Case: Patient becomes a liability when nonadherant to prescribed tests
MC, a 42-year-old woman (G1P1001), presents for an office visit. As the medical assistant hands you the chart, she says, “Good luck with this one. She yelled at me because you were 20 minutes behind schedule. She didn’t like sitting in the waiting room.” You greet the patient, obtain her medical history, proceed with a physical examination, and outline a management plan. You recall from the chart that you operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the operating room (OR) for a laparotomy to control bleeding. The patient has not brought this up since being discharged from the hospital. 

During the current office visit, the esprit de corps in the consultation room is a bit uncomfortable, and you sense the patient is not happy. You leave the examination room and discuss the management plan with the nurse, who then returns to the patient to review the plan. The patient is unhappy with the battery of tests you have ordered but tells the nurse that she will comply.

One week later the nurse follows up with the patient by phone because she has not obtained the requested lab tests. The nurse reports to you, “She read me the riot act: ‘Why do I need all these tests? They are expensive.’ The patient indicated that she has no understanding as to why the tests were ordered in the first place.” After a discussion with you, the nurse calls the patient back in an effort to clarify her understanding of the need for the tests. The patient hangs up on her in the middle of the conversation.

The office manager tracks you down to discuss this patient. “Enough is enough,” she exclaims. “This patient is harassing the staff. She told the nurse what tests she herself believes are best and that those are the only ones she will comply with.” Your office manager states that this patient is “a liability.”

What are your choices at this point? You have thought about picking up the phone and calling her. You have considered ending her relationship with your practice. You ask yourself again, what is the best approach?

Patients have the legal right to “dismiss” or change health care providers at any time and for almost any reason without notice. But that right is not reciprocal—clinicians have a legal duty not to abandon a patient and an ethical duty to promote continuity of patient care. A clinician may dismiss a patient from his or her practice (other than for a discriminatory reason that violates ethical or legal limitations), but it must be done in the proper way.

We examine the legal, practical, and ethical issues in dismissing a patient, and how to do it without unnecessary risk. In addition, we will look at a new issue that sometimes arises in these circumstances—managed care limitations.
 

Legal and medical issues
Why would you end a clinician−patient relationship?
There are a number of reasons for dismissing a patient, including^1,2:

The legal details vary from state to state, but fortunately there is sufficient similarity that best practices can be determined. The law starts with the proposition that ordinarily professionals may choose their patients or clients. There are limits, however, in state and federal law. A clinician may not discriminate based, for example, on ethnicity, religion, gender, or sexual orientation. In addition, the Americans with Disabilities Act limits the basis for not providing care to a patient.³

Limiting factors when dismissing a patient
Once a patient has been accepted and a professional relationship has begun, the clinician has a duty of continued care and must act reasonably to end the relationship in a way that protects the patient’s well-being. 

Other recognized limitations to the ending of a treatment relationship exist. These are:

Abandonment
The legal and ethical issues are essentially related to “abandonment”—dismissing a patient improperly. Technically, abandonment is a form of negligence (the clinician does not act reasonably to protect the patient’s interests). The Oklahoma Supreme Court put it clearly: “When further medical and/or surgical attention is needed, a physician may terminate the doctor−patient relationship only after giving reasonable notice and affording an ample opportunity for the patient to secure other medical attention from other physicians” (emphasis added).^4–6

How to end a patient relationship
Always send a letter
Two elements must be taken into account when dismissing a patient:

Together, these elements mean that the intention of ending the clinician−patient relationship and the importance of finding an alternative care provider must be clearly communicated to the patient. That communication needs to be in writing—both to get the patient’s attention and as clear proof of what was said.

Some experts suggest that the best process is to have a face-to-face meeting with the patient followed by a letter. A goal of such a meeting is to make the parting as amicable as possible. It may seem more professional for a clinician to communicate such an important matter in person. The risk is that it may become a confrontation that exacerbates the situation because one or both parties may have some built-up emotion. It, therefore, depends on the circumstances as to whether such a meeting is desirable. Even if there is an oral conversation, it must be followed up with a letter to the patient.

A reasonable time frame to give the patient to find another clinician is commonly a maximum of 30 days of follow-up and emergency care. A set period of time may be a legitimate starting point but it needs to be adjusted in lieu of special circumstances, such as the availability of other similar specialists in the vicinity who are taking new patients or managed care complications. A specific time period should be indicated, along with an agreement to provide care during that time period in “emergency” or “urgent” circumstances. Of course, ongoing care also should be continued for a reasonable time (30 days is often reasonable, as mentioned). It may be best to also discuss any specific ongoing issues that should be attended to (such as the recommended tests in our opening case). 

There is disagreement among experts as to whether a general statement of the reasons for ending the care relationship should be included in the letter. The argument for doing so is that, without a stated reason, the patient may call to ask why. The other side of the argument is that it adds an element of accusation; the patient undoubtedly knows what the problem is. Not writing down the reasons seems the better part of valor, especially if there has been an oral conversation.^7,8

The box above provides an example of a letter to a patient (but not a model). Experts agree that the letter should be sent by certified mail with return receipt. Should the patient reject the letter, a regular delivery letter should be sent with full documentation kept in the file of the time and place it was mailed.

Managed care considerations
A consideration of increasing importance is managed care. Before taking any action, ensure that the managed care contract(s) (including federal or state government programs) have provisions concerning patient dismissals. These may be as simple as notifying the organization as to any time limits for care or of the process of dismissal. 

Make sure your staff knows
Your scheduling staff needs to know with clarity the rules for scheduling (or not scheduling) this patient in the future. As a general matter, the better course of action is to allow an appointment if the patient reports that it is an emergency, whether the staff believes it is or not. In such cases it may be good to document to the patient that the emergency care does not constitute reestablishing a regular clinician−patient relationship.

Document everything
The patient’s record, at a minimum, should contain a copy of the letter sent to the patient and a log of any conversations with her about ending the relationship. Keep your own notes concerning the disruption or problems with the patient over time. 

Are there risks of a malpractice lawsuit?
The abandonment claim is, of course, one possibility for a malpractice lawsuit. That is why documentation and careful communication are so important. This is one area in which having legal advice when developing a letter template should be part of the ongoing relationship with a health law attorney. 

There is another malpractice risk illustrated in our hypothetical case. The physician “operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the OR and laparotomy to control bleeding.”  Malpractice claims (as opposed to actual malpractice occurrences) most often arise because of bad communication with patients or when patients feel ignored. The clinician is thus between a rock and a hard place. On one hand, by ending this relationship, the clinician could well precipitate a claim based primarily on the earlier “maloccurrence.” On the other hand, continuing to treat a patient who is resisting care and creating problems with the staff has its own difficulties. It may be time for the health care professional to discuss the matter with an attorney.

Although not present in this hypothetical case, ending a patient relationship because of nonpayment of professional fees is also a touchy situation. It can be one of the other precipitating events for malpractice claims, and calls for special care.

Tread with care
Having to dismiss a patient is almost always a difficult process. The decision neither can be made lightly nor implemented sloppily. Because it is difficult, it calls on professionals to be particularly careful to not cut essential corners.⁹ 

Case: Resolved
You ask the nurse to note the details of her follow-up phone conversation with the patient in the chart. You then call MC to explain the importance of the tests. She says she is unavailable to talk right now, so you ask her to come in for an appointment, free of charge. The patient makes an appointment but does not show.

You send a letter by certified mail describing the medical necessity for the tests and that her lack of adherence and refusal to come to the office have compelled you to end your clinician−patient relationship. You write that she should immediately identify another health care professional and suggest that she contact her managed care organization for assistance. You note that, should there be a medical emergency or urgent care needed in the next 30 days, you will provide that care. You enclose a release of medical records form in the letter.

In the patient’s record you note the details of the phone conversation and ask the office manager to add that the patient was a no show for her appointment. You include a copy of the certified letter and proof of mailing in the chart.

Two weeks later, the office manager reports that she is sending the patient’s records to another physician upon receipt of the release of medical records form from the patient.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Case: Patient becomes a liability when nonadherant to prescribed tests
MC, a 42-year-old woman (G1P1001), presents for an office visit. As the medical assistant hands you the chart, she says, “Good luck with this one. She yelled at me because you were 20 minutes behind schedule. She didn’t like sitting in the waiting room.” You greet the patient, obtain her medical history, proceed with a physical examination, and outline a management plan. You recall from the chart that you operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the operating room (OR) for a laparotomy to control bleeding. The patient has not brought this up since being discharged from the hospital. 

During the current office visit, the esprit de corps in the consultation room is a bit uncomfortable, and you sense the patient is not happy. You leave the examination room and discuss the management plan with the nurse, who then returns to the patient to review the plan. The patient is unhappy with the battery of tests you have ordered but tells the nurse that she will comply.

One week later the nurse follows up with the patient by phone because she has not obtained the requested lab tests. The nurse reports to you, “She read me the riot act: ‘Why do I need all these tests? They are expensive.’ The patient indicated that she has no understanding as to why the tests were ordered in the first place.” After a discussion with you, the nurse calls the patient back in an effort to clarify her understanding of the need for the tests. The patient hangs up on her in the middle of the conversation.

The office manager tracks you down to discuss this patient. “Enough is enough,” she exclaims. “This patient is harassing the staff. She told the nurse what tests she herself believes are best and that those are the only ones she will comply with.” Your office manager states that this patient is “a liability.”

What are your choices at this point? You have thought about picking up the phone and calling her. You have considered ending her relationship with your practice. You ask yourself again, what is the best approach?

Patients have the legal right to “dismiss” or change health care providers at any time and for almost any reason without notice. But that right is not reciprocal—clinicians have a legal duty not to abandon a patient and an ethical duty to promote continuity of patient care. A clinician may dismiss a patient from his or her practice (other than for a discriminatory reason that violates ethical or legal limitations), but it must be done in the proper way.

We examine the legal, practical, and ethical issues in dismissing a patient, and how to do it without unnecessary risk. In addition, we will look at a new issue that sometimes arises in these circumstances—managed care limitations.
 

Legal and medical issues
Why would you end a clinician−patient relationship?
There are a number of reasons for dismissing a patient, including^1,2:

The legal details vary from state to state, but fortunately there is sufficient similarity that best practices can be determined. The law starts with the proposition that ordinarily professionals may choose their patients or clients. There are limits, however, in state and federal law. A clinician may not discriminate based, for example, on ethnicity, religion, gender, or sexual orientation. In addition, the Americans with Disabilities Act limits the basis for not providing care to a patient.³

Limiting factors when dismissing a patient
Once a patient has been accepted and a professional relationship has begun, the clinician has a duty of continued care and must act reasonably to end the relationship in a way that protects the patient’s well-being. 

Other recognized limitations to the ending of a treatment relationship exist. These are:

Abandonment
The legal and ethical issues are essentially related to “abandonment”—dismissing a patient improperly. Technically, abandonment is a form of negligence (the clinician does not act reasonably to protect the patient’s interests). The Oklahoma Supreme Court put it clearly: “When further medical and/or surgical attention is needed, a physician may terminate the doctor−patient relationship only after giving reasonable notice and affording an ample opportunity for the patient to secure other medical attention from other physicians” (emphasis added).^4–6

How to end a patient relationship
Always send a letter
Two elements must be taken into account when dismissing a patient:

Together, these elements mean that the intention of ending the clinician−patient relationship and the importance of finding an alternative care provider must be clearly communicated to the patient. That communication needs to be in writing—both to get the patient’s attention and as clear proof of what was said.

Some experts suggest that the best process is to have a face-to-face meeting with the patient followed by a letter. A goal of such a meeting is to make the parting as amicable as possible. It may seem more professional for a clinician to communicate such an important matter in person. The risk is that it may become a confrontation that exacerbates the situation because one or both parties may have some built-up emotion. It, therefore, depends on the circumstances as to whether such a meeting is desirable. Even if there is an oral conversation, it must be followed up with a letter to the patient.

A reasonable time frame to give the patient to find another clinician is commonly a maximum of 30 days of follow-up and emergency care. A set period of time may be a legitimate starting point but it needs to be adjusted in lieu of special circumstances, such as the availability of other similar specialists in the vicinity who are taking new patients or managed care complications. A specific time period should be indicated, along with an agreement to provide care during that time period in “emergency” or “urgent” circumstances. Of course, ongoing care also should be continued for a reasonable time (30 days is often reasonable, as mentioned). It may be best to also discuss any specific ongoing issues that should be attended to (such as the recommended tests in our opening case). 

There is disagreement among experts as to whether a general statement of the reasons for ending the care relationship should be included in the letter. The argument for doing so is that, without a stated reason, the patient may call to ask why. The other side of the argument is that it adds an element of accusation; the patient undoubtedly knows what the problem is. Not writing down the reasons seems the better part of valor, especially if there has been an oral conversation.^7,8

The box above provides an example of a letter to a patient (but not a model). Experts agree that the letter should be sent by certified mail with return receipt. Should the patient reject the letter, a regular delivery letter should be sent with full documentation kept in the file of the time and place it was mailed.

Managed care considerations
A consideration of increasing importance is managed care. Before taking any action, ensure that the managed care contract(s) (including federal or state government programs) have provisions concerning patient dismissals. These may be as simple as notifying the organization as to any time limits for care or of the process of dismissal. 

Make sure your staff knows
Your scheduling staff needs to know with clarity the rules for scheduling (or not scheduling) this patient in the future. As a general matter, the better course of action is to allow an appointment if the patient reports that it is an emergency, whether the staff believes it is or not. In such cases it may be good to document to the patient that the emergency care does not constitute reestablishing a regular clinician−patient relationship.

Document everything
The patient’s record, at a minimum, should contain a copy of the letter sent to the patient and a log of any conversations with her about ending the relationship. Keep your own notes concerning the disruption or problems with the patient over time. 

Are there risks of a malpractice lawsuit?
The abandonment claim is, of course, one possibility for a malpractice lawsuit. That is why documentation and careful communication are so important. This is one area in which having legal advice when developing a letter template should be part of the ongoing relationship with a health law attorney. 

There is another malpractice risk illustrated in our hypothetical case. The physician “operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the OR and laparotomy to control bleeding.”  Malpractice claims (as opposed to actual malpractice occurrences) most often arise because of bad communication with patients or when patients feel ignored. The clinician is thus between a rock and a hard place. On one hand, by ending this relationship, the clinician could well precipitate a claim based primarily on the earlier “maloccurrence.” On the other hand, continuing to treat a patient who is resisting care and creating problems with the staff has its own difficulties. It may be time for the health care professional to discuss the matter with an attorney.

Although not present in this hypothetical case, ending a patient relationship because of nonpayment of professional fees is also a touchy situation. It can be one of the other precipitating events for malpractice claims, and calls for special care.

Tread with care
Having to dismiss a patient is almost always a difficult process. The decision neither can be made lightly nor implemented sloppily. Because it is difficult, it calls on professionals to be particularly careful to not cut essential corners.⁹ 

Case: Resolved
You ask the nurse to note the details of her follow-up phone conversation with the patient in the chart. You then call MC to explain the importance of the tests. She says she is unavailable to talk right now, so you ask her to come in for an appointment, free of charge. The patient makes an appointment but does not show.

You send a letter by certified mail describing the medical necessity for the tests and that her lack of adherence and refusal to come to the office have compelled you to end your clinician−patient relationship. You write that she should immediately identify another health care professional and suggest that she contact her managed care organization for assistance. You note that, should there be a medical emergency or urgent care needed in the next 30 days, you will provide that care. You enclose a release of medical records form in the letter.

In the patient’s record you note the details of the phone conversation and ask the office manager to add that the patient was a no show for her appointment. You include a copy of the certified letter and proof of mailing in the chart.

Two weeks later, the office manager reports that she is sending the patient’s records to another physician upon receipt of the release of medical records form from the patient.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Case: Patient becomes a liability when nonadherant to prescribed tests
MC, a 42-year-old woman (G1P1001), presents for an office visit. As the medical assistant hands you the chart, she says, “Good luck with this one. She yelled at me because you were 20 minutes behind schedule. She didn’t like sitting in the waiting room.” You greet the patient, obtain her medical history, proceed with a physical examination, and outline a management plan. You recall from the chart that you operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the operating room (OR) for a laparotomy to control bleeding. The patient has not brought this up since being discharged from the hospital. 

During the current office visit, the esprit de corps in the consultation room is a bit uncomfortable, and you sense the patient is not happy. You leave the examination room and discuss the management plan with the nurse, who then returns to the patient to review the plan. The patient is unhappy with the battery of tests you have ordered but tells the nurse that she will comply.

One week later the nurse follows up with the patient by phone because she has not obtained the requested lab tests. The nurse reports to you, “She read me the riot act: ‘Why do I need all these tests? They are expensive.’ The patient indicated that she has no understanding as to why the tests were ordered in the first place.” After a discussion with you, the nurse calls the patient back in an effort to clarify her understanding of the need for the tests. The patient hangs up on her in the middle of the conversation.

The office manager tracks you down to discuss this patient. “Enough is enough,” she exclaims. “This patient is harassing the staff. She told the nurse what tests she herself believes are best and that those are the only ones she will comply with.” Your office manager states that this patient is “a liability.”

What are your choices at this point? You have thought about picking up the phone and calling her. You have considered ending her relationship with your practice. You ask yourself again, what is the best approach?

Patients have the legal right to “dismiss” or change health care providers at any time and for almost any reason without notice. But that right is not reciprocal—clinicians have a legal duty not to abandon a patient and an ethical duty to promote continuity of patient care. A clinician may dismiss a patient from his or her practice (other than for a discriminatory reason that violates ethical or legal limitations), but it must be done in the proper way.

We examine the legal, practical, and ethical issues in dismissing a patient, and how to do it without unnecessary risk. In addition, we will look at a new issue that sometimes arises in these circumstances—managed care limitations.
 

Legal and medical issues
Why would you end a clinician−patient relationship?
There are a number of reasons for dismissing a patient, including^1,2:

The legal details vary from state to state, but fortunately there is sufficient similarity that best practices can be determined. The law starts with the proposition that ordinarily professionals may choose their patients or clients. There are limits, however, in state and federal law. A clinician may not discriminate based, for example, on ethnicity, religion, gender, or sexual orientation. In addition, the Americans with Disabilities Act limits the basis for not providing care to a patient.³

Limiting factors when dismissing a patient
Once a patient has been accepted and a professional relationship has begun, the clinician has a duty of continued care and must act reasonably to end the relationship in a way that protects the patient’s well-being. 

Other recognized limitations to the ending of a treatment relationship exist. These are:

Abandonment
The legal and ethical issues are essentially related to “abandonment”—dismissing a patient improperly. Technically, abandonment is a form of negligence (the clinician does not act reasonably to protect the patient’s interests). The Oklahoma Supreme Court put it clearly: “When further medical and/or surgical attention is needed, a physician may terminate the doctor−patient relationship only after giving reasonable notice and affording an ample opportunity for the patient to secure other medical attention from other physicians” (emphasis added).^4–6

How to end a patient relationship
Always send a letter
Two elements must be taken into account when dismissing a patient:

Together, these elements mean that the intention of ending the clinician−patient relationship and the importance of finding an alternative care provider must be clearly communicated to the patient. That communication needs to be in writing—both to get the patient’s attention and as clear proof of what was said.

Some experts suggest that the best process is to have a face-to-face meeting with the patient followed by a letter. A goal of such a meeting is to make the parting as amicable as possible. It may seem more professional for a clinician to communicate such an important matter in person. The risk is that it may become a confrontation that exacerbates the situation because one or both parties may have some built-up emotion. It, therefore, depends on the circumstances as to whether such a meeting is desirable. Even if there is an oral conversation, it must be followed up with a letter to the patient.

A reasonable time frame to give the patient to find another clinician is commonly a maximum of 30 days of follow-up and emergency care. A set period of time may be a legitimate starting point but it needs to be adjusted in lieu of special circumstances, such as the availability of other similar specialists in the vicinity who are taking new patients or managed care complications. A specific time period should be indicated, along with an agreement to provide care during that time period in “emergency” or “urgent” circumstances. Of course, ongoing care also should be continued for a reasonable time (30 days is often reasonable, as mentioned). It may be best to also discuss any specific ongoing issues that should be attended to (such as the recommended tests in our opening case). 

There is disagreement among experts as to whether a general statement of the reasons for ending the care relationship should be included in the letter. The argument for doing so is that, without a stated reason, the patient may call to ask why. The other side of the argument is that it adds an element of accusation; the patient undoubtedly knows what the problem is. Not writing down the reasons seems the better part of valor, especially if there has been an oral conversation.^7,8

The box above provides an example of a letter to a patient (but not a model). Experts agree that the letter should be sent by certified mail with return receipt. Should the patient reject the letter, a regular delivery letter should be sent with full documentation kept in the file of the time and place it was mailed.

Managed care considerations
A consideration of increasing importance is managed care. Before taking any action, ensure that the managed care contract(s) (including federal or state government programs) have provisions concerning patient dismissals. These may be as simple as notifying the organization as to any time limits for care or of the process of dismissal. 

Make sure your staff knows
Your scheduling staff needs to know with clarity the rules for scheduling (or not scheduling) this patient in the future. As a general matter, the better course of action is to allow an appointment if the patient reports that it is an emergency, whether the staff believes it is or not. In such cases it may be good to document to the patient that the emergency care does not constitute reestablishing a regular clinician−patient relationship.

Document everything
The patient’s record, at a minimum, should contain a copy of the letter sent to the patient and a log of any conversations with her about ending the relationship. Keep your own notes concerning the disruption or problems with the patient over time. 

Are there risks of a malpractice lawsuit?
The abandonment claim is, of course, one possibility for a malpractice lawsuit. That is why documentation and careful communication are so important. This is one area in which having legal advice when developing a letter template should be part of the ongoing relationship with a health law attorney. 

There is another malpractice risk illustrated in our hypothetical case. The physician “operated on her 8 months ago and there was a complication/maloccurrence in which postoperative bleeding necessitated return to the OR and laparotomy to control bleeding.”  Malpractice claims (as opposed to actual malpractice occurrences) most often arise because of bad communication with patients or when patients feel ignored. The clinician is thus between a rock and a hard place. On one hand, by ending this relationship, the clinician could well precipitate a claim based primarily on the earlier “maloccurrence.” On the other hand, continuing to treat a patient who is resisting care and creating problems with the staff has its own difficulties. It may be time for the health care professional to discuss the matter with an attorney.

Although not present in this hypothetical case, ending a patient relationship because of nonpayment of professional fees is also a touchy situation. It can be one of the other precipitating events for malpractice claims, and calls for special care.

Tread with care
Having to dismiss a patient is almost always a difficult process. The decision neither can be made lightly nor implemented sloppily. Because it is difficult, it calls on professionals to be particularly careful to not cut essential corners.⁹ 

Case: Resolved
You ask the nurse to note the details of her follow-up phone conversation with the patient in the chart. You then call MC to explain the importance of the tests. She says she is unavailable to talk right now, so you ask her to come in for an appointment, free of charge. The patient makes an appointment but does not show.

You send a letter by certified mail describing the medical necessity for the tests and that her lack of adherence and refusal to come to the office have compelled you to end your clinician−patient relationship. You write that she should immediately identify another health care professional and suggest that she contact her managed care organization for assistance. You note that, should there be a medical emergency or urgent care needed in the next 30 days, you will provide that care. You enclose a release of medical records form in the letter.

In the patient’s record you note the details of the phone conversation and ask the office manager to add that the patient was a no show for her appointment. You include a copy of the certified letter and proof of mailing in the chart.

Two weeks later, the office manager reports that she is sending the patient’s records to another physician upon receipt of the release of medical records form from the patient.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Congratulations, OBG Management readers! After years of hard work and collective advocacy on your part, the US Congress finally passed, and President Barack Obama quickly signed into law, a permanent repeal of the Medicare Sustainable Growth Rate (SGR) physician payment system. Yes, celebrations are in order.

The US House of Representatives passed the bill, HR 2, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), sponsored by American College of Obstetricians and Gynecologists (ACOG) Fellow and US Rep. ­Michael ­Burgess (R-TX), on March 26, with 382 Republicans and Democrats voting “Yes.” The Senate followed, on April 14, and agreed with the House to repeal, forever, the Medicare SGR, passing the Burgess bill without amendment, on a bipartisan vote of 92–8. With only hours to go before the scheduled 21.2% cut took effect, the President signed the bill, now Public Law (PL) 114-10, on April 16. The President noted that he was “proud to sign the bill into law.” ACOG is proud to have been such an important part of this landmark moment.

SGR: the perennial nemesis of physicians
The SGR has wreaked havoc on medicine and patient care for 15 years or more. Approximately 30,000 ObGyns participate in Medicare, and many private health insurers use Medicare payment policies, as does TriCare, the nation’s health care coverage for military members and their families. The SGR’s effect was felt widely across medicine, making it nearly impossible for physician practices to invest in health information technology and other patient safety advances, or even to plan for the next year or continue accepting Medicare patients.

When it was introduced last year, HR 2 was supported by more than 600 national and state medical societies and specialty organizations, plus patient and provider organizations, policy think tanks, and advocacy groups across the political spectrum.

ACOG Fellows petitioned their members of Congress with incredible passion, perseverance, and commitment to put an end to the SGR wrecking ball. Hundreds flew into Washington, DC, sent thousands of emails, made phone calls, wrote letters, and personally lobbied at home and in the halls of Congress.

Special kudos, too, to our champions in Congress, and there are many, led by ACOG Fellows and US Reps. Dr. Burgess and Phil Roe, MD (R-TN). Burgess wrote the House bill and, together with Roe, pushed nonstop to get this bill over the finish line. It wouldn’t have happened without them.

ACOG worked tirelessly on its own and in coalition with the American Medical Association, surgical groups, and many other partners. We were able to win important provisions in the statute that we anticipate will greatly help ObGyns successfully transition to this new payment system.

PL114-10 replaces the SGR with a new payment system intended to promote care coordination and quality improvement and lead to better health for our nation’s seniors. Congress developed this new payment plan with the physician community, rather than imposing it on us. That’s why throughout the statute, we see repeated requirements that the Secretary of Health and Human Services must develop quality measures, alternative payment models, and a host of key aspects with input from and in consultation with physicians and the relevant medical specialties, ensuring that physicians retain their preeminent roles in these areas. Funding is provided for quality measure development at $15 million per year from 2015 to 2019.

This law will likely change physician practices more than the ACA ever will, and Congress agreed that physicians should be integral to its development to ensure that they can continue to thrive and provide high-quality care and access for their patients.

Let’s take a closer look at the new Medicare payment system—especially what it will mean for your practice.

What the new law does
Important provisions

MACRA stabilizes the Medicare payment system by permanently repealing the SGR and scheduling payments into the future:

Two payment system options reward continuous quality improvement
Option 1: MIPS. MACRA consolidates and expands pay-for-performance incentives within the old SGR fee-for-service system, creating the new MIPS. Under MIPS, the Physician Quality Reporting System (PQRS), electronic health record (EHR) meaningful use incentive program, and physician value-based modifiers (VBMs) become a single program. In 2019, a physician’s individual score on these measures will be used to adjust his or her Medicare payments, and the penalties previously associated with these programs come to an end.

MACRA creates 4 categories of measures that are weighted to calculate an individual physician’s MIPS score:

Physicians will only be assessed on the categories, measures, and activities that apply to them. A physician’s composite score (0–100) will be compared with a performance threshold that reflects all physicians. Those who score above the threshold will receive increased payments; those who score below the threshold will receive reduced payments. Physicians will know these thresholds in advance and will know the score they must reach to avoid penalties and win higher reimbursements in each performance period.

As physicians as a whole improve their performance, the threshold will move with them. So each year, physicians will have the incentive to keep improving their quality, resource use, clinical improvement, and EHR use. A physician’s payment adjustment in one year will not affect his or her payment adjustment in the next year.

The range of potential payment adjustments based on MIPS performance measures increases each year through 2022. Providers who have high scores are rewarded with a 4% increase in 2019. By 2022, the reward is 9%. The program is budget-neutral, so total positive adjustments across all providers will equal total negative adjustments across all providers to poor performers. Separate funds are set aside to reward the highest performers, who will earn bonuses of up to 10% of their fee-for-service payment rate from 2019 through 2024, as well as to help low performers improve and qualify for increased payments from 2016 through 2020.

Help for physicians includes:

Option 2: APMs. Physicians can earn higher fees by opting out of MIPS fee for service and participating in APMs. The law defines qualifying APMs as those that require participating providers to take on “more than nominal” financial risk, report quality measures, and use certified EHR technology.

APMs will cover multiple services, show that they can limit the growth of spending, and use performance-based methods of compensation. These and other provisions will likely continue the trend away from physicians practicing in solo or small-group fee-for-service practices into risk-based multispecialty settings that are subject to increased management and oversight.

From 2019 to 2024, qualified APM physicians will receive a 5% annual lump sum bonus based on their prior year’s physician fee-schedule payments plus shared savings from participation. This bonus is based on patient volume, not just revenue, to make it easier for ObGyns to qualify. To make the bonus widely available, the Secretary of Health and Human Services must test APMs designed for specific specialties and physicians in small practices. As in MIPS, top APM performers will also receive an additional bonus.

To qualify, physicians must meet increasing thresholds for the percentage of their revenue that they receive through APMs. Those who are below but near the required level of APM revenue can be exempted from MIPS adjustments.

Who pays the bill?
Medicare beneficiaries pay more
The new law increases the percentage of Medicare Parts B and D premiums that high-income beneficiaries must pay beginning in 2018:

This change will affect about 2% of Medicare beneficiaries; half of all Medicare beneficiaries currently have annual incomes below $26,000.¹

Medigap “first-dollar coverage” will end
Many Medigap plans on the market today provide “first-dollar coverage” for beneficiaries, which means that the plans pay the deductibles and copayments so that the beneficiaries have no out-of-pocket costs. Beginning in 2020, Medigap plans will only be available to cover costs above the Medicare Part B deductible, currently $147 per year, for new Medigap enrollees. Many lawmakers thought it was important for Medicare beneficiaries to have “skin in the game.”

The law cuts payments for some providers
To partially offset the cost of repealing the SGR, MACRA cuts Medicare payments to hospitals and postacute providers. It:

The law extends many programs
These programs are vital to support the future ObGyn workforce and access to health care. Among these programs are:

Next steps
It’s very important that ObGyns and other physicians use these early years to understand and get ready for the new payment systems. ACOG is developing educational material for our members, and will work closely with our colleague medical organizations and the Department of Health and Human Services to develop key aspects of the law and ensure that it is properly implemented to work for physicians and patients.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Congratulations, OBG Management readers! After years of hard work and collective advocacy on your part, the US Congress finally passed, and President Barack Obama quickly signed into law, a permanent repeal of the Medicare Sustainable Growth Rate (SGR) physician payment system. Yes, celebrations are in order.

The US House of Representatives passed the bill, HR 2, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), sponsored by American College of Obstetricians and Gynecologists (ACOG) Fellow and US Rep. ­Michael ­Burgess (R-TX), on March 26, with 382 Republicans and Democrats voting “Yes.” The Senate followed, on April 14, and agreed with the House to repeal, forever, the Medicare SGR, passing the Burgess bill without amendment, on a bipartisan vote of 92–8. With only hours to go before the scheduled 21.2% cut took effect, the President signed the bill, now Public Law (PL) 114-10, on April 16. The President noted that he was “proud to sign the bill into law.” ACOG is proud to have been such an important part of this landmark moment.

SGR: the perennial nemesis of physicians
The SGR has wreaked havoc on medicine and patient care for 15 years or more. Approximately 30,000 ObGyns participate in Medicare, and many private health insurers use Medicare payment policies, as does TriCare, the nation’s health care coverage for military members and their families. The SGR’s effect was felt widely across medicine, making it nearly impossible for physician practices to invest in health information technology and other patient safety advances, or even to plan for the next year or continue accepting Medicare patients.

When it was introduced last year, HR 2 was supported by more than 600 national and state medical societies and specialty organizations, plus patient and provider organizations, policy think tanks, and advocacy groups across the political spectrum.

ACOG Fellows petitioned their members of Congress with incredible passion, perseverance, and commitment to put an end to the SGR wrecking ball. Hundreds flew into Washington, DC, sent thousands of emails, made phone calls, wrote letters, and personally lobbied at home and in the halls of Congress.

Special kudos, too, to our champions in Congress, and there are many, led by ACOG Fellows and US Reps. Dr. Burgess and Phil Roe, MD (R-TN). Burgess wrote the House bill and, together with Roe, pushed nonstop to get this bill over the finish line. It wouldn’t have happened without them.

ACOG worked tirelessly on its own and in coalition with the American Medical Association, surgical groups, and many other partners. We were able to win important provisions in the statute that we anticipate will greatly help ObGyns successfully transition to this new payment system.

PL114-10 replaces the SGR with a new payment system intended to promote care coordination and quality improvement and lead to better health for our nation’s seniors. Congress developed this new payment plan with the physician community, rather than imposing it on us. That’s why throughout the statute, we see repeated requirements that the Secretary of Health and Human Services must develop quality measures, alternative payment models, and a host of key aspects with input from and in consultation with physicians and the relevant medical specialties, ensuring that physicians retain their preeminent roles in these areas. Funding is provided for quality measure development at $15 million per year from 2015 to 2019.

This law will likely change physician practices more than the ACA ever will, and Congress agreed that physicians should be integral to its development to ensure that they can continue to thrive and provide high-quality care and access for their patients.

Let’s take a closer look at the new Medicare payment system—especially what it will mean for your practice.

What the new law does
Important provisions

MACRA stabilizes the Medicare payment system by permanently repealing the SGR and scheduling payments into the future:

Two payment system options reward continuous quality improvement
Option 1: MIPS. MACRA consolidates and expands pay-for-performance incentives within the old SGR fee-for-service system, creating the new MIPS. Under MIPS, the Physician Quality Reporting System (PQRS), electronic health record (EHR) meaningful use incentive program, and physician value-based modifiers (VBMs) become a single program. In 2019, a physician’s individual score on these measures will be used to adjust his or her Medicare payments, and the penalties previously associated with these programs come to an end.

MACRA creates 4 categories of measures that are weighted to calculate an individual physician’s MIPS score:

Physicians will only be assessed on the categories, measures, and activities that apply to them. A physician’s composite score (0–100) will be compared with a performance threshold that reflects all physicians. Those who score above the threshold will receive increased payments; those who score below the threshold will receive reduced payments. Physicians will know these thresholds in advance and will know the score they must reach to avoid penalties and win higher reimbursements in each performance period.

As physicians as a whole improve their performance, the threshold will move with them. So each year, physicians will have the incentive to keep improving their quality, resource use, clinical improvement, and EHR use. A physician’s payment adjustment in one year will not affect his or her payment adjustment in the next year.

The range of potential payment adjustments based on MIPS performance measures increases each year through 2022. Providers who have high scores are rewarded with a 4% increase in 2019. By 2022, the reward is 9%. The program is budget-neutral, so total positive adjustments across all providers will equal total negative adjustments across all providers to poor performers. Separate funds are set aside to reward the highest performers, who will earn bonuses of up to 10% of their fee-for-service payment rate from 2019 through 2024, as well as to help low performers improve and qualify for increased payments from 2016 through 2020.

Help for physicians includes:

Option 2: APMs. Physicians can earn higher fees by opting out of MIPS fee for service and participating in APMs. The law defines qualifying APMs as those that require participating providers to take on “more than nominal” financial risk, report quality measures, and use certified EHR technology.

APMs will cover multiple services, show that they can limit the growth of spending, and use performance-based methods of compensation. These and other provisions will likely continue the trend away from physicians practicing in solo or small-group fee-for-service practices into risk-based multispecialty settings that are subject to increased management and oversight.

From 2019 to 2024, qualified APM physicians will receive a 5% annual lump sum bonus based on their prior year’s physician fee-schedule payments plus shared savings from participation. This bonus is based on patient volume, not just revenue, to make it easier for ObGyns to qualify. To make the bonus widely available, the Secretary of Health and Human Services must test APMs designed for specific specialties and physicians in small practices. As in MIPS, top APM performers will also receive an additional bonus.

To qualify, physicians must meet increasing thresholds for the percentage of their revenue that they receive through APMs. Those who are below but near the required level of APM revenue can be exempted from MIPS adjustments.

Who pays the bill?
Medicare beneficiaries pay more
The new law increases the percentage of Medicare Parts B and D premiums that high-income beneficiaries must pay beginning in 2018:

This change will affect about 2% of Medicare beneficiaries; half of all Medicare beneficiaries currently have annual incomes below $26,000.¹

Medigap “first-dollar coverage” will end
Many Medigap plans on the market today provide “first-dollar coverage” for beneficiaries, which means that the plans pay the deductibles and copayments so that the beneficiaries have no out-of-pocket costs. Beginning in 2020, Medigap plans will only be available to cover costs above the Medicare Part B deductible, currently $147 per year, for new Medigap enrollees. Many lawmakers thought it was important for Medicare beneficiaries to have “skin in the game.”

The law cuts payments for some providers
To partially offset the cost of repealing the SGR, MACRA cuts Medicare payments to hospitals and postacute providers. It:

The law extends many programs
These programs are vital to support the future ObGyn workforce and access to health care. Among these programs are:

Next steps
It’s very important that ObGyns and other physicians use these early years to understand and get ready for the new payment systems. ACOG is developing educational material for our members, and will work closely with our colleague medical organizations and the Department of Health and Human Services to develop key aspects of the law and ensure that it is properly implemented to work for physicians and patients.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Congratulations, OBG Management readers! After years of hard work and collective advocacy on your part, the US Congress finally passed, and President Barack Obama quickly signed into law, a permanent repeal of the Medicare Sustainable Growth Rate (SGR) physician payment system. Yes, celebrations are in order.

The US House of Representatives passed the bill, HR 2, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), sponsored by American College of Obstetricians and Gynecologists (ACOG) Fellow and US Rep. ­Michael ­Burgess (R-TX), on March 26, with 382 Republicans and Democrats voting “Yes.” The Senate followed, on April 14, and agreed with the House to repeal, forever, the Medicare SGR, passing the Burgess bill without amendment, on a bipartisan vote of 92–8. With only hours to go before the scheduled 21.2% cut took effect, the President signed the bill, now Public Law (PL) 114-10, on April 16. The President noted that he was “proud to sign the bill into law.” ACOG is proud to have been such an important part of this landmark moment.

SGR: the perennial nemesis of physicians
The SGR has wreaked havoc on medicine and patient care for 15 years or more. Approximately 30,000 ObGyns participate in Medicare, and many private health insurers use Medicare payment policies, as does TriCare, the nation’s health care coverage for military members and their families. The SGR’s effect was felt widely across medicine, making it nearly impossible for physician practices to invest in health information technology and other patient safety advances, or even to plan for the next year or continue accepting Medicare patients.

When it was introduced last year, HR 2 was supported by more than 600 national and state medical societies and specialty organizations, plus patient and provider organizations, policy think tanks, and advocacy groups across the political spectrum.

ACOG Fellows petitioned their members of Congress with incredible passion, perseverance, and commitment to put an end to the SGR wrecking ball. Hundreds flew into Washington, DC, sent thousands of emails, made phone calls, wrote letters, and personally lobbied at home and in the halls of Congress.

Special kudos, too, to our champions in Congress, and there are many, led by ACOG Fellows and US Reps. Dr. Burgess and Phil Roe, MD (R-TN). Burgess wrote the House bill and, together with Roe, pushed nonstop to get this bill over the finish line. It wouldn’t have happened without them.

ACOG worked tirelessly on its own and in coalition with the American Medical Association, surgical groups, and many other partners. We were able to win important provisions in the statute that we anticipate will greatly help ObGyns successfully transition to this new payment system.

PL114-10 replaces the SGR with a new payment system intended to promote care coordination and quality improvement and lead to better health for our nation’s seniors. Congress developed this new payment plan with the physician community, rather than imposing it on us. That’s why throughout the statute, we see repeated requirements that the Secretary of Health and Human Services must develop quality measures, alternative payment models, and a host of key aspects with input from and in consultation with physicians and the relevant medical specialties, ensuring that physicians retain their preeminent roles in these areas. Funding is provided for quality measure development at $15 million per year from 2015 to 2019.

This law will likely change physician practices more than the ACA ever will, and Congress agreed that physicians should be integral to its development to ensure that they can continue to thrive and provide high-quality care and access for their patients.

Let’s take a closer look at the new Medicare payment system—especially what it will mean for your practice.

What the new law does
Important provisions

MACRA stabilizes the Medicare payment system by permanently repealing the SGR and scheduling payments into the future:

Two payment system options reward continuous quality improvement
Option 1: MIPS. MACRA consolidates and expands pay-for-performance incentives within the old SGR fee-for-service system, creating the new MIPS. Under MIPS, the Physician Quality Reporting System (PQRS), electronic health record (EHR) meaningful use incentive program, and physician value-based modifiers (VBMs) become a single program. In 2019, a physician’s individual score on these measures will be used to adjust his or her Medicare payments, and the penalties previously associated with these programs come to an end.

MACRA creates 4 categories of measures that are weighted to calculate an individual physician’s MIPS score:

Physicians will only be assessed on the categories, measures, and activities that apply to them. A physician’s composite score (0–100) will be compared with a performance threshold that reflects all physicians. Those who score above the threshold will receive increased payments; those who score below the threshold will receive reduced payments. Physicians will know these thresholds in advance and will know the score they must reach to avoid penalties and win higher reimbursements in each performance period.

As physicians as a whole improve their performance, the threshold will move with them. So each year, physicians will have the incentive to keep improving their quality, resource use, clinical improvement, and EHR use. A physician’s payment adjustment in one year will not affect his or her payment adjustment in the next year.

The range of potential payment adjustments based on MIPS performance measures increases each year through 2022. Providers who have high scores are rewarded with a 4% increase in 2019. By 2022, the reward is 9%. The program is budget-neutral, so total positive adjustments across all providers will equal total negative adjustments across all providers to poor performers. Separate funds are set aside to reward the highest performers, who will earn bonuses of up to 10% of their fee-for-service payment rate from 2019 through 2024, as well as to help low performers improve and qualify for increased payments from 2016 through 2020.

Help for physicians includes:

Option 2: APMs. Physicians can earn higher fees by opting out of MIPS fee for service and participating in APMs. The law defines qualifying APMs as those that require participating providers to take on “more than nominal” financial risk, report quality measures, and use certified EHR technology.

APMs will cover multiple services, show that they can limit the growth of spending, and use performance-based methods of compensation. These and other provisions will likely continue the trend away from physicians practicing in solo or small-group fee-for-service practices into risk-based multispecialty settings that are subject to increased management and oversight.

From 2019 to 2024, qualified APM physicians will receive a 5% annual lump sum bonus based on their prior year’s physician fee-schedule payments plus shared savings from participation. This bonus is based on patient volume, not just revenue, to make it easier for ObGyns to qualify. To make the bonus widely available, the Secretary of Health and Human Services must test APMs designed for specific specialties and physicians in small practices. As in MIPS, top APM performers will also receive an additional bonus.

To qualify, physicians must meet increasing thresholds for the percentage of their revenue that they receive through APMs. Those who are below but near the required level of APM revenue can be exempted from MIPS adjustments.

Who pays the bill?
Medicare beneficiaries pay more
The new law increases the percentage of Medicare Parts B and D premiums that high-income beneficiaries must pay beginning in 2018:

This change will affect about 2% of Medicare beneficiaries; half of all Medicare beneficiaries currently have annual incomes below $26,000.¹

Medigap “first-dollar coverage” will end
Many Medigap plans on the market today provide “first-dollar coverage” for beneficiaries, which means that the plans pay the deductibles and copayments so that the beneficiaries have no out-of-pocket costs. Beginning in 2020, Medigap plans will only be available to cover costs above the Medicare Part B deductible, currently $147 per year, for new Medigap enrollees. Many lawmakers thought it was important for Medicare beneficiaries to have “skin in the game.”

The law cuts payments for some providers
To partially offset the cost of repealing the SGR, MACRA cuts Medicare payments to hospitals and postacute providers. It:

The law extends many programs
These programs are vital to support the future ObGyn workforce and access to health care. Among these programs are:

Next steps
It’s very important that ObGyns and other physicians use these early years to understand and get ready for the new payment systems. ACOG is developing educational material for our members, and will work closely with our colleague medical organizations and the Department of Health and Human Services to develop key aspects of the law and ensure that it is properly implemented to work for physicians and patients.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Warfarin tablets

Anticoagulant bridge therapy may be harmful for patients with a low to moderate risk of venous thromboembolism (VTE), according to research published in JAMA Internal Medicine.

The study included more than 1000 patients with VTE who had to stop receiving warfarin prior to a procedure.

Investigators compared outcomes in patients who received bridge therapy—a short-acting anticoagulant during the periprocedural period—and patients who did not.

Nathan Clark, PharmD, of Kaiser Permanente Colorado in Aurora, and his colleagues conducted this research.

They examined the electronic medical records of 1178 patients with VTE who underwent 1812 invasive diagnostic or surgical procedures between January 2006 and March 2012 that required the interruption of warfarin.

The investigators divided patients into 3 groups based on their annual risk of VTE recurrence without anticoagulant therapy. Seventy-nine percent of patients were categorized as low-risk, 17.9% as moderate-risk, and 3.1% as high-risk.

The team then divided patients according to the use of bridge therapy. Of the 1812 procedures, 555 included bridge therapy, and 1257 did not.

Patients in the bridged group had a significantly higher incidence of clinically relevant bleeding at 30 days than patients in the non-bridged group—2.7% and 0.2%, respectively (P=0.01).

When the investigators assessed patients according to VTE risk, they found the increased incidence of bleeding in the bridged group was significant among low-risk patients (2.0% vs 0.1%, P<0.001) and moderate-risk patients (4.6% vs 0%, P=0.004) but not high-risk patients (5.6% vs 4.8%, P=0.90).

On the other hand, there was no significant difference in VTE recurrence between the bridged and non-bridged groups—for all risk categories (0 vs 3 cases, P=0.56), low-risk patients (0 vs 2, P=0.37), moderate-risk patients (0 vs 1, P=0.48), or high-risk patients (0 vs 0, P>0.99)

The investigators said further research is needed to identify patient and procedure-related characteristics associated with the highest risk for perioperative VTE recurrence where targeted bridge therapy may be beneficial.

Warfarin tablets

Anticoagulant bridge therapy may be harmful for patients with a low to moderate risk of venous thromboembolism (VTE), according to research published in JAMA Internal Medicine.

The study included more than 1000 patients with VTE who had to stop receiving warfarin prior to a procedure.

Investigators compared outcomes in patients who received bridge therapy—a short-acting anticoagulant during the periprocedural period—and patients who did not.

Nathan Clark, PharmD, of Kaiser Permanente Colorado in Aurora, and his colleagues conducted this research.

They examined the electronic medical records of 1178 patients with VTE who underwent 1812 invasive diagnostic or surgical procedures between January 2006 and March 2012 that required the interruption of warfarin.

The investigators divided patients into 3 groups based on their annual risk of VTE recurrence without anticoagulant therapy. Seventy-nine percent of patients were categorized as low-risk, 17.9% as moderate-risk, and 3.1% as high-risk.

The team then divided patients according to the use of bridge therapy. Of the 1812 procedures, 555 included bridge therapy, and 1257 did not.

Patients in the bridged group had a significantly higher incidence of clinically relevant bleeding at 30 days than patients in the non-bridged group—2.7% and 0.2%, respectively (P=0.01).

When the investigators assessed patients according to VTE risk, they found the increased incidence of bleeding in the bridged group was significant among low-risk patients (2.0% vs 0.1%, P<0.001) and moderate-risk patients (4.6% vs 0%, P=0.004) but not high-risk patients (5.6% vs 4.8%, P=0.90).

On the other hand, there was no significant difference in VTE recurrence between the bridged and non-bridged groups—for all risk categories (0 vs 3 cases, P=0.56), low-risk patients (0 vs 2, P=0.37), moderate-risk patients (0 vs 1, P=0.48), or high-risk patients (0 vs 0, P>0.99)

The investigators said further research is needed to identify patient and procedure-related characteristics associated with the highest risk for perioperative VTE recurrence where targeted bridge therapy may be beneficial.

Warfarin tablets

Anticoagulant bridge therapy may be harmful for patients with a low to moderate risk of venous thromboembolism (VTE), according to research published in JAMA Internal Medicine.

The study included more than 1000 patients with VTE who had to stop receiving warfarin prior to a procedure.

Investigators compared outcomes in patients who received bridge therapy—a short-acting anticoagulant during the periprocedural period—and patients who did not.

Nathan Clark, PharmD, of Kaiser Permanente Colorado in Aurora, and his colleagues conducted this research.

They examined the electronic medical records of 1178 patients with VTE who underwent 1812 invasive diagnostic or surgical procedures between January 2006 and March 2012 that required the interruption of warfarin.

The investigators divided patients into 3 groups based on their annual risk of VTE recurrence without anticoagulant therapy. Seventy-nine percent of patients were categorized as low-risk, 17.9% as moderate-risk, and 3.1% as high-risk.

The team then divided patients according to the use of bridge therapy. Of the 1812 procedures, 555 included bridge therapy, and 1257 did not.

Patients in the bridged group had a significantly higher incidence of clinically relevant bleeding at 30 days than patients in the non-bridged group—2.7% and 0.2%, respectively (P=0.01).

When the investigators assessed patients according to VTE risk, they found the increased incidence of bleeding in the bridged group was significant among low-risk patients (2.0% vs 0.1%, P<0.001) and moderate-risk patients (4.6% vs 0%, P=0.004) but not high-risk patients (5.6% vs 4.8%, P=0.90).

On the other hand, there was no significant difference in VTE recurrence between the bridged and non-bridged groups—for all risk categories (0 vs 3 cases, P=0.56), low-risk patients (0 vs 2, P=0.37), moderate-risk patients (0 vs 1, P=0.48), or high-risk patients (0 vs 0, P>0.99)

The investigators said further research is needed to identify patient and procedure-related characteristics associated with the highest risk for perioperative VTE recurrence where targeted bridge therapy may be beneficial.

Preparation for HSCT

Photo by Chad McNeeley

Research has shown that caring for cancer patients after hematopoietic stem cell transplant (HSCT) can have negative psychological effects on the caregiver, but results of a new study suggest a psychosocial intervention could change that.

The trial showed that counseling sessions focused on stress management could significantly reduce stress, anxiety, depression, and mood disturbance among these caregivers.

“The first 100 days after a stem cell transplant is a critical period for patients, in which caregivers are called upon to deliver around-the-clock care, providing support for patients’ everyday needs and also patients’ emotional health, but who takes care of the caregivers?” asked Mark Laudenslager, PhD, of the University of Colorado Denver.

To address this problem, Dr Laudenslager and his colleagues studied 148 caregivers of patients who underwent allogeneic HSCT. The team described this research in Bone Marrow Transplantation.

The caregivers were randomized to a group that was offered a psychosocial intervention (n=74) and a group that received standard treatment, in which mental health support services were available but not required (n=74).

In the experimental group, caregivers attended 8 sessions on stress management. These one-on-one sessions focused on understanding stress and its physical consequences, changing roles as caregivers, cognitive behavioral stress management, pacing respiration, and identifying social support. The researchers call this intervention PsychoEducation, Paced Respiration and Relaxation (PEPRR).

After a patient underwent HSCT, Dr Laudenslager and his colleagues used several questionnaires to follow the trajectory of caregiver distress over time. The questionnaires were used to measure stress, depression, anxiety, mood disturbance, sleep quality, and other mental health outcomes.

There was no significant difference in stress or other mental health measures between the 2 treatment groups at baseline.

However, at 3 months after transplant, caregivers in the PEPRR group saw some significant improvements over caregivers in the standard treatment group.

The PEPRR group had less stress according to the Perceived Stress Scale (P=0.039), less depression according to the Center for Epidemiologic Studies Depression test (P=0.016), less anxiety according to the State-Trait Anxiety Inventory-State questionnaire (P=0.0009), and less mood disturbance according to the Profile of Mood States-Total Mood Disturbance test (P=0.039).

Overall caregiver distress (composite scores from the questionnaires) was significantly lower in the PEPRR group than the standard treatment group (P=0.019).

However, there was no significant difference in caregiver well-being (composite scores) or scores on the Caregiver Reaction Assessment, Pittsburgh Sleep Quality Index, Short Form 36 Health Survey, or Impact of Events scale.

Still, the other improvements caregivers experienced suggest PEPRR is a promising intervention, Dr Laudenslager said.

He and his colleagues are now recruiting subjects for a follow-up study (NCT02037568) focused on evaluating quality of life in allogeneic HSCT recipients whose caregivers participate in programs similar to the PEPRR intervention.

Preparation for HSCT

Photo by Chad McNeeley

Research has shown that caring for cancer patients after hematopoietic stem cell transplant (HSCT) can have negative psychological effects on the caregiver, but results of a new study suggest a psychosocial intervention could change that.

The trial showed that counseling sessions focused on stress management could significantly reduce stress, anxiety, depression, and mood disturbance among these caregivers.

“The first 100 days after a stem cell transplant is a critical period for patients, in which caregivers are called upon to deliver around-the-clock care, providing support for patients’ everyday needs and also patients’ emotional health, but who takes care of the caregivers?” asked Mark Laudenslager, PhD, of the University of Colorado Denver.

To address this problem, Dr Laudenslager and his colleagues studied 148 caregivers of patients who underwent allogeneic HSCT. The team described this research in Bone Marrow Transplantation.

The caregivers were randomized to a group that was offered a psychosocial intervention (n=74) and a group that received standard treatment, in which mental health support services were available but not required (n=74).

In the experimental group, caregivers attended 8 sessions on stress management. These one-on-one sessions focused on understanding stress and its physical consequences, changing roles as caregivers, cognitive behavioral stress management, pacing respiration, and identifying social support. The researchers call this intervention PsychoEducation, Paced Respiration and Relaxation (PEPRR).

After a patient underwent HSCT, Dr Laudenslager and his colleagues used several questionnaires to follow the trajectory of caregiver distress over time. The questionnaires were used to measure stress, depression, anxiety, mood disturbance, sleep quality, and other mental health outcomes.

There was no significant difference in stress or other mental health measures between the 2 treatment groups at baseline.

However, at 3 months after transplant, caregivers in the PEPRR group saw some significant improvements over caregivers in the standard treatment group.

The PEPRR group had less stress according to the Perceived Stress Scale (P=0.039), less depression according to the Center for Epidemiologic Studies Depression test (P=0.016), less anxiety according to the State-Trait Anxiety Inventory-State questionnaire (P=0.0009), and less mood disturbance according to the Profile of Mood States-Total Mood Disturbance test (P=0.039).

Overall caregiver distress (composite scores from the questionnaires) was significantly lower in the PEPRR group than the standard treatment group (P=0.019).

However, there was no significant difference in caregiver well-being (composite scores) or scores on the Caregiver Reaction Assessment, Pittsburgh Sleep Quality Index, Short Form 36 Health Survey, or Impact of Events scale.

Still, the other improvements caregivers experienced suggest PEPRR is a promising intervention, Dr Laudenslager said.

He and his colleagues are now recruiting subjects for a follow-up study (NCT02037568) focused on evaluating quality of life in allogeneic HSCT recipients whose caregivers participate in programs similar to the PEPRR intervention.

Preparation for HSCT

Photo by Chad McNeeley

Research has shown that caring for cancer patients after hematopoietic stem cell transplant (HSCT) can have negative psychological effects on the caregiver, but results of a new study suggest a psychosocial intervention could change that.

The trial showed that counseling sessions focused on stress management could significantly reduce stress, anxiety, depression, and mood disturbance among these caregivers.

“The first 100 days after a stem cell transplant is a critical period for patients, in which caregivers are called upon to deliver around-the-clock care, providing support for patients’ everyday needs and also patients’ emotional health, but who takes care of the caregivers?” asked Mark Laudenslager, PhD, of the University of Colorado Denver.

To address this problem, Dr Laudenslager and his colleagues studied 148 caregivers of patients who underwent allogeneic HSCT. The team described this research in Bone Marrow Transplantation.

The caregivers were randomized to a group that was offered a psychosocial intervention (n=74) and a group that received standard treatment, in which mental health support services were available but not required (n=74).

In the experimental group, caregivers attended 8 sessions on stress management. These one-on-one sessions focused on understanding stress and its physical consequences, changing roles as caregivers, cognitive behavioral stress management, pacing respiration, and identifying social support. The researchers call this intervention PsychoEducation, Paced Respiration and Relaxation (PEPRR).

After a patient underwent HSCT, Dr Laudenslager and his colleagues used several questionnaires to follow the trajectory of caregiver distress over time. The questionnaires were used to measure stress, depression, anxiety, mood disturbance, sleep quality, and other mental health outcomes.

There was no significant difference in stress or other mental health measures between the 2 treatment groups at baseline.

However, at 3 months after transplant, caregivers in the PEPRR group saw some significant improvements over caregivers in the standard treatment group.

The PEPRR group had less stress according to the Perceived Stress Scale (P=0.039), less depression according to the Center for Epidemiologic Studies Depression test (P=0.016), less anxiety according to the State-Trait Anxiety Inventory-State questionnaire (P=0.0009), and less mood disturbance according to the Profile of Mood States-Total Mood Disturbance test (P=0.039).

Overall caregiver distress (composite scores from the questionnaires) was significantly lower in the PEPRR group than the standard treatment group (P=0.019).

However, there was no significant difference in caregiver well-being (composite scores) or scores on the Caregiver Reaction Assessment, Pittsburgh Sleep Quality Index, Short Form 36 Health Survey, or Impact of Events scale.

Still, the other improvements caregivers experienced suggest PEPRR is a promising intervention, Dr Laudenslager said.

He and his colleagues are now recruiting subjects for a follow-up study (NCT02037568) focused on evaluating quality of life in allogeneic HSCT recipients whose caregivers participate in programs similar to the PEPRR intervention.

Micrograph showing HL

LONDON—Results of a small, phase 1 trial suggest CD30-directed chimeric antigen receptor (CAR) T-cell therapy is feasible in patients with aggressive Hodgkin lymphoma (HL).

The trial included 7 patients with relapsed or refractory HL.

Five of the patients achieved stable disease or better after infusions of CAR T cells, and the researchers said treatment-related adverse events were manageable.

William (Wei) Cao, PhD, of Cellular Biomedicine Group, presented these results at the 10th Annual World Stem Cells & Regenerative Medicine Congress.

The research was funded by Cellular Biomedicine Group, the company developing the CAR T-cell therapy (known as CBM-C30.1), as well as by grants from the National Natural Science Foundation of China and the National Basic Science and Development Program of China.

The trial included 7 patients with progressive HL. Two patients had stage III disease, and 5 had stage IV. The patients had a median of 16 prior treatments (range, 8-24) and limited prognosis (several months to less than 2-year survival) with currently available therapies.

The patients received escalating doses of autologous T cells transduced with a CD30-directed CAR moiety for 3 to 5 days, following a conditioning regimen. The researchers measured the level of CAR transgenes in peripheral blood and biopsied tumor tissues by quantitative PCR.

Two patients achieved a partial response to CAR T-cell therapy, and 3 attained stable disease. So the therapy resulted in an overall disease control rate of 71.4% (5/7) and an objective response rate of 28.6% (2/7).

Stable disease lasted 2 months in 2 of the patients and more than 3.5 months in the third patient. Partial response lasted more than 2 months in 1 patient and more than 3.5 months in the other.

Dr Cao said adverse events consisted largely of fever and were manageable with medical intervention. One patient experienced 5-day self-limiting arthralgia, myalgia, and dual knee swelling 2 weeks after cell infusion. There were no delayed or severe adverse events.

“We are very encouraged by the efficacy and toxicity profile of our CAR-T CD30 technology,” Dr Cao said, “given that the [patients] were diagnosed with stage III and IV Hodgkin’s lymphoma.”

Micrograph showing HL

LONDON—Results of a small, phase 1 trial suggest CD30-directed chimeric antigen receptor (CAR) T-cell therapy is feasible in patients with aggressive Hodgkin lymphoma (HL).

The trial included 7 patients with relapsed or refractory HL.

Five of the patients achieved stable disease or better after infusions of CAR T cells, and the researchers said treatment-related adverse events were manageable.

William (Wei) Cao, PhD, of Cellular Biomedicine Group, presented these results at the 10th Annual World Stem Cells & Regenerative Medicine Congress.

The research was funded by Cellular Biomedicine Group, the company developing the CAR T-cell therapy (known as CBM-C30.1), as well as by grants from the National Natural Science Foundation of China and the National Basic Science and Development Program of China.

The trial included 7 patients with progressive HL. Two patients had stage III disease, and 5 had stage IV. The patients had a median of 16 prior treatments (range, 8-24) and limited prognosis (several months to less than 2-year survival) with currently available therapies.

The patients received escalating doses of autologous T cells transduced with a CD30-directed CAR moiety for 3 to 5 days, following a conditioning regimen. The researchers measured the level of CAR transgenes in peripheral blood and biopsied tumor tissues by quantitative PCR.

Two patients achieved a partial response to CAR T-cell therapy, and 3 attained stable disease. So the therapy resulted in an overall disease control rate of 71.4% (5/7) and an objective response rate of 28.6% (2/7).

Stable disease lasted 2 months in 2 of the patients and more than 3.5 months in the third patient. Partial response lasted more than 2 months in 1 patient and more than 3.5 months in the other.

Dr Cao said adverse events consisted largely of fever and were manageable with medical intervention. One patient experienced 5-day self-limiting arthralgia, myalgia, and dual knee swelling 2 weeks after cell infusion. There were no delayed or severe adverse events.

“We are very encouraged by the efficacy and toxicity profile of our CAR-T CD30 technology,” Dr Cao said, “given that the [patients] were diagnosed with stage III and IV Hodgkin’s lymphoma.”

Micrograph showing HL

LONDON—Results of a small, phase 1 trial suggest CD30-directed chimeric antigen receptor (CAR) T-cell therapy is feasible in patients with aggressive Hodgkin lymphoma (HL).

The trial included 7 patients with relapsed or refractory HL.

Five of the patients achieved stable disease or better after infusions of CAR T cells, and the researchers said treatment-related adverse events were manageable.

William (Wei) Cao, PhD, of Cellular Biomedicine Group, presented these results at the 10th Annual World Stem Cells & Regenerative Medicine Congress.

The research was funded by Cellular Biomedicine Group, the company developing the CAR T-cell therapy (known as CBM-C30.1), as well as by grants from the National Natural Science Foundation of China and the National Basic Science and Development Program of China.

The trial included 7 patients with progressive HL. Two patients had stage III disease, and 5 had stage IV. The patients had a median of 16 prior treatments (range, 8-24) and limited prognosis (several months to less than 2-year survival) with currently available therapies.

The patients received escalating doses of autologous T cells transduced with a CD30-directed CAR moiety for 3 to 5 days, following a conditioning regimen. The researchers measured the level of CAR transgenes in peripheral blood and biopsied tumor tissues by quantitative PCR.

Two patients achieved a partial response to CAR T-cell therapy, and 3 attained stable disease. So the therapy resulted in an overall disease control rate of 71.4% (5/7) and an objective response rate of 28.6% (2/7).

Stable disease lasted 2 months in 2 of the patients and more than 3.5 months in the third patient. Partial response lasted more than 2 months in 1 patient and more than 3.5 months in the other.

Dr Cao said adverse events consisted largely of fever and were manageable with medical intervention. One patient experienced 5-day self-limiting arthralgia, myalgia, and dual knee swelling 2 weeks after cell infusion. There were no delayed or severe adverse events.

“We are very encouraged by the efficacy and toxicity profile of our CAR-T CD30 technology,” Dr Cao said, “given that the [patients] were diagnosed with stage III and IV Hodgkin’s lymphoma.”

Blood for transfusion

Photo by Elise Amendola

A patient blood management (PBM) program can reduce transfusion use, cut costs, and improve outcomes in cardiac surgery patients, according to a single-center study.

A PBM program instituted at Eastern Maine Medical Center (EMMC) in Bangor substantially decreased the use of blood products, the loss of red blood cells, the length of hospital stays, the incidence of acute kidney injury, and direct costs.

Irwin Gross, MD, of EMMC, and his colleagues reported these results in Transfusion.

The team compared clinical and transfusion data from cardiac surgery patients treated at the center before the PBM program began (July 2006-March 2007) and after (April 2007-September 2012).

EMMC’s PBM initiative involved pre- and post-operative anemia management, a more restrictive transfusion threshold, the use of single-unit transfusions when necessary, and other measures.

The researchers analyzed data on 2662 patients, 387 treated before the PBM program began and 2275 treated after.

As expected, the rate of transfusions decreased after the PBM program began. The rate of red blood cell transfusion decreased from 39.3% to 20.8% (P<0.001), the rate of fresh-frozen plasma transfusion decreased from 18.3% to 6.5% (P<0.001), and the rate of platelet transfusion decreased from 17.8% to 9.8% (P<0.001).

Red blood cell loss decreased from a median of 721 mL to 552 mL (P<0.001), and pre-transfusion hemoglobin decreased from a mean of 7.2 ± 1.4 g/dL to 6.6 ± 1.2 g/dL (P<0.001).

Patients saw a decrease in the incidence of post-operative kidney injury from 7.6% to 5.0% (P=0.039) and a decrease in the median length of hospital stay from 10 days to 8 days (P<0.001).

Total adjusted direct costs decreased after the program began as well, falling from a median of $39,709 to $36,906 (P< 0.001).

There was no significant difference in the rate of hospital mortality or the incidence of cerebral vascular accident before and after the PBM program began.

Blood for transfusion

Photo by Elise Amendola

A patient blood management (PBM) program can reduce transfusion use, cut costs, and improve outcomes in cardiac surgery patients, according to a single-center study.

A PBM program instituted at Eastern Maine Medical Center (EMMC) in Bangor substantially decreased the use of blood products, the loss of red blood cells, the length of hospital stays, the incidence of acute kidney injury, and direct costs.

Irwin Gross, MD, of EMMC, and his colleagues reported these results in Transfusion.

The team compared clinical and transfusion data from cardiac surgery patients treated at the center before the PBM program began (July 2006-March 2007) and after (April 2007-September 2012).

EMMC’s PBM initiative involved pre- and post-operative anemia management, a more restrictive transfusion threshold, the use of single-unit transfusions when necessary, and other measures.

The researchers analyzed data on 2662 patients, 387 treated before the PBM program began and 2275 treated after.

As expected, the rate of transfusions decreased after the PBM program began. The rate of red blood cell transfusion decreased from 39.3% to 20.8% (P<0.001), the rate of fresh-frozen plasma transfusion decreased from 18.3% to 6.5% (P<0.001), and the rate of platelet transfusion decreased from 17.8% to 9.8% (P<0.001).

Red blood cell loss decreased from a median of 721 mL to 552 mL (P<0.001), and pre-transfusion hemoglobin decreased from a mean of 7.2 ± 1.4 g/dL to 6.6 ± 1.2 g/dL (P<0.001).

Patients saw a decrease in the incidence of post-operative kidney injury from 7.6% to 5.0% (P=0.039) and a decrease in the median length of hospital stay from 10 days to 8 days (P<0.001).

Total adjusted direct costs decreased after the program began as well, falling from a median of $39,709 to $36,906 (P< 0.001).

There was no significant difference in the rate of hospital mortality or the incidence of cerebral vascular accident before and after the PBM program began.

Blood for transfusion

Photo by Elise Amendola

A patient blood management (PBM) program can reduce transfusion use, cut costs, and improve outcomes in cardiac surgery patients, according to a single-center study.

A PBM program instituted at Eastern Maine Medical Center (EMMC) in Bangor substantially decreased the use of blood products, the loss of red blood cells, the length of hospital stays, the incidence of acute kidney injury, and direct costs.

Irwin Gross, MD, of EMMC, and his colleagues reported these results in Transfusion.

The team compared clinical and transfusion data from cardiac surgery patients treated at the center before the PBM program began (July 2006-March 2007) and after (April 2007-September 2012).

EMMC’s PBM initiative involved pre- and post-operative anemia management, a more restrictive transfusion threshold, the use of single-unit transfusions when necessary, and other measures.

The researchers analyzed data on 2662 patients, 387 treated before the PBM program began and 2275 treated after.

As expected, the rate of transfusions decreased after the PBM program began. The rate of red blood cell transfusion decreased from 39.3% to 20.8% (P<0.001), the rate of fresh-frozen plasma transfusion decreased from 18.3% to 6.5% (P<0.001), and the rate of platelet transfusion decreased from 17.8% to 9.8% (P<0.001).

Red blood cell loss decreased from a median of 721 mL to 552 mL (P<0.001), and pre-transfusion hemoglobin decreased from a mean of 7.2 ± 1.4 g/dL to 6.6 ± 1.2 g/dL (P<0.001).

Patients saw a decrease in the incidence of post-operative kidney injury from 7.6% to 5.0% (P=0.039) and a decrease in the median length of hospital stay from 10 days to 8 days (P<0.001).

Total adjusted direct costs decreased after the program began as well, falling from a median of $39,709 to $36,906 (P< 0.001).

There was no significant difference in the rate of hospital mortality or the incidence of cerebral vascular accident before and after the PBM program began.

Pedicle subtraction osteotomies (PSOs) have been used in the treatment of multiple spinal conditions involving a fixed sagittal imbalance, such as degenerative scoliosis, idiopathic scoliosis, posttraumatic deformities, iatrogenic flatback syndrome, and ankylosing spondylitis. The procedure was first described by Thomasen¹ for the treatment of ankylosing spondylitis. More recently, multiple centers have reported the expanded use and good success of PSO in the treatment of fixed sagittal imbalance of other etiologies.^2,3 According to Bridwell and colleagues,² lumbar lordosis can be increased 34.1°, and sagittal plumb line can be improved 13.5 cm.

PSO is a complex, extensive surgery most often performed in the revision setting. Multiple authors have described the technique for PSO.^4,5 There are significant technical challenges and many complications, including neurologic deficits, pseudarthrosis of adjacent levels, and wound infections.⁶ Short-term challenges include a large loss of blood, 2.4 L on average, according to Bridwell and colleagues.⁶ Time of closure of the osteotomy gap is a crucial point in the surgery. Blood loss, often large, slows only after the gap is closed and stabilized.

In this article, we describe a technique in which an additional rod or pedicle screw construct is used at the periosteotomy levels to close the osteotomy gap during PSO and simplify subsequent instrumentation. In addition, we report our experience with the procedure.

Materials and Methods

Seventeen consecutive patients (mean age, 58 years; range, 12-81 years) with fixed sagittal imbalance were treated with lumbar PSO. The indication in all cases was flatback syndrome after previous spinal surgery. Mean follow-up was 13 months. Mean number of prior surgeries was 3. Thirteen PSOs were performed at L3, and 4 were performed at L2.

Radiographic data were collected from before surgery, in the immediate postoperative period, and at final follow-up. All the radiographs were standing films. Established radiographic parameters were measured: thoracic kyphosis from T5 to T12, lumbar lordosis from L1 to S1, PSO angle (1 level above to 1 level below osteotomy level), sagittal plumb line (from center of C7 body to posterosuperior aspect of S1 body), and coronal plumb line (from center of C7 body to center of S1 body).²

Good clinical outcomes in the treatment of spinal disorders require careful attention to the alignment of the spine in the sagittal plane.^7,8 When evaluating the preoperative radiographs, we measured and documented pelvic parameters. Figure 1A shows how pelvic incidence was determined. We measured this as the angle between a line drawn from the center of the S1 endplate to the center of the femoral head and the perpendicular off the S1 endplate. Figure 1B shows pelvic tilt as determined by the angle between a line drawn from the center of S1 to the femoral head and a vertical line originating from the center of the femoral head. Figure 1C shows the sacral slope, which we measured as the angle between a line drawn parallel to the endplate of S1 and its intersection with a horizontal line.

Surgical Technique

The overall surgical technique for PSO has been well described.^4,5 Here we describe the “outrigger” modification to osteotomy closure (Figures 2, 3).

Most of our 17 cases were revisions. In these cases, new fixation points are first established. All fixation points that will be needed for the final fusion are placed. If a pedicle above or below the osteotomy level is not suitable for a screw, it can be skipped.

Wide decompression of the involved level is performed from pedicle to pedicle, ensuring that the nerve roots are completely decompressed. The dissection is then continued around the lateral wall of the vertebral body. While the neural elements are protected with gentle retraction, the pedicle and a portion of the posterior aspect of the vertebral body are removed with a combination of a rongeur and reverse-angle curettes. Resection of the vertebral body can be facilitated by attaching a short rod to the pedicle screws on either side of the osteotomy level and using it to provide gentle distraction.

Once sufficient bone has been removed to close the osteotomy, short rods are placed in the pedicle screws in the level above and the level below the osteotomy site. These rods are attached with offset connectors that allow the rods to be placed lateral to the screws. Before the surgical procedure is started, the patient is positioned on 2 sets of posts separated by the break in the table. The break in the table allows flexion to accommodate the preoperative kyphosis and allows hyperextension to help close the osteotomy site. Now, with the osteotomy site ready for closure, the table is gradually positioned in extension along with a combination of posterior pressure and compression between the pedicle screws above and below the osteotomy. Once the osteotomy is adequately compressed, the short rods are tightened, holding the osteotomy in good position. With the osteotomy held by the short rods and table positioning, decompression of the neural elements is confirmed and hemostasis obtained.

Final instrumentation is then performed with long rods that can bypass the osteotomized levels, allowing for simpler contouring. If desired, a cross connector can be placed between the long rod of the fusion construct and the short rod holding the osteotomy. The rest of the fusion procedure is completed in standard fashion with at least 1 subfascial drain.

Results

Our 17 patients’ results are summarized in the Table. Mean sagittal plumb line improved from 17.7 cm (range, 5.9 to 29 cm) before surgery to 4.5 cm (range, –0.2 to 12.9 cm) after surgery, for a mean improvement of 13.2 cm. At final follow-up, mean sagittal plumb line was 5.1 cm (range, –1.4 to 10.2 cm).

Mean lumbar lordosis improved from 10° (range, –14° to 34°) before surgery to 49° (range, 36° to 63°) after surgery, for a mean improvement of 39°. Mean PSO angle improved from 3° (range, –36° to 23°) before surgery to 41° (range, 25° to 65°) after surgery, for a mean improvement of 38°. At final follow-up, mean lumbar lordosis remained at 47° (range, 26° to 64°), and mean PSO angle was 39° (range, 24° to 59°).

Mean thoracic kyphosis improved from 18° (range, –8° to 52°) before surgery to 30° (range, 3° to 58°) after surgery, for a mean improvement of 12°. At final follow-up, mean thoracic kyphosis was 31° (range, 2° to 57°).

Fourteen patients did not have complications during the study period. Of the 3 patients with complications, 1 had an early infection, treated effectively with irrigation and débridement and intravenous antibiotics; 1 had a late deep infection, treated with multiple débridements, hardware removal, and, eventually, suppressive antibiotics; and 1 had cauda equina syndrome (caused by extensive scar tissue on the dura, which buckled with restoration of lordosis leading to cord compression), treated with duraplasty, which resulted in full neurologic recovery.

Discussion

In the present series of patients, the described technique for facilitating PSO for correction of sagittal imbalance was effective, and complications were similar to those previously reported.

The benefit of the outrigger construct is that it allows controlled compression of the osteotomy site and can be left in place at time of final instrumentation, locking in compression and correction. Other techniques involve removing the temporary rod and replacing it with final instrumentation^4,5—an extra step that complicates instrumentation of the additional levels of the fusion construct and possibly adds pedicle screw stress and contributes to loosening when the new rod is reduced to the pedicle screw. The final long rod construct can bypass the osteotomy levels and allow for simpler instrumentation.

 Mean age was 58 years in this series versus 52.4 years in the series reported by Bridwell and colleagues.² Given the higher mean age of our patients, though no objective measures of bone quality were available, this technique is likely applicable to patients with poor bone quality.

The complications we have reported are in line with those reported in previous series, and maintenance of radiographic parameters at final follow-up indicates that this osteotomy technique allows for solid fusion constructs.

The outrigger technique for controlling PSO closure is an effective method that simplifies instrumentation during a complex revision case.

Pedicle subtraction osteotomies (PSOs) have been used in the treatment of multiple spinal conditions involving a fixed sagittal imbalance, such as degenerative scoliosis, idiopathic scoliosis, posttraumatic deformities, iatrogenic flatback syndrome, and ankylosing spondylitis. The procedure was first described by Thomasen¹ for the treatment of ankylosing spondylitis. More recently, multiple centers have reported the expanded use and good success of PSO in the treatment of fixed sagittal imbalance of other etiologies.^2,3 According to Bridwell and colleagues,² lumbar lordosis can be increased 34.1°, and sagittal plumb line can be improved 13.5 cm.

PSO is a complex, extensive surgery most often performed in the revision setting. Multiple authors have described the technique for PSO.^4,5 There are significant technical challenges and many complications, including neurologic deficits, pseudarthrosis of adjacent levels, and wound infections.⁶ Short-term challenges include a large loss of blood, 2.4 L on average, according to Bridwell and colleagues.⁶ Time of closure of the osteotomy gap is a crucial point in the surgery. Blood loss, often large, slows only after the gap is closed and stabilized.

In this article, we describe a technique in which an additional rod or pedicle screw construct is used at the periosteotomy levels to close the osteotomy gap during PSO and simplify subsequent instrumentation. In addition, we report our experience with the procedure.

Materials and Methods

Seventeen consecutive patients (mean age, 58 years; range, 12-81 years) with fixed sagittal imbalance were treated with lumbar PSO. The indication in all cases was flatback syndrome after previous spinal surgery. Mean follow-up was 13 months. Mean number of prior surgeries was 3. Thirteen PSOs were performed at L3, and 4 were performed at L2.

Radiographic data were collected from before surgery, in the immediate postoperative period, and at final follow-up. All the radiographs were standing films. Established radiographic parameters were measured: thoracic kyphosis from T5 to T12, lumbar lordosis from L1 to S1, PSO angle (1 level above to 1 level below osteotomy level), sagittal plumb line (from center of C7 body to posterosuperior aspect of S1 body), and coronal plumb line (from center of C7 body to center of S1 body).²

Good clinical outcomes in the treatment of spinal disorders require careful attention to the alignment of the spine in the sagittal plane.^7,8 When evaluating the preoperative radiographs, we measured and documented pelvic parameters. Figure 1A shows how pelvic incidence was determined. We measured this as the angle between a line drawn from the center of the S1 endplate to the center of the femoral head and the perpendicular off the S1 endplate. Figure 1B shows pelvic tilt as determined by the angle between a line drawn from the center of S1 to the femoral head and a vertical line originating from the center of the femoral head. Figure 1C shows the sacral slope, which we measured as the angle between a line drawn parallel to the endplate of S1 and its intersection with a horizontal line.

Surgical Technique

The overall surgical technique for PSO has been well described.^4,5 Here we describe the “outrigger” modification to osteotomy closure (Figures 2, 3).

Most of our 17 cases were revisions. In these cases, new fixation points are first established. All fixation points that will be needed for the final fusion are placed. If a pedicle above or below the osteotomy level is not suitable for a screw, it can be skipped.

Wide decompression of the involved level is performed from pedicle to pedicle, ensuring that the nerve roots are completely decompressed. The dissection is then continued around the lateral wall of the vertebral body. While the neural elements are protected with gentle retraction, the pedicle and a portion of the posterior aspect of the vertebral body are removed with a combination of a rongeur and reverse-angle curettes. Resection of the vertebral body can be facilitated by attaching a short rod to the pedicle screws on either side of the osteotomy level and using it to provide gentle distraction.

Once sufficient bone has been removed to close the osteotomy, short rods are placed in the pedicle screws in the level above and the level below the osteotomy site. These rods are attached with offset connectors that allow the rods to be placed lateral to the screws. Before the surgical procedure is started, the patient is positioned on 2 sets of posts separated by the break in the table. The break in the table allows flexion to accommodate the preoperative kyphosis and allows hyperextension to help close the osteotomy site. Now, with the osteotomy site ready for closure, the table is gradually positioned in extension along with a combination of posterior pressure and compression between the pedicle screws above and below the osteotomy. Once the osteotomy is adequately compressed, the short rods are tightened, holding the osteotomy in good position. With the osteotomy held by the short rods and table positioning, decompression of the neural elements is confirmed and hemostasis obtained.

Final instrumentation is then performed with long rods that can bypass the osteotomized levels, allowing for simpler contouring. If desired, a cross connector can be placed between the long rod of the fusion construct and the short rod holding the osteotomy. The rest of the fusion procedure is completed in standard fashion with at least 1 subfascial drain.

Results

Our 17 patients’ results are summarized in the Table. Mean sagittal plumb line improved from 17.7 cm (range, 5.9 to 29 cm) before surgery to 4.5 cm (range, –0.2 to 12.9 cm) after surgery, for a mean improvement of 13.2 cm. At final follow-up, mean sagittal plumb line was 5.1 cm (range, –1.4 to 10.2 cm).

Mean lumbar lordosis improved from 10° (range, –14° to 34°) before surgery to 49° (range, 36° to 63°) after surgery, for a mean improvement of 39°. Mean PSO angle improved from 3° (range, –36° to 23°) before surgery to 41° (range, 25° to 65°) after surgery, for a mean improvement of 38°. At final follow-up, mean lumbar lordosis remained at 47° (range, 26° to 64°), and mean PSO angle was 39° (range, 24° to 59°).

Mean thoracic kyphosis improved from 18° (range, –8° to 52°) before surgery to 30° (range, 3° to 58°) after surgery, for a mean improvement of 12°. At final follow-up, mean thoracic kyphosis was 31° (range, 2° to 57°).

Fourteen patients did not have complications during the study period. Of the 3 patients with complications, 1 had an early infection, treated effectively with irrigation and débridement and intravenous antibiotics; 1 had a late deep infection, treated with multiple débridements, hardware removal, and, eventually, suppressive antibiotics; and 1 had cauda equina syndrome (caused by extensive scar tissue on the dura, which buckled with restoration of lordosis leading to cord compression), treated with duraplasty, which resulted in full neurologic recovery.

Discussion

In the present series of patients, the described technique for facilitating PSO for correction of sagittal imbalance was effective, and complications were similar to those previously reported.

The benefit of the outrigger construct is that it allows controlled compression of the osteotomy site and can be left in place at time of final instrumentation, locking in compression and correction. Other techniques involve removing the temporary rod and replacing it with final instrumentation^4,5—an extra step that complicates instrumentation of the additional levels of the fusion construct and possibly adds pedicle screw stress and contributes to loosening when the new rod is reduced to the pedicle screw. The final long rod construct can bypass the osteotomy levels and allow for simpler instrumentation.

 Mean age was 58 years in this series versus 52.4 years in the series reported by Bridwell and colleagues.² Given the higher mean age of our patients, though no objective measures of bone quality were available, this technique is likely applicable to patients with poor bone quality.

The complications we have reported are in line with those reported in previous series, and maintenance of radiographic parameters at final follow-up indicates that this osteotomy technique allows for solid fusion constructs.

The outrigger technique for controlling PSO closure is an effective method that simplifies instrumentation during a complex revision case.

Pedicle subtraction osteotomies (PSOs) have been used in the treatment of multiple spinal conditions involving a fixed sagittal imbalance, such as degenerative scoliosis, idiopathic scoliosis, posttraumatic deformities, iatrogenic flatback syndrome, and ankylosing spondylitis. The procedure was first described by Thomasen¹ for the treatment of ankylosing spondylitis. More recently, multiple centers have reported the expanded use and good success of PSO in the treatment of fixed sagittal imbalance of other etiologies.^2,3 According to Bridwell and colleagues,² lumbar lordosis can be increased 34.1°, and sagittal plumb line can be improved 13.5 cm.

PSO is a complex, extensive surgery most often performed in the revision setting. Multiple authors have described the technique for PSO.^4,5 There are significant technical challenges and many complications, including neurologic deficits, pseudarthrosis of adjacent levels, and wound infections.⁶ Short-term challenges include a large loss of blood, 2.4 L on average, according to Bridwell and colleagues.⁶ Time of closure of the osteotomy gap is a crucial point in the surgery. Blood loss, often large, slows only after the gap is closed and stabilized.

In this article, we describe a technique in which an additional rod or pedicle screw construct is used at the periosteotomy levels to close the osteotomy gap during PSO and simplify subsequent instrumentation. In addition, we report our experience with the procedure.

Materials and Methods

Seventeen consecutive patients (mean age, 58 years; range, 12-81 years) with fixed sagittal imbalance were treated with lumbar PSO. The indication in all cases was flatback syndrome after previous spinal surgery. Mean follow-up was 13 months. Mean number of prior surgeries was 3. Thirteen PSOs were performed at L3, and 4 were performed at L2.

Radiographic data were collected from before surgery, in the immediate postoperative period, and at final follow-up. All the radiographs were standing films. Established radiographic parameters were measured: thoracic kyphosis from T5 to T12, lumbar lordosis from L1 to S1, PSO angle (1 level above to 1 level below osteotomy level), sagittal plumb line (from center of C7 body to posterosuperior aspect of S1 body), and coronal plumb line (from center of C7 body to center of S1 body).²

Good clinical outcomes in the treatment of spinal disorders require careful attention to the alignment of the spine in the sagittal plane.^7,8 When evaluating the preoperative radiographs, we measured and documented pelvic parameters. Figure 1A shows how pelvic incidence was determined. We measured this as the angle between a line drawn from the center of the S1 endplate to the center of the femoral head and the perpendicular off the S1 endplate. Figure 1B shows pelvic tilt as determined by the angle between a line drawn from the center of S1 to the femoral head and a vertical line originating from the center of the femoral head. Figure 1C shows the sacral slope, which we measured as the angle between a line drawn parallel to the endplate of S1 and its intersection with a horizontal line.

Surgical Technique

The overall surgical technique for PSO has been well described.^4,5 Here we describe the “outrigger” modification to osteotomy closure (Figures 2, 3).

Most of our 17 cases were revisions. In these cases, new fixation points are first established. All fixation points that will be needed for the final fusion are placed. If a pedicle above or below the osteotomy level is not suitable for a screw, it can be skipped.

Wide decompression of the involved level is performed from pedicle to pedicle, ensuring that the nerve roots are completely decompressed. The dissection is then continued around the lateral wall of the vertebral body. While the neural elements are protected with gentle retraction, the pedicle and a portion of the posterior aspect of the vertebral body are removed with a combination of a rongeur and reverse-angle curettes. Resection of the vertebral body can be facilitated by attaching a short rod to the pedicle screws on either side of the osteotomy level and using it to provide gentle distraction.

Once sufficient bone has been removed to close the osteotomy, short rods are placed in the pedicle screws in the level above and the level below the osteotomy site. These rods are attached with offset connectors that allow the rods to be placed lateral to the screws. Before the surgical procedure is started, the patient is positioned on 2 sets of posts separated by the break in the table. The break in the table allows flexion to accommodate the preoperative kyphosis and allows hyperextension to help close the osteotomy site. Now, with the osteotomy site ready for closure, the table is gradually positioned in extension along with a combination of posterior pressure and compression between the pedicle screws above and below the osteotomy. Once the osteotomy is adequately compressed, the short rods are tightened, holding the osteotomy in good position. With the osteotomy held by the short rods and table positioning, decompression of the neural elements is confirmed and hemostasis obtained.

Final instrumentation is then performed with long rods that can bypass the osteotomized levels, allowing for simpler contouring. If desired, a cross connector can be placed between the long rod of the fusion construct and the short rod holding the osteotomy. The rest of the fusion procedure is completed in standard fashion with at least 1 subfascial drain.

Results

Our 17 patients’ results are summarized in the Table. Mean sagittal plumb line improved from 17.7 cm (range, 5.9 to 29 cm) before surgery to 4.5 cm (range, –0.2 to 12.9 cm) after surgery, for a mean improvement of 13.2 cm. At final follow-up, mean sagittal plumb line was 5.1 cm (range, –1.4 to 10.2 cm).

Mean lumbar lordosis improved from 10° (range, –14° to 34°) before surgery to 49° (range, 36° to 63°) after surgery, for a mean improvement of 39°. Mean PSO angle improved from 3° (range, –36° to 23°) before surgery to 41° (range, 25° to 65°) after surgery, for a mean improvement of 38°. At final follow-up, mean lumbar lordosis remained at 47° (range, 26° to 64°), and mean PSO angle was 39° (range, 24° to 59°).

Mean thoracic kyphosis improved from 18° (range, –8° to 52°) before surgery to 30° (range, 3° to 58°) after surgery, for a mean improvement of 12°. At final follow-up, mean thoracic kyphosis was 31° (range, 2° to 57°).

Fourteen patients did not have complications during the study period. Of the 3 patients with complications, 1 had an early infection, treated effectively with irrigation and débridement and intravenous antibiotics; 1 had a late deep infection, treated with multiple débridements, hardware removal, and, eventually, suppressive antibiotics; and 1 had cauda equina syndrome (caused by extensive scar tissue on the dura, which buckled with restoration of lordosis leading to cord compression), treated with duraplasty, which resulted in full neurologic recovery.

Discussion

In the present series of patients, the described technique for facilitating PSO for correction of sagittal imbalance was effective, and complications were similar to those previously reported.

The benefit of the outrigger construct is that it allows controlled compression of the osteotomy site and can be left in place at time of final instrumentation, locking in compression and correction. Other techniques involve removing the temporary rod and replacing it with final instrumentation^4,5—an extra step that complicates instrumentation of the additional levels of the fusion construct and possibly adds pedicle screw stress and contributes to loosening when the new rod is reduced to the pedicle screw. The final long rod construct can bypass the osteotomy levels and allow for simpler instrumentation.

 Mean age was 58 years in this series versus 52.4 years in the series reported by Bridwell and colleagues.² Given the higher mean age of our patients, though no objective measures of bone quality were available, this technique is likely applicable to patients with poor bone quality.

The complications we have reported are in line with those reported in previous series, and maintenance of radiographic parameters at final follow-up indicates that this osteotomy technique allows for solid fusion constructs.

The outrigger technique for controlling PSO closure is an effective method that simplifies instrumentation during a complex revision case.

In the United States, surgeons perform an estimated 200,000 anterior cruciate ligament reconstructions (ACLRs) each year. Over the past decade, there has been a surge in interest in defining anterior cruciate ligament (ACL) anatomy to guide ACLR. With this renewed interest in the anatomical features of the ACL, particularly the insertion site, many authors have advocated an approach for complete or near-complete “footprint restoration” for anatomical ACLR.^1,2 Some have recommended a double-bundle (DB) technique that completely “fills” the footprint, but it is seldom used. Others have proposed centralizing the femoral tunnel position within the ACL footprint in the hope of capturing the function of both the anteromedial (AM) and posterolateral (PL) bundles.^1,3,4 Indeed, a primary surgical goal of most anatomical ACLR techniques is creation of a femoral tunnel based off the anatomical centrum (center point) of the ACL femoral footprint.^3,5 With a single-bundle technique, the femoral socket is localized in the center of the entire footprint; with a DB technique, sockets are created in the centrums of both the AM and PL bundles.

Because of the complex shape of the native ACL, however, the strategy of restoring the femoral footprint with use of either a central tunnel or a DB approach has been challenged. The femoral footprint is 3.5 times larger than the midsubstance of the ACL.⁶ Detailed anatomical dissections have recently demonstrated that the femoral origin of the ACL has a stout anterior band of fibers with a fanlike extension posteriorly.⁷ As the ACL fibers extend off the bony footprint, they form a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick.^2,8 Within this structure, there is no clear separation of the AM and PL bundles. The presence of this structure makes sense given the anatomical constraints inherent in the notch. Indeed, the space for the native ACL is narrow, as the posterior cruciate ligament (PCL) occupies that largest portion of the notch with the knee in full extension, leaving only a thin, 5-mm slot through which the ACL must pass.⁹ Therefore, filling the femoral footprint with a tubular ACL graft probably does not reproduce the dynamic 3-dimensional morphology of the ACL.

In light of the discrepancy between the sizes of the femoral footprint and the midsubstance of the native ACL, it seems reasonable that optimizing the position of the ACL femoral tunnel may be more complex than simply centralizing the tunnel within the footprint or attempting to maximize footprint coverage. In this article, we amalgamate the lessons of 4 decades of ACL research into 5 points for strategic femoral tunnel positioning, based on anatomical, histologic, isometric, biomechanical, and clinical data. These points are summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension.

1. Anatomy Considerations

In response to study results demonstrating that some transtibial ACLRs were associated with nonanatomical placement of the femoral tunnel—resulting in vertical graft placement, PCL impingement, and recurrent rotational instability^10-16—investigators have reexamined both the anatomy of the femoral origin of the native ACL and the ACL graft. Specifically, a large body of research has been devoted to characterizing the osseous landmarks of the femoral origin of the ACL¹⁷ and the dimensions of the femoral footprint.³ In addition, authors have supported the concept that the ACL contains 2 functional bundles, AM and PL.^5,17 Several osseous landmarks have been identified as defining the boundaries of the femoral footprint. The lateral intercondylar ridge is the most anterior aspect of the femoral footprint and was first defined by Clancy.¹⁸ More recently, the lateral bifurcate ridge, which separates the AM and PL bundle insertion sites, was described¹⁹ (Figure 1A).

These osseous ridges delineate the location of the femoral footprint. Studies have shown that ACL fibers attach from the lateral intercondylar ridge on the anterior border of the femoral footprint and extend posteriorly to the cartilage of the lateral femoral condyle (Figure 1B).

ACL fibers from this oblong footprint are organized such that the midsubstance of the ACL is narrower than the femoral footprint. Anatomical dissections have demonstrated that, though the femoral footprint is oval, the native ACL forms a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick as it takes off from the bone.^8,20 There is a resulting discrepancy between the femoral footprint size and shape and the morphology of the native ACL, and placing a tunnel in the center of the footprint or “filling the footprint” with ACL graft may not reproduce the morphology or function of the native ACL. Given this size mismatch, strategic decisions need to be made to place the femoral tunnel in a specific region of the femoral footprint to optimize its function.

2. Histologic Findings

Histologic analysis has further clarified the relationship between the femoral footprint and functional aspects of the native ACL. The femoral origin of the ACL has distinct direct and indirect insertions, as demonstrated by histology and 3-dimensional volume-rendered computed tomography.²¹ The direct insertion consists of dense collagen fibers anterior in the footprint that is attached to a bony depression immediately posterior to the lateral intercondylar ridge.¹⁹ Sasaki and colleagues²² found that these direct fibers extended a mean (SD) of 5.3 (1.1) mm posteriorly but did not continue to the posterior femoral articular cartilage. The indirect insertion consists of more posterior collagen fibers that extend to and blend into the articular cartilage of the posterior aspect of the lateral femoral condyle. Mean (SD) width of this membrane-like tissue, located between the direct insertion and the posterior femoral articular cartilage, was found by Sasaki and colleagues²²  to be 4.4 (0.5) mm anteroposteriorly(Figure 2). This anterior band of ACL tissue with the direct insertion histologically corresponds to the fibers in the anterior, more isometric region of the femoral footprint. Conversely, the more posterior band of fibers with its indirect insertion histologically corresponds to the more anisometric region and is seen macroscopically as a fanlike projection extending to the posterior articular cartilage.⁷

The dense collagen fibers of the direct insertion and the more membrane-like indirect insertion regions of the femoral footprint of the native ACL suggest that these regions have different load-sharing characteristics. The direct fibers of the insertion form a firm, fixed attachment that allows for gradual load distribution into the subchondral bone. From a biomechanical point of view, this attachment is extremely important, a key ligament–bone link transmitting mechanical load to the joint.²³ A recent kinematic analysis revealed that the indirect fibers in the posterior region of the footprint, adjacent to the posterior articular cartilage, contribute minimally to restraint of tibial translation and rotations during stability examination.²⁴ This suggests it may be strategically wise to place a tunnel in the direct insertion region of the footprint—eccentrically anterior (high) in the footprint rather than in the centrum.

3. Isometric Considerations

Forty years ago, Artmann and Wirth²⁵ reported that a nearly isometric region existed in the femur such that there is minimal elongation of the native ACL during knee motion. The biomechanical rationale for choosing an isometric region of an ACL graft is that it will maintain function throughout the range of flexion and extension. A nonisometric graft would be expected to slacken during a large portion of the flexion cycle and not restrain anterior translation of the tibia, or, if fixed at the wrong flexion angle, it could capture the knee and cause graft failure by excessive tension. These 2 theoretical undesirable effects from nonisometric graft placement are supported by many experimental and clinical studies demonstrating that nonisometric femoral tunnel placement at time of surgery can cause recurrent anterior laxity of the knee.^26-28 Multiple studies have further clarified that the isometric characteristics of an ACL graft are largely determined by femoral positioning. The most isometric region of the femoral footprint is consistently shown to be localized eccentrically within the footprint, in a relatively narrow bandlike region that is proximal (deep) and anterior (along the lateral intercondylar ridge within the footprint)^19,29,30 (Figure 3).

A large body of literature has demonstrated that a tunnel placed in the center of the femoral footprint is less isometric than a tunnel in the more anterior region.^25,29,31,32 Indeed, the anterior position (high in the footprint) identified by Hefzy and colleagues²⁹ demonstrated minimal anisometry with 1 to 4 mm of length change through the range of motion. In contrast, a central tunnel would be expected to demonstrate 5 to 7 mm of length change, whereas a lower graft (in the PL region of the footprint) would demonstrate about 1 cm of length change through the range of motion.^31,32 As such, central grafts, or grafts placed in the PL portion of the femoral footprint, would be expected to see high tension or graft forces as the knee is flexed, or to lose tension completely if the graft is fixed at full extension.³²

Importantly, Markolf and colleagues³³ reported that the native ACL does not behave exactly in a so-called isometric fashion during the last 30° of extension. They showed that about 3 mm of retraction of a trial wire into the joint during the last 30° of extension (as measured with an isometer) is reasonable to achieve graft length changes approximating those of the intact ACL. Given this important caveat, a primary goal for ACLR is placement of the femoral tunnel within this isometric region so that the length change in the ACL graft is minimized to 3 mm from 30° to full flexion. In addition, results of a time-zero biomechanical study suggested better rotational control with anatomical femoral tunnel position than with an isometric femoral tunnel³⁴ placed outside the femoral footprint. Therefore, maximizing isometry alone is not the goal; placing the graft in the most isometric region within the anatomical femoral footprint is desired. This isometric region in the footprint is in the histologic region that corresponds to the direct fibers. Again, this region is eccentrically located in the anterior (high) and proximal (deep) portion of the footprint.

4. Biomechanical Considerations

Multiple cadaveric studies have investigated the relationship between femoral tunnel positioning and time-zero stability. These studies often demonstrated superior time-zero control of knee stability, particularly in pivot type maneuvers, with a femoral tunnel placed more centrally in the femoral footprint than with a tunnel placed outside the footprint.^34-37 However, an emerging body of literature is finding no significant difference in time-zero stability between an anteriorly placed femoral tunnel within the anatomical footprint (eccentrically located in the footprint) and a centrally placed graft.^38,39 Returning to the more isometric tunnel position, still within the femoral footprint, would be expected to confer the benefits of an anatomically based graft position with the advantageous profile of improved isometry, as compared with a centrally placed or PL graft. Biomechanical studies⁴⁰ have documented that ACL graft fibers placed posteriorly (low) in the footprint cause high graft forces in extension and, in some cases, graft rupture (Figure 4). Accordingly, the importance of reconstructing the posterior region of the footprint to better control time-zero stability is questioned.⁴¹

In addition to time-zero control of the stability examination, restoring the low tension-flexion pattern in the ACL graft to replicate the tension-flexion behavior of the native ACL is a fundamental biomechanical principle of ACLR.^15,33,42,43 These studies have demonstrated that a femoral tunnel localized anterior (high) and proximal (deep) within the footprint better replicates the tension-flexion behavior of the native ACL, as compared with strategies that attempt to anatomically “fill the footprint.”⁴⁰ Together, these studies have demonstrated that an eccentric position in the footprint, in the anterior (high) and proximal (deep) region, not only maximizes isometry and restores the direct fibers, but provides favorable time-zero stability and a low tension-flexion pattern biomechanically, particularly as compared with a tunnel in the more central or posterior region of the footprint.

5. Clinical Data

Clinical studies of the traditional transtibial ACLR have shown good results.^44,45 However, when the tibial tunnel in the coronal plane was drilled vertical with respect to the medial joint line of the tibia, the transtibially placed femoral tunnel migrated anterior to the anatomical femoral footprint, often on the roof of the notch.^10,14 This nonanatomical, vertical placement of the femoral tunnel led to failed normalization of knee kinematics.^46-50 Indeed, a higher tension-flexion pattern was found in this nonanatomical “roof” position for the femoral tunnel as compared with the native ACL—a pattern that can result in either loss of flexion or recurrent instability.^13,15,51

Clinical results of techniques used to create an anatomical ACLR centrally within the footprint have been mixed. Registry data showed that the revision rate at 4 years was higher with the AM portal technique (5.16%) than with transtibial drilling (3.20%).⁵² This higher rate may be associated with the more central placement of the femoral tunnel with the AM portal technique than with the transtibial technique, as shown in vivo with high-resolution magnetic resonance imaging.¹² Recent reports have documented a higher rate of failure with DB or central ACLR approaches than with traditional transtibial techniques.⁵³ As mentioned, in contrast to a more isometric position, a central femoral tunnel position would be expected to demonstrate 5 to 7 mm of length change, whereas moving the graft more posterior in the footprint (closer to the articular cartilage) would result in more than 1 cm of length change through the range of motion.^31,32 As such, these more central grafts, or grafts placed even lower (more posterior) in the footprint, would be expected to see high tension in extension (if fixed in flexion), or to lose tension completely during flexion (if the graft is fixed at full extension).³² This may be a mechanistic cause of the high failure rate in the more posterior bundles of the DB approach.⁵⁴

Together, these clinical data suggest that the femoral tunnel should be placed within the anatomical footprint of the ACL. However, within the footprint, a more eccentric femoral tunnel position capturing the isometric and direct region of the insertion may be preferable to a more central or posterior (low region) position.

Summary

Anatomical, histologic, isometric, biomechanical, and clinical data from more than 4 decades collectively point to an optimal position for the femoral tunnel within the femoral footprint. This position can be summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension (Figure 5).

In vivo and in vitro studies as well as surgical experience suggest a need to avoid both (a) the nonanatomical vertical (roof) femoral tunnel placement that causes PCL impingement, high tension in the ACL graft in flexion, and ultimately graft stretch-out with instability and (b) the femoral tunnel placement in the posterior (lowest) region of the footprint that causes high tension in extension and can result in graft stretch-out with instability.^13,15,39,40 The transtibial and AM portal techniques can both be effective in properly placing the femoral tunnel and restoring motion, stability, and function to the knee. Their effectiveness, however, depends on correct placement of the femoral tunnel. We think coming studies will focus on single-bundle ACLR and will be designed to improve the reliability of the transtibial and AM portal techniques for placing a femoral tunnel in keeping with the principles summarized by the I.D.E.A.L. acronym.

In the United States, surgeons perform an estimated 200,000 anterior cruciate ligament reconstructions (ACLRs) each year. Over the past decade, there has been a surge in interest in defining anterior cruciate ligament (ACL) anatomy to guide ACLR. With this renewed interest in the anatomical features of the ACL, particularly the insertion site, many authors have advocated an approach for complete or near-complete “footprint restoration” for anatomical ACLR.^1,2 Some have recommended a double-bundle (DB) technique that completely “fills” the footprint, but it is seldom used. Others have proposed centralizing the femoral tunnel position within the ACL footprint in the hope of capturing the function of both the anteromedial (AM) and posterolateral (PL) bundles.^1,3,4 Indeed, a primary surgical goal of most anatomical ACLR techniques is creation of a femoral tunnel based off the anatomical centrum (center point) of the ACL femoral footprint.^3,5 With a single-bundle technique, the femoral socket is localized in the center of the entire footprint; with a DB technique, sockets are created in the centrums of both the AM and PL bundles.

Because of the complex shape of the native ACL, however, the strategy of restoring the femoral footprint with use of either a central tunnel or a DB approach has been challenged. The femoral footprint is 3.5 times larger than the midsubstance of the ACL.⁶ Detailed anatomical dissections have recently demonstrated that the femoral origin of the ACL has a stout anterior band of fibers with a fanlike extension posteriorly.⁷ As the ACL fibers extend off the bony footprint, they form a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick.^2,8 Within this structure, there is no clear separation of the AM and PL bundles. The presence of this structure makes sense given the anatomical constraints inherent in the notch. Indeed, the space for the native ACL is narrow, as the posterior cruciate ligament (PCL) occupies that largest portion of the notch with the knee in full extension, leaving only a thin, 5-mm slot through which the ACL must pass.⁹ Therefore, filling the femoral footprint with a tubular ACL graft probably does not reproduce the dynamic 3-dimensional morphology of the ACL.

In light of the discrepancy between the sizes of the femoral footprint and the midsubstance of the native ACL, it seems reasonable that optimizing the position of the ACL femoral tunnel may be more complex than simply centralizing the tunnel within the footprint or attempting to maximize footprint coverage. In this article, we amalgamate the lessons of 4 decades of ACL research into 5 points for strategic femoral tunnel positioning, based on anatomical, histologic, isometric, biomechanical, and clinical data. These points are summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension.

1. Anatomy Considerations

In response to study results demonstrating that some transtibial ACLRs were associated with nonanatomical placement of the femoral tunnel—resulting in vertical graft placement, PCL impingement, and recurrent rotational instability^10-16—investigators have reexamined both the anatomy of the femoral origin of the native ACL and the ACL graft. Specifically, a large body of research has been devoted to characterizing the osseous landmarks of the femoral origin of the ACL¹⁷ and the dimensions of the femoral footprint.³ In addition, authors have supported the concept that the ACL contains 2 functional bundles, AM and PL.^5,17 Several osseous landmarks have been identified as defining the boundaries of the femoral footprint. The lateral intercondylar ridge is the most anterior aspect of the femoral footprint and was first defined by Clancy.¹⁸ More recently, the lateral bifurcate ridge, which separates the AM and PL bundle insertion sites, was described¹⁹ (Figure 1A).

These osseous ridges delineate the location of the femoral footprint. Studies have shown that ACL fibers attach from the lateral intercondylar ridge on the anterior border of the femoral footprint and extend posteriorly to the cartilage of the lateral femoral condyle (Figure 1B).

ACL fibers from this oblong footprint are organized such that the midsubstance of the ACL is narrower than the femoral footprint. Anatomical dissections have demonstrated that, though the femoral footprint is oval, the native ACL forms a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick as it takes off from the bone.^8,20 There is a resulting discrepancy between the femoral footprint size and shape and the morphology of the native ACL, and placing a tunnel in the center of the footprint or “filling the footprint” with ACL graft may not reproduce the morphology or function of the native ACL. Given this size mismatch, strategic decisions need to be made to place the femoral tunnel in a specific region of the femoral footprint to optimize its function.

2. Histologic Findings

Histologic analysis has further clarified the relationship between the femoral footprint and functional aspects of the native ACL. The femoral origin of the ACL has distinct direct and indirect insertions, as demonstrated by histology and 3-dimensional volume-rendered computed tomography.²¹ The direct insertion consists of dense collagen fibers anterior in the footprint that is attached to a bony depression immediately posterior to the lateral intercondylar ridge.¹⁹ Sasaki and colleagues²² found that these direct fibers extended a mean (SD) of 5.3 (1.1) mm posteriorly but did not continue to the posterior femoral articular cartilage. The indirect insertion consists of more posterior collagen fibers that extend to and blend into the articular cartilage of the posterior aspect of the lateral femoral condyle. Mean (SD) width of this membrane-like tissue, located between the direct insertion and the posterior femoral articular cartilage, was found by Sasaki and colleagues²²  to be 4.4 (0.5) mm anteroposteriorly(Figure 2). This anterior band of ACL tissue with the direct insertion histologically corresponds to the fibers in the anterior, more isometric region of the femoral footprint. Conversely, the more posterior band of fibers with its indirect insertion histologically corresponds to the more anisometric region and is seen macroscopically as a fanlike projection extending to the posterior articular cartilage.⁷

The dense collagen fibers of the direct insertion and the more membrane-like indirect insertion regions of the femoral footprint of the native ACL suggest that these regions have different load-sharing characteristics. The direct fibers of the insertion form a firm, fixed attachment that allows for gradual load distribution into the subchondral bone. From a biomechanical point of view, this attachment is extremely important, a key ligament–bone link transmitting mechanical load to the joint.²³ A recent kinematic analysis revealed that the indirect fibers in the posterior region of the footprint, adjacent to the posterior articular cartilage, contribute minimally to restraint of tibial translation and rotations during stability examination.²⁴ This suggests it may be strategically wise to place a tunnel in the direct insertion region of the footprint—eccentrically anterior (high) in the footprint rather than in the centrum.

3. Isometric Considerations

Forty years ago, Artmann and Wirth²⁵ reported that a nearly isometric region existed in the femur such that there is minimal elongation of the native ACL during knee motion. The biomechanical rationale for choosing an isometric region of an ACL graft is that it will maintain function throughout the range of flexion and extension. A nonisometric graft would be expected to slacken during a large portion of the flexion cycle and not restrain anterior translation of the tibia, or, if fixed at the wrong flexion angle, it could capture the knee and cause graft failure by excessive tension. These 2 theoretical undesirable effects from nonisometric graft placement are supported by many experimental and clinical studies demonstrating that nonisometric femoral tunnel placement at time of surgery can cause recurrent anterior laxity of the knee.^26-28 Multiple studies have further clarified that the isometric characteristics of an ACL graft are largely determined by femoral positioning. The most isometric region of the femoral footprint is consistently shown to be localized eccentrically within the footprint, in a relatively narrow bandlike region that is proximal (deep) and anterior (along the lateral intercondylar ridge within the footprint)^19,29,30 (Figure 3).

A large body of literature has demonstrated that a tunnel placed in the center of the femoral footprint is less isometric than a tunnel in the more anterior region.^25,29,31,32 Indeed, the anterior position (high in the footprint) identified by Hefzy and colleagues²⁹ demonstrated minimal anisometry with 1 to 4 mm of length change through the range of motion. In contrast, a central tunnel would be expected to demonstrate 5 to 7 mm of length change, whereas a lower graft (in the PL region of the footprint) would demonstrate about 1 cm of length change through the range of motion.^31,32 As such, central grafts, or grafts placed in the PL portion of the femoral footprint, would be expected to see high tension or graft forces as the knee is flexed, or to lose tension completely if the graft is fixed at full extension.³²

Importantly, Markolf and colleagues³³ reported that the native ACL does not behave exactly in a so-called isometric fashion during the last 30° of extension. They showed that about 3 mm of retraction of a trial wire into the joint during the last 30° of extension (as measured with an isometer) is reasonable to achieve graft length changes approximating those of the intact ACL. Given this important caveat, a primary goal for ACLR is placement of the femoral tunnel within this isometric region so that the length change in the ACL graft is minimized to 3 mm from 30° to full flexion. In addition, results of a time-zero biomechanical study suggested better rotational control with anatomical femoral tunnel position than with an isometric femoral tunnel³⁴ placed outside the femoral footprint. Therefore, maximizing isometry alone is not the goal; placing the graft in the most isometric region within the anatomical femoral footprint is desired. This isometric region in the footprint is in the histologic region that corresponds to the direct fibers. Again, this region is eccentrically located in the anterior (high) and proximal (deep) portion of the footprint.

4. Biomechanical Considerations

Multiple cadaveric studies have investigated the relationship between femoral tunnel positioning and time-zero stability. These studies often demonstrated superior time-zero control of knee stability, particularly in pivot type maneuvers, with a femoral tunnel placed more centrally in the femoral footprint than with a tunnel placed outside the footprint.^34-37 However, an emerging body of literature is finding no significant difference in time-zero stability between an anteriorly placed femoral tunnel within the anatomical footprint (eccentrically located in the footprint) and a centrally placed graft.^38,39 Returning to the more isometric tunnel position, still within the femoral footprint, would be expected to confer the benefits of an anatomically based graft position with the advantageous profile of improved isometry, as compared with a centrally placed or PL graft. Biomechanical studies⁴⁰ have documented that ACL graft fibers placed posteriorly (low) in the footprint cause high graft forces in extension and, in some cases, graft rupture (Figure 4). Accordingly, the importance of reconstructing the posterior region of the footprint to better control time-zero stability is questioned.⁴¹

In addition to time-zero control of the stability examination, restoring the low tension-flexion pattern in the ACL graft to replicate the tension-flexion behavior of the native ACL is a fundamental biomechanical principle of ACLR.^15,33,42,43 These studies have demonstrated that a femoral tunnel localized anterior (high) and proximal (deep) within the footprint better replicates the tension-flexion behavior of the native ACL, as compared with strategies that attempt to anatomically “fill the footprint.”⁴⁰ Together, these studies have demonstrated that an eccentric position in the footprint, in the anterior (high) and proximal (deep) region, not only maximizes isometry and restores the direct fibers, but provides favorable time-zero stability and a low tension-flexion pattern biomechanically, particularly as compared with a tunnel in the more central or posterior region of the footprint.

5. Clinical Data

Clinical studies of the traditional transtibial ACLR have shown good results.^44,45 However, when the tibial tunnel in the coronal plane was drilled vertical with respect to the medial joint line of the tibia, the transtibially placed femoral tunnel migrated anterior to the anatomical femoral footprint, often on the roof of the notch.^10,14 This nonanatomical, vertical placement of the femoral tunnel led to failed normalization of knee kinematics.^46-50 Indeed, a higher tension-flexion pattern was found in this nonanatomical “roof” position for the femoral tunnel as compared with the native ACL—a pattern that can result in either loss of flexion or recurrent instability.^13,15,51

Clinical results of techniques used to create an anatomical ACLR centrally within the footprint have been mixed. Registry data showed that the revision rate at 4 years was higher with the AM portal technique (5.16%) than with transtibial drilling (3.20%).⁵² This higher rate may be associated with the more central placement of the femoral tunnel with the AM portal technique than with the transtibial technique, as shown in vivo with high-resolution magnetic resonance imaging.¹² Recent reports have documented a higher rate of failure with DB or central ACLR approaches than with traditional transtibial techniques.⁵³ As mentioned, in contrast to a more isometric position, a central femoral tunnel position would be expected to demonstrate 5 to 7 mm of length change, whereas moving the graft more posterior in the footprint (closer to the articular cartilage) would result in more than 1 cm of length change through the range of motion.^31,32 As such, these more central grafts, or grafts placed even lower (more posterior) in the footprint, would be expected to see high tension in extension (if fixed in flexion), or to lose tension completely during flexion (if the graft is fixed at full extension).³² This may be a mechanistic cause of the high failure rate in the more posterior bundles of the DB approach.⁵⁴

Together, these clinical data suggest that the femoral tunnel should be placed within the anatomical footprint of the ACL. However, within the footprint, a more eccentric femoral tunnel position capturing the isometric and direct region of the insertion may be preferable to a more central or posterior (low region) position.

Summary

Anatomical, histologic, isometric, biomechanical, and clinical data from more than 4 decades collectively point to an optimal position for the femoral tunnel within the femoral footprint. This position can be summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension (Figure 5).

In vivo and in vitro studies as well as surgical experience suggest a need to avoid both (a) the nonanatomical vertical (roof) femoral tunnel placement that causes PCL impingement, high tension in the ACL graft in flexion, and ultimately graft stretch-out with instability and (b) the femoral tunnel placement in the posterior (lowest) region of the footprint that causes high tension in extension and can result in graft stretch-out with instability.^13,15,39,40 The transtibial and AM portal techniques can both be effective in properly placing the femoral tunnel and restoring motion, stability, and function to the knee. Their effectiveness, however, depends on correct placement of the femoral tunnel. We think coming studies will focus on single-bundle ACLR and will be designed to improve the reliability of the transtibial and AM portal techniques for placing a femoral tunnel in keeping with the principles summarized by the I.D.E.A.L. acronym.

In the United States, surgeons perform an estimated 200,000 anterior cruciate ligament reconstructions (ACLRs) each year. Over the past decade, there has been a surge in interest in defining anterior cruciate ligament (ACL) anatomy to guide ACLR. With this renewed interest in the anatomical features of the ACL, particularly the insertion site, many authors have advocated an approach for complete or near-complete “footprint restoration” for anatomical ACLR.^1,2 Some have recommended a double-bundle (DB) technique that completely “fills” the footprint, but it is seldom used. Others have proposed centralizing the femoral tunnel position within the ACL footprint in the hope of capturing the function of both the anteromedial (AM) and posterolateral (PL) bundles.^1,3,4 Indeed, a primary surgical goal of most anatomical ACLR techniques is creation of a femoral tunnel based off the anatomical centrum (center point) of the ACL femoral footprint.^3,5 With a single-bundle technique, the femoral socket is localized in the center of the entire footprint; with a DB technique, sockets are created in the centrums of both the AM and PL bundles.

Because of the complex shape of the native ACL, however, the strategy of restoring the femoral footprint with use of either a central tunnel or a DB approach has been challenged. The femoral footprint is 3.5 times larger than the midsubstance of the ACL.⁶ Detailed anatomical dissections have recently demonstrated that the femoral origin of the ACL has a stout anterior band of fibers with a fanlike extension posteriorly.⁷ As the ACL fibers extend off the bony footprint, they form a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick.^2,8 Within this structure, there is no clear separation of the AM and PL bundles. The presence of this structure makes sense given the anatomical constraints inherent in the notch. Indeed, the space for the native ACL is narrow, as the posterior cruciate ligament (PCL) occupies that largest portion of the notch with the knee in full extension, leaving only a thin, 5-mm slot through which the ACL must pass.⁹ Therefore, filling the femoral footprint with a tubular ACL graft probably does not reproduce the dynamic 3-dimensional morphology of the ACL.

In light of the discrepancy between the sizes of the femoral footprint and the midsubstance of the native ACL, it seems reasonable that optimizing the position of the ACL femoral tunnel may be more complex than simply centralizing the tunnel within the footprint or attempting to maximize footprint coverage. In this article, we amalgamate the lessons of 4 decades of ACL research into 5 points for strategic femoral tunnel positioning, based on anatomical, histologic, isometric, biomechanical, and clinical data. These points are summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension.

1. Anatomy Considerations

In response to study results demonstrating that some transtibial ACLRs were associated with nonanatomical placement of the femoral tunnel—resulting in vertical graft placement, PCL impingement, and recurrent rotational instability^10-16—investigators have reexamined both the anatomy of the femoral origin of the native ACL and the ACL graft. Specifically, a large body of research has been devoted to characterizing the osseous landmarks of the femoral origin of the ACL¹⁷ and the dimensions of the femoral footprint.³ In addition, authors have supported the concept that the ACL contains 2 functional bundles, AM and PL.^5,17 Several osseous landmarks have been identified as defining the boundaries of the femoral footprint. The lateral intercondylar ridge is the most anterior aspect of the femoral footprint and was first defined by Clancy.¹⁸ More recently, the lateral bifurcate ridge, which separates the AM and PL bundle insertion sites, was described¹⁹ (Figure 1A).

These osseous ridges delineate the location of the femoral footprint. Studies have shown that ACL fibers attach from the lateral intercondylar ridge on the anterior border of the femoral footprint and extend posteriorly to the cartilage of the lateral femoral condyle (Figure 1B).

ACL fibers from this oblong footprint are organized such that the midsubstance of the ACL is narrower than the femoral footprint. Anatomical dissections have demonstrated that, though the femoral footprint is oval, the native ACL forms a flat, ribbonlike structure 9 to 16 mm wide and only 2 to 4 mm thick as it takes off from the bone.^8,20 There is a resulting discrepancy between the femoral footprint size and shape and the morphology of the native ACL, and placing a tunnel in the center of the footprint or “filling the footprint” with ACL graft may not reproduce the morphology or function of the native ACL. Given this size mismatch, strategic decisions need to be made to place the femoral tunnel in a specific region of the femoral footprint to optimize its function.

2. Histologic Findings

Histologic analysis has further clarified the relationship between the femoral footprint and functional aspects of the native ACL. The femoral origin of the ACL has distinct direct and indirect insertions, as demonstrated by histology and 3-dimensional volume-rendered computed tomography.²¹ The direct insertion consists of dense collagen fibers anterior in the footprint that is attached to a bony depression immediately posterior to the lateral intercondylar ridge.¹⁹ Sasaki and colleagues²² found that these direct fibers extended a mean (SD) of 5.3 (1.1) mm posteriorly but did not continue to the posterior femoral articular cartilage. The indirect insertion consists of more posterior collagen fibers that extend to and blend into the articular cartilage of the posterior aspect of the lateral femoral condyle. Mean (SD) width of this membrane-like tissue, located between the direct insertion and the posterior femoral articular cartilage, was found by Sasaki and colleagues²²  to be 4.4 (0.5) mm anteroposteriorly(Figure 2). This anterior band of ACL tissue with the direct insertion histologically corresponds to the fibers in the anterior, more isometric region of the femoral footprint. Conversely, the more posterior band of fibers with its indirect insertion histologically corresponds to the more anisometric region and is seen macroscopically as a fanlike projection extending to the posterior articular cartilage.⁷

The dense collagen fibers of the direct insertion and the more membrane-like indirect insertion regions of the femoral footprint of the native ACL suggest that these regions have different load-sharing characteristics. The direct fibers of the insertion form a firm, fixed attachment that allows for gradual load distribution into the subchondral bone. From a biomechanical point of view, this attachment is extremely important, a key ligament–bone link transmitting mechanical load to the joint.²³ A recent kinematic analysis revealed that the indirect fibers in the posterior region of the footprint, adjacent to the posterior articular cartilage, contribute minimally to restraint of tibial translation and rotations during stability examination.²⁴ This suggests it may be strategically wise to place a tunnel in the direct insertion region of the footprint—eccentrically anterior (high) in the footprint rather than in the centrum.

3. Isometric Considerations

Forty years ago, Artmann and Wirth²⁵ reported that a nearly isometric region existed in the femur such that there is minimal elongation of the native ACL during knee motion. The biomechanical rationale for choosing an isometric region of an ACL graft is that it will maintain function throughout the range of flexion and extension. A nonisometric graft would be expected to slacken during a large portion of the flexion cycle and not restrain anterior translation of the tibia, or, if fixed at the wrong flexion angle, it could capture the knee and cause graft failure by excessive tension. These 2 theoretical undesirable effects from nonisometric graft placement are supported by many experimental and clinical studies demonstrating that nonisometric femoral tunnel placement at time of surgery can cause recurrent anterior laxity of the knee.^26-28 Multiple studies have further clarified that the isometric characteristics of an ACL graft are largely determined by femoral positioning. The most isometric region of the femoral footprint is consistently shown to be localized eccentrically within the footprint, in a relatively narrow bandlike region that is proximal (deep) and anterior (along the lateral intercondylar ridge within the footprint)^19,29,30 (Figure 3).

A large body of literature has demonstrated that a tunnel placed in the center of the femoral footprint is less isometric than a tunnel in the more anterior region.^25,29,31,32 Indeed, the anterior position (high in the footprint) identified by Hefzy and colleagues²⁹ demonstrated minimal anisometry with 1 to 4 mm of length change through the range of motion. In contrast, a central tunnel would be expected to demonstrate 5 to 7 mm of length change, whereas a lower graft (in the PL region of the footprint) would demonstrate about 1 cm of length change through the range of motion.^31,32 As such, central grafts, or grafts placed in the PL portion of the femoral footprint, would be expected to see high tension or graft forces as the knee is flexed, or to lose tension completely if the graft is fixed at full extension.³²

Importantly, Markolf and colleagues³³ reported that the native ACL does not behave exactly in a so-called isometric fashion during the last 30° of extension. They showed that about 3 mm of retraction of a trial wire into the joint during the last 30° of extension (as measured with an isometer) is reasonable to achieve graft length changes approximating those of the intact ACL. Given this important caveat, a primary goal for ACLR is placement of the femoral tunnel within this isometric region so that the length change in the ACL graft is minimized to 3 mm from 30° to full flexion. In addition, results of a time-zero biomechanical study suggested better rotational control with anatomical femoral tunnel position than with an isometric femoral tunnel³⁴ placed outside the femoral footprint. Therefore, maximizing isometry alone is not the goal; placing the graft in the most isometric region within the anatomical femoral footprint is desired. This isometric region in the footprint is in the histologic region that corresponds to the direct fibers. Again, this region is eccentrically located in the anterior (high) and proximal (deep) portion of the footprint.

4. Biomechanical Considerations

Multiple cadaveric studies have investigated the relationship between femoral tunnel positioning and time-zero stability. These studies often demonstrated superior time-zero control of knee stability, particularly in pivot type maneuvers, with a femoral tunnel placed more centrally in the femoral footprint than with a tunnel placed outside the footprint.^34-37 However, an emerging body of literature is finding no significant difference in time-zero stability between an anteriorly placed femoral tunnel within the anatomical footprint (eccentrically located in the footprint) and a centrally placed graft.^38,39 Returning to the more isometric tunnel position, still within the femoral footprint, would be expected to confer the benefits of an anatomically based graft position with the advantageous profile of improved isometry, as compared with a centrally placed or PL graft. Biomechanical studies⁴⁰ have documented that ACL graft fibers placed posteriorly (low) in the footprint cause high graft forces in extension and, in some cases, graft rupture (Figure 4). Accordingly, the importance of reconstructing the posterior region of the footprint to better control time-zero stability is questioned.⁴¹

In addition to time-zero control of the stability examination, restoring the low tension-flexion pattern in the ACL graft to replicate the tension-flexion behavior of the native ACL is a fundamental biomechanical principle of ACLR.^15,33,42,43 These studies have demonstrated that a femoral tunnel localized anterior (high) and proximal (deep) within the footprint better replicates the tension-flexion behavior of the native ACL, as compared with strategies that attempt to anatomically “fill the footprint.”⁴⁰ Together, these studies have demonstrated that an eccentric position in the footprint, in the anterior (high) and proximal (deep) region, not only maximizes isometry and restores the direct fibers, but provides favorable time-zero stability and a low tension-flexion pattern biomechanically, particularly as compared with a tunnel in the more central or posterior region of the footprint.

5. Clinical Data

Clinical studies of the traditional transtibial ACLR have shown good results.^44,45 However, when the tibial tunnel in the coronal plane was drilled vertical with respect to the medial joint line of the tibia, the transtibially placed femoral tunnel migrated anterior to the anatomical femoral footprint, often on the roof of the notch.^10,14 This nonanatomical, vertical placement of the femoral tunnel led to failed normalization of knee kinematics.^46-50 Indeed, a higher tension-flexion pattern was found in this nonanatomical “roof” position for the femoral tunnel as compared with the native ACL—a pattern that can result in either loss of flexion or recurrent instability.^13,15,51

Clinical results of techniques used to create an anatomical ACLR centrally within the footprint have been mixed. Registry data showed that the revision rate at 4 years was higher with the AM portal technique (5.16%) than with transtibial drilling (3.20%).⁵² This higher rate may be associated with the more central placement of the femoral tunnel with the AM portal technique than with the transtibial technique, as shown in vivo with high-resolution magnetic resonance imaging.¹² Recent reports have documented a higher rate of failure with DB or central ACLR approaches than with traditional transtibial techniques.⁵³ As mentioned, in contrast to a more isometric position, a central femoral tunnel position would be expected to demonstrate 5 to 7 mm of length change, whereas moving the graft more posterior in the footprint (closer to the articular cartilage) would result in more than 1 cm of length change through the range of motion.^31,32 As such, these more central grafts, or grafts placed even lower (more posterior) in the footprint, would be expected to see high tension in extension (if fixed in flexion), or to lose tension completely during flexion (if the graft is fixed at full extension).³² This may be a mechanistic cause of the high failure rate in the more posterior bundles of the DB approach.⁵⁴

Together, these clinical data suggest that the femoral tunnel should be placed within the anatomical footprint of the ACL. However, within the footprint, a more eccentric femoral tunnel position capturing the isometric and direct region of the insertion may be preferable to a more central or posterior (low region) position.

Summary

Anatomical, histologic, isometric, biomechanical, and clinical data from more than 4 decades collectively point to an optimal position for the femoral tunnel within the femoral footprint. This position can be summarized by the acronym I.D.E.A.L., which refers to placing a femoral tunnel in a position that reproduces the Isometry of the native ACL, that covers the fibers of the Direct insertion histologically, that is Eccentrically located in the anterior (high) and proximal (deep) region of the footprint, that is Anatomical (within the footprint), and that replicates the Low tension-flexion pattern of the native ACL throughout the range of flexion and extension (Figure 5).

In vivo and in vitro studies as well as surgical experience suggest a need to avoid both (a) the nonanatomical vertical (roof) femoral tunnel placement that causes PCL impingement, high tension in the ACL graft in flexion, and ultimately graft stretch-out with instability and (b) the femoral tunnel placement in the posterior (lowest) region of the footprint that causes high tension in extension and can result in graft stretch-out with instability.^13,15,39,40 The transtibial and AM portal techniques can both be effective in properly placing the femoral tunnel and restoring motion, stability, and function to the knee. Their effectiveness, however, depends on correct placement of the femoral tunnel. We think coming studies will focus on single-bundle ACLR and will be designed to improve the reliability of the transtibial and AM portal techniques for placing a femoral tunnel in keeping with the principles summarized by the I.D.E.A.L. acronym.

Osteoarthritic (OA) knees with varus deformities commonly present with tight, contracted medial collateral ligaments and soft-tissue sleeves.¹ More severe varus deformities require more extensive medial releases on the concave side to optimize flexion-extension gaps. Excessive soft-tissue releases in milder varus deformities can result in medial instability in flexion and extension.^2-4 Misjudgments in soft-tissue release can therefore lead to knee instability, an important cause of early total knee arthroplasty (TKA) failures.^2,5,6 Some authors have reported difficulty in coronal plane balancing in knees with preoperative varus deformity of more than 20°.^4,7

Surgeons often refer to varus as a description of coronal mal­alignment, mainly with the knee in extension. In the surgical setting, however, descriptions are given regarding differential medial soft-tissue tightness in extension and flexion. Balancing the knee in extension may not necessarily balance the knee in flexion. Thus, there is the concept of extension and flexion varus, which has not been well described in the literature. Releases on the anterior medial and posterior medial aspects of the proximal tibia have differential effects on flexion and extension gaps, respectively.²

Intraoperative alignment certainly has a pivotal role in component longevity.⁸ Since its advent in the 1990s, use of computer navigation in TKA has offered new hope for improving component alignment. Some authors routinely use computer navigation for intraoperative soft-tissue releases.⁹ A recent meta-analysis found that computer-navigated surgery is associated with fewer outliers in final component alignment compared with conventional TKA.¹⁰

Increased use of computer navigation in TKA at our institution in recent years has come with the observation that knees with severe extension varus seem to have correspondingly more severe flexion varus. Before computer navigation, coronal alignment of knees in flexion was almost impossible to measure because of the spatial alignment of the knees in that position.

We conducted a study to evaluate the relationship of extension and flexion varus in OA knees and to determine whether severity of fixed flexion deformity (FFD) in the sagittal plane correlates with severity of coronal plane varus deformity. We hypothesized that there would be differential varus in flexion and extension and that increasing knee extension varus would correlate closely with knee flexion varus beyond a certain tibiofemoral angle. We also hypothesized that severity of sagittal plane deformity will correlate with the severity of coronal plane deformity.

Patients and Methods

Data Collection

After this study was approved by our institution’s ethics review committee, we prospectively collected data from 403 consecutive computer-navigated TKAs performed at our institution between November 2008 and August 2011. Dr. Tan, who was not the primary physician, retrospectively analyzed the radiographic and navigation data.

Each patient’s knee varus-valgus angles were captured by Dr. Teo, an adult reconstruction surgeon, in standard fashion from maximal extension to 0º, 30º, 45º, 60º, 90º, and maximal flexion. An example of standard data capture appears in Table 1. With varus-hyperextension defined as –0.5° or less (more negative), neutral as 0°, and valgus-flexion as 0.5° or more, there were 362 varus knees, 41 valgus knees, and no neutral knees.

Study inclusion criteria were OA and varus deformity. Exclusion criteria were rheumatoid arthritis, other types of inflammatory arthritis, neuromuscular disorders, knees with valgus angulation, and incomplete data (Table 2). Figure 1 summarizes the inclusion/exclusion process, which left 317 knees available for study. Cases of incomplete data were likely due to computer errors or to inadvertent movement when navigation data were being acquired during surgery.

In conventional TKA, the main objective is to equalize flexion-extension gaps with knee at 90° flexion and 0° extension. The ability to achieve this often implies the knee will be balanced throughout its range of motion (ROM). From the data for the 317 study knees, 3 sets of values were extracted: varus angles from maximal knee extension (extension varus), varus angles from 90° knee flexion (flexion varus), and maximal knee extension. All knees were able to achieve 90° flexion.

Power Calculation

Our analysis used a correlation coefficient (r) of at least 0.5 at a 5% level of significance and power of 80%. With 317 knees, the study was more than adequately powered for significance.

Surgical and Navigation Technique

All patients underwent either general or regional anesthesia for their surgeries, which were performed by Dr. Teo. Standard medial parapatellar arthrotomy was performed. Navigation pins were then inserted into the femur and tibia outside the knee wound. Anatomical reference points were digitized per routine navigation requirements. (The reference for varus-valgus alignment of the femur is the mechanical femur axis defined by the digitized hip center and knee center, and the reference for varus-valgus alignment of the tibia is the mechanical tibia axis defined by the digitized tibia center and calculated ankle center. The ankle center is calculated by dividing the digitized transmalleolar axis according to a ratio of 56% lateral to 44% medial with the inherent navigation software.) Our institution uses an imageless navigation system (Navigation System II; Stryker Orthopedics, Mahwah, New Jersey).

The leg was then brought from maximal knee extension to maximal knee flexion to assess preoperative ROM, which indicates inherent flexion contracture or hyperextension. Varus-valgus measurements of the knee were then generated as part of the navigation software protocol. These measurements were obtained without additional varus or valgus stress applied to the knee and before any bony resection. The rest of the operation was completed using navigation to guide bony resection and soft-tissue balancing. The final components used were all cemented cruciate-substituting TKA implants. After component insertion, the knee was again brought through ROM from maximal knee extension to maximal knee flexion to assess postoperative ROM before wound closure.

Extension and Flexion Varus

As none of the patients in the flexion varus dataset (range, –0.5° to –19°) had a varus deformity of more than 20° at 90° flexion, we used a cutoff of 10° to divide these patients into 2 subgroups: less than 10° (237 knees) and 10° or more (80 knees). The extension varus dataset ranged from –0.5° to –24°. Incremental values of –0.5° to –24° in this dataset were then analyzed against the 90° flexion varus subgroups using logistic regression. A scatterplot of the relationship between extension and flexion varus is shown in Figure 2. The probability function was then derived and a probability graph plotted.

FFD and Extension and Flexion Varus

Maximal knee extension, obtained from intraoperative navigation measurements, ranged from –9° (hyperextension) to 33° (FFD) and maximal knee flexion ranged from 90° to 146°. Ninety-two knees had slight hyperextension, and 6 were neutral. Of the 317 OA knees with varus deformity, 219 (69%) had FFD. This sagittal plane alignment parameter was analyzed against coronal plane alignment in maximal knee extension and 90° knee flexion to determine if increasing severity of FFD corresponds with increasing extension or flexion varus.

Statistical Analysis

Statistical analysis was performed with Stata 10.1 (Statacorp, College Station, Texas). Significance was set at P < .05.

Results

Extension and Flexion Varus

Patient demographic data are listed in Table 3. Univariate logistic regression analysis revealed that age (P = .110), body mass index (P = .696), and sex (P = .584) did not affect the association between preoperative extension and flexion varus.

Mean (SD) preoperative extension varus was –9.9° (4.80°), and mean (SD) preoperative flexion 90° varus was –7.02° (3.74°). Linear regression of the data showed a significant positive correlation between preoperative extension varus and flexion varus (Pearson correlation coefficient, 0.57; P < .0001). The probability function was determined as follows: Probability of having flexion varus of more than 10° = 1 / (1 + e–z), where z = –4.014 – 0.265 × extension varus. Plotting the probability graph of flexion varus against varus angles at maximal knee extension from the probability formula yielded a sigmoid graph (Figure 3). The most linear part of the graph corresponds to the 10° to 20° of extension varus (solid line), demonstrating an almost linear increase in the probability of having more than 10° flexion varus with increasing extension varus from 10° to 20°. For extension varus of 20° or more, the probability of having flexion varus of more than 10° approaches 1.

FFD and Extension and Flexion Varus

Mean (SD) preoperative maximal knee extension (analogous to FFD) was 4.41° (7.50°), mean (SD) extension varus was –9.9° (4.80°), and mean (SD) 90° flexion varus was –7.02° (3.74°). We did not find any correlation between preoperative FFD and preoperative flexion varus (r = –0.02; P = .6583) or extension varus (r = –0.11; P = .046) (Figure 4).

Postoperative Alignment

Of the 317 OA knees, 18 had incomplete navigation-acquired postoperative alignment data. The postoperative alignment of the other 299 knees at various degrees of knee flexion is illustrated with a box-and-whisker plot (Figure 5).

Knees With Severe Extension Varus

Fourteen of the 15 knees with severe extension varus (>20°) had flexion varus of more than 9° (range, –9° to –17.5°, with only 1 outlier, at –5°). For the 15 patients, maximal knee extension ranged from –9° hyperextension to 27.5° FFD. Six knees had slight hyperextension, and 9 had FFD demonstrating large variability in sagittal alignment. Despite severe preoperative coronal deformity, all 15 knees had satisfactory deformity correction. Preoperative and postoperative knee alignment data for these 15 knees appear in Table 4 and Figure 6, respectively.

Discussion

OA varus knees represent a majority of the cases being managed by orthopedic surgeons. Soft-tissue contractures involving the medial collateral ligament (MCL), posteromedial capsule, pes anserinus, and semimembranosus muscle are commonly encountered. Bone loss may also occur on the tibial and femoral joint surfaces in knees with severe angular deformity. In an OA varus knee, bone loss tends to be mainly on the medial tibial plateau and usually on the posterior aspect of the tibia because flexion contractures often are concomitant with these marked deformities.¹¹ Therefore, a varus deformity is apparent whether the knee is extended or flexed. Our results showed a correlation between extension and flexion varus in OA varus knees. In contrast, for a valgus deformity, as bone loss can occur on both the tibial and femoral surfaces,¹¹ a similar correlation may not be seen. For that reason, and because there were only 41 valgus knees in this study, they were excluded. For FFD, soft-tissue contractures often involve both the posterior capsule and the posterior cruciate ligament (PCL). Posterior osteophytes often cause tenting of the posterior capsule in knees with FFD. Anteriorly, growth of osteophytes at the tibial spine and intercondylar notch of the femur can result in bony causes of restricted knee extension.¹²

One would expect increased coronal plane angular deformity to correspond to more severe FFD in the sagittal plane because the same pathology affects soft tissue or bones in an OA knee in both planes. Interestingly, our study results proved otherwise. FFD did not correlate with degree of extension or flexion varus severity. This phenomenon has not been described in the literature likely because clinical measurements of flexion varus and FFD were difficult to perform because of the spatial alignment of the knee in flexion. In recent years, however, computer navigation technology has made such measurements possible.

Mihalko and colleagues² established that soft-tissue releases on different parts of the proximal tibia have different effects on soft-tissue balancing in flexion and extension. In knees with extension varus, more releases are required on the posterior medial aspect of the tibia (the posterior oblique fibers of the superficial MCL, the posteromedial capsule, and, sometimes, the semimembranosus), whereas knees with flexion varus require more releases on the anterior medial aspect of the tibia (the deep MCL, the anterior fibers of the superficial MCL, and, sometimes, the pes anserinus attachment).¹³ Consequently, soft-tissue stabilizers seem to have different functions in flexion and extension and cannot reliably be released solely in extension or flexion for optimal gap balancing during TKA.² Other authors, in cadaveric studies, have found that a larger amount of coronal deformity correction is achieved with more distal soft-tissue releases from the joint line.^9,14 Surgical techniques for correcting FFD include removal of prominent anterior and posterior osteophytes, posterior capsular releases, sometimes PCL sacrifices, and even gastrocnemius recession.¹²

In our study, all 14 patients with severe extension and correspondingly severe flexion varus needed not only modest posterior medial soft-tissue releases for the severe extension varus, but also modest anterior medial releases for the flexion varus. The respective soft-tissue releases were confirmed in real time with computer navigation sequentially after bony resection and osteophyte removal. With this method, we restored final postoperative alignment to within 3° of the mechanical axis (Figure 6). Our experience here led us to believe that, with these patients, modest anterior medial and posterior medial releases could be performed at the start of surgery, as severe extension varus (>20°) almost certainly equates to severe flexion varus (>10°). Therein lies the clinical relevance of our study. However, not all patients with severe coronal plane deformity have correspondingly severe sagittal plane deformity in the form of FFD, as illustrated in our study. Therefore, not all patients with severe varus knee deformity need aggressive posterior capsular release or PCL recession to correct FFD. Some patients have mild hyperextension, which can be attributed partly to the postanesthesia effects of soft-tissue laxity. It is unclear exactly how much anesthesia contributes to this difference in sagittal alignment, though the majority of our patients had FFD. It is not our intent here to discuss the surgical techniques of soft-tissue balancing or to advocate routine use of computer navigation.

Many factors (eg, medial femoral condyle bone loss, medial tibial plateau bone loss, femur or tibia bowing, medial soft-tissue contracture) can contribute to varus malalignment. Current navigation technology cannot isolate the causes of varus alignment, and we did not intend to investigate them in this study. Our primary aim was to assess for a correlation between overall extension varus alignment and expected flexion varus. We also wanted to analyze the correlation between FFD and the coronal plane alignment, in extension and flexion, contributed by the combined bony and soft-tissue components in OA varus knees.

The strengths of this study are that it was a single-surgeon series with knee data from consecutive patients who had computer-navigated TKA. Patient data were prospectively generated from the navigation software and retrospectively analyzed. All navigation alignment was performed by a single surgeon, thereby eliminating examination bias during the time knee alignment data were being obtained. The study was adequately powered and had a large number of patients for data analysis. The authors believe that this is the first study to analyze alignment in both the coronal and sagittal plane in varus OA knees.

We acknowledge a few limitations in our study. Although several investigators have found that navigation can be used to achieve accurate postoperative alignment,^10,15,16 subtle errors may be inadvertently introduced at different points of alignment measurement. These error points include identification of visually selected anatomical landmarks; kinematic registration of hip, knee, and ankle; and intraoperative changes in the navigation environment (eg, inadvertent movement of pins or rigid bodies). In addition, different surgeons have different techniques for kinematic registration. However, the surgeries in our study were performed by the same surgeon, so this confounding factor was effectively removed. Another limitation was that navigation alignment was obtained during surgery, when patients were under anesthesia and in a supine, non-weight-bearing position, whereas routine clinical weight-bearing radiographs are taken with nonanesthetized patients and this might overestimate the deformities intraoperatively. However, all parameters were measured in the same patient under the same anesthetic effects, so this should not have affected the analyses. Most surgeons would make an intraoperative assessment of the severity of any deformity before the surgery proper anyway. Nevertheless, some authors have found that knee alignment obtained with intraoperative navigation correlated well with alignment obtained with weight-bearing radiographs.^17,18

Conclusion

Our study results showed that, in OA varus knees, extension varus highly correlated with flexion varus. However, there was no correlation between FFD and coronal plane varus deformity.

Osteoarthritic (OA) knees with varus deformities commonly present with tight, contracted medial collateral ligaments and soft-tissue sleeves.¹ More severe varus deformities require more extensive medial releases on the concave side to optimize flexion-extension gaps. Excessive soft-tissue releases in milder varus deformities can result in medial instability in flexion and extension.^2-4 Misjudgments in soft-tissue release can therefore lead to knee instability, an important cause of early total knee arthroplasty (TKA) failures.^2,5,6 Some authors have reported difficulty in coronal plane balancing in knees with preoperative varus deformity of more than 20°.^4,7

Surgeons often refer to varus as a description of coronal mal­alignment, mainly with the knee in extension. In the surgical setting, however, descriptions are given regarding differential medial soft-tissue tightness in extension and flexion. Balancing the knee in extension may not necessarily balance the knee in flexion. Thus, there is the concept of extension and flexion varus, which has not been well described in the literature. Releases on the anterior medial and posterior medial aspects of the proximal tibia have differential effects on flexion and extension gaps, respectively.²

Intraoperative alignment certainly has a pivotal role in component longevity.⁸ Since its advent in the 1990s, use of computer navigation in TKA has offered new hope for improving component alignment. Some authors routinely use computer navigation for intraoperative soft-tissue releases.⁹ A recent meta-analysis found that computer-navigated surgery is associated with fewer outliers in final component alignment compared with conventional TKA.¹⁰

Increased use of computer navigation in TKA at our institution in recent years has come with the observation that knees with severe extension varus seem to have correspondingly more severe flexion varus. Before computer navigation, coronal alignment of knees in flexion was almost impossible to measure because of the spatial alignment of the knees in that position.

We conducted a study to evaluate the relationship of extension and flexion varus in OA knees and to determine whether severity of fixed flexion deformity (FFD) in the sagittal plane correlates with severity of coronal plane varus deformity. We hypothesized that there would be differential varus in flexion and extension and that increasing knee extension varus would correlate closely with knee flexion varus beyond a certain tibiofemoral angle. We also hypothesized that severity of sagittal plane deformity will correlate with the severity of coronal plane deformity.

Patients and Methods

Data Collection

After this study was approved by our institution’s ethics review committee, we prospectively collected data from 403 consecutive computer-navigated TKAs performed at our institution between November 2008 and August 2011. Dr. Tan, who was not the primary physician, retrospectively analyzed the radiographic and navigation data.

Each patient’s knee varus-valgus angles were captured by Dr. Teo, an adult reconstruction surgeon, in standard fashion from maximal extension to 0º, 30º, 45º, 60º, 90º, and maximal flexion. An example of standard data capture appears in Table 1. With varus-hyperextension defined as –0.5° or less (more negative), neutral as 0°, and valgus-flexion as 0.5° or more, there were 362 varus knees, 41 valgus knees, and no neutral knees.

Study inclusion criteria were OA and varus deformity. Exclusion criteria were rheumatoid arthritis, other types of inflammatory arthritis, neuromuscular disorders, knees with valgus angulation, and incomplete data (Table 2). Figure 1 summarizes the inclusion/exclusion process, which left 317 knees available for study. Cases of incomplete data were likely due to computer errors or to inadvertent movement when navigation data were being acquired during surgery.

In conventional TKA, the main objective is to equalize flexion-extension gaps with knee at 90° flexion and 0° extension. The ability to achieve this often implies the knee will be balanced throughout its range of motion (ROM). From the data for the 317 study knees, 3 sets of values were extracted: varus angles from maximal knee extension (extension varus), varus angles from 90° knee flexion (flexion varus), and maximal knee extension. All knees were able to achieve 90° flexion.

Power Calculation

Our analysis used a correlation coefficient (r) of at least 0.5 at a 5% level of significance and power of 80%. With 317 knees, the study was more than adequately powered for significance.

Surgical and Navigation Technique

All patients underwent either general or regional anesthesia for their surgeries, which were performed by Dr. Teo. Standard medial parapatellar arthrotomy was performed. Navigation pins were then inserted into the femur and tibia outside the knee wound. Anatomical reference points were digitized per routine navigation requirements. (The reference for varus-valgus alignment of the femur is the mechanical femur axis defined by the digitized hip center and knee center, and the reference for varus-valgus alignment of the tibia is the mechanical tibia axis defined by the digitized tibia center and calculated ankle center. The ankle center is calculated by dividing the digitized transmalleolar axis according to a ratio of 56% lateral to 44% medial with the inherent navigation software.) Our institution uses an imageless navigation system (Navigation System II; Stryker Orthopedics, Mahwah, New Jersey).

The leg was then brought from maximal knee extension to maximal knee flexion to assess preoperative ROM, which indicates inherent flexion contracture or hyperextension. Varus-valgus measurements of the knee were then generated as part of the navigation software protocol. These measurements were obtained without additional varus or valgus stress applied to the knee and before any bony resection. The rest of the operation was completed using navigation to guide bony resection and soft-tissue balancing. The final components used were all cemented cruciate-substituting TKA implants. After component insertion, the knee was again brought through ROM from maximal knee extension to maximal knee flexion to assess postoperative ROM before wound closure.

Extension and Flexion Varus

As none of the patients in the flexion varus dataset (range, –0.5° to –19°) had a varus deformity of more than 20° at 90° flexion, we used a cutoff of 10° to divide these patients into 2 subgroups: less than 10° (237 knees) and 10° or more (80 knees). The extension varus dataset ranged from –0.5° to –24°. Incremental values of –0.5° to –24° in this dataset were then analyzed against the 90° flexion varus subgroups using logistic regression. A scatterplot of the relationship between extension and flexion varus is shown in Figure 2. The probability function was then derived and a probability graph plotted.

FFD and Extension and Flexion Varus

Maximal knee extension, obtained from intraoperative navigation measurements, ranged from –9° (hyperextension) to 33° (FFD) and maximal knee flexion ranged from 90° to 146°. Ninety-two knees had slight hyperextension, and 6 were neutral. Of the 317 OA knees with varus deformity, 219 (69%) had FFD. This sagittal plane alignment parameter was analyzed against coronal plane alignment in maximal knee extension and 90° knee flexion to determine if increasing severity of FFD corresponds with increasing extension or flexion varus.

Statistical Analysis

Statistical analysis was performed with Stata 10.1 (Statacorp, College Station, Texas). Significance was set at P < .05.

Results

Extension and Flexion Varus

Patient demographic data are listed in Table 3. Univariate logistic regression analysis revealed that age (P = .110), body mass index (P = .696), and sex (P = .584) did not affect the association between preoperative extension and flexion varus.

Mean (SD) preoperative extension varus was –9.9° (4.80°), and mean (SD) preoperative flexion 90° varus was –7.02° (3.74°). Linear regression of the data showed a significant positive correlation between preoperative extension varus and flexion varus (Pearson correlation coefficient, 0.57; P < .0001). The probability function was determined as follows: Probability of having flexion varus of more than 10° = 1 / (1 + e–z), where z = –4.014 – 0.265 × extension varus. Plotting the probability graph of flexion varus against varus angles at maximal knee extension from the probability formula yielded a sigmoid graph (Figure 3). The most linear part of the graph corresponds to the 10° to 20° of extension varus (solid line), demonstrating an almost linear increase in the probability of having more than 10° flexion varus with increasing extension varus from 10° to 20°. For extension varus of 20° or more, the probability of having flexion varus of more than 10° approaches 1.

FFD and Extension and Flexion Varus

Mean (SD) preoperative maximal knee extension (analogous to FFD) was 4.41° (7.50°), mean (SD) extension varus was –9.9° (4.80°), and mean (SD) 90° flexion varus was –7.02° (3.74°). We did not find any correlation between preoperative FFD and preoperative flexion varus (r = –0.02; P = .6583) or extension varus (r = –0.11; P = .046) (Figure 4).

Postoperative Alignment

Of the 317 OA knees, 18 had incomplete navigation-acquired postoperative alignment data. The postoperative alignment of the other 299 knees at various degrees of knee flexion is illustrated with a box-and-whisker plot (Figure 5).

Knees With Severe Extension Varus

Fourteen of the 15 knees with severe extension varus (>20°) had flexion varus of more than 9° (range, –9° to –17.5°, with only 1 outlier, at –5°). For the 15 patients, maximal knee extension ranged from –9° hyperextension to 27.5° FFD. Six knees had slight hyperextension, and 9 had FFD demonstrating large variability in sagittal alignment. Despite severe preoperative coronal deformity, all 15 knees had satisfactory deformity correction. Preoperative and postoperative knee alignment data for these 15 knees appear in Table 4 and Figure 6, respectively.

Discussion

OA varus knees represent a majority of the cases being managed by orthopedic surgeons. Soft-tissue contractures involving the medial collateral ligament (MCL), posteromedial capsule, pes anserinus, and semimembranosus muscle are commonly encountered. Bone loss may also occur on the tibial and femoral joint surfaces in knees with severe angular deformity. In an OA varus knee, bone loss tends to be mainly on the medial tibial plateau and usually on the posterior aspect of the tibia because flexion contractures often are concomitant with these marked deformities.¹¹ Therefore, a varus deformity is apparent whether the knee is extended or flexed. Our results showed a correlation between extension and flexion varus in OA varus knees. In contrast, for a valgus deformity, as bone loss can occur on both the tibial and femoral surfaces,¹¹ a similar correlation may not be seen. For that reason, and because there were only 41 valgus knees in this study, they were excluded. For FFD, soft-tissue contractures often involve both the posterior capsule and the posterior cruciate ligament (PCL). Posterior osteophytes often cause tenting of the posterior capsule in knees with FFD. Anteriorly, growth of osteophytes at the tibial spine and intercondylar notch of the femur can result in bony causes of restricted knee extension.¹²

One would expect increased coronal plane angular deformity to correspond to more severe FFD in the sagittal plane because the same pathology affects soft tissue or bones in an OA knee in both planes. Interestingly, our study results proved otherwise. FFD did not correlate with degree of extension or flexion varus severity. This phenomenon has not been described in the literature likely because clinical measurements of flexion varus and FFD were difficult to perform because of the spatial alignment of the knee in flexion. In recent years, however, computer navigation technology has made such measurements possible.

Mihalko and colleagues² established that soft-tissue releases on different parts of the proximal tibia have different effects on soft-tissue balancing in flexion and extension. In knees with extension varus, more releases are required on the posterior medial aspect of the tibia (the posterior oblique fibers of the superficial MCL, the posteromedial capsule, and, sometimes, the semimembranosus), whereas knees with flexion varus require more releases on the anterior medial aspect of the tibia (the deep MCL, the anterior fibers of the superficial MCL, and, sometimes, the pes anserinus attachment).¹³ Consequently, soft-tissue stabilizers seem to have different functions in flexion and extension and cannot reliably be released solely in extension or flexion for optimal gap balancing during TKA.² Other authors, in cadaveric studies, have found that a larger amount of coronal deformity correction is achieved with more distal soft-tissue releases from the joint line.^9,14 Surgical techniques for correcting FFD include removal of prominent anterior and posterior osteophytes, posterior capsular releases, sometimes PCL sacrifices, and even gastrocnemius recession.¹²

In our study, all 14 patients with severe extension and correspondingly severe flexion varus needed not only modest posterior medial soft-tissue releases for the severe extension varus, but also modest anterior medial releases for the flexion varus. The respective soft-tissue releases were confirmed in real time with computer navigation sequentially after bony resection and osteophyte removal. With this method, we restored final postoperative alignment to within 3° of the mechanical axis (Figure 6). Our experience here led us to believe that, with these patients, modest anterior medial and posterior medial releases could be performed at the start of surgery, as severe extension varus (>20°) almost certainly equates to severe flexion varus (>10°). Therein lies the clinical relevance of our study. However, not all patients with severe coronal plane deformity have correspondingly severe sagittal plane deformity in the form of FFD, as illustrated in our study. Therefore, not all patients with severe varus knee deformity need aggressive posterior capsular release or PCL recession to correct FFD. Some patients have mild hyperextension, which can be attributed partly to the postanesthesia effects of soft-tissue laxity. It is unclear exactly how much anesthesia contributes to this difference in sagittal alignment, though the majority of our patients had FFD. It is not our intent here to discuss the surgical techniques of soft-tissue balancing or to advocate routine use of computer navigation.

Many factors (eg, medial femoral condyle bone loss, medial tibial plateau bone loss, femur or tibia bowing, medial soft-tissue contracture) can contribute to varus malalignment. Current navigation technology cannot isolate the causes of varus alignment, and we did not intend to investigate them in this study. Our primary aim was to assess for a correlation between overall extension varus alignment and expected flexion varus. We also wanted to analyze the correlation between FFD and the coronal plane alignment, in extension and flexion, contributed by the combined bony and soft-tissue components in OA varus knees.

The strengths of this study are that it was a single-surgeon series with knee data from consecutive patients who had computer-navigated TKA. Patient data were prospectively generated from the navigation software and retrospectively analyzed. All navigation alignment was performed by a single surgeon, thereby eliminating examination bias during the time knee alignment data were being obtained. The study was adequately powered and had a large number of patients for data analysis. The authors believe that this is the first study to analyze alignment in both the coronal and sagittal plane in varus OA knees.

We acknowledge a few limitations in our study. Although several investigators have found that navigation can be used to achieve accurate postoperative alignment,^10,15,16 subtle errors may be inadvertently introduced at different points of alignment measurement. These error points include identification of visually selected anatomical landmarks; kinematic registration of hip, knee, and ankle; and intraoperative changes in the navigation environment (eg, inadvertent movement of pins or rigid bodies). In addition, different surgeons have different techniques for kinematic registration. However, the surgeries in our study were performed by the same surgeon, so this confounding factor was effectively removed. Another limitation was that navigation alignment was obtained during surgery, when patients were under anesthesia and in a supine, non-weight-bearing position, whereas routine clinical weight-bearing radiographs are taken with nonanesthetized patients and this might overestimate the deformities intraoperatively. However, all parameters were measured in the same patient under the same anesthetic effects, so this should not have affected the analyses. Most surgeons would make an intraoperative assessment of the severity of any deformity before the surgery proper anyway. Nevertheless, some authors have found that knee alignment obtained with intraoperative navigation correlated well with alignment obtained with weight-bearing radiographs.^17,18

Conclusion

Our study results showed that, in OA varus knees, extension varus highly correlated with flexion varus. However, there was no correlation between FFD and coronal plane varus deformity.

Osteoarthritic (OA) knees with varus deformities commonly present with tight, contracted medial collateral ligaments and soft-tissue sleeves.¹ More severe varus deformities require more extensive medial releases on the concave side to optimize flexion-extension gaps. Excessive soft-tissue releases in milder varus deformities can result in medial instability in flexion and extension.^2-4 Misjudgments in soft-tissue release can therefore lead to knee instability, an important cause of early total knee arthroplasty (TKA) failures.^2,5,6 Some authors have reported difficulty in coronal plane balancing in knees with preoperative varus deformity of more than 20°.^4,7

Surgeons often refer to varus as a description of coronal mal­alignment, mainly with the knee in extension. In the surgical setting, however, descriptions are given regarding differential medial soft-tissue tightness in extension and flexion. Balancing the knee in extension may not necessarily balance the knee in flexion. Thus, there is the concept of extension and flexion varus, which has not been well described in the literature. Releases on the anterior medial and posterior medial aspects of the proximal tibia have differential effects on flexion and extension gaps, respectively.²

Intraoperative alignment certainly has a pivotal role in component longevity.⁸ Since its advent in the 1990s, use of computer navigation in TKA has offered new hope for improving component alignment. Some authors routinely use computer navigation for intraoperative soft-tissue releases.⁹ A recent meta-analysis found that computer-navigated surgery is associated with fewer outliers in final component alignment compared with conventional TKA.¹⁰

Increased use of computer navigation in TKA at our institution in recent years has come with the observation that knees with severe extension varus seem to have correspondingly more severe flexion varus. Before computer navigation, coronal alignment of knees in flexion was almost impossible to measure because of the spatial alignment of the knees in that position.

We conducted a study to evaluate the relationship of extension and flexion varus in OA knees and to determine whether severity of fixed flexion deformity (FFD) in the sagittal plane correlates with severity of coronal plane varus deformity. We hypothesized that there would be differential varus in flexion and extension and that increasing knee extension varus would correlate closely with knee flexion varus beyond a certain tibiofemoral angle. We also hypothesized that severity of sagittal plane deformity will correlate with the severity of coronal plane deformity.

Patients and Methods

Data Collection

After this study was approved by our institution’s ethics review committee, we prospectively collected data from 403 consecutive computer-navigated TKAs performed at our institution between November 2008 and August 2011. Dr. Tan, who was not the primary physician, retrospectively analyzed the radiographic and navigation data.

Each patient’s knee varus-valgus angles were captured by Dr. Teo, an adult reconstruction surgeon, in standard fashion from maximal extension to 0º, 30º, 45º, 60º, 90º, and maximal flexion. An example of standard data capture appears in Table 1. With varus-hyperextension defined as –0.5° or less (more negative), neutral as 0°, and valgus-flexion as 0.5° or more, there were 362 varus knees, 41 valgus knees, and no neutral knees.

Study inclusion criteria were OA and varus deformity. Exclusion criteria were rheumatoid arthritis, other types of inflammatory arthritis, neuromuscular disorders, knees with valgus angulation, and incomplete data (Table 2). Figure 1 summarizes the inclusion/exclusion process, which left 317 knees available for study. Cases of incomplete data were likely due to computer errors or to inadvertent movement when navigation data were being acquired during surgery.

In conventional TKA, the main objective is to equalize flexion-extension gaps with knee at 90° flexion and 0° extension. The ability to achieve this often implies the knee will be balanced throughout its range of motion (ROM). From the data for the 317 study knees, 3 sets of values were extracted: varus angles from maximal knee extension (extension varus), varus angles from 90° knee flexion (flexion varus), and maximal knee extension. All knees were able to achieve 90° flexion.

Power Calculation

Our analysis used a correlation coefficient (r) of at least 0.5 at a 5% level of significance and power of 80%. With 317 knees, the study was more than adequately powered for significance.

Surgical and Navigation Technique

All patients underwent either general or regional anesthesia for their surgeries, which were performed by Dr. Teo. Standard medial parapatellar arthrotomy was performed. Navigation pins were then inserted into the femur and tibia outside the knee wound. Anatomical reference points were digitized per routine navigation requirements. (The reference for varus-valgus alignment of the femur is the mechanical femur axis defined by the digitized hip center and knee center, and the reference for varus-valgus alignment of the tibia is the mechanical tibia axis defined by the digitized tibia center and calculated ankle center. The ankle center is calculated by dividing the digitized transmalleolar axis according to a ratio of 56% lateral to 44% medial with the inherent navigation software.) Our institution uses an imageless navigation system (Navigation System II; Stryker Orthopedics, Mahwah, New Jersey).

The leg was then brought from maximal knee extension to maximal knee flexion to assess preoperative ROM, which indicates inherent flexion contracture or hyperextension. Varus-valgus measurements of the knee were then generated as part of the navigation software protocol. These measurements were obtained without additional varus or valgus stress applied to the knee and before any bony resection. The rest of the operation was completed using navigation to guide bony resection and soft-tissue balancing. The final components used were all cemented cruciate-substituting TKA implants. After component insertion, the knee was again brought through ROM from maximal knee extension to maximal knee flexion to assess postoperative ROM before wound closure.

Extension and Flexion Varus

As none of the patients in the flexion varus dataset (range, –0.5° to –19°) had a varus deformity of more than 20° at 90° flexion, we used a cutoff of 10° to divide these patients into 2 subgroups: less than 10° (237 knees) and 10° or more (80 knees). The extension varus dataset ranged from –0.5° to –24°. Incremental values of –0.5° to –24° in this dataset were then analyzed against the 90° flexion varus subgroups using logistic regression. A scatterplot of the relationship between extension and flexion varus is shown in Figure 2. The probability function was then derived and a probability graph plotted.

FFD and Extension and Flexion Varus

Maximal knee extension, obtained from intraoperative navigation measurements, ranged from –9° (hyperextension) to 33° (FFD) and maximal knee flexion ranged from 90° to 146°. Ninety-two knees had slight hyperextension, and 6 were neutral. Of the 317 OA knees with varus deformity, 219 (69%) had FFD. This sagittal plane alignment parameter was analyzed against coronal plane alignment in maximal knee extension and 90° knee flexion to determine if increasing severity of FFD corresponds with increasing extension or flexion varus.

Statistical Analysis

Statistical analysis was performed with Stata 10.1 (Statacorp, College Station, Texas). Significance was set at P < .05.

Results

Extension and Flexion Varus

Patient demographic data are listed in Table 3. Univariate logistic regression analysis revealed that age (P = .110), body mass index (P = .696), and sex (P = .584) did not affect the association between preoperative extension and flexion varus.

Mean (SD) preoperative extension varus was –9.9° (4.80°), and mean (SD) preoperative flexion 90° varus was –7.02° (3.74°). Linear regression of the data showed a significant positive correlation between preoperative extension varus and flexion varus (Pearson correlation coefficient, 0.57; P < .0001). The probability function was determined as follows: Probability of having flexion varus of more than 10° = 1 / (1 + e–z), where z = –4.014 – 0.265 × extension varus. Plotting the probability graph of flexion varus against varus angles at maximal knee extension from the probability formula yielded a sigmoid graph (Figure 3). The most linear part of the graph corresponds to the 10° to 20° of extension varus (solid line), demonstrating an almost linear increase in the probability of having more than 10° flexion varus with increasing extension varus from 10° to 20°. For extension varus of 20° or more, the probability of having flexion varus of more than 10° approaches 1.

FFD and Extension and Flexion Varus

Mean (SD) preoperative maximal knee extension (analogous to FFD) was 4.41° (7.50°), mean (SD) extension varus was –9.9° (4.80°), and mean (SD) 90° flexion varus was –7.02° (3.74°). We did not find any correlation between preoperative FFD and preoperative flexion varus (r = –0.02; P = .6583) or extension varus (r = –0.11; P = .046) (Figure 4).

Postoperative Alignment

Of the 317 OA knees, 18 had incomplete navigation-acquired postoperative alignment data. The postoperative alignment of the other 299 knees at various degrees of knee flexion is illustrated with a box-and-whisker plot (Figure 5).

Knees With Severe Extension Varus

Fourteen of the 15 knees with severe extension varus (>20°) had flexion varus of more than 9° (range, –9° to –17.5°, with only 1 outlier, at –5°). For the 15 patients, maximal knee extension ranged from –9° hyperextension to 27.5° FFD. Six knees had slight hyperextension, and 9 had FFD demonstrating large variability in sagittal alignment. Despite severe preoperative coronal deformity, all 15 knees had satisfactory deformity correction. Preoperative and postoperative knee alignment data for these 15 knees appear in Table 4 and Figure 6, respectively.

Discussion

OA varus knees represent a majority of the cases being managed by orthopedic surgeons. Soft-tissue contractures involving the medial collateral ligament (MCL), posteromedial capsule, pes anserinus, and semimembranosus muscle are commonly encountered. Bone loss may also occur on the tibial and femoral joint surfaces in knees with severe angular deformity. In an OA varus knee, bone loss tends to be mainly on the medial tibial plateau and usually on the posterior aspect of the tibia because flexion contractures often are concomitant with these marked deformities.¹¹ Therefore, a varus deformity is apparent whether the knee is extended or flexed. Our results showed a correlation between extension and flexion varus in OA varus knees. In contrast, for a valgus deformity, as bone loss can occur on both the tibial and femoral surfaces,¹¹ a similar correlation may not be seen. For that reason, and because there were only 41 valgus knees in this study, they were excluded. For FFD, soft-tissue contractures often involve both the posterior capsule and the posterior cruciate ligament (PCL). Posterior osteophytes often cause tenting of the posterior capsule in knees with FFD. Anteriorly, growth of osteophytes at the tibial spine and intercondylar notch of the femur can result in bony causes of restricted knee extension.¹²

One would expect increased coronal plane angular deformity to correspond to more severe FFD in the sagittal plane because the same pathology affects soft tissue or bones in an OA knee in both planes. Interestingly, our study results proved otherwise. FFD did not correlate with degree of extension or flexion varus severity. This phenomenon has not been described in the literature likely because clinical measurements of flexion varus and FFD were difficult to perform because of the spatial alignment of the knee in flexion. In recent years, however, computer navigation technology has made such measurements possible.

Mihalko and colleagues² established that soft-tissue releases on different parts of the proximal tibia have different effects on soft-tissue balancing in flexion and extension. In knees with extension varus, more releases are required on the posterior medial aspect of the tibia (the posterior oblique fibers of the superficial MCL, the posteromedial capsule, and, sometimes, the semimembranosus), whereas knees with flexion varus require more releases on the anterior medial aspect of the tibia (the deep MCL, the anterior fibers of the superficial MCL, and, sometimes, the pes anserinus attachment).¹³ Consequently, soft-tissue stabilizers seem to have different functions in flexion and extension and cannot reliably be released solely in extension or flexion for optimal gap balancing during TKA.² Other authors, in cadaveric studies, have found that a larger amount of coronal deformity correction is achieved with more distal soft-tissue releases from the joint line.^9,14 Surgical techniques for correcting FFD include removal of prominent anterior and posterior osteophytes, posterior capsular releases, sometimes PCL sacrifices, and even gastrocnemius recession.¹²

In our study, all 14 patients with severe extension and correspondingly severe flexion varus needed not only modest posterior medial soft-tissue releases for the severe extension varus, but also modest anterior medial releases for the flexion varus. The respective soft-tissue releases were confirmed in real time with computer navigation sequentially after bony resection and osteophyte removal. With this method, we restored final postoperative alignment to within 3° of the mechanical axis (Figure 6). Our experience here led us to believe that, with these patients, modest anterior medial and posterior medial releases could be performed at the start of surgery, as severe extension varus (>20°) almost certainly equates to severe flexion varus (>10°). Therein lies the clinical relevance of our study. However, not all patients with severe coronal plane deformity have correspondingly severe sagittal plane deformity in the form of FFD, as illustrated in our study. Therefore, not all patients with severe varus knee deformity need aggressive posterior capsular release or PCL recession to correct FFD. Some patients have mild hyperextension, which can be attributed partly to the postanesthesia effects of soft-tissue laxity. It is unclear exactly how much anesthesia contributes to this difference in sagittal alignment, though the majority of our patients had FFD. It is not our intent here to discuss the surgical techniques of soft-tissue balancing or to advocate routine use of computer navigation.

Many factors (eg, medial femoral condyle bone loss, medial tibial plateau bone loss, femur or tibia bowing, medial soft-tissue contracture) can contribute to varus malalignment. Current navigation technology cannot isolate the causes of varus alignment, and we did not intend to investigate them in this study. Our primary aim was to assess for a correlation between overall extension varus alignment and expected flexion varus. We also wanted to analyze the correlation between FFD and the coronal plane alignment, in extension and flexion, contributed by the combined bony and soft-tissue components in OA varus knees.

The strengths of this study are that it was a single-surgeon series with knee data from consecutive patients who had computer-navigated TKA. Patient data were prospectively generated from the navigation software and retrospectively analyzed. All navigation alignment was performed by a single surgeon, thereby eliminating examination bias during the time knee alignment data were being obtained. The study was adequately powered and had a large number of patients for data analysis. The authors believe that this is the first study to analyze alignment in both the coronal and sagittal plane in varus OA knees.

We acknowledge a few limitations in our study. Although several investigators have found that navigation can be used to achieve accurate postoperative alignment,^10,15,16 subtle errors may be inadvertently introduced at different points of alignment measurement. These error points include identification of visually selected anatomical landmarks; kinematic registration of hip, knee, and ankle; and intraoperative changes in the navigation environment (eg, inadvertent movement of pins or rigid bodies). In addition, different surgeons have different techniques for kinematic registration. However, the surgeries in our study were performed by the same surgeon, so this confounding factor was effectively removed. Another limitation was that navigation alignment was obtained during surgery, when patients were under anesthesia and in a supine, non-weight-bearing position, whereas routine clinical weight-bearing radiographs are taken with nonanesthetized patients and this might overestimate the deformities intraoperatively. However, all parameters were measured in the same patient under the same anesthetic effects, so this should not have affected the analyses. Most surgeons would make an intraoperative assessment of the severity of any deformity before the surgery proper anyway. Nevertheless, some authors have found that knee alignment obtained with intraoperative navigation correlated well with alignment obtained with weight-bearing radiographs.^17,18

Conclusion

Our study results showed that, in OA varus knees, extension varus highly correlated with flexion varus. However, there was no correlation between FFD and coronal plane varus deformity.