell A. The use of metal-backed patellar prostheses in total knee arthroplasty. Clin Orthop Relat Res. 1990;260:52-55.
3. Evanich CJ, Tkach TK, von Glinski S, Camargo MP, Hofmann AA. 6- to 10-year experience using countersunk metal-backed patellas. J Arthroplasty. 1997;12(2):149-154.
4. Schwartz AJ, Della Vale CJ, Rosenberg AG, Jacobs JJ, Berger RA, Galante JO. Cruciate-retaining TKA using a third-generation system with a four-pegged tibial component: a minimum 10-year followup note. Clin Orthop Relat Res. 2010;468(8):2160-2167.
5. Bisschop R, Brouwer RW, Van Raay JJ. Total knee arthroplasty in younger patients: a 13-year follow-up study. Orthopedics. 2010;33(12):876-880.
6. Dixon MC, Brown RR, Parsch D, Scott RD. Modular fixed-bearing total knee arthroplasty with retention of the posterior cruciate ligament. A study of patients followed for a minimum of fifteen years. J Bone Joint Surg Am. 2005;87(3):598-603.
7. Brick GW, Scott RD. The patellofemoral component of total knee arthroplasty. Clin Orthop Relat Res. 1988;231)163-178.
8. Garcia RM, Kraay MJ, Goldberg VM. Isolated all-polyethylene patellar revisions for metal-backed patellar failure. Clin Orthop Relat Res. 2008;466(11):2784-2789.
9. Rosenberg AG, Andriacchi TP, Barden R, Galante JO. Patellar component failure in cementless total knee arthroplasty. Clin Orthop Relat Res. 1988;(236):106-114.
10. Stulberg SD, Stulberg BN, Hamati Y, Tsao A. Failure mechanisms of metal-backed patellar components. Clin Orthop Relat Res. 1988;236:88-105.
11. Sundfeldt M, Johansson CB, Regner L, Albrektsson T, Carlsson LV. Long-term results of a cementless knee prosthesis with a metal-backed patellar component: clinical and radiological follow-up with histology from retrieved components. J Long Term Eff Med Implants. 2003;13(4):341-354.
12. Kraay MJ, Darr OJ, Salata MJ, Goldberg VM. Outcome of metal-backed cementless patellar components: the effect of implant design. Clin Orthop Relat Res. 2001;392:239-244.
13. Jensen LN, Lund B, Gotfredsen K. Bone growth into a revised porous-coated patellar implant. Acta Orthop Scand. 1990;61(3):213-216.
14. Hsu HP, Walker PS. Wear and deformation of patellar components in total knee arthroplasty. Clin Orthop Relat Res. 1989;246:260-265.
15. Jordan LR, Sorrells RB, Jordan LC, Olivo JL. The long-term results of a metal-backed mobile bearing patella. Clin Orthop Relat Res. 2005;436:111-118.
16. Ewald FC. The Knee Society total knee arthroplasty roentgenographic evaluation and scoring system. Clin Orthop Relat Res. 1989;248:9-12.
17. Bayley JC, Scott RD, Ewald FC, Holmes GB Jr. Failure of the metal-backed patellar component after total knee replacement. J Bone Joint Surg Am. 1988;70(5):668-674.
18. Lombardi AV Jr, Engh GA, Volz RG, Albrigo JL, Brainard BJ. Fracture/dissociation of the polyethylene in metal-backed patellar components in total knee arthroplasty. J Bone Joint Surg Am. 1988;70(5):675-679.
19. Moreland JR. Mechanisms of failure in total knee arthroplasty. Clin Orthop Relat Res. 1988;226:49-64.
20. Francke EI, Lachiewicz PF. Failure of a cemented all-polyethylene patellar component of a press-fit condylar total knee arthroplasty. J Arthroplasty. 2000;15(2):234-237.
21. Stulberg BN, Wright TM, Stoller AP, Mimnaugh KL, Mason JJ. Bilateral patellar component shear failure of highly cross-linked polyethylene components: report of a case and laboratory analysis of failure mechanisms. J Arthroplasty. 2012;27(5):789-796.
1. Firestone TP, Teeny SM, Krackow KA, Hungerford DS. The clinical and roentgenographic results of cementless porous-coated patellar fixation. Clin Orthop Relat Res. 1991;273:184-189.
2. Laskin RS, Bucknell A. The use of metal-backed patellar prostheses in total knee arthroplasty. Clin Orthop Relat Res. 1990;260:52-55.
3. Evanich CJ, Tkach TK, von Glinski S, Camargo MP, Hofmann AA. 6- to 10-year experience using countersunk metal-backed patellas. J Arthroplasty. 1997;12(2):149-154.
