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Is aspirin the best way to prevent blood clots after THA/TKA?
CHICAGO – Patients discharged to facilities rather than to home after total hip arthroplasty (THA) or total knee arthroplasty (TKA) may need more potent chemoprophylaxis than aspirin to prevent blood clots, new data suggest.
Researchers led by Stefano Muscatelli, MD, an orthopedist at Michigan Medicine, Ann Arbor, first aimed to determine whether there was an increase in risk of venous thromboembolism (VTE) in patients who were discharged to facilities such as a skilled nursing facility or inpatient rehabilitation facility, compared with those discharged to home after THA or TKA.
The second aim was to determine whether VTE risk differed between home- and non–home-discharge patients when stratified by the chemoprophylaxis prescribed to prevent VTE.
Findings were presented at the annual meeting of the American Academy of Orthopaedic Surgeons by coauthor Michael McHugh, MD, also an orthopedist at Michigan Medicine in Ann Arbor.
The agents were categorized in three groups: aspirin only; more aggressive anticoagulants, including warfarin, factor Xa inhibitor, direct thrombin inhibitor, low-molecular-weight heparin, pentasaccharide, or antiplatelet agents, with or without concurrent aspirin; and other regimens.
The researchers found that rates of VTE were higher among patients discharged to facilities.
Of 6,411 patients included in the study, the overall rate of VTE was 1.05%. Among home-discharge patients (n = 5445), rates of VTE were significantly lower than among patients discharged to facilities (n = 966) (0.83% vs. 2.26%; P < .001).
However, the researchers found there was no difference in VTE rates between non-home and home discharge in patients who received more aggressive chemoprophylaxis.
Among discharged patients who received only aspirin, rates of VTE among those discharged to home were significantly lower compared to those discharged to facilities (0.76% vs. 3.83%; P < .001).
“Smoking, BMI [body mass index], procedure type, and preoperative anticoagulation were not associated with the outcome of VTE,” Dr. McHugh said.
“Although we found VTE to continue to be an uncommon complication, non-home discharge is independently associated with higher rates of VTE. Patients should be encouraged to discharge home, but those discharged to non-home facilities after total joint arthroplasty should be considered for more potent chemoprophylaxis than aspirin,” he concluded.
Stuart J. Fischer, MD, with Summit (N.J.) Orthopaedics and Sports Medicine, who was not part of the study, told this news organization that he found the results inconclusive.
He said there is the potential for confounding because “the people who are sent to a facility after total hip or total knee are inherently less mobile and less able to take care of themselves, so they are at a higher risk for VTE. They are going to be more static.”
Dr. Fischer noted that over the past few years, there has been a movement away from anticoagulation with more aggressive agents toward aspirin, for several reasons. Providers don’t have to monitor aspirin use and can instruct patients to take it once or twice a day. Initial data seem to show that it protects well against VTE.
“The question is, in certain population of patients, is it enough? And that’s where the data are unclear,” Dr. Fischer said.
“It’s certainly a useful study, and we need to find out which methods of anticoagulation are most effective in each setting,” he said.
Limitations include that it was a retrospective review and that adverse events from more aggressive chemoprophylaxis agents were not assessed. Prophylactic regimens were chosen at the discretion of the treating surgeon.
The researchers excluded bilateral cases, conversion arthroplasty, hip hemiarthroplasty, unicompartmental knee arthroplasty, and deaths.
Dr. Muscatelli and Dr. McHugh reported no relevant financial relationships. A coauthor reported being a paid consultant for DePuy and Zimmer. Dr. Fischer reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
CHICAGO – Patients discharged to facilities rather than to home after total hip arthroplasty (THA) or total knee arthroplasty (TKA) may need more potent chemoprophylaxis than aspirin to prevent blood clots, new data suggest.
Researchers led by Stefano Muscatelli, MD, an orthopedist at Michigan Medicine, Ann Arbor, first aimed to determine whether there was an increase in risk of venous thromboembolism (VTE) in patients who were discharged to facilities such as a skilled nursing facility or inpatient rehabilitation facility, compared with those discharged to home after THA or TKA.
The second aim was to determine whether VTE risk differed between home- and non–home-discharge patients when stratified by the chemoprophylaxis prescribed to prevent VTE.
Findings were presented at the annual meeting of the American Academy of Orthopaedic Surgeons by coauthor Michael McHugh, MD, also an orthopedist at Michigan Medicine in Ann Arbor.
The agents were categorized in three groups: aspirin only; more aggressive anticoagulants, including warfarin, factor Xa inhibitor, direct thrombin inhibitor, low-molecular-weight heparin, pentasaccharide, or antiplatelet agents, with or without concurrent aspirin; and other regimens.
The researchers found that rates of VTE were higher among patients discharged to facilities.
Of 6,411 patients included in the study, the overall rate of VTE was 1.05%. Among home-discharge patients (n = 5445), rates of VTE were significantly lower than among patients discharged to facilities (n = 966) (0.83% vs. 2.26%; P < .001).
However, the researchers found there was no difference in VTE rates between non-home and home discharge in patients who received more aggressive chemoprophylaxis.
Among discharged patients who received only aspirin, rates of VTE among those discharged to home were significantly lower compared to those discharged to facilities (0.76% vs. 3.83%; P < .001).
“Smoking, BMI [body mass index], procedure type, and preoperative anticoagulation were not associated with the outcome of VTE,” Dr. McHugh said.
“Although we found VTE to continue to be an uncommon complication, non-home discharge is independently associated with higher rates of VTE. Patients should be encouraged to discharge home, but those discharged to non-home facilities after total joint arthroplasty should be considered for more potent chemoprophylaxis than aspirin,” he concluded.
Stuart J. Fischer, MD, with Summit (N.J.) Orthopaedics and Sports Medicine, who was not part of the study, told this news organization that he found the results inconclusive.
He said there is the potential for confounding because “the people who are sent to a facility after total hip or total knee are inherently less mobile and less able to take care of themselves, so they are at a higher risk for VTE. They are going to be more static.”
Dr. Fischer noted that over the past few years, there has been a movement away from anticoagulation with more aggressive agents toward aspirin, for several reasons. Providers don’t have to monitor aspirin use and can instruct patients to take it once or twice a day. Initial data seem to show that it protects well against VTE.
“The question is, in certain population of patients, is it enough? And that’s where the data are unclear,” Dr. Fischer said.
“It’s certainly a useful study, and we need to find out which methods of anticoagulation are most effective in each setting,” he said.
Limitations include that it was a retrospective review and that adverse events from more aggressive chemoprophylaxis agents were not assessed. Prophylactic regimens were chosen at the discretion of the treating surgeon.
The researchers excluded bilateral cases, conversion arthroplasty, hip hemiarthroplasty, unicompartmental knee arthroplasty, and deaths.
Dr. Muscatelli and Dr. McHugh reported no relevant financial relationships. A coauthor reported being a paid consultant for DePuy and Zimmer. Dr. Fischer reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
CHICAGO – Patients discharged to facilities rather than to home after total hip arthroplasty (THA) or total knee arthroplasty (TKA) may need more potent chemoprophylaxis than aspirin to prevent blood clots, new data suggest.
Researchers led by Stefano Muscatelli, MD, an orthopedist at Michigan Medicine, Ann Arbor, first aimed to determine whether there was an increase in risk of venous thromboembolism (VTE) in patients who were discharged to facilities such as a skilled nursing facility or inpatient rehabilitation facility, compared with those discharged to home after THA or TKA.
The second aim was to determine whether VTE risk differed between home- and non–home-discharge patients when stratified by the chemoprophylaxis prescribed to prevent VTE.
Findings were presented at the annual meeting of the American Academy of Orthopaedic Surgeons by coauthor Michael McHugh, MD, also an orthopedist at Michigan Medicine in Ann Arbor.
The agents were categorized in three groups: aspirin only; more aggressive anticoagulants, including warfarin, factor Xa inhibitor, direct thrombin inhibitor, low-molecular-weight heparin, pentasaccharide, or antiplatelet agents, with or without concurrent aspirin; and other regimens.
The researchers found that rates of VTE were higher among patients discharged to facilities.
Of 6,411 patients included in the study, the overall rate of VTE was 1.05%. Among home-discharge patients (n = 5445), rates of VTE were significantly lower than among patients discharged to facilities (n = 966) (0.83% vs. 2.26%; P < .001).
However, the researchers found there was no difference in VTE rates between non-home and home discharge in patients who received more aggressive chemoprophylaxis.
Among discharged patients who received only aspirin, rates of VTE among those discharged to home were significantly lower compared to those discharged to facilities (0.76% vs. 3.83%; P < .001).
“Smoking, BMI [body mass index], procedure type, and preoperative anticoagulation were not associated with the outcome of VTE,” Dr. McHugh said.
“Although we found VTE to continue to be an uncommon complication, non-home discharge is independently associated with higher rates of VTE. Patients should be encouraged to discharge home, but those discharged to non-home facilities after total joint arthroplasty should be considered for more potent chemoprophylaxis than aspirin,” he concluded.
Stuart J. Fischer, MD, with Summit (N.J.) Orthopaedics and Sports Medicine, who was not part of the study, told this news organization that he found the results inconclusive.
He said there is the potential for confounding because “the people who are sent to a facility after total hip or total knee are inherently less mobile and less able to take care of themselves, so they are at a higher risk for VTE. They are going to be more static.”
Dr. Fischer noted that over the past few years, there has been a movement away from anticoagulation with more aggressive agents toward aspirin, for several reasons. Providers don’t have to monitor aspirin use and can instruct patients to take it once or twice a day. Initial data seem to show that it protects well against VTE.
“The question is, in certain population of patients, is it enough? And that’s where the data are unclear,” Dr. Fischer said.
“It’s certainly a useful study, and we need to find out which methods of anticoagulation are most effective in each setting,” he said.
Limitations include that it was a retrospective review and that adverse events from more aggressive chemoprophylaxis agents were not assessed. Prophylactic regimens were chosen at the discretion of the treating surgeon.
The researchers excluded bilateral cases, conversion arthroplasty, hip hemiarthroplasty, unicompartmental knee arthroplasty, and deaths.
Dr. Muscatelli and Dr. McHugh reported no relevant financial relationships. A coauthor reported being a paid consultant for DePuy and Zimmer. Dr. Fischer reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
AT AAOS 2022
Stress tests before knee, hip replacement surgeries down, with no ill effects
Cardiac stress testing before hip and knee replacements has dropped steadily since 2006, according to results from a new study that also showed major cardiac complications to be low in the absence of stress testing – even among people with established risk factors.
Routine stress testing before noncardiac surgeries has come under fire in recent decades as an overuse of resources and a burden on patients. Practice guidelines issued in 2007 and 2014 by the American College of Cardiology and the American Heart Association sought to limit the use of preoperative testing to patients with specific cardiovascular risk factors who might have their management changed by the test results.
For their study, published online in JAMA Cardiology, Daniel S. Rubin, MD, of the University of Chicago and colleagues looked at employee-based insurance data, which included Medicare Advantage claims, for more than 800,000 total hip or knee arthroplasties (28% hip and 72% knee replacements) conducted between 2004 and 2017.
While some 10% of the cohort (mean age 62, 58% women) received a stress test in the 2 months before surgery, the investigators found that the frequency of preoperative stress testing dropped annually starting in late 2006, when it peaked at about 14%, to about 7% in 2017. Older age, male sex and a Revised Cardiac Risk Index score of 1 or greater were all associated with a higher likelihood of being tested.
The overall frequency of myocardial infarction or cardiac arrest was 0.24%, occurring in 1,677 of 686,067 patients. While the rate was higher in patients with at least one RCRI condition, this did not differ significantly between those who received a preoperative stress test and those who did not (0.60%; 221 of 36,554 vs. 0.57%; 694 of 122,466 patients.
The 2007 and 2014 ACC/AHA guidelines make clear that patients with zero RCRI conditions – which comprise a history of ischemic heart disease, heart failure, insulin therapy for diabetes, cerebrovascular disease, or chronic kidney disease – should not receive a stress test before an intermediate-risk surgery such as a hip or knee replacement. But in this study, Dr. Rubin and his colleagues found that almost half of patients who had no RCRI risk factors were stress tested anyway. This means, Dr. Rubin said in an interview, that “there’s still room for improvement” in reducing testing.
“I never want to question how a physician chooses to practice, but I have to applaud physicians for reining in the use of this test. We’re using less of this test and yet the incidence of myocardial infarction and cardiac arrest is also going down, which also calls into question whether we’re getting better at choosing the right patients for the test; or the test doesn’t impact outcomes; or overall health of these patients is improving,” he said.
One surprise finding in the study, Dr. Rubin noted, was a higher rate of complications among people without RCRI conditions who were stress tested, compared with those who were not, with a mean complication rate of 0.27%, compared with 0.14% among those who did not receive a test (P < .001). “The RCRI doesn’t capture certain things,” Dr. Rubin said. “And we know that no risk stratification tool is going to capture everything.”
The RCRI, he noted, is based on a clinical history. “If you haven’t been diagnosed yet, it won’t appear as a risk factor, even if you’re clearly at risk. The question then becomes for a physician, do you do the test or not? On a day-to-day basis it’s hard to make that decision because you want what’s best for the individual patient – and it’s hard to generalize from a study of 800,000 people what’s right for that one patient. That said, it doesn’t appear that stress testing improves outcomes and a decrease in testing appears appropriate.”
Dr. Rubin and his colleagues described as a weakness of their study that it did not capture the full scope of preoperative stress testing among Medicare patients, who are older and therefore more likely to be tested.
That the 2007 and 2014 practice guidelines bore on the drop in testing was not demonstrated by Dr. Rubin and colleagues’ study, which saw declines begin even before the guidelines were published. Nonetheless, the results appear to validate the approach advocated in the guidelines, said guideline coauthor Joshua Beckman, MD, of Vanderbilt University, whose recent research has focused on identifying risk factors for MI after noncardiac surgery.
“I hope that the guidelines have helped in changing the culture for the use of preoperative stress testing as a regular thing,” Dr. Beckman said in an interview. “In fact, the guidelines say you shouldn’t do anything before an operation that you wouldn’t do anyway. So these findings are certainly in agreement with what we’re suggesting and support the idea that unless you have something that is unstable or active, stress testing isn’t likely to help.”
Annemarie Thompson, MD, of Duke University in Durham, N.C., another coauthor on the 2014 guidelines, commented in an interview that Dr. Rubin and colleagues’ findings of a doubled rate of complications among people without RCRI conditions who were stress tested, compared with those who were not might mean something “other than just sheer overuse or overordering of tests inappropriately.”
Rather, she said, physicians might be seeing something in the clinic that cannot be captured by a screening tool reliant on existing diagnoses. “Maybe when they’re sitting in front of you in a clinic, they’re so immobile that you’re left wondering. Or maybe they haven’t been seen by a doctor in a long time,” Dr. Thompson said. “So they don’t have diagnoses if they haven’t been followed. I think what [this finding] shows is that clinicians are detecting something. They may not know what it is. But we have to give a little wiggle room to the clinician who is sitting there looking at a patient who looks like they may not make it through surgery.”
Dr. Thompson said it would be helpful, after a big-data study like this one, to go through the clinical histories of those patients – in this study fewer than 100 – who had no RCRI risk factors and yet were stress tested and ended up having complications. “Until then we’re not going to solve the mystery,” she said. “But it’s a very, very interesting study.”
Dr. Rubin is the president of DRDR Mobile Health, a company that creates mobile applications for health care and from which he has not received compensation. One of his coauthors on the study, Dr. Peter Nagele, reported fee income from Roche Diagnostics. Dr. Beckman disclosed personal fees from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and other pharmaceutical manufacturers. Dr. Thompson has no disclosures.
SOURCE: Rubin et al. JAMA Cardiol. 2020 Sep 30. doi: 10.1001/jamacardio.2020.4311.
Cardiac stress testing before hip and knee replacements has dropped steadily since 2006, according to results from a new study that also showed major cardiac complications to be low in the absence of stress testing – even among people with established risk factors.
Routine stress testing before noncardiac surgeries has come under fire in recent decades as an overuse of resources and a burden on patients. Practice guidelines issued in 2007 and 2014 by the American College of Cardiology and the American Heart Association sought to limit the use of preoperative testing to patients with specific cardiovascular risk factors who might have their management changed by the test results.
For their study, published online in JAMA Cardiology, Daniel S. Rubin, MD, of the University of Chicago and colleagues looked at employee-based insurance data, which included Medicare Advantage claims, