A young couple already has decided to bring their as-yet-unborn child to your group. Now they are interviewing each member in hopes of finding a primary care physician who will best fit their expectations. Their second question for you is, “How do you feel about letting a baby cry itself to sleep?”

You sense that their question is a Rorschach test and a sneaky attempt to peer into what makes you tick. But let’s pretend for a moment that you are seized by a brain cramp and fail to do the obvious by turning the question around and asking them about how they feel about sleep training. Instead, you shoot from the hip. How would you respond?

Would you tell them that allowing a child to cry himself to sleep is neither dangerous nor cruel? Nor does it commit the child to a life of insecurity and emotional imbalance. In your opinion, if done correctly, it is usually the quickest and least painful way to help a child develop healthy sleep habits.

Or would you tell them that their child’s cry means that he needs something, and it is their responsibility to meet that need? That you believe letting a child cry himself to sleep is cruel and that it is better to let a child develop the skill of falling to sleep naturally at his own pace.

Because you neglected to first determine where these parents are coming from, regardless of which end of the spectrum you favor, your candid, nuance-free answer is likely to be a problem for somebody. If you revealed that you are a let-’em-cry proponent, the parents who were looking for a sensitive, child-centered pediatrician will quickly cross you off their list. However, if the parents choose you because you presented yourself as a let-nature-take-its-time pediatrician, they may have narrowed their options when their baby fails to settle in easily.

The challenge of how best to advise parents about infant sleep problems is a prime example of when practicing primary care medicine becomes an art. The answer to the let-’em-cry … or not dilemma is saturated with emotion and pretty much devoid of supporting scientific data. My gut, my personality, and 40 years of experience tell me that, more often than not, letting children cry themselves to sleep is the better approach. However, experience also has told me to keep my mouth shut when the topic of infant sleep is painted in the black-and-white question of let ‘em cry … or not.

The best approach is to learn as much as possible about the baby’s parents. Do they have similar or widely differing tolerances for a crying infant? I won’t really learn this until the parenting game has begun. Will I be able to convince these parents that, while it may be their responsibility to meet their crying child’s needs, one of those needs is the need to fall asleep? Or will I be wasting my time by trying to change their instincts?

Regardless of your own bias, your advice must be tailored to each individual family’s strengths and vulnerabilities, including the child’s temperament and the parents’ emotional resilience and tolerance for crying. Just as when we are counseling a mother who is nearing the end of her struggle with breastfeeding, a pediatrician must be prepared to become a chameleon and leave his or her bias behind.

One of the best strategies for avoiding that treacherous let-’em-cry … or not fork in the road is to promote good sleep habits from the beginning. When a baby is gaining weight, I encourage mothers to shorten feedings so that the baby finishes most feedings sated and drowsy but not fully asleep. I urge parents who find that a pacifier helps to use it only when the child is in his crib and to create a dim light, minimal-stimulation environment from around 7 p.m. to 7 a.m. By encouraging families to adopt these and other sleep-friendly practices early, I can often avoid revealing the ugly truth that, at my core, I am really a let-’em-cry guy.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

A young couple already has decided to bring their as-yet-unborn child to your group. Now they are interviewing each member in hopes of finding a primary care physician who will best fit their expectations. Their second question for you is, “How do you feel about letting a baby cry itself to sleep?”

You sense that their question is a Rorschach test and a sneaky attempt to peer into what makes you tick. But let’s pretend for a moment that you are seized by a brain cramp and fail to do the obvious by turning the question around and asking them about how they feel about sleep training. Instead, you shoot from the hip. How would you respond?

Would you tell them that allowing a child to cry himself to sleep is neither dangerous nor cruel? Nor does it commit the child to a life of insecurity and emotional imbalance. In your opinion, if done correctly, it is usually the quickest and least painful way to help a child develop healthy sleep habits.

Or would you tell them that their child’s cry means that he needs something, and it is their responsibility to meet that need? That you believe letting a child cry himself to sleep is cruel and that it is better to let a child develop the skill of falling to sleep naturally at his own pace.

Because you neglected to first determine where these parents are coming from, regardless of which end of the spectrum you favor, your candid, nuance-free answer is likely to be a problem for somebody. If you revealed that you are a let-’em-cry proponent, the parents who were looking for a sensitive, child-centered pediatrician will quickly cross you off their list. However, if the parents choose you because you presented yourself as a let-nature-take-its-time pediatrician, they may have narrowed their options when their baby fails to settle in easily.

The challenge of how best to advise parents about infant sleep problems is a prime example of when practicing primary care medicine becomes an art. The answer to the let-’em-cry … or not dilemma is saturated with emotion and pretty much devoid of supporting scientific data. My gut, my personality, and 40 years of experience tell me that, more often than not, letting children cry themselves to sleep is the better approach. However, experience also has told me to keep my mouth shut when the topic of infant sleep is painted in the black-and-white question of let ‘em cry … or not.

The best approach is to learn as much as possible about the baby’s parents. Do they have similar or widely differing tolerances for a crying infant? I won’t really learn this until the parenting game has begun. Will I be able to convince these parents that, while it may be their responsibility to meet their crying child’s needs, one of those needs is the need to fall asleep? Or will I be wasting my time by trying to change their instincts?

Regardless of your own bias, your advice must be tailored to each individual family’s strengths and vulnerabilities, including the child’s temperament and the parents’ emotional resilience and tolerance for crying. Just as when we are counseling a mother who is nearing the end of her struggle with breastfeeding, a pediatrician must be prepared to become a chameleon and leave his or her bias behind.

One of the best strategies for avoiding that treacherous let-’em-cry … or not fork in the road is to promote good sleep habits from the beginning. When a baby is gaining weight, I encourage mothers to shorten feedings so that the baby finishes most feedings sated and drowsy but not fully asleep. I urge parents who find that a pacifier helps to use it only when the child is in his crib and to create a dim light, minimal-stimulation environment from around 7 p.m. to 7 a.m. By encouraging families to adopt these and other sleep-friendly practices early, I can often avoid revealing the ugly truth that, at my core, I am really a let-’em-cry guy.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

A young couple already has decided to bring their as-yet-unborn child to your group. Now they are interviewing each member in hopes of finding a primary care physician who will best fit their expectations. Their second question for you is, “How do you feel about letting a baby cry itself to sleep?”

You sense that their question is a Rorschach test and a sneaky attempt to peer into what makes you tick. But let’s pretend for a moment that you are seized by a brain cramp and fail to do the obvious by turning the question around and asking them about how they feel about sleep training. Instead, you shoot from the hip. How would you respond?

Would you tell them that allowing a child to cry himself to sleep is neither dangerous nor cruel? Nor does it commit the child to a life of insecurity and emotional imbalance. In your opinion, if done correctly, it is usually the quickest and least painful way to help a child develop healthy sleep habits.

Or would you tell them that their child’s cry means that he needs something, and it is their responsibility to meet that need? That you believe letting a child cry himself to sleep is cruel and that it is better to let a child develop the skill of falling to sleep naturally at his own pace.

Because you neglected to first determine where these parents are coming from, regardless of which end of the spectrum you favor, your candid, nuance-free answer is likely to be a problem for somebody. If you revealed that you are a let-’em-cry proponent, the parents who were looking for a sensitive, child-centered pediatrician will quickly cross you off their list. However, if the parents choose you because you presented yourself as a let-nature-take-its-time pediatrician, they may have narrowed their options when their baby fails to settle in easily.

The challenge of how best to advise parents about infant sleep problems is a prime example of when practicing primary care medicine becomes an art. The answer to the let-’em-cry … or not dilemma is saturated with emotion and pretty much devoid of supporting scientific data. My gut, my personality, and 40 years of experience tell me that, more often than not, letting children cry themselves to sleep is the better approach. However, experience also has told me to keep my mouth shut when the topic of infant sleep is painted in the black-and-white question of let ‘em cry … or not.

The best approach is to learn as much as possible about the baby’s parents. Do they have similar or widely differing tolerances for a crying infant? I won’t really learn this until the parenting game has begun. Will I be able to convince these parents that, while it may be their responsibility to meet their crying child’s needs, one of those needs is the need to fall asleep? Or will I be wasting my time by trying to change their instincts?

Regardless of your own bias, your advice must be tailored to each individual family’s strengths and vulnerabilities, including the child’s temperament and the parents’ emotional resilience and tolerance for crying. Just as when we are counseling a mother who is nearing the end of her struggle with breastfeeding, a pediatrician must be prepared to become a chameleon and leave his or her bias behind.

One of the best strategies for avoiding that treacherous let-’em-cry … or not fork in the road is to promote good sleep habits from the beginning. When a baby is gaining weight, I encourage mothers to shorten feedings so that the baby finishes most feedings sated and drowsy but not fully asleep. I urge parents who find that a pacifier helps to use it only when the child is in his crib and to create a dim light, minimal-stimulation environment from around 7 p.m. to 7 a.m. By encouraging families to adopt these and other sleep-friendly practices early, I can often avoid revealing the ugly truth that, at my core, I am really a let-’em-cry guy.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

The prevalence of methicillin-resistant Staphylococcus aureus colonization among asymptomatic athletes is more than three times higher than the rate reported for the community population overall, a systematic review and meta-analysis showed.

Investigators searched PubMed and EMBASE looking for studies on MRSA colonization among the athletic community. They did not include studies involving individuals who previously were infected or had active MRSA infections. The database search yielded 382 studies, and of those, 15 were included in the meta-analysis, reported Dr. Styliani Karanika of Rhode Island Hospital’s infectious diseases division at Brown University, Providence, R.I. (Clin Infect Dis. 2016 April 18. doi: 10.1093/cid/ciw240).

©Photo Researchers/NHGRI

By conducting a statistical analysis among 1,495 screened asymptomatic athletic team members (athletes and staff), Dr. Karanika and colleagues were able to see how the prevalence of MRSA colonization differed among athletes by level of playing experience and sport. The investigators found that the 6% prevalence of MRSA colonization among asymptomatic athletes was comparable to the prevalence among patients on dialysis (6%) and those with HIV (6.9%). Among college athletes, the 13% prevalence of MRSA was almost twice the rate found among patients in intensive care units (7%).

When it came to individual sports, the highest prevalence was found in wrestling (22%), followed by football (8%) and basketball (8%). The risk for subsequent MRSA skin and soft tissue infection among colonized athletes was more than seven times higher than the risk of MRSA skin and soft tissue infection among noncolonized athletes within a 3-month follow-up period upon documented MRSA colonization. Decolonization treatment was effective in reducing the risk of infection in colonized individuals.

“Our findings highlight the importance of controlling the spread of MRSA in the athletic setting, particularly among collegiate athletes,” Dr. Karanika said in an interview.

Dr. Karanika noted that athletes are more susceptible to MRSA because of the frequency of skin abrasions, close contact, shared equipment and training facilities, and poor hygiene practices that can result from the intense demands and time restrictions. Because the prevalence of MRSA colonization is high among this group, coaches, athletes, and athletic trainers should be aware of the early symptoms of a MRSA skin and soft tissue infection, and they should be educated about proper hygiene and prevention and control protocols to halt the spread of MRSA.

Though researchers found decolonization to be effective at reducing the risk of subsequent infection, they believe more research is needed to determine the durability and feasibility of decolonization regimens. Until these protocols are established, they said, strategies including implementing MRSA surveillance in athletes, environmental surveys, and regularly occurring physical examinations of athletes over the course of the season might help break the cycle of MRSA colonization-infection-transmission in athletic settings.

The investigators declared no conflicts of interest.

The prevalence of methicillin-resistant Staphylococcus aureus colonization among asymptomatic athletes is more than three times higher than the rate reported for the community population overall, a systematic review and meta-analysis showed.

Investigators searched PubMed and EMBASE looking for studies on MRSA colonization among the athletic community. They did not include studies involving individuals who previously were infected or had active MRSA infections. The database search yielded 382 studies, and of those, 15 were included in the meta-analysis, reported Dr. Styliani Karanika of Rhode Island Hospital’s infectious diseases division at Brown University, Providence, R.I. (Clin Infect Dis. 2016 April 18. doi: 10.1093/cid/ciw240).

©Photo Researchers/NHGRI

By conducting a statistical analysis among 1,495 screened asymptomatic athletic team members (athletes and staff), Dr. Karanika and colleagues were able to see how the prevalence of MRSA colonization differed among athletes by level of playing experience and sport. The investigators found that the 6% prevalence of MRSA colonization among asymptomatic athletes was comparable to the prevalence among patients on dialysis (6%) and those with HIV (6.9%). Among college athletes, the 13% prevalence of MRSA was almost twice the rate found among patients in intensive care units (7%).

When it came to individual sports, the highest prevalence was found in wrestling (22%), followed by football (8%) and basketball (8%). The risk for subsequent MRSA skin and soft tissue infection among colonized athletes was more than seven times higher than the risk of MRSA skin and soft tissue infection among noncolonized athletes within a 3-month follow-up period upon documented MRSA colonization. Decolonization treatment was effective in reducing the risk of infection in colonized individuals.

“Our findings highlight the importance of controlling the spread of MRSA in the athletic setting, particularly among collegiate athletes,” Dr. Karanika said in an interview.

Dr. Karanika noted that athletes are more susceptible to MRSA because of the frequency of skin abrasions, close contact, shared equipment and training facilities, and poor hygiene practices that can result from the intense demands and time restrictions. Because the prevalence of MRSA colonization is high among this group, coaches, athletes, and athletic trainers should be aware of the early symptoms of a MRSA skin and soft tissue infection, and they should be educated about proper hygiene and prevention and control protocols to halt the spread of MRSA.

Though researchers found decolonization to be effective at reducing the risk of subsequent infection, they believe more research is needed to determine the durability and feasibility of decolonization regimens. Until these protocols are established, they said, strategies including implementing MRSA surveillance in athletes, environmental surveys, and regularly occurring physical examinations of athletes over the course of the season might help break the cycle of MRSA colonization-infection-transmission in athletic settings.

The investigators declared no conflicts of interest.

The prevalence of methicillin-resistant Staphylococcus aureus colonization among asymptomatic athletes is more than three times higher than the rate reported for the community population overall, a systematic review and meta-analysis showed.

Investigators searched PubMed and EMBASE looking for studies on MRSA colonization among the athletic community. They did not include studies involving individuals who previously were infected or had active MRSA infections. The database search yielded 382 studies, and of those, 15 were included in the meta-analysis, reported Dr. Styliani Karanika of Rhode Island Hospital’s infectious diseases division at Brown University, Providence, R.I. (Clin Infect Dis. 2016 April 18. doi: 10.1093/cid/ciw240).

©Photo Researchers/NHGRI

By conducting a statistical analysis among 1,495 screened asymptomatic athletic team members (athletes and staff), Dr. Karanika and colleagues were able to see how the prevalence of MRSA colonization differed among athletes by level of playing experience and sport. The investigators found that the 6% prevalence of MRSA colonization among asymptomatic athletes was comparable to the prevalence among patients on dialysis (6%) and those with HIV (6.9%). Among college athletes, the 13% prevalence of MRSA was almost twice the rate found among patients in intensive care units (7%).

When it came to individual sports, the highest prevalence was found in wrestling (22%), followed by football (8%) and basketball (8%). The risk for subsequent MRSA skin and soft tissue infection among colonized athletes was more than seven times higher than the risk of MRSA skin and soft tissue infection among noncolonized athletes within a 3-month follow-up period upon documented MRSA colonization. Decolonization treatment was effective in reducing the risk of infection in colonized individuals.

“Our findings highlight the importance of controlling the spread of MRSA in the athletic setting, particularly among collegiate athletes,” Dr. Karanika said in an interview.

Dr. Karanika noted that athletes are more susceptible to MRSA because of the frequency of skin abrasions, close contact, shared equipment and training facilities, and poor hygiene practices that can result from the intense demands and time restrictions. Because the prevalence of MRSA colonization is high among this group, coaches, athletes, and athletic trainers should be aware of the early symptoms of a MRSA skin and soft tissue infection, and they should be educated about proper hygiene and prevention and control protocols to halt the spread of MRSA.

Though researchers found decolonization to be effective at reducing the risk of subsequent infection, they believe more research is needed to determine the durability and feasibility of decolonization regimens. Until these protocols are established, they said, strategies including implementing MRSA surveillance in athletes, environmental surveys, and regularly occurring physical examinations of athletes over the course of the season might help break the cycle of MRSA colonization-infection-transmission in athletic settings.

The investigators declared no conflicts of interest.

Adding telephone coaching to a home-based physiotherapist-prescribed activity program does not increase the pain and function benefits of such a program alone in knee osteoarthritis, a randomized controlled trial shows.

Kim L. Bennell, Ph.D., and her associates recruited volunteers who were aged 50 years and older, had knee pain rated at 4 or higher on an 11-point scale, and were classified as sedentary. One group participated in both coaching and the home-based physiotherapy program; the other participated in the home-based physiotherapy program alone.

©decade3d/Thinkstock

Overall,142 (85%), 136 (81%), and 128 (76%) participants completed 6-, 12-, and 18-month measurements. In the 6-month outcomes, no significance differences were found between the two groups in average pain (mean difference, 0.4 units) or in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) function (1.8 units). In addition, there was no change between group differences observed at either 12 or 18 months. At 6 months, however, both groups showed large significant and clinically important improvements from baseline in the primary outcomes of pain and function, reported Dr. Bennell of the Centre for Health, Exercise and Sports Medicine at the University of Melbourne.

Reseachers also examined secondary outcomes and found there was no significant difference for change in numeric rating scale walking pain, WOMAC pain, or quality-of-life scores at any time.

“Improving exercise adherence was an aim of our coaching intervention given that adherence is positively linked to clinical outcomes in knee OA,” the reseachers concluded. “Our study provides novel information about the effects of telephone coaching alongside a physiotherapy prescribed physical activity and exercise program and extends the limited research in telephone coaching for OA.”

Read the full study in Arthritis Care & Research (doi: 10.1002/acr.22915).

[email protected]

Adding telephone coaching to a home-based physiotherapist-prescribed activity program does not increase the pain and function benefits of such a program alone in knee osteoarthritis, a randomized controlled trial shows.

Kim L. Bennell, Ph.D., and her associates recruited volunteers who were aged 50 years and older, had knee pain rated at 4 or higher on an 11-point scale, and were classified as sedentary. One group participated in both coaching and the home-based physiotherapy program; the other participated in the home-based physiotherapy program alone.

©decade3d/Thinkstock

Overall,142 (85%), 136 (81%), and 128 (76%) participants completed 6-, 12-, and 18-month measurements. In the 6-month outcomes, no significance differences were found between the two groups in average pain (mean difference, 0.4 units) or in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) function (1.8 units). In addition, there was no change between group differences observed at either 12 or 18 months. At 6 months, however, both groups showed large significant and clinically important improvements from baseline in the primary outcomes of pain and function, reported Dr. Bennell of the Centre for Health, Exercise and Sports Medicine at the University of Melbourne.

Reseachers also examined secondary outcomes and found there was no significant difference for change in numeric rating scale walking pain, WOMAC pain, or quality-of-life scores at any time.

“Improving exercise adherence was an aim of our coaching intervention given that adherence is positively linked to clinical outcomes in knee OA,” the reseachers concluded. “Our study provides novel information about the effects of telephone coaching alongside a physiotherapy prescribed physical activity and exercise program and extends the limited research in telephone coaching for OA.”

Read the full study in Arthritis Care & Research (doi: 10.1002/acr.22915).

[email protected]

Adding telephone coaching to a home-based physiotherapist-prescribed activity program does not increase the pain and function benefits of such a program alone in knee osteoarthritis, a randomized controlled trial shows.

Kim L. Bennell, Ph.D., and her associates recruited volunteers who were aged 50 years and older, had knee pain rated at 4 or higher on an 11-point scale, and were classified as sedentary. One group participated in both coaching and the home-based physiotherapy program; the other participated in the home-based physiotherapy program alone.

©decade3d/Thinkstock

Overall,142 (85%), 136 (81%), and 128 (76%) participants completed 6-, 12-, and 18-month measurements. In the 6-month outcomes, no significance differences were found between the two groups in average pain (mean difference, 0.4 units) or in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) function (1.8 units). In addition, there was no change between group differences observed at either 12 or 18 months. At 6 months, however, both groups showed large significant and clinically important improvements from baseline in the primary outcomes of pain and function, reported Dr. Bennell of the Centre for Health, Exercise and Sports Medicine at the University of Melbourne.

Reseachers also examined secondary outcomes and found there was no significant difference for change in numeric rating scale walking pain, WOMAC pain, or quality-of-life scores at any time.

“Improving exercise adherence was an aim of our coaching intervention given that adherence is positively linked to clinical outcomes in knee OA,” the reseachers concluded. “Our study provides novel information about the effects of telephone coaching alongside a physiotherapy prescribed physical activity and exercise program and extends the limited research in telephone coaching for OA.”

Read the full study in Arthritis Care & Research (doi: 10.1002/acr.22915).

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

CHICAGO – Stroke risk in diabetic women with restless legs syndrome (RLS) is triple that of diabetic men with the sensorimotor disease, Zoe Heis reported at the annual meeting of the American College of Cardiology.

The mechanism underlying this marked gender discrepancy in risk requires further investigation, as does the highly practical question of whether improved diabetic control can reduce the stroke risk, said Ms. Heis of the Center for Integrative Research on Cardiovascular Aging at Aurora Health Care in Milwaukee.

She presented a retrospective cohort study of 385 patients diagnosed with RLS during 2011-2013 at a community sleep center using the International RLS Study Group criteria. Along with 770 propensity-matched controls, they were followed until mid-2015. At baseline, 40% of the RLS patients had diabetes and 70% had hypertension, as did 32% and 63% of controls, respectively.

Stroke occurred in 7.5% of the RLS group and 4.2% of matched controls. The presence of diabetes more than doubled the stroke risk in both groups.

The risk of stroke was 18.2% in diabetic women with RLS and 7% in diabetic men with RLS. In a multivariate analysis that controlled for potential confounding factors, this translated to a threefold increased stroke risk.

Diabetes was associated with a doubling of stroke risk in subjects without RLS, but the risk was similar in men and women, according to Ms. Heis.

In addition to diabetes and female gender, the other major predictor of increased stroke risk in patients with RLS was, not surprisingly, hypertension. It was associated with a 13-fold increased likelihood of stroke, she noted.

RLS was initially linked to increased risk of coronary heart disease in a report from the Nurses’ Health Study (Circulation. 2012 Oct 2;126[14]:1689-94). In 2015, another research group linked more severe RLS to an increased risk of stroke. Ms. Heis and her coinvestigators carried out the current study to test their hypothesis that, since diabetes is a condition that accelerates cardiovascular disease, the endocrine disorder would boost stroke risk more in subjects with RLS than in those without it.

Ms. Heis reported having no financial conflicts regarding her study, which was conducted free of commercial support.

[email protected]

A successful hospitalist program requires strong leadership from the floor to the C-suite. SHM’s Leadership Academy prepares clinical and academic leaders with vital skills traditionally not taught in medical school or typical residency programs. This year’s meeting will be held from October 24 to 27 at Disney’s BoardWalk Inn in Lake Buena Vista, Fla. Courses offered include:

• Leadership Foundations: Evaluate your personal leadership strengths and weaknesses, understand key hospital drivers, and more.
• Advanced Leadership: Influential Management: Learn the skills needed to drive culture change through specific leadership behaviors and actions as well as financial storytelling.

  (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

•  Advanced Leadership: Mastering Teamwork: Learn to critically assess program growth opportunities, lead and motivate teams, and design effective communication strategies. (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

Build the skills and resources necessary to successfully lead and manage a hospital medicine program now and in the future. Learn more at www.shmleadershipacademy.org.

A successful hospitalist program requires strong leadership from the floor to the C-suite. SHM’s Leadership Academy prepares clinical and academic leaders with vital skills traditionally not taught in medical school or typical residency programs. This year’s meeting will be held from October 24 to 27 at Disney’s BoardWalk Inn in Lake Buena Vista, Fla. Courses offered include:

• Leadership Foundations: Evaluate your personal leadership strengths and weaknesses, understand key hospital drivers, and more.
• Advanced Leadership: Influential Management: Learn the skills needed to drive culture change through specific leadership behaviors and actions as well as financial storytelling.

  (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

•  Advanced Leadership: Mastering Teamwork: Learn to critically assess program growth opportunities, lead and motivate teams, and design effective communication strategies. (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

Build the skills and resources necessary to successfully lead and manage a hospital medicine program now and in the future. Learn more at www.shmleadershipacademy.org.

A successful hospitalist program requires strong leadership from the floor to the C-suite. SHM’s Leadership Academy prepares clinical and academic leaders with vital skills traditionally not taught in medical school or typical residency programs. This year’s meeting will be held from October 24 to 27 at Disney’s BoardWalk Inn in Lake Buena Vista, Fla. Courses offered include:

• Leadership Foundations: Evaluate your personal leadership strengths and weaknesses, understand key hospital drivers, and more.
• Advanced Leadership: Influential Management: Learn the skills needed to drive culture change through specific leadership behaviors and actions as well as financial storytelling.

  (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

•  Advanced Leadership: Mastering Teamwork: Learn to critically assess program growth opportunities, lead and motivate teams, and design effective communication strategies. (Prerequisite: Leadership Foundations or an advanced management degree upon course director approval.)

Build the skills and resources necessary to successfully lead and manage a hospital medicine program now and in the future. Learn more at www.shmleadershipacademy.org.

Eric Howell, MD, MHM, recently was promoted to professor of medicine at Johns Hopkins University in Baltimore. Dr. Howell serves as division director of the Collaborative Inpatient Medicine Service (CIMS) at Johns Hopkins Bayview Medical Center. He is a past president of SHM and currently a senior physician advisor for the society.

 

Aric Groshong, MD, is the first pediatric hospitalist at CHI Mercy Health Mercy Medical Center in Roseburg, Ore. Dr. Groshong previously served the Roseburg community through his private practice for 21 years. CHI Mercy Health Mercy Medical Center is a 174-bed acute-care hospital serving southwestern Oregon since 1909.

 

Michael Malek, MD, is the new chief medical officer of Hope Hospice in Dublin, Calif. Dr. Malek is a hospitalist who most recently served as lead hospitalist for the Palo Alto Medical Foundation in Dublin. He also served as an associate medical director of Hope Hospice from 2005 to 2013.

 

 

Chris Moriates, MD, was appointed assistant dean of healthcare value and associate professor in the department of internal medicine at the new Dell Medical School at the University of Texas at Austin. Most recently, Dr. Moriates served as an assistant professor in the hospital medicine division at the University of California, San Francisco (UCSF). Dr. Moriates also serves as the director of implementation initiatives at Costs of Care, a global nonprofit organization focused on delivering better care at a lower cost.

Ted Pennel, MD, has been named the new chief hospitalist of Gordon Hospital in Calhoun, Ga. He previously served as chief hospitalist at Redmond Regional Medical Center in Rome, Ga. Dr. Pennel has been affiliated with Gordon Hospital, a 69-bed community hospital in the Adventist Health system, since 1988.

 

 

Gina Puglisi, MD, received the 2016 Summit Award from EmCare, a hospitalist management company based in Dallas. Dr. Puglisi is a hospitalist at Nyack Hospital in Nyack, N.Y. Each year, EmCare chooses a single outstanding hospitalist from across the country to receive the award.

 

 

Bedri Yusuf, MD, SFHM, is the new vice president and chief physician executive for Gwinnett Medical Group in Lawrenceville, Ga. Dr. Yusuf most recently served as vice president of Gwinnett Medical Center’s medical staff and co-director of the hospitalist program there. Dr. Yusuf has been a hospitalist at Gwinnett since 2006.

Business Moves

Winter Haven Hospital in Winter Haven, Fla., is now offering pediatric hospitalist services thanks to an agreement with Watson Clinic, based in Lakeland, Fla. The new pediatric unit consists of eight beds and is supervised by three pediatric hospitalists. Winter Haven Hospital is a 468-bed nonprofit hospital and is one of 14 hospitals in the BayCare Health System, which serves the greater Tampa Bay region of Florida.

TeamHealth has been recognized by Becker’s Hospital Review as one of “150 Great Places to Work in Healthcare.” TeamHealth also made the list of “The World’s Most Admired Companies” by Fortune magazine for the second year in a row. TeamHealth is a physician management company based in Knoxville, Tenn., with more than 3,400 acute- and post-acute-care facilities and physician groups across the country. TeamHealth was founded in 1979.

Ob Hospitalist Group (OBHG), based in Greenville, S.C., recently announced eight new ob-gyn hospitalist programs. OBHG’s new programs reside at the following hospitals: Alexian Brothers Women & Children’s Hospital in Hoffman Estates, Ill.; Baylor Medical Center at Carrollton in Carrollton, Texas; Florida Hospital Tampa in Tampa, Fla.; JFK Medical Center in Atlantis, Fla.; Memorial Hospital Central in Colorado Springs, Colo.; Mother Frances Hospital Tyler in Tyler, Texas; Northridge Hospital Medical Center in Northridge, Calif.; and Salinas Valley Memorial Hospital in Salinas, Calif. OBHG has been staffing ob-gyn hospitalists since 2006.

Eric Howell, MD, MHM, recently was promoted to professor of medicine at Johns Hopkins University in Baltimore. Dr. Howell serves as division director of the Collaborative Inpatient Medicine Service (CIMS) at Johns Hopkins Bayview Medical Center. He is a past president of SHM and currently a senior physician advisor for the society.

 

Aric Groshong, MD, is the first pediatric hospitalist at CHI Mercy Health Mercy Medical Center in Roseburg, Ore. Dr. Groshong previously served the Roseburg community through his private practice for 21 years. CHI Mercy Health Mercy Medical Center is a 174-bed acute-care hospital serving southwestern Oregon since 1909.

 

Michael Malek, MD, is the new chief medical officer of Hope Hospice in Dublin, Calif. Dr. Malek is a hospitalist who most recently served as lead hospitalist for the Palo Alto Medical Foundation in Dublin. He also served as an associate medical director of Hope Hospice from 2005 to 2013.

 

 

Chris Moriates, MD, was appointed assistant dean of healthcare value and associate professor in the department of internal medicine at the new Dell Medical School at the University of Texas at Austin. Most recently, Dr. Moriates served as an assistant professor in the hospital medicine division at the University of California, San Francisco (UCSF). Dr. Moriates also serves as the director of implementation initiatives at Costs of Care, a global nonprofit organization focused on delivering better care at a lower cost.

Ted Pennel, MD, has been named the new chief hospitalist of Gordon Hospital in Calhoun, Ga. He previously served as chief hospitalist at Redmond Regional Medical Center in Rome, Ga. Dr. Pennel has been affiliated with Gordon Hospital, a 69-bed community hospital in the Adventist Health system, since 1988.

 

 

Gina Puglisi, MD, received the 2016 Summit Award from EmCare, a hospitalist management company based in Dallas. Dr. Puglisi is a hospitalist at Nyack Hospital in Nyack, N.Y. Each year, EmCare chooses a single outstanding hospitalist from across the country to receive the award.

 

 

Bedri Yusuf, MD, SFHM, is the new vice president and chief physician executive for Gwinnett Medical Group in Lawrenceville, Ga. Dr. Yusuf most recently served as vice president of Gwinnett Medical Center’s medical staff and co-director of the hospitalist program there. Dr. Yusuf has been a hospitalist at Gwinnett since 2006.

Business Moves

Winter Haven Hospital in Winter Haven, Fla., is now offering pediatric hospitalist services thanks to an agreement with Watson Clinic, based in Lakeland, Fla. The new pediatric unit consists of eight beds and is supervised by three pediatric hospitalists. Winter Haven Hospital is a 468-bed nonprofit hospital and is one of 14 hospitals in the BayCare Health System, which serves the greater Tampa Bay region of Florida.

TeamHealth has been recognized by Becker’s Hospital Review as one of “150 Great Places to Work in Healthcare.” TeamHealth also made the list of “The World’s Most Admired Companies” by Fortune magazine for the second year in a row. TeamHealth is a physician management company based in Knoxville, Tenn., with more than 3,400 acute- and post-acute-care facilities and physician groups across the country. TeamHealth was founded in 1979.

Ob Hospitalist Group (OBHG), based in Greenville, S.C., recently announced eight new ob-gyn hospitalist programs. OBHG’s new programs reside at the following hospitals: Alexian Brothers Women & Children’s Hospital in Hoffman Estates, Ill.; Baylor Medical Center at Carrollton in Carrollton, Texas; Florida Hospital Tampa in Tampa, Fla.; JFK Medical Center in Atlantis, Fla.; Memorial Hospital Central in Colorado Springs, Colo.; Mother Frances Hospital Tyler in Tyler, Texas; Northridge Hospital Medical Center in Northridge, Calif.; and Salinas Valley Memorial Hospital in Salinas, Calif. OBHG has been staffing ob-gyn hospitalists since 2006.

Eric Howell, MD, MHM, recently was promoted to professor of medicine at Johns Hopkins University in Baltimore. Dr. Howell serves as division director of the Collaborative Inpatient Medicine Service (CIMS) at Johns Hopkins Bayview Medical Center. He is a past president of SHM and currently a senior physician advisor for the society.

 

Aric Groshong, MD, is the first pediatric hospitalist at CHI Mercy Health Mercy Medical Center in Roseburg, Ore. Dr. Groshong previously served the Roseburg community through his private practice for 21 years. CHI Mercy Health Mercy Medical Center is a 174-bed acute-care hospital serving southwestern Oregon since 1909.

 

Michael Malek, MD, is the new chief medical officer of Hope Hospice in Dublin, Calif. Dr. Malek is a hospitalist who most recently served as lead hospitalist for the Palo Alto Medical Foundation in Dublin. He also served as an associate medical director of Hope Hospice from 2005 to 2013.

 

 

Chris Moriates, MD, was appointed assistant dean of healthcare value and associate professor in the department of internal medicine at the new Dell Medical School at the University of Texas at Austin. Most recently, Dr. Moriates served as an assistant professor in the hospital medicine division at the University of California, San Francisco (UCSF). Dr. Moriates also serves as the director of implementation initiatives at Costs of Care, a global nonprofit organization focused on delivering better care at a lower cost.

Ted Pennel, MD, has been named the new chief hospitalist of Gordon Hospital in Calhoun, Ga. He previously served as chief hospitalist at Redmond Regional Medical Center in Rome, Ga. Dr. Pennel has been affiliated with Gordon Hospital, a 69-bed community hospital in the Adventist Health system, since 1988.

 

 

Gina Puglisi, MD, received the 2016 Summit Award from EmCare, a hospitalist management company based in Dallas. Dr. Puglisi is a hospitalist at Nyack Hospital in Nyack, N.Y. Each year, EmCare chooses a single outstanding hospitalist from across the country to receive the award.

 

 

Bedri Yusuf, MD, SFHM, is the new vice president and chief physician executive for Gwinnett Medical Group in Lawrenceville, Ga. Dr. Yusuf most recently served as vice president of Gwinnett Medical Center’s medical staff and co-director of the hospitalist program there. Dr. Yusuf has been a hospitalist at Gwinnett since 2006.

Business Moves

Winter Haven Hospital in Winter Haven, Fla., is now offering pediatric hospitalist services thanks to an agreement with Watson Clinic, based in Lakeland, Fla. The new pediatric unit consists of eight beds and is supervised by three pediatric hospitalists. Winter Haven Hospital is a 468-bed nonprofit hospital and is one of 14 hospitals in the BayCare Health System, which serves the greater Tampa Bay region of Florida.

TeamHealth has been recognized by Becker’s Hospital Review as one of “150 Great Places to Work in Healthcare.” TeamHealth also made the list of “The World’s Most Admired Companies” by Fortune magazine for the second year in a row. TeamHealth is a physician management company based in Knoxville, Tenn., with more than 3,400 acute- and post-acute-care facilities and physician groups across the country. TeamHealth was founded in 1979.

Ob Hospitalist Group (OBHG), based in Greenville, S.C., recently announced eight new ob-gyn hospitalist programs. OBHG’s new programs reside at the following hospitals: Alexian Brothers Women & Children’s Hospital in Hoffman Estates, Ill.; Baylor Medical Center at Carrollton in Carrollton, Texas; Florida Hospital Tampa in Tampa, Fla.; JFK Medical Center in Atlantis, Fla.; Memorial Hospital Central in Colorado Springs, Colo.; Mother Frances Hospital Tyler in Tyler, Texas; Northridge Hospital Medical Center in Northridge, Calif.; and Salinas Valley Memorial Hospital in Salinas, Calif. OBHG has been staffing ob-gyn hospitalists since 2006.

Case

A 66-year-old man with diabetes mellitus type 2 and hypertension underwent left total knee replacement. Several hours after surgery, the patient developed atrial fibrillation (AF). He was asymptomatic, and reversible causes of AF were ruled out. Approximately 18 hours later, he spontaneously reverted back to sinus rhythm. Should this patient, who has no known prior history of AF and a CHA2DS2-VASc score of 3, be started on anticoagulation?

Background

Hospitalists are commonly consulted for evaluation and management of postoperative atrial fibrillation (POAF). The incidence of new-onset AF associated with non-cardiac surgery is approximately 2% and may be more frequent in an elderly population.1 The increased adrenergic tone associated with surgery is thought to elicit AF in some patients. POAF has also been associated with positive fluid balance, electrolyte abnormalities, and hypoxemia.2 Some of these patients will spontaneously revert back to sinus rhythm after these issues are reversed. Others will go on to develop chronic or paroxysmal AF that persists indefinitely. It is also likely that some patients with POAF, in fact, already had asymptomatic AF that was simply undetected prior to hospitalization.

Hospitalists are faced with the difficult task of determining which patients with POAF will benefit from either short-term or long-term anticoagulation. This has not been well studied in postsurgical patients, in contrast to medical patients in whom stroke risk from AF has been very well-characterized. The decision may be further complicated by bleeding risk (associated with either some surgeries or with patient-dependent factors).3

It is worth noting that following major cardiac or thoracic surgery, POAF is common; the incidence ranges from 10% to 60%. In these cases, POAF may be triggered by transient atrial ischemia or by postoperative inflammation and may have a different natural history from POAF in non-cardiac surgery patients in terms of both reversibility and stroke risk. More retrospective data are available regarding cardiothoracic surgery patients.

Previous American Heart Association (AHA) and American College of Cardiology (ACC) guidelines stated that POAF lasting longer than 48 hours warranted anticoagulation. This recommendation was removed from the newest update. The 2014 updated AHA/ACC guidelines are less absolute and now state only that “it is reasonable to administer antithrombotic medication in patients who developed postoperative AF, as recommended for nonsurgical patients” (Level of Evidence: B) in regard to cardiothoracic surgery.4

There is no specific recommendation regarding POAF for non-cardiac surgery patients. The current guidelines are likely purposefully vague due to the lack of direct evidence. The following is a review of the existing literature and a suggested approach to anticoagulation in POAF.

Review

How common is postoperative atrial fibrillation? New-onset AF during hospitalization is known to occur in association with many acute conditions including surgery, infection, and myocardial infarction. About half of the cases of in-hospital new-onset AF are associated with surgery. AF is more commonly seen in surgery that involves the thoracic cavity and cardiac structures. In a cross-sectional epidemiologic study of 22 million patients in California, 20.8% of patients undergoing cardiac surgery developed POAF compared with only 1.3% of patients undergoing non-cardiac surgery.5 A smaller study of non-cardiac surgery patients found a 30-day POAF incidence of 0.37%.2

Does postoperative atrial fibrillation increase the short-term risk of stroke? A major concern in AF is the risk of stroke. It is well-established that prolonged or recurrent AF increases the risk for stroke over months or years, but do short episodes of POAF increase stroke risk to a significant degree? Most of the studies in the literature focus on perioperative stroke risk specifically in cardiothoracic surgery. A prospective study of 4,000 patients undergoing cardiac surgery found that the in-hospital postoperative stroke risk was 3.3% in patients with POAF compared to 1.4% in patients without POAF (P<0.01).6 Similar outcomes were seen in a VA study looking at patients who underwent open heart surgery: Stroke risk was 5.3% at six months in POAF patients compared to 2.4% in those without POAF.7 Another study of coronary artery bypass graft (CABG) patients with a follow-up of almost six years showed a stroke risk of 12.1% in POAF patients compared to 8.4% in those without POAF.8

 

It is not clear that all of the increase in stroke risk is a direct effect of POAF. Indeed, in a retrospective analysis of almost 3,000 CABG patients, 1.1% suffered a stroke during their hospital stay. Fewer than half of those had a cardiac rhythm other than sinus rhythm. In the 15 stroke patients who developed POAF, nine presented with stroke symptoms prior to the first episode of AF.9 The authors suggest that aggressive anticoagulation for POAF would not have prevented most of these events.

Furthermore, the rate of in-hospital stroke after non-cardiac surgery is probably much lower, though it has not been as well studied. These data raise some questions as to the benefit of anticoagulation in the immediate postoperative period, though it is difficult to draw firm conclusions without randomized data.

What about non-cardiac surgery? There is less evidence available for patients undergoing non-cardiac surgery, but the few studies that do exist also point to higher stroke risk in patients with POAF. A large population-based study using ICD codes found that the one-year risk of stroke for patients with POAF after non-cardiac surgery was 1.47% compared to 0.36% in non-cardiac surgery patients without POAF (P<0.001). Based on these data, the long-term stroke risk after POAF in non-cardiac surgery patients is similar to that of medical AF patients with a CHA2DS2-VASc score of 2. The authors of this study suggest that transient POAF after non-cardiac surgery may carry a long-term stroke risk similar to any other AF diagnosis.10 However, this study design is subject to significant ascertainment bias (i.e., they may have unintentionally captured some patients with preexisting or prolonged AF), and further research is needed to better delineate this risk.

Does increased stroke risk translate into increased mortality? In a retrospective study of 17,000 patients, El-Chami et al found that POAF after CABG was associated with decreased survival after one year (90% versus 96%) and 10 years (55% versus 70%).11 However, those patients who develop POAF may be sicker overall.

Another study showed that death due to stroke occurred in 4.2% of POAF patients compared to 0.2% of non-POAF patients in a five-year period.12 Based on these studies, POAF is likely associated with increased mortality, but there may be other unaccounted variables. Nevertheless, the increased mortality associated with POAF in these populations is similar to that seen for non-surgical population-based studies13 and provides support that those with newly diagnosed AF in the post-surgical setting should at least be followed closely to assess for recurrence.

What is a patient’s risk of developing atrial fibrillation later in life? When we choose to anticoagulate patients with POAF, we then have to determine whether they should be committed to long-term anticoagulation. It is thought that many cases of POAF are transient; however, some patients will go on to have persistent or paroxysmal AF after discharge.

A retrospective study examined 571 patients who underwent CABG, 30% of whom had POAF during the index admission. After five years of follow-up, 25% of those with POAF were diagnosed with paroxysmal or persistent AF after discharge compared to only 3% of patients without POAF. Researchers did this by looking at the most recent ECG, if done in the last year, or by obtaining a new ECG at the five-year point.12 By this method, it is probable that some diagnoses of paroxysmal AF were missed.

In another study of about 300 CABG patients, about 20% of patients with POAF also went on to develop post-discharge AF, defined as symptomatic AF that led to medical evaluation. As in the previous study, it is likely that there were undetected episodes of AF.14 Thus, in cardiothoracic surgery patients, some but not all of whom develop POAF have recurrent or ongoing AF. For this reason, if anticoagulation is started, it may be reasonable to stop anticoagulation after weeks or months if ongoing AF is not apparent.

 

What is the risk of postoperative bleeding if anticoagulation is started? Any decision about the benefits of anticoagulation must be weighed against the risks, most notably the risk of serious or life-threatening bleeding. This risk may be heightened in the immediate perioperative period. Discussions should always take place with our surgical colleagues about type of surgery, intraoperative complications, and postoperative risk of bleeding.

Anticoagulation, if indicated, should not be started until postoperative bleeding risk is deemed appropriately low. That said, the 2015 BRIDGE trial (looking at the benefits and risks of “bridging” patients before surgery) provides some peripheral but meaningful information about postoperative bleeding risk. In this study, patients with preexisting AF who underwent low-bleeding-risk surgery and were bridged on day one after surgery with therapeutic doses of unfractionated or low-molecular-weight heparin had a significantly higher risk of postoperative bleeding compared to non-bridged patients, with a number needed to harm of 50.15 It may be reasonable—and likely safer—to wait a couple days to start anticoagulation for patients with POAF.

What is the expert’s opinion? We asked one of our cardiac electrophysiologists what her approach is to this situation. In general, if a patient has a low stroke risk and is in AF for fewer than 24 hours, it is reasonable to defer anticoagulation and follow as an outpatient. Regardless of risk, if AF is sustained for more than 24 hours, we recommend at least four weeks of anticoagulation and close outpatient follow-up, which should include a period of ambulatory monitoring to determine the need for continued anticoagulation. We also recommend considering what comprises the patient’s stroke risk.

For example, if the CHA2DS2-VASc score is 2 but the points come from being a female with coronary artery disease, we would consider forgoing anticoagulation but arranging for an outpatient cardiac monitor with cardiology follow-up. If the patient has a history of stroke or TIA, we recommend continuing anticoagulation indefinitely.

Back to the Case

Given our patient’s episode of POAF lasted fewer than 24 hours, it would be reasonable to hold off starting anticoagulation, but he should be followed as an outpatient with ambulatory monitoring at a minimum, monitoring for recurrence. If he were to develop recurrent AF, then he would warrant anticoagulation based on an annual stroke risk of 3.2% as determined by a CHA2DS2-VASc score of 3.

Bottom Line

Our strategy is as follows: If a patient has a low stroke risk (i.e., CHA2DS2-VASc score <2) and is in AF for fewer than 24 hours, anticoagulation is not started, but outpatient follow-up is arranged to monitor symptoms. Regardless of stroke risk, if a patient is in AF for more than 24 hours, we initiate and continue anticoagulation for a minimum of four weeks and arrange outpatient follow-up with a period of ambulatory monitoring to determine need for continued anticoagulation. If a patient has a high stroke risk (CHA2DS2-VASc >2) or if their risk factors include a history of stroke or TIA, anticoagulation is started and continued indefinitely. Risk-benefit discussion is held with the patient, especially with regard to bleeding risk, prior to anticoagulation initiation. If the individual patient’s situation presents further nuance, we ask for the assistance of our cardiology or cardiac electrophysiology colleagues.

Final Thought

None of the mentioned studies investigated or included newer oral anticoagulants. Risk-benefit ratios may change (potentially considerably) with these agents. Further study is needed. We expect, in due time, studies will look at the question of POAF in regard to newer anticoagulant agents, and perhaps then our decision making will change. TH

---

 

Dr. Evavold is a resident in the hospitalist training program, while Dr. Lessing and Dr. Merritt are hospitalists in the Department of Internal Medicine at the University of Colorado. Dr. Tzou is a cardiologist in the section of electrophysiology at the University of Colorado.

References:

1. POISE Study Group, Devereaux PJ, Yang H, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. Lancet. 2008;371(9627):1839-1847. doi:10.1016/s0140-6736(08)60601-7.
2. Christians K, Wu B, Quebbeman E, Brasel K. Postoperative atrial fibrillation in noncardiothoracic surgical patients. Am J Surg. 2001;182(6):713-715. doi:10.1016/s0002-9610(01)00799-1.
3. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010;138(5):1093-1100. doi:10.1378/chest.10-0134.
4. Fleisher L, Beckman J, Brown K, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 2002 guidelines on perioperative cardiovascular evaluation for noncardiac surgery). Circulation. 2007;116(17):e418-e500. doi:10.1161/circulationaha.107.185699.
5. Walkey A, Benjamin E, Lubitz S. New-onset atrial fibrillation during hospitalization. J Am Coll Cardiol. 2014;64(22):2432-2433. doi:10.1016/j.jacc.2014.09.034.
6. Creswell L, Schuessler R, Rosenbloom M, Cox J. Hazards of postoperative atrial arrhythmias. Ann Thorac Surg. 1993;56(3):539-549. doi:10.1016/0003-4975(93)90894-n.
7. Almassi G, Schowalter T, Nicolosi A, et al. Atrial fibrillation after cardiac surgery: a major morbid event? Ann Surg. 1997;226(4):501-513.
8. Horwich P, Buth K, Légaré J. New onset postoperative atrial fibrillation is associated with a long-term risk for stroke and death following cardiac surgery. J Card Surg. 2013;28(1):8-13. doi:10.1111/jocs.12033.
9. Kollar A, Lick S, Vasquez K, Conti V. Relationship of atrial fibrillation and stroke after coronary artery bypass graft surgery: when is anticoagulation indicated? Ann Thorac Surg. 2006;82(2):515-523. doi:10.1016/j.athoracsur.2006.03.037.
10. Gialdini G, Nearing K, Bhave P, et al. Perioperative atrial fibrillation and the long-term risk of ischemic stroke. JAMA. 2014;312(6):616. doi:10.1001/jama.2014.9143.
11. El-Chami M, Kilgo P, Thourani V, et al. New-onset atrial fibrillation predicts long-term mortality after coronary artery bypass graft. J Am Coll Cardiol. 2010;55(13):1370-1376. doi:10.1016/j.jacc.2009.10.058.
12. Ahlsson A, Fengsrud E, Bodin L, Englund A. Postoperative atrial fibrillation in patients undergoing aortocoronary bypass surgery carries an eightfold risk of future atrial fibrillation and a doubled cardiovascular mortality. Euro J Cardiothorac Surg. 2010;37(6):1353-1359. doi:10.1016/j.ejcts.2009.12.033.
13. Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98(10):946-952.
14. Antonelli D, Peres D, Freedberg N, Feldman A, Rosenfeld T. Incidence of postdischarge symptomatic paroxysmal atrial fibrillation in patients who underwent coronary artery bypass graft: long-term follow-up. Pacing Clin Electrophysiol. 2004;27(3):365-367. doi:10.1111/j.1540-8159.2004.00443.x.
15. Douketis J, Spyropoulos A, Kaatz S, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015;373(9):823-833. doi:10.1056/nejmoa1501035.

Case

A 66-year-old man with diabetes mellitus type 2 and hypertension underwent left total knee replacement. Several hours after surgery, the patient developed atrial fibrillation (AF). He was asymptomatic, and reversible causes of AF were ruled out. Approximately 18 hours later, he spontaneously reverted back to sinus rhythm. Should this patient, who has no known prior history of AF and a CHA2DS2-VASc score of 3, be started on anticoagulation?

Background

Hospitalists are commonly consulted for evaluation and management of postoperative atrial fibrillation (POAF). The incidence of new-onset AF associated with non-cardiac surgery is approximately 2% and may be more frequent in an elderly population.1 The increased adrenergic tone associated with surgery is thought to elicit AF in some patients. POAF has also been associated with positive fluid balance, electrolyte abnormalities, and hypoxemia.2 Some of these patients will spontaneously revert back to sinus rhythm after these issues are reversed. Others will go on to develop chronic or paroxysmal AF that persists indefinitely. It is also likely that some patients with POAF, in fact, already had asymptomatic AF that was simply undetected prior to hospitalization.

Hospitalists are faced with the difficult task of determining which patients with POAF will benefit from either short-term or long-term anticoagulation. This has not been well studied in postsurgical patients, in contrast to medical patients in whom stroke risk from AF has been very well-characterized. The decision may be further complicated by bleeding risk (associated with either some surgeries or with patient-dependent factors).3

It is worth noting that following major cardiac or thoracic surgery, POAF is common; the incidence ranges from 10% to 60%. In these cases, POAF may be triggered by transient atrial ischemia or by postoperative inflammation and may have a different natural history from POAF in non-cardiac surgery patients in terms of both reversibility and stroke risk. More retrospective data are available regarding cardiothoracic surgery patients.

Previous American Heart Association (AHA) and American College of Cardiology (ACC) guidelines stated that POAF lasting longer than 48 hours warranted anticoagulation. This recommendation was removed from the newest update. The 2014 updated AHA/ACC guidelines are less absolute and now state only that “it is reasonable to administer antithrombotic medication in patients who developed postoperative AF, as recommended for nonsurgical patients” (Level of Evidence: B) in regard to cardiothoracic surgery.4

There is no specific recommendation regarding POAF for non-cardiac surgery patients. The current guidelines are likely purposefully vague due to the lack of direct evidence. The following is a review of the existing literature and a suggested approach to anticoagulation in POAF.

Review

How common is postoperative atrial fibrillation? New-onset AF during hospitalization is known to occur in association with many acute conditions including surgery, infection, and myocardial infarction. About half of the cases of in-hospital new-onset AF are associated with surgery. AF is more commonly seen in surgery that involves the thoracic cavity and cardiac structures. In a cross-sectional epidemiologic study of 22 million patients in California, 20.8% of patients undergoing cardiac surgery developed POAF compared with only 1.3% of patients undergoing non-cardiac surgery.5 A smaller study of non-cardiac surgery patients found a 30-day POAF incidence of 0.37%.2

Does postoperative atrial fibrillation increase the short-term risk of stroke? A major concern in AF is the risk of stroke. It is well-established that prolonged or recurrent AF increases the risk for stroke over months or years, but do short episodes of POAF increase stroke risk to a significant degree? Most of the studies in the literature focus on perioperative stroke risk specifically in cardiothoracic surgery. A prospective study of 4,000 patients undergoing cardiac surgery found that the in-hospital postoperative stroke risk was 3.3% in patients with POAF compared to 1.4% in patients without POAF (P<0.01).6 Similar outcomes were seen in a VA study looking at patients who underwent open heart surgery: Stroke risk was 5.3% at six months in POAF patients compared to 2.4% in those without POAF.7 Another study of coronary artery bypass graft (CABG) patients with a follow-up of almost six years showed a stroke risk of 12.1% in POAF patients compared to 8.4% in those without POAF.8

 

It is not clear that all of the increase in stroke risk is a direct effect of POAF. Indeed, in a retrospective analysis of almost 3,000 CABG patients, 1.1% suffered a stroke during their hospital stay. Fewer than half of those had a cardiac rhythm other than sinus rhythm. In the 15 stroke patients who developed POAF, nine presented with stroke symptoms prior to the first episode of AF.9 The authors suggest that aggressive anticoagulation for POAF would not have prevented most of these events.

Furthermore, the rate of in-hospital stroke after non-cardiac surgery is probably much lower, though it has not been as well studied. These data raise some questions as to the benefit of anticoagulation in the immediate postoperative period, though it is difficult to draw firm conclusions without randomized data.

What about non-cardiac surgery? There is less evidence available for patients undergoing non-cardiac surgery, but the few studies that do exist also point to higher stroke risk in patients with POAF. A large population-based study using ICD codes found that the one-year risk of stroke for patients with POAF after non-cardiac surgery was 1.47% compared to 0.36% in non-cardiac surgery patients without POAF (P<0.001). Based on these data, the long-term stroke risk after POAF in non-cardiac surgery patients is similar to that of medical AF patients with a CHA2DS2-VASc score of 2. The authors of this study suggest that transient POAF after non-cardiac surgery may carry a long-term stroke risk similar to any other AF diagnosis.10 However, this study design is subject to significant ascertainment bias (i.e., they may have unintentionally captured some patients with preexisting or prolonged AF), and further research is needed to better delineate this risk.

Does increased stroke risk translate into increased mortality? In a retrospective study of 17,000 patients, El-Chami et al found that POAF after CABG was associated with decreased survival after one year (90% versus 96%) and 10 years (55% versus 70%).11 However, those patients who develop POAF may be sicker overall.

Another study showed that death due to stroke occurred in 4.2% of POAF patients compared to 0.2% of non-POAF patients in a five-year period.12 Based on these studies, POAF is likely associated with increased mortality, but there may be other unaccounted variables. Nevertheless, the increased mortality associated with POAF in these populations is similar to that seen for non-surgical population-based studies13 and provides support that those with newly diagnosed AF in the post-surgical setting should at least be followed closely to assess for recurrence.

What is a patient’s risk of developing atrial fibrillation later in life? When we choose to anticoagulate patients with POAF, we then have to determine whether they should be committed to long-term anticoagulation. It is thought that many cases of POAF are transient; however, some patients will go on to have persistent or paroxysmal AF after discharge.

A retrospective study examined 571 patients who underwent CABG, 30% of whom had POAF during the index admission. After five years of follow-up, 25% of those with POAF were diagnosed with paroxysmal or persistent AF after discharge compared to only 3% of patients without POAF. Researchers did this by looking at the most recent ECG, if done in the last year, or by obtaining a new ECG at the five-year point.12 By this method, it is probable that some diagnoses of paroxysmal AF were missed.

In another study of about 300 CABG patients, about 20% of patients with POAF also went on to develop post-discharge AF, defined as symptomatic AF that led to medical evaluation. As in the previous study, it is likely that there were undetected episodes of AF.14 Thus, in cardiothoracic surgery patients, some but not all of whom develop POAF have recurrent or ongoing AF. For this reason, if anticoagulation is started, it may be reasonable to stop anticoagulation after weeks or months if ongoing AF is not apparent.

 

What is the risk of postoperative bleeding if anticoagulation is started? Any decision about the benefits of anticoagulation must be weighed against the risks, most notably the risk of serious or life-threatening bleeding. This risk may be heightened in the immediate perioperative period. Discussions should always take place with our surgical colleagues about type of surgery, intraoperative complications, and postoperative risk of bleeding.

Anticoagulation, if indicated, should not be started until postoperative bleeding risk is deemed appropriately low. That said, the 2015 BRIDGE trial (looking at the benefits and risks of “bridging” patients before surgery) provides some peripheral but meaningful information about postoperative bleeding risk. In this study, patients with preexisting AF who underwent low-bleeding-risk surgery and were bridged on day one after surgery with therapeutic doses of unfractionated or low-molecular-weight heparin had a significantly higher risk of postoperative bleeding compared to non-bridged patients, with a number needed to harm of 50.15 It may be reasonable—and likely safer—to wait a couple days to start anticoagulation for patients with POAF.

What is the expert’s opinion? We asked one of our cardiac electrophysiologists what her approach is to this situation. In general, if a patient has a low stroke risk and is in AF for fewer than 24 hours, it is reasonable to defer anticoagulation and follow as an outpatient. Regardless of risk, if AF is sustained for more than 24 hours, we recommend at least four weeks of anticoagulation and close outpatient follow-up, which should include a period of ambulatory monitoring to determine the need for continued anticoagulation. We also recommend considering what comprises the patient’s stroke risk.

For example, if the CHA2DS2-VASc score is 2 but the points come from being a female with coronary artery disease, we would consider forgoing anticoagulation but arranging for an outpatient cardiac monitor with cardiology follow-up. If the patient has a history of stroke or TIA, we recommend continuing anticoagulation indefinitely.

Back to the Case

Given our patient’s episode of POAF lasted fewer than 24 hours, it would be reasonable to hold off starting anticoagulation, but he should be followed as an outpatient with ambulatory monitoring at a minimum, monitoring for recurrence. If he were to develop recurrent AF, then he would warrant anticoagulation based on an annual stroke risk of 3.2% as determined by a CHA2DS2-VASc score of 3.

Bottom Line

Our strategy is as follows: If a patient has a low stroke risk (i.e., CHA2DS2-VASc score <2) and is in AF for fewer than 24 hours, anticoagulation is not started, but outpatient follow-up is arranged to monitor symptoms. Regardless of stroke risk, if a patient is in AF for more than 24 hours, we initiate and continue anticoagulation for a minimum of four weeks and arrange outpatient follow-up with a period of ambulatory monitoring to determine need for continued anticoagulation. If a patient has a high stroke risk (CHA2DS2-VASc >2) or if their risk factors include a history of stroke or TIA, anticoagulation is started and continued indefinitely. Risk-benefit discussion is held with the patient, especially with regard to bleeding risk, prior to anticoagulation initiation. If the individual patient’s situation presents further nuance, we ask for the assistance of our cardiology or cardiac electrophysiology colleagues.

Final Thought

None of the mentioned studies investigated or included newer oral anticoagulants. Risk-benefit ratios may change (potentially considerably) with these agents. Further study is needed. We expect, in due time, studies will look at the question of POAF in regard to newer anticoagulant agents, and perhaps then our decision making will change. TH

---

 

Dr. Evavold is a resident in the hospitalist training program, while Dr. Lessing and Dr. Merritt are hospitalists in the Department of Internal Medicine at the University of Colorado. Dr. Tzou is a cardiologist in the section of electrophysiology at the University of Colorado.

References:

1. POISE Study Group, Devereaux PJ, Yang H, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. Lancet. 2008;371(9627):1839-1847. doi:10.1016/s0140-6736(08)60601-7.
2. Christians K, Wu B, Quebbeman E, Brasel K. Postoperative atrial fibrillation in noncardiothoracic surgical patients. Am J Surg. 2001;182(6):713-715. doi:10.1016/s0002-9610(01)00799-1.
3. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010;138(5):1093-1100. doi:10.1378/chest.10-0134.
4. Fleisher L, Beckman J, Brown K, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 2002 guidelines on perioperative cardiovascular evaluation for noncardiac surgery). Circulation. 2007;116(17):e418-e500. doi:10.1161/circulationaha.107.185699.
5. Walkey A, Benjamin E, Lubitz S. New-onset atrial fibrillation during hospitalization. J Am Coll Cardiol. 2014;64(22):2432-2433. doi:10.1016/j.jacc.2014.09.034.
6. Creswell L, Schuessler R, Rosenbloom M, Cox J. Hazards of postoperative atrial arrhythmias. Ann Thorac Surg. 1993;56(3):539-549. doi:10.1016/0003-4975(93)90894-n.
7. Almassi G, Schowalter T, Nicolosi A, et al. Atrial fibrillation after cardiac surgery: a major morbid event? Ann Surg. 1997;226(4):501-513.
8. Horwich P, Buth K, Légaré J. New onset postoperative atrial fibrillation is associated with a long-term risk for stroke and death following cardiac surgery. J Card Surg. 2013;28(1):8-13. doi:10.1111/jocs.12033.
9. Kollar A, Lick S, Vasquez K, Conti V. Relationship of atrial fibrillation and stroke after coronary artery bypass graft surgery: when is anticoagulation indicated? Ann Thorac Surg. 2006;82(2):515-523. doi:10.1016/j.athoracsur.2006.03.037.
10. Gialdini G, Nearing K, Bhave P, et al. Perioperative atrial fibrillation and the long-term risk of ischemic stroke. JAMA. 2014;312(6):616. doi:10.1001/jama.2014.9143.
11. El-Chami M, Kilgo P, Thourani V, et al. New-onset atrial fibrillation predicts long-term mortality after coronary artery bypass graft. J Am Coll Cardiol. 2010;55(13):1370-1376. doi:10.1016/j.jacc.2009.10.058.
12. Ahlsson A, Fengsrud E, Bodin L, Englund A. Postoperative atrial fibrillation in patients undergoing aortocoronary bypass surgery carries an eightfold risk of future atrial fibrillation and a doubled cardiovascular mortality. Euro J Cardiothorac Surg. 2010;37(6):1353-1359. doi:10.1016/j.ejcts.2009.12.033.
13. Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98(10):946-952.
14. Antonelli D, Peres D, Freedberg N, Feldman A, Rosenfeld T. Incidence of postdischarge symptomatic paroxysmal atrial fibrillation in patients who underwent coronary artery bypass graft: long-term follow-up. Pacing Clin Electrophysiol. 2004;27(3):365-367. doi:10.1111/j.1540-8159.2004.00443.x.
15. Douketis J, Spyropoulos A, Kaatz S, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015;373(9):823-833. doi:10.1056/nejmoa1501035.

Case

A 66-year-old man with diabetes mellitus type 2 and hypertension underwent left total knee replacement. Several hours after surgery, the patient developed atrial fibrillation (AF). He was asymptomatic, and reversible causes of AF were ruled out. Approximately 18 hours later, he spontaneously reverted back to sinus rhythm. Should this patient, who has no known prior history of AF and a CHA2DS2-VASc score of 3, be started on anticoagulation?

Background

Hospitalists are commonly consulted for evaluation and management of postoperative atrial fibrillation (POAF). The incidence of new-onset AF associated with non-cardiac surgery is approximately 2% and may be more frequent in an elderly population.1 The increased adrenergic tone associated with surgery is thought to elicit AF in some patients. POAF has also been associated with positive fluid balance, electrolyte abnormalities, and hypoxemia.2 Some of these patients will spontaneously revert back to sinus rhythm after these issues are reversed. Others will go on to develop chronic or paroxysmal AF that persists indefinitely. It is also likely that some patients with POAF, in fact, already had asymptomatic AF that was simply undetected prior to hospitalization.

Hospitalists are faced with the difficult task of determining which patients with POAF will benefit from either short-term or long-term anticoagulation. This has not been well studied in postsurgical patients, in contrast to medical patients in whom stroke risk from AF has been very well-characterized. The decision may be further complicated by bleeding risk (associated with either some surgeries or with patient-dependent factors).3

It is worth noting that following major cardiac or thoracic surgery, POAF is common; the incidence ranges from 10% to 60%. In these cases, POAF may be triggered by transient atrial ischemia or by postoperative inflammation and may have a different natural history from POAF in non-cardiac surgery patients in terms of both reversibility and stroke risk. More retrospective data are available regarding cardiothoracic surgery patients.

Previous American Heart Association (AHA) and American College of Cardiology (ACC) guidelines stated that POAF lasting longer than 48 hours warranted anticoagulation. This recommendation was removed from the newest update. The 2014 updated AHA/ACC guidelines are less absolute and now state only that “it is reasonable to administer antithrombotic medication in patients who developed postoperative AF, as recommended for nonsurgical patients” (Level of Evidence: B) in regard to cardiothoracic surgery.4

There is no specific recommendation regarding POAF for non-cardiac surgery patients. The current guidelines are likely purposefully vague due to the lack of direct evidence. The following is a review of the existing literature and a suggested approach to anticoagulation in POAF.

Review

How common is postoperative atrial fibrillation? New-onset AF during hospitalization is known to occur in association with many acute conditions including surgery, infection, and myocardial infarction. About half of the cases of in-hospital new-onset AF are associated with surgery. AF is more commonly seen in surgery that involves the thoracic cavity and cardiac structures. In a cross-sectional epidemiologic study of 22 million patients in California, 20.8% of patients undergoing cardiac surgery developed POAF compared with only 1.3% of patients undergoing non-cardiac surgery.5 A smaller study of non-cardiac surgery patients found a 30-day POAF incidence of 0.37%.2

Does postoperative atrial fibrillation increase the short-term risk of stroke? A major concern in AF is the risk of stroke. It is well-established that prolonged or recurrent AF increases the risk for stroke over months or years, but do short episodes of POAF increase stroke risk to a significant degree? Most of the studies in the literature focus on perioperative stroke risk specifically in cardiothoracic surgery. A prospective study of 4,000 patients undergoing cardiac surgery found that the in-hospital postoperative stroke risk was 3.3% in patients with POAF compared to 1.4% in patients without POAF (P<0.01).6 Similar outcomes were seen in a VA study looking at patients who underwent open heart surgery: Stroke risk was 5.3% at six months in POAF patients compared to 2.4% in those without POAF.7 Another study of coronary artery bypass graft (CABG) patients with a follow-up of almost six years showed a stroke risk of 12.1% in POAF patients compared to 8.4% in those without POAF.8

 

It is not clear that all of the increase in stroke risk is a direct effect of POAF. Indeed, in a retrospective analysis of almost 3,000 CABG patients, 1.1% suffered a stroke during their hospital stay. Fewer than half of those had a cardiac rhythm other than sinus rhythm. In the 15 stroke patients who developed POAF, nine presented with stroke symptoms prior to the first episode of AF.9 The authors suggest that aggressive anticoagulation for POAF would not have prevented most of these events.

Furthermore, the rate of in-hospital stroke after non-cardiac surgery is probably much lower, though it has not been as well studied. These data raise some questions as to the benefit of anticoagulation in the immediate postoperative period, though it is difficult to draw firm conclusions without randomized data.

What about non-cardiac surgery? There is less evidence available for patients undergoing non-cardiac surgery, but the few studies that do exist also point to higher stroke risk in patients with POAF. A large population-based study using ICD codes found that the one-year risk of stroke for patients with POAF after non-cardiac surgery was 1.47% compared to 0.36% in non-cardiac surgery patients without POAF (P<0.001). Based on these data, the long-term stroke risk after POAF in non-cardiac surgery patients is similar to that of medical AF patients with a CHA2DS2-VASc score of 2. The authors of this study suggest that transient POAF after non-cardiac surgery may carry a long-term stroke risk similar to any other AF diagnosis.10 However, this study design is subject to significant ascertainment bias (i.e., they may have unintentionally captured some patients with preexisting or prolonged AF), and further research is needed to better delineate this risk.

Does increased stroke risk translate into increased mortality? In a retrospective study of 17,000 patients, El-Chami et al found that POAF after CABG was associated with decreased survival after one year (90% versus 96%) and 10 years (55% versus 70%).11 However, those patients who develop POAF may be sicker overall.

Another study showed that death due to stroke occurred in 4.2% of POAF patients compared to 0.2% of non-POAF patients in a five-year period.12 Based on these studies, POAF is likely associated with increased mortality, but there may be other unaccounted variables. Nevertheless, the increased mortality associated with POAF in these populations is similar to that seen for non-surgical population-based studies13 and provides support that those with newly diagnosed AF in the post-surgical setting should at least be followed closely to assess for recurrence.

What is a patient’s risk of developing atrial fibrillation later in life? When we choose to anticoagulate patients with POAF, we then have to determine whether they should be committed to long-term anticoagulation. It is thought that many cases of POAF are transient; however, some patients will go on to have persistent or paroxysmal AF after discharge.

A retrospective study examined 571 patients who underwent CABG, 30% of whom had POAF during the index admission. After five years of follow-up, 25% of those with POAF were diagnosed with paroxysmal or persistent AF after discharge compared to only 3% of patients without POAF. Researchers did this by looking at the most recent ECG, if done in the last year, or by obtaining a new ECG at the five-year point.12 By this method, it is probable that some diagnoses of paroxysmal AF were missed.

In another study of about 300 CABG patients, about 20% of patients with POAF also went on to develop post-discharge AF, defined as symptomatic AF that led to medical evaluation. As in the previous study, it is likely that there were undetected episodes of AF.14 Thus, in cardiothoracic surgery patients, some but not all of whom develop POAF have recurrent or ongoing AF. For this reason, if anticoagulation is started, it may be reasonable to stop anticoagulation after weeks or months if ongoing AF is not apparent.

 

What is the risk of postoperative bleeding if anticoagulation is started? Any decision about the benefits of anticoagulation must be weighed against the risks, most notably the risk of serious or life-threatening bleeding. This risk may be heightened in the immediate perioperative period. Discussions should always take place with our surgical colleagues about type of surgery, intraoperative complications, and postoperative risk of bleeding.

Anticoagulation, if indicated, should not be started until postoperative bleeding risk is deemed appropriately low. That said, the 2015 BRIDGE trial (looking at the benefits and risks of “bridging” patients before surgery) provides some peripheral but meaningful information about postoperative bleeding risk. In this study, patients with preexisting AF who underwent low-bleeding-risk surgery and were bridged on day one after surgery with therapeutic doses of unfractionated or low-molecular-weight heparin had a significantly higher risk of postoperative bleeding compared to non-bridged patients, with a number needed to harm of 50.15 It may be reasonable—and likely safer—to wait a couple days to start anticoagulation for patients with POAF.

What is the expert’s opinion? We asked one of our cardiac electrophysiologists what her approach is to this situation. In general, if a patient has a low stroke risk and is in AF for fewer than 24 hours, it is reasonable to defer anticoagulation and follow as an outpatient. Regardless of risk, if AF is sustained for more than 24 hours, we recommend at least four weeks of anticoagulation and close outpatient follow-up, which should include a period of ambulatory monitoring to determine the need for continued anticoagulation. We also recommend considering what comprises the patient’s stroke risk.

For example, if the CHA2DS2-VASc score is 2 but the points come from being a female with coronary artery disease, we would consider forgoing anticoagulation but arranging for an outpatient cardiac monitor with cardiology follow-up. If the patient has a history of stroke or TIA, we recommend continuing anticoagulation indefinitely.

Back to the Case

Given our patient’s episode of POAF lasted fewer than 24 hours, it would be reasonable to hold off starting anticoagulation, but he should be followed as an outpatient with ambulatory monitoring at a minimum, monitoring for recurrence. If he were to develop recurrent AF, then he would warrant anticoagulation based on an annual stroke risk of 3.2% as determined by a CHA2DS2-VASc score of 3.

Bottom Line

Our strategy is as follows: If a patient has a low stroke risk (i.e., CHA2DS2-VASc score <2) and is in AF for fewer than 24 hours, anticoagulation is not started, but outpatient follow-up is arranged to monitor symptoms. Regardless of stroke risk, if a patient is in AF for more than 24 hours, we initiate and continue anticoagulation for a minimum of four weeks and arrange outpatient follow-up with a period of ambulatory monitoring to determine need for continued anticoagulation. If a patient has a high stroke risk (CHA2DS2-VASc >2) or if their risk factors include a history of stroke or TIA, anticoagulation is started and continued indefinitely. Risk-benefit discussion is held with the patient, especially with regard to bleeding risk, prior to anticoagulation initiation. If the individual patient’s situation presents further nuance, we ask for the assistance of our cardiology or cardiac electrophysiology colleagues.

Final Thought

None of the mentioned studies investigated or included newer oral anticoagulants. Risk-benefit ratios may change (potentially considerably) with these agents. Further study is needed. We expect, in due time, studies will look at the question of POAF in regard to newer anticoagulant agents, and perhaps then our decision making will change. TH

---

 

Dr. Evavold is a resident in the hospitalist training program, while Dr. Lessing and Dr. Merritt are hospitalists in the Department of Internal Medicine at the University of Colorado. Dr. Tzou is a cardiologist in the section of electrophysiology at the University of Colorado.

References:

1. POISE Study Group, Devereaux PJ, Yang H, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. Lancet. 2008;371(9627):1839-1847. doi:10.1016/s0140-6736(08)60601-7.
2. Christians K, Wu B, Quebbeman E, Brasel K. Postoperative atrial fibrillation in noncardiothoracic surgical patients. Am J Surg. 2001;182(6):713-715. doi:10.1016/s0002-9610(01)00799-1.
3. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010;138(5):1093-1100. doi:10.1378/chest.10-0134.
4. Fleisher L, Beckman J, Brown K, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 2002 guidelines on perioperative cardiovascular evaluation for noncardiac surgery). Circulation. 2007;116(17):e418-e500. doi:10.1161/circulationaha.107.185699.
5. Walkey A, Benjamin E, Lubitz S. New-onset atrial fibrillation during hospitalization. J Am Coll Cardiol. 2014;64(22):2432-2433. doi:10.1016/j.jacc.2014.09.034.
6. Creswell L, Schuessler R, Rosenbloom M, Cox J. Hazards of postoperative atrial arrhythmias. Ann Thorac Surg. 1993;56(3):539-549. doi:10.1016/0003-4975(93)90894-n.
7. Almassi G, Schowalter T, Nicolosi A, et al. Atrial fibrillation after cardiac surgery: a major morbid event? Ann Surg. 1997;226(4):501-513.
8. Horwich P, Buth K, Légaré J. New onset postoperative atrial fibrillation is associated with a long-term risk for stroke and death following cardiac surgery. J Card Surg. 2013;28(1):8-13. doi:10.1111/jocs.12033.
9. Kollar A, Lick S, Vasquez K, Conti V. Relationship of atrial fibrillation and stroke after coronary artery bypass graft surgery: when is anticoagulation indicated? Ann Thorac Surg. 2006;82(2):515-523. doi:10.1016/j.athoracsur.2006.03.037.
10. Gialdini G, Nearing K, Bhave P, et al. Perioperative atrial fibrillation and the long-term risk of ischemic stroke. JAMA. 2014;312(6):616. doi:10.1001/jama.2014.9143.
11. El-Chami M, Kilgo P, Thourani V, et al. New-onset atrial fibrillation predicts long-term mortality after coronary artery bypass graft. J Am Coll Cardiol. 2010;55(13):1370-1376. doi:10.1016/j.jacc.2009.10.058.
12. Ahlsson A, Fengsrud E, Bodin L, Englund A. Postoperative atrial fibrillation in patients undergoing aortocoronary bypass surgery carries an eightfold risk of future atrial fibrillation and a doubled cardiovascular mortality. Euro J Cardiothorac Surg. 2010;37(6):1353-1359. doi:10.1016/j.ejcts.2009.12.033.
13. Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98(10):946-952.
14. Antonelli D, Peres D, Freedberg N, Feldman A, Rosenfeld T. Incidence of postdischarge symptomatic paroxysmal atrial fibrillation in patients who underwent coronary artery bypass graft: long-term follow-up. Pacing Clin Electrophysiol. 2004;27(3):365-367. doi:10.1111/j.1540-8159.2004.00443.x.
15. Douketis J, Spyropoulos A, Kaatz S, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015;373(9):823-833. doi:10.1056/nejmoa1501035.

A group of US physicians has called for the creation of a publicly financed, single-payer national health program that would cover all Americans for all medically necessary care.

The proposal, which was drafted by a panel of 39 physicians, was announced in an editorial published in the American Journal of Public Health.

The proposal currently has more than 2000 signatures from physicians practicing in 48 states and the District of Columbia.

“Our nation is at a crossroads,” said Adam Gaffney, MD, a pulmonary disease and critical care specialist in Boston, Massachusetts, who is lead author of the editorial and co-chair of the working group that drafted the proposal.

“Despite the passage of the Affordable Care Act 6 years ago, 30 million Americans remain uninsured, an even greater number are underinsured, financial barriers to care like co-pays and deductibles are rising, bureaucracy is growing, provider networks are narrowing, and medical costs are continuing to climb.”

Dr Gaffney and his colleagues described their publicly financed, single-payer national health program (NHP) as follows.

Patients could choose to visit any doctor and hospital. Most hospitals and clinics would remain privately owned and operated, receiving a budget from the NHP to cover all operating costs. Physicians could continue to practice on a fee-for-service basis or receive salaries from group practices, hospitals, or clinics.

The program would be paid for by combining current sources of government health spending into a single fund with new taxes that would be fully offset by reductions in premiums and out-of-pocket spending. Co-pays and deductibles would be eliminated.

The single-payer program would save about $500 billion annually by eliminating the high overhead and profits of insurance firms and the paperwork they require from hospitals and doctors.

The administrative savings of the system would fully offset the costs of covering the uninsured and upgraded coverage for everyone else—eg, full coverage of prescription drugs, dental care, and long-term care. Savings would also be redirected to currently underfunded health priorities, particularly public health.

The “single payer” would be in a position to negotiate lower prices for medications and other medical supplies.

More details and documents related to the physicians’ proposal are available on the Physicians for a National Health Program website.

The Physicians for a National Health Program is a nonpartisan, nonprofit research and education organization founded in 1987. The organization had no role in funding the aforementioned proposal or editorial.

A group of US physicians has called for the creation of a publicly financed, single-payer national health program that would cover all Americans for all medically necessary care.

The proposal, which was drafted by a panel of 39 physicians, was announced in an editorial published in the American Journal of Public Health.

The proposal currently has more than 2000 signatures from physicians practicing in 48 states and the District of Columbia.

“Our nation is at a crossroads,” said Adam Gaffney, MD, a pulmonary disease and critical care specialist in Boston, Massachusetts, who is lead author of the editorial and co-chair of the working group that drafted the proposal.

“Despite the passage of the Affordable Care Act 6 years ago, 30 million Americans remain uninsured, an even greater number are underinsured, financial barriers to care like co-pays and deductibles are rising, bureaucracy is growing, provider networks are narrowing, and medical costs are continuing to climb.”

Dr Gaffney and his colleagues described their publicly financed, single-payer national health program (NHP) as follows.

Patients could choose to visit any doctor and hospital. Most hospitals and clinics would remain privately owned and operated, receiving a budget from the NHP to cover all operating costs. Physicians could continue to practice on a fee-for-service basis or receive salaries from group practices, hospitals, or clinics.

The program would be paid for by combining current sources of government health spending into a single fund with new taxes that would be fully offset by reductions in premiums and out-of-pocket spending. Co-pays and deductibles would be eliminated.

The single-payer program would save about $500 billion annually by eliminating the high overhead and profits of insurance firms and the paperwork they require from hospitals and doctors.

The administrative savings of the system would fully offset the costs of covering the uninsured and upgraded coverage for everyone else—eg, full coverage of prescription drugs, dental care, and long-term care. Savings would also be redirected to currently underfunded health priorities, particularly public health.

The “single payer” would be in a position to negotiate lower prices for medications and other medical supplies.

More details and documents related to the physicians’ proposal are available on the Physicians for a National Health Program website.

The Physicians for a National Health Program is a nonpartisan, nonprofit research and education organization founded in 1987. The organization had no role in funding the aforementioned proposal or editorial.

A group of US physicians has called for the creation of a publicly financed, single-payer national health program that would cover all Americans for all medically necessary care.

The proposal, which was drafted by a panel of 39 physicians, was announced in an editorial published in the American Journal of Public Health.

The proposal currently has more than 2000 signatures from physicians practicing in 48 states and the District of Columbia.

“Our nation is at a crossroads,” said Adam Gaffney, MD, a pulmonary disease and critical care specialist in Boston, Massachusetts, who is lead author of the editorial and co-chair of the working group that drafted the proposal.

“Despite the passage of the Affordable Care Act 6 years ago, 30 million Americans remain uninsured, an even greater number are underinsured, financial barriers to care like co-pays and deductibles are rising, bureaucracy is growing, provider networks are narrowing, and medical costs are continuing to climb.”

Dr Gaffney and his colleagues described their publicly financed, single-payer national health program (NHP) as follows.

Patients could choose to visit any doctor and hospital. Most hospitals and clinics would remain privately owned and operated, receiving a budget from the NHP to cover all operating costs. Physicians could continue to practice on a fee-for-service basis or receive salaries from group practices, hospitals, or clinics.

The program would be paid for by combining current sources of government health spending into a single fund with new taxes that would be fully offset by reductions in premiums and out-of-pocket spending. Co-pays and deductibles would be eliminated.

The single-payer program would save about $500 billion annually by eliminating the high overhead and profits of insurance firms and the paperwork they require from hospitals and doctors.

The administrative savings of the system would fully offset the costs of covering the uninsured and upgraded coverage for everyone else—eg, full coverage of prescription drugs, dental care, and long-term care. Savings would also be redirected to currently underfunded health priorities, particularly public health.

The “single payer” would be in a position to negotiate lower prices for medications and other medical supplies.

More details and documents related to the physicians’ proposal are available on the Physicians for a National Health Program website.

The Physicians for a National Health Program is a nonpartisan, nonprofit research and education organization founded in 1987. The organization had no role in funding the aforementioned proposal or editorial.

GLASGOW – Older adults are more than seven times as likely to develop knee osteoarthritis if they had anterior knee pain as adolescents, according to the results of a case-control study.

The adjusted odds ratio for patellofemoral osteoarthritis (PFOA) was 7.5 if there was prior adolescent anterior knee pain. Although the 95% confidence interval was wide (1.51-36.94) the association was significant (P = .014). Adjustment had been made for the potential confounding factors of previous patellar dislocation, prior surgery, and patient-reported knee instability; before this adjustment the OR was 20.2 (95% CI, 3.34-11.67).

©pixologicstudio/Thinkstock

Patellar dislocation during adolescence also was found to be a significant risk factor for later PFOA (aOR, 3.2; 95% CI, 1.25-9.18; P = .016).

“Adolescent anterior knee pain represents a constellation of symptoms and had always been thought of as benign and self-limiting,” Henry Conchie, a medical student at the University of Bristol (England), said at the British Society for Rheumatology annual conference.

“I think the take-home message from our research is really that this traditional view of benign pathology associated with adolescent anterior knee pain and patellar dislocation must be challenged and when seen in clinical practice we now encourage the acknowledgment of the potentially severe consequences in the future,” Mr. Conchie said.

A link between adolescent anterior knee pain and later PFOA has previously been suggested but there are few data to support this observation, he explained. So the aim of the current study was to look at this in more detail in a group of patients from the knee arthroplasty database at Southmead Hospital in Bristol.

Questionnaires that asked about a variety of symptoms and knee pain were sent to 190 patients in the database who had undergone patellofemoral arthroplasty and so had severe, isolated, and radiologically confirmed PFOA. Questionnaires also were sent to 445 patients who had undergone arthroplasty for unicompartmental tibiofemoral arthritis to serve as the control group.

A subanalysis was performed to look at the mean age of the first dislocation and the investigators found that patients with PFOA were likely to be much younger than controls, with a 44-year difference observed between the groups.

“This adds some weight to the theory that this process [PFOA] begins much earlier than once thought – at a younger age,” Mr. Conchie suggested.

The study subjects were surveyed 1-4 years after their operation, so patient recall could have affected the results, but the use of the unicompartmental tibiofemoral arthritis patients as controls should have reduced this potential bias, he said. The fact that they had gone through an arthroplasty meant that they would have had very similar experiences to the PFOA group in terms of pain.

Although only severe OA cases and arthritis controls were used, the team believes that the findings are robust as these were clearly defined patient groups, albeit at the end of the disease spectrum.

“Thought can now turn to etiological mechanisms underlying these relationships, and I think it is likely that anatomical etiologies such as patellar outer and trochlear dysplasia can define both the pain and instability in youth as well as the patellofemoral osteoarthritis in later life,” Mr. Conchie proposed. Further research to look at this would be needed in future.

During the Q&A following his presentation, Dr. Eileen Baildam of Alder Hey Children’s Hospital in Liverpool, England, commented that she had looked at the persistence of pain in patients with adolescent anterior knee pain some years ago and found that, 10-20 years later, 60% were still experiencing pain.

The chair of the session, Dr. Joyce Davidson of the Royal Hospital for Sick Children in Glasgow, summed up by saying: “I think we do see lots of patients and maybe we just need to be aware that this may not be as benign as we think, and certainly we should be looking for abnormal patellae and being very aware of it in young people.”

Mr. Conchie and his coauthors had nothing to disclose.

GLASGOW – Older adults are more than seven times as likely to develop knee osteoarthritis if they had anterior knee pain as adolescents, according to the results of a case-control study.

The adjusted odds ratio for patellofemoral osteoarthritis (PFOA) was 7.5 if there was prior adolescent anterior knee pain. Although the 95% confidence interval was wide (1.51-36.94) the association was significant (P = .014). Adjustment had been made for the potential confounding factors of previous patellar dislocation, prior surgery, and patient-reported knee instability; before this adjustment the OR was 20.2 (95% CI, 3.34-11.67).

©pixologicstudio/Thinkstock

Patellar dislocation during adolescence also was found to be a significant risk factor for later PFOA (aOR, 3.2; 95% CI, 1.25-9.18; P = .016).

“Adolescent anterior knee pain represents a constellation of symptoms and had always been thought of as benign and self-limiting,” Henry Conchie, a medical student at the University of Bristol (England), said at the British Society for Rheumatology annual conference.

“I think the take-home message from our research is really that this traditional view of benign pathology associated with adolescent anterior knee pain and patellar dislocation must be challenged and when seen in clinical practice we now encourage the acknowledgment of the potentially severe consequences in the future,” Mr. Conchie said.

A link between adolescent anterior knee pain and later PFOA has previously been suggested but there are few data to support this observation, he explained. So the aim of the current study was to look at this in more detail in a group of patients from the knee arthroplasty database at Southmead Hospital in Bristol.

Questionnaires that asked about a variety of symptoms and knee pain were sent to 190 patients in the database who had undergone patellofemoral arthroplasty and so had severe, isolated, and radiologically confirmed PFOA. Questionnaires also were sent to 445 patients who had undergone arthroplasty for unicompartmental tibiofemoral arthritis to serve as the control group.

A subanalysis was performed to look at the mean age of the first dislocation and the investigators found that patients with PFOA were likely to be much younger than controls, with a 44-year difference observed between the groups.

“This adds some weight to the theory that this process [PFOA] begins much earlier than once thought – at a younger age,” Mr. Conchie suggested.

The study subjects were surveyed 1-4 years after their operation, so patient recall could have affected the results, but the use of the unicompartmental tibiofemoral arthritis patients as controls should have reduced this potential bias, he said. The fact that they had gone through an arthroplasty meant that they would have had very similar experiences to the PFOA group in terms of pain.

Although only severe OA cases and arthritis controls were used, the team believes that the findings are robust as these were clearly defined patient groups, albeit at the end of the disease spectrum.

“Thought can now turn to etiological mechanisms underlying these relationships, and I think it is likely that anatomical etiologies such as patellar outer and trochlear dysplasia can define both the pain and instability in youth as well as the patellofemoral osteoarthritis in later life,” Mr. Conchie proposed. Further research to look at this would be needed in future.

During the Q&A following his presentation, Dr. Eileen Baildam of Alder Hey Children’s Hospital in Liverpool, England, commented that she had looked at the persistence of pain in patients with adolescent anterior knee pain some years ago and found that, 10-20 years later, 60% were still experiencing pain.

The chair of the session, Dr. Joyce Davidson of the Royal Hospital for Sick Children in Glasgow, summed up by saying: “I think we do see lots of patients and maybe we just need to be aware that this may not be as benign as we think, and certainly we should be looking for abnormal patellae and being very aware of it in young people.”

Mr. Conchie and his coauthors had nothing to disclose.

GLASGOW – Older adults are more than seven times as likely to develop knee osteoarthritis if they had anterior knee pain as adolescents, according to the results of a case-control study.

The adjusted odds ratio for patellofemoral osteoarthritis (PFOA) was 7.5 if there was prior adolescent anterior knee pain. Although the 95% confidence interval was wide (1.51-36.94) the association was significant (P = .014). Adjustment had been made for the potential confounding factors of previous patellar dislocation, prior surgery, and patient-reported knee instability; before this adjustment the OR was 20.2 (95% CI, 3.34-11.67).

©pixologicstudio/Thinkstock

Patellar dislocation during adolescence also was found to be a significant risk factor for later PFOA (aOR, 3.2; 95% CI, 1.25-9.18; P = .016).

“Adolescent anterior knee pain represents a constellation of symptoms and had always been thought of as benign and self-limiting,” Henry Conchie, a medical student at the University of Bristol (England), said at the British Society for Rheumatology annual conference.

“I think the take-home message from our research is really that this traditional view of benign pathology associated with adolescent anterior knee pain and patellar dislocation must be challenged and when seen in clinical practice we now encourage the acknowledgment of the potentially severe consequences in the future,” Mr. Conchie said.

A link between adolescent anterior knee pain and later PFOA has previously been suggested but there are few data to support this observation, he explained. So the aim of the current study was to look at this in more detail in a group of patients from the knee arthroplasty database at Southmead Hospital in Bristol.

Questionnaires that asked about a variety of symptoms and knee pain were sent to 190 patients in the database who had undergone patellofemoral arthroplasty and so had severe, isolated, and radiologically confirmed PFOA. Questionnaires also were sent to 445 patients who had undergone arthroplasty for unicompartmental tibiofemoral arthritis to serve as the control group.

A subanalysis was performed to look at the mean age of the first dislocation and the investigators found that patients with PFOA were likely to be much younger than controls, with a 44-year difference observed between the groups.

“This adds some weight to the theory that this process [PFOA] begins much earlier than once thought – at a younger age,” Mr. Conchie suggested.

The study subjects were surveyed 1-4 years after their operation, so patient recall could have affected the results, but the use of the unicompartmental tibiofemoral arthritis patients as controls should have reduced this potential bias, he said. The fact that they had gone through an arthroplasty meant that they would have had very similar experiences to the PFOA group in terms of pain.

Although only severe OA cases and arthritis controls were used, the team believes that the findings are robust as these were clearly defined patient groups, albeit at the end of the disease spectrum.

“Thought can now turn to etiological mechanisms underlying these relationships, and I think it is likely that anatomical etiologies such as patellar outer and trochlear dysplasia can define both the pain and instability in youth as well as the patellofemoral osteoarthritis in later life,” Mr. Conchie proposed. Further research to look at this would be needed in future.

During the Q&A following his presentation, Dr. Eileen Baildam of Alder Hey Children’s Hospital in Liverpool, England, commented that she had looked at the persistence of pain in patients with adolescent anterior knee pain some years ago and found that, 10-20 years later, 60% were still experiencing pain.

The chair of the session, Dr. Joyce Davidson of the Royal Hospital for Sick Children in Glasgow, summed up by saying: “I think we do see lots of patients and maybe we just need to be aware that this may not be as benign as we think, and certainly we should be looking for abnormal patellae and being very aware of it in young people.”

Mr. Conchie and his coauthors had nothing to disclose.