4. Schwartz AJ, Della Vale CJ, Rosenberg AG, Jacobs JJ, Berger RA, Galante JO. Cruciate-retaining TKA using a third-generation system with a four-pegged tibial component: a minimum 10-year followup note. Clin Orthop Relat Res. 2010;468(8):2160-2167.
5. Bisschop R, Brouwer RW, Van Raay JJ. Total knee arthroplasty in younger patients: a 13-year follow-up study. Orthopedics. 2010;33(12):876-880.
6. Dixon MC, Brown RR, Parsch D, Scott RD. Modular fixed-bearing total knee arthroplasty with retention of the posterior cruciate ligament. A study of patients followed for a minimum of fifteen years. J Bone Joint Surg Am. 2005;87(3):598-603.
7. Brick GW, Scott RD. The patellofemoral component of total knee arthroplasty. Clin Orthop Relat Res. 1988;231)163-178.
8. Garcia RM, Kraay MJ, Goldberg VM. Isolated all-polyethylene patellar revisions for metal-backed patellar failure. Clin Orthop Relat Res. 2008;466(11):2784-2789.
9. Rosenberg AG, Andriacchi TP, Barden R, Galante JO. Patellar component failure in cementless total knee arthroplasty. Clin Orthop Relat Res. 1988;(236):106-114.
10. Stulberg SD, Stulberg BN, Hamati Y, Tsao A. Failure mechanisms of metal-backed patellar components. Clin Orthop Relat Res. 1988;236:88-105.
11. Sundfeldt M, Johansson CB, Regner L, Albrektsson T, Carlsson LV. Long-term results of a cementless knee prosthesis with a metal-backed patellar component: clinical and radiological follow-up with histology from retrieved components. J Long Term Eff Med Implants. 2003;13(4):341-354.
12. Kraay MJ, Darr OJ, Salata MJ, Goldberg VM. Outcome of metal-backed cementless patellar components: the effect of implant design. Clin Orthop Relat Res. 2001;392:239-244.
13. Jensen LN, Lund B, Gotfredsen K. Bone growth into a revised porous-coated patellar implant. Acta Orthop Scand. 1990;61(3):213-216.
14. Hsu HP, Walker PS. Wear and deformation of patellar components in total knee arthroplasty. Clin Orthop Relat Res. 1989;246:260-265.
15. Jordan LR, Sorrells RB, Jordan LC, Olivo JL. The long-term results of a metal-backed mobile bearing patella. Clin Orthop Relat Res. 2005;436:111-118.
16. Ewald FC. The Knee Society total knee arthroplasty roentgenographic evaluation and scoring system. Clin Orthop Relat Res. 1989;248:9-12.
17. Bayley JC, Scott RD, Ewald FC, Holmes GB Jr. Failure of the metal-backed patellar component after total knee replacement. J Bone Joint Surg Am. 1988;70(5):668-674.
18. Lombardi AV Jr, Engh GA, Volz RG, Albrigo JL, Brainard BJ. Fracture/dissociation of the polyethylene in metal-backed patellar components in total knee arthroplasty. J Bone Joint Surg Am. 1988;70(5):675-679.
19. Moreland JR. Mechanisms of failure in total knee arthroplasty. Clin Orthop Relat Res. 1988;226:49-64.
20. Francke EI, Lachiewicz PF. Failure of a cemented all-polyethylene patellar component of a press-fit condylar total knee arthroplasty. J Arthroplasty. 2000;15(2):234-237.
21. Stulberg BN, Wright TM, Stoller AP, Mimnaugh KL, Mason JJ. Bilateral patellar component shear failure of highly cross-linked polyethylene components: report of a case and laboratory analysis of failure mechanisms. J Arthroplasty. 2012;27(5):789-796.
The view from my office: How psychiatry residency programs have changed
As I approach my twentieth year as Residency Program Coordinator in the Department of Psychiatry at Saint Louis University School of Medicine, I’ve been reflecting on the many changes that have occurred: within our residency program; in the requirements that all residency programs must meet to continue as an Accreditation Council for Graduate Medical Education (ACGME)-accredited program; and in the overall scope of psychiatry residency training.
What has changed
During my time as Residency Program Coordinator, I have assisted 5 program directors and 3 associate program directors with day-to-day details of residency training. Our residency program has had couples, and a father and son; some residents even married each other while still in training.
The Electronic Residency Application System was not available until 2001; before that, applicants interested in being invited for an interview with a psychiatry residency program had to mail in their applications for review. This was a time-consuming, tedious process. In addition, residency programs today are required to use the American Board of Psychiatry and Neurology (ABPN) PreCERT credentialing program to verify training—instead of (as in the past) simply submitting a letter to ABPN that detailed the rotations and clinical skills examinations completed.
Residency programs have gone from evaluating residents by using the 6 competencies to the Milestones requirement from ACGME, which is the newest system of measuring residents’ competencies. Every month, the program faculty meets to discuss the progress of 1 of the classes of residents and the residents who are completing an individual self-assessment. Milestone scores for each resident are then reported to ACGME.
At one time, a resident’s files could be stored in a 2-inch binder; now, we need a 4-inch binder to accommodate required documentation! I am relieved—as, I am sure, many other residency program coordinators are—that residency programs are no longer required to prepare a Program Information Form but, instead, perform a self-study and, every 10 years, have a site visit. Last, every academic year, the Residency Program Coordinator is required to enter the incoming residents’ information into the graduate medical education track, ACGME, and PreCERT Web site systems.
Rewards of my position
As Residency Program Coordinator, I’ve had the rewarding experience of meeting physicians from all over the world without having to travel to other countries. Because I have a 3- or 4-year relationship with residents, I serve them in various roles: mentor, mother, confidante, motivator, and friend. As much as the job is rewarding, being the Residency Program Coordinator can, on some days, be overwhelming, particularly because I need to think “out of the box” to streamline decisions and thus avoid conflicts with program rotations and didactic schedules.
As I approach my twentieth year as Residency Program Coordinator in the Department of Psychiatry at Saint Louis University School of Medicine, I’ve been reflecting on the many changes that have occurred: within our residency program; in the requirements that all residency programs must meet to continue as an Accreditation Council for Graduate Medical Education (ACGME)-accredited program; and in the overall scope of psychiatry residency training.
What has changed
During my time as Residency Program Coordinator, I have assisted 5 program directors and 3 associate program directors with day-to-day details of residency training. Our residency program has had couples, and a father and son; some residents even married each other while still in training.
The Electronic Residency Application System was not available until 2001; before that, applicants interested in being invited for an interview with a psychiatry residency program had to mail in their applications for review. This was a time-consuming, tedious process. In addition, residency programs today are required to use the American Board of Psychiatry and Neurology (ABPN) PreCERT credentialing program to verify training—instead of (as in the past) simply submitting a letter to ABPN that detailed the rotations and clinical skills examinations completed.
Residency programs have gone from evaluating residents by using the 6 competencies to the Milestones requirement from ACGME, which is the newest system of measuring residents’ competencies. Every month, the program faculty meets to discuss the progress of 1 of the classes of residents and the residents who are completing an individual self-assessment. Milestone scores for each resident are then reported to ACGME.
At one time, a resident’s files could be stored in a 2-inch binder; now, we need a 4-inch binder to accommodate required documentation! I am relieved—as, I am sure, many other residency program coordinators are—that residency programs are no longer required to prepare a Program Information Form but, instead, perform a self-study and, every 10 years, have a site visit. Last, every academic year, the Residency Program Coordinator is required to enter the incoming residents’ information into the graduate medical education track, ACGME, and PreCERT Web site systems.
Rewards of my position
As Residency Program Coordinator, I’ve had the rewarding experience of meeting physicians from all over the world without having to travel to other countries. Because I have a 3- or 4-year relationship with residents, I serve them in various roles: mentor, mother, confidante, motivator, and friend. As much as the job is rewarding, being the Residency Program Coordinator can, on some days, be overwhelming, particularly because I need to think “out of the box” to streamline decisions and thus avoid conflicts with program rotations and didactic schedules.
As I approach my twentieth year as Residency Program Coordinator in the Department of Psychiatry at Saint Louis University School of Medicine, I’ve been reflecting on the many changes that have occurred: within our residency program; in the requirements that all residency programs must meet to continue as an Accreditation Council for Graduate Medical Education (ACGME)-accredited program; and in the overall scope of psychiatry residency training.
What has changed
During my time as Residency Program Coordinator, I have assisted 5 program directors and 3 associate program directors with day-to-day details of residency training. Our residency program has had couples, and a father and son; some residents even married each other while still in training.
The Electronic Residency Application System was not available until 2001; before that, applicants interested in being invited for an interview with a psychiatry residency program had to mail in their applications for review. This was a time-consuming, tedious process. In addition, residency programs today are required to use the American Board of Psychiatry and Neurology (ABPN) PreCERT credentialing program to verify training—instead of (as in the past) simply submitting a letter to ABPN that detailed the rotations and clinical skills examinations completed.
Residency programs have gone from evaluating residents by using the 6 competencies to the Milestones requirement from ACGME, which is the newest system of measuring residents’ competencies. Every month, the program faculty meets to discuss the progress of 1 of the classes of residents and the residents who are completing an individual self-assessment. Milestone scores for each resident are then reported to ACGME.
At one time, a resident’s files could be stored in a 2-inch binder; now, we need a 4-inch binder to accommodate required documentation! I am relieved—as, I am sure, many other residency program coordinators are—that residency programs are no longer required to prepare a Program Information Form but, instead, perform a self-study and, every 10 years, have a site visit. Last, every academic year, the Residency Program Coordinator is required to enter the incoming residents’ information into the graduate medical education track, ACGME, and PreCERT Web site systems.
Rewards of my position
As Residency Program Coordinator, I’ve had the rewarding experience of meeting physicians from all over the world without having to travel to other countries. Because I have a 3- or 4-year relationship with residents, I serve them in various roles: mentor, mother, confidante, motivator, and friend. As much as the job is rewarding, being the Residency Program Coordinator can, on some days, be overwhelming, particularly because I need to think “out of the box” to streamline decisions and thus avoid conflicts with program rotations and didactic schedules.
Subpectoral Biceps Tenodesis
Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.1 Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.2 Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.1 Neviaser and colleagues3 correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.4
Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.
Examination and Indications
Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.5 Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.
Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.6 Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues7 reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.
Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.8 Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.
Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.
Surgical Technique
When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues9 reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues10 reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.2 We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.
Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.12 Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.1 For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.
No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues15 found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.15
Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.
After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.18 Despite the ease of performing this type of fixation, Mazzocca and colleagues19 found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)20 and soft-tissue tenodesis to the rotator interval or conjoined tendon.21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.
Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues23 and Ozalay and colleagues24 evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues25 compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors26,27 have presented conflicting laboratory data, and Millett and colleagues28 reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.19,23-25,29
Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.
Postoperative Rehabilitation
The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues5 and Mazzocca and colleagues31 recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.
For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.32 For overhead athletes, Werner and colleagues33 advocated a throwing program starting 3 to 4 months after surgery.
Outcomes and Complications
Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes32,34,35 and has a low complication rate.5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues32 found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues28 reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues34 compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.
Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.41 In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues39 found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues28 reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues32 documented 1 fixation failure (2%) 1 year after interference screw fixation.
Werner and colleagues34 encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.37,42 In a recent biomechanical study, however, Euler and colleagues40 found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues37 and Dein and colleagues42 presented case reports of humeral fracture after biceps tenodesis with an interference screw.
For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues43 and Gregory and colleagues44 showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues44 revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues45 performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.
Conclusion
LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.
1. Friedman DJ, Dunn JC, Higgins LD, Warner JJP. Proximal biceps tendon: injuries and management. Sports Med Arthrosc. 2008;16(3):162-169.
2. Nho SJ, Strauss EJ, Lenart BA, et al. Long head of the biceps tendinopathy: diagnosis and management. J Am Acad Orthop Surg. 2010;18(11):645-656.
3. Neviaser TJ, Neviaser RJ, Neviaser JS, Neviaser JS. The four-in-one arthroplasty for the painful arc syndrome. Clin Orthop Relat Res. 1982;163:107-112.
4. Patton WC, McCluskey GM 3rd. Biceps tendinitis and subluxation. Clin Sports Med. 2001;20(3):505-529.
5. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.
6. Bennett WF. Arthroscopic repair of isolated subscapularis tears: a prospective cohort with 2- to 4-year follow-up. Arthroscopy. 2003;19(2):131-143.
7. Dines DM, Warren RF, Inglis AE, Pavlov H. The coracoid impingement syndrome. Bone Joint J Br. 1990;72(2):314-316.
8. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
9. Boileau P, Baqué F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am. 2007;89(4):747-757.
10. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
11. Boileau P, Neyton L. Arthroscopic tenodesis for lesions of the long head of the biceps. Oper Orthop Traumatol. 2005;17(6):601-623.
12. Moon SC, Cho NS, Rhee YG. Analysis of “hidden lesions” of the extra-articular biceps after subpectoral biceps tenodesis: the subpectoral portion as the optimal tenodesis site. Am J Sports Med. 2015;43(1):63-68.
13. Sanders B, Lavery K, Pennington S, Warner JJP. Biceps tendon tenodesis: success with proximal versus distal fixation (SS-16). Arthroscopy. 2008;24(6 suppl):e9.
14. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
15. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
16. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
17. Jarrett CD, McClelland WB, Xerogeanes JW. Minimally invasive proximal biceps tenodesis: an anatomical study for optimal placement and safe surgical technique. J Shoulder Elbow Surg. 2011;20(3):477-480.
18. Mazzocca AD, Noerdlinger MA, Romeo AA. Mini open and subpectoral biceps tenodesis. Oper Tech Sports Med. 2003;11(1):24-31.
19. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
20. Froimson AI, O I. Keyhole tenodesis of biceps origin at the shoulder. Clin Orthop Relat Res. 1975;(112):245-249.
21. Sekiya JK, Elkousy HA, Rodosky MW. Arthroscopic biceps tenodesis using the percutaneous intra-articular transtendon technique. Arthroscopy. 2003;19(10):1137-1141.
22. Verma NN, Drakos M, O’Brien SJ. Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy. 2005;21(6):764.
23. Kilicoglu O, Koyuncu O, Demirhan M, et al. Time-dependent changes in failure loads of 3 biceps tenodesis techniques: in vivo study in a sheep model. Am J Sports Med. 2005;33(10):1536-1544.
24. Ozalay M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
25. Patzer T, Santo G, Olender GD, Wellmann M, Hurschler C, Schofer MD. Suprapectoral or subpectoral position for biceps tenodesis: biomechanical comparison of four different techniques in both positions. J Shoulder Elbow Surg. 2012;21(1):116-125.
26. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
27. Tashjian RZ, Henninger HB. Biomechanical evaluation of subpectoral biceps tenodesis: dual suture anchor versus interference screw fixation. J Shoulder Elbow Surg. 2013;22(10):1408-1412.
28. Millett PJ, Sanders B, Gobezie R, Braun S, Warner JJP. Interference screw vs. suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(1):121.
29. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
30. Slabaugh MA, Frank RM, Van Thiel GS, et al. Biceps tenodesis with interference screw fixation: a biomechanical comparison of screw length and diameter. Arthroscopy. 2011;27(2):161-166.
31. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
32. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
33. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
34. Werner BC, Evans CL, Holzgrefe RE, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of minimum 2-year clinical outcomes. Am J Sports Med. 2014;42(11):2583-2590.
35. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
36. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis: a report of 4 cases. Am J Sports Med. 2013;41(9):2048-2053.
37. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
38. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
39. Abtahi AM, Granger EK, Tashjian RZ. Complications after subpectoral biceps tenodesis using a dual suture anchor technique. Int J Shoulder Surg. 2014;8(2):47-50.
40. Euler SA, Smith SD, Williams BT, Dornan GJ, Millett PJ, Wijdicks CA. Biomechanical analysis of subpectoral biceps tenodesis: effect of screw malpositioning on proximal humeral strength. Am J Sports Med. 2015;43(1):69-74.
41. Carofino BC, Brogan DM, Kircher MF, et al. Iatrogenic nerve injuries during shoulder surgery. J Bone Joint Surg Am. 2013;95(18):1667-1674.
42. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis. Am J Sports Med. 2014;42(4):877-879.
43. Heckman DS, Creighton RA, Romeo AA. Management of failed biceps tenodesis or tenotomy: causation and treatment. Sports Med Arthrosc. 2010;18(3):173-180.
44. Gregory JM, Harwood DP, Gochanour E, Sherman SL, Romeo AA. Clinical outcomes of revision biceps tenodesis. Int J Shoulder Surg. 2012;6(2):45-50.
45. Anthony SG, McCormick F, Gross DJ, Golijanin P, Provencher MT. Biceps tenodesis for long head of the biceps after auto-rupture or failed surgical tenotomy: results in an active population. J Shoulder Elbow Surg. 2015;24(2):e36-e40.
Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.1 Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.2 Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.1 Neviaser and colleagues3 correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.4
Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.
Examination and Indications
Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.5 Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.
Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.6 Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues7 reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.
Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.8 Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.
Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.
Surgical Technique
When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues9 reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues10 reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.2 We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.
Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.12 Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.1 For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.
No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues15 found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.15
Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.
After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.18 Despite the ease of performing this type of fixation, Mazzocca and colleagues19 found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)20 and soft-tissue tenodesis to the rotator interval or conjoined tendon.21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.
Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues23 and Ozalay and colleagues24 evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues25 compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors26,27 have presented conflicting laboratory data, and Millett and colleagues28 reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.19,23-25,29
Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.
Postoperative Rehabilitation
The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues5 and Mazzocca and colleagues31 recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.
For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.32 For overhead athletes, Werner and colleagues33 advocated a throwing program starting 3 to 4 months after surgery.
Outcomes and Complications
Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes32,34,35 and has a low complication rate.5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues32 found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues28 reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues34 compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.
Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.41 In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues39 found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues28 reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues32 documented 1 fixation failure (2%) 1 year after interference screw fixation.
Werner and colleagues34 encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.37,42 In a recent biomechanical study, however, Euler and colleagues40 found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues37 and Dein and colleagues42 presented case reports of humeral fracture after biceps tenodesis with an interference screw.
For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues43 and Gregory and colleagues44 showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues44 revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues45 performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.
Conclusion
LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.
Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.1 Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.2 Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.1 Neviaser and colleagues3 correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.4
Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.
Examination and Indications
Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.5 Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.
Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.6 Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues7 reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.
Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.8 Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.
Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.
Surgical Technique
When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues9 reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues10 reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.2 We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.
Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.12 Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.1 For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.
No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues15 found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.15
Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.
After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.18 Despite the ease of performing this type of fixation, Mazzocca and colleagues19 found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)20 and soft-tissue tenodesis to the rotator interval or conjoined tendon.21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.
Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues23 and Ozalay and colleagues24 evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues25 compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors26,27 have presented conflicting laboratory data, and Millett and colleagues28 reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.19,23-25,29
Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.
Postoperative Rehabilitation
The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues5 and Mazzocca and colleagues31 recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.
For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.32 For overhead athletes, Werner and colleagues33 advocated a throwing program starting 3 to 4 months after surgery.
Outcomes and Complications
Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes32,34,35 and has a low complication rate.5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues32 found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues28 reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues34 compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.
Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.41 In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues39 found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues28 reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues32 documented 1 fixation failure (2%) 1 year after interference screw fixation.
Werner and colleagues34 encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.37,42 In a recent biomechanical study, however, Euler and colleagues40 found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues37 and Dein and colleagues42 presented case reports of humeral fracture after biceps tenodesis with an interference screw.
For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues43 and Gregory and colleagues44 showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues44 revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues45 performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.
Conclusion
LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.
1. Friedman DJ, Dunn JC, Higgins LD, Warner JJP. Proximal biceps tendon: injuries and management. Sports Med Arthrosc. 2008;16(3):162-169.
2. Nho SJ, Strauss EJ, Lenart BA, et al. Long head of the biceps tendinopathy: diagnosis and management. J Am Acad Orthop Surg. 2010;18(11):645-656.
3. Neviaser TJ, Neviaser RJ, Neviaser JS, Neviaser JS. The four-in-one arthroplasty for the painful arc syndrome. Clin Orthop Relat Res. 1982;163:107-112.
4. Patton WC, McCluskey GM 3rd. Biceps tendinitis and subluxation. Clin Sports Med. 2001;20(3):505-529.
5. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.
6. Bennett WF. Arthroscopic repair of isolated subscapularis tears: a prospective cohort with 2- to 4-year follow-up. Arthroscopy. 2003;19(2):131-143.
7. Dines DM, Warren RF, Inglis AE, Pavlov H. The coracoid impingement syndrome. Bone Joint J Br. 1990;72(2):314-316.
8. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
9. Boileau P, Baqué F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am. 2007;89(4):747-757.
10. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
11. Boileau P, Neyton L. Arthroscopic tenodesis for lesions of the long head of the biceps. Oper Orthop Traumatol. 2005;17(6):601-623.
12. Moon SC, Cho NS, Rhee YG. Analysis of “hidden lesions” of the extra-articular biceps after subpectoral biceps tenodesis: the subpectoral portion as the optimal tenodesis site. Am J Sports Med. 2015;43(1):63-68.
13. Sanders B, Lavery K, Pennington S, Warner JJP. Biceps tendon tenodesis: success with proximal versus distal fixation (SS-16). Arthroscopy. 2008;24(6 suppl):e9.
14. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
15. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
16. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
17. Jarrett CD, McClelland WB, Xerogeanes JW. Minimally invasive proximal biceps tenodesis: an anatomical study for optimal placement and safe surgical technique. J Shoulder Elbow Surg. 2011;20(3):477-480.
18. Mazzocca AD, Noerdlinger MA, Romeo AA. Mini open and subpectoral biceps tenodesis. Oper Tech Sports Med. 2003;11(1):24-31.
19. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
20. Froimson AI, O I. Keyhole tenodesis of biceps origin at the shoulder. Clin Orthop Relat Res. 1975;(112):245-249.
21. Sekiya JK, Elkousy HA, Rodosky MW. Arthroscopic biceps tenodesis using the percutaneous intra-articular transtendon technique. Arthroscopy. 2003;19(10):1137-1141.
22. Verma NN, Drakos M, O’Brien SJ. Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy. 2005;21(6):764.
23. Kilicoglu O, Koyuncu O, Demirhan M, et al. Time-dependent changes in failure loads of 3 biceps tenodesis techniques: in vivo study in a sheep model. Am J Sports Med. 2005;33(10):1536-1544.
24. Ozalay M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
25. Patzer T, Santo G, Olender GD, Wellmann M, Hurschler C, Schofer MD. Suprapectoral or subpectoral position for biceps tenodesis: biomechanical comparison of four different techniques in both positions. J Shoulder Elbow Surg. 2012;21(1):116-125.
26. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
27. Tashjian RZ, Henninger HB. Biomechanical evaluation of subpectoral biceps tenodesis: dual suture anchor versus interference screw fixation. J Shoulder Elbow Surg. 2013;22(10):1408-1412.
28. Millett PJ, Sanders B, Gobezie R, Braun S, Warner JJP. Interference screw vs. suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(1):121.
29. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
30. Slabaugh MA, Frank RM, Van Thiel GS, et al. Biceps tenodesis with interference screw fixation: a biomechanical comparison of screw length and diameter. Arthroscopy. 2011;27(2):161-166.
31. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
32. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
33. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
34. Werner BC, Evans CL, Holzgrefe RE, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of minimum 2-year clinical outcomes. Am J Sports Med. 2014;42(11):2583-2590.
35. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
36. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis: a report of 4 cases. Am J Sports Med. 2013;41(9):2048-2053.
37. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
38. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
39. Abtahi AM, Granger EK, Tashjian RZ. Complications after subpectoral biceps tenodesis using a dual suture anchor technique. Int J Shoulder Surg. 2014;8(2):47-50.
40. Euler SA, Smith SD, Williams BT, Dornan GJ, Millett PJ, Wijdicks CA. Biomechanical analysis of subpectoral biceps tenodesis: effect of screw malpositioning on proximal humeral strength. Am J Sports Med. 2015;43(1):69-74.
41. Carofino BC, Brogan DM, Kircher MF, et al. Iatrogenic nerve injuries during shoulder surgery. J Bone Joint Surg Am. 2013;95(18):1667-1674.
42. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis. Am J Sports Med. 2014;42(4):877-879.
43. Heckman DS, Creighton RA, Romeo AA. Management of failed biceps tenodesis or tenotomy: causation and treatment. Sports Med Arthrosc. 2010;18(3):173-180.
44. Gregory JM, Harwood DP, Gochanour E, Sherman SL, Romeo AA. Clinical outcomes of revision biceps tenodesis. Int J Shoulder Surg. 2012;6(2):45-50.
45. Anthony SG, McCormick F, Gross DJ, Golijanin P, Provencher MT. Biceps tenodesis for long head of the biceps after auto-rupture or failed surgical tenotomy: results in an active population. J Shoulder Elbow Surg. 2015;24(2):e36-e40.
1. Friedman DJ, Dunn JC, Higgins LD, Warner JJP. Proximal biceps tendon: injuries and management. Sports Med Arthrosc. 2008;16(3):162-169.
2. Nho SJ, Strauss EJ, Lenart BA, et al. Long head of the biceps tendinopathy: diagnosis and management. J Am Acad Orthop Surg. 2010;18(11):645-656.
3. Neviaser TJ, Neviaser RJ, Neviaser JS, Neviaser JS. The four-in-one arthroplasty for the painful arc syndrome. Clin Orthop Relat Res. 1982;163:107-112.
4. Patton WC, McCluskey GM 3rd. Biceps tendinitis and subluxation. Clin Sports Med. 2001;20(3):505-529.
5. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.
6. Bennett WF. Arthroscopic repair of isolated subscapularis tears: a prospective cohort with 2- to 4-year follow-up. Arthroscopy. 2003;19(2):131-143.
7. Dines DM, Warren RF, Inglis AE, Pavlov H. The coracoid impingement syndrome. Bone Joint J Br. 1990;72(2):314-316.
8. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
9. Boileau P, Baqué F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am. 2007;89(4):747-757.
10. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
11. Boileau P, Neyton L. Arthroscopic tenodesis for lesions of the long head of the biceps. Oper Orthop Traumatol. 2005;17(6):601-623.
12. Moon SC, Cho NS, Rhee YG. Analysis of “hidden lesions” of the extra-articular biceps after subpectoral biceps tenodesis: the subpectoral portion as the optimal tenodesis site. Am J Sports Med. 2015;43(1):63-68.
13. Sanders B, Lavery K, Pennington S, Warner JJP. Biceps tendon tenodesis: success with proximal versus distal fixation (SS-16). Arthroscopy. 2008;24(6 suppl):e9.
14. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
15. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
16. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
17. Jarrett CD, McClelland WB, Xerogeanes JW. Minimally invasive proximal biceps tenodesis: an anatomical study for optimal placement and safe surgical technique. J Shoulder Elbow Surg. 2011;20(3):477-480.
18. Mazzocca AD, Noerdlinger MA, Romeo AA. Mini open and subpectoral biceps tenodesis. Oper Tech Sports Med. 2003;11(1):24-31.
19. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.
20. Froimson AI, O I. Keyhole tenodesis of biceps origin at the shoulder. Clin Orthop Relat Res. 1975;(112):245-249.
21. Sekiya JK, Elkousy HA, Rodosky MW. Arthroscopic biceps tenodesis using the percutaneous intra-articular transtendon technique. Arthroscopy. 2003;19(10):1137-1141.
22. Verma NN, Drakos M, O’Brien SJ. Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy. 2005;21(6):764.
23. Kilicoglu O, Koyuncu O, Demirhan M, et al. Time-dependent changes in failure loads of 3 biceps tenodesis techniques: in vivo study in a sheep model. Am J Sports Med. 2005;33(10):1536-1544.
24. Ozalay M, Akpinar S, Karaeminogullari O, et al. Mechanical strength of four different biceps tenodesis techniques. Arthroscopy. 2005;21(8):992-998.
25. Patzer T, Santo G, Olender GD, Wellmann M, Hurschler C, Schofer MD. Suprapectoral or subpectoral position for biceps tenodesis: biomechanical comparison of four different techniques in both positions. J Shoulder Elbow Surg. 2012;21(1):116-125.
26. Buchholz A, Martetschläger F, Siebenlist S, et al. Biomechanical comparison of intramedullary cortical button fixation and interference screw technique for subpectoral biceps tenodesis. Arthroscopy. 2013;29(5):845-853.
27. Tashjian RZ, Henninger HB. Biomechanical evaluation of subpectoral biceps tenodesis: dual suture anchor versus interference screw fixation. J Shoulder Elbow Surg. 2013;22(10):1408-1412.
28. Millett PJ, Sanders B, Gobezie R, Braun S, Warner JJP. Interference screw vs. suture anchor fixation for open subpectoral biceps tenodesis: does it matter? BMC Musculoskelet Disord. 2008;9(1):121.
29. Sethi PM, Rajaram A, Beitzel K, Hackett TR, Chowaniec DM, Mazzocca AD. Biomechanical performance of subpectoral biceps tenodesis: a comparison of interference screw fixation, cortical button fixation, and interference screw diameter. J Shoulder Elbow Surg. 2013;22(4):451-457.
30. Slabaugh MA, Frank RM, Van Thiel GS, et al. Biceps tenodesis with interference screw fixation: a biomechanical comparison of screw length and diameter. Arthroscopy. 2011;27(2):161-166.
31. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.
32. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
33. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
34. Werner BC, Evans CL, Holzgrefe RE, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of minimum 2-year clinical outcomes. Am J Sports Med. 2014;42(11):2583-2590.
35. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
36. Rhee PC, Spinner RJ, Bishop AT, Shin AY. Iatrogenic brachial plexus injuries associated with open subpectoral biceps tenodesis: a report of 4 cases. Am J Sports Med. 2013;41(9):2048-2053.
37. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
38. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
39. Abtahi AM, Granger EK, Tashjian RZ. Complications after subpectoral biceps tenodesis using a dual suture anchor technique. Int J Shoulder Surg. 2014;8(2):47-50.
40. Euler SA, Smith SD, Williams BT, Dornan GJ, Millett PJ, Wijdicks CA. Biomechanical analysis of subpectoral biceps tenodesis: effect of screw malpositioning on proximal humeral strength. Am J Sports Med. 2015;43(1):69-74.
41. Carofino BC, Brogan DM, Kircher MF, et al. Iatrogenic nerve injuries during shoulder surgery. J Bone Joint Surg Am. 2013;95(18):1667-1674.
42. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis. Am J Sports Med. 2014;42(4):877-879.
43. Heckman DS, Creighton RA, Romeo AA. Management of failed biceps tenodesis or tenotomy: causation and treatment. Sports Med Arthrosc. 2010;18(3):173-180.
44. Gregory JM, Harwood DP, Gochanour E, Sherman SL, Romeo AA. Clinical outcomes of revision biceps tenodesis. Int J Shoulder Surg. 2012;6(2):45-50.
45. Anthony SG, McCormick F, Gross DJ, Golijanin P, Provencher MT. Biceps tenodesis for long head of the biceps after auto-rupture or failed surgical tenotomy: results in an active population. J Shoulder Elbow Surg. 2015;24(2):e36-e40.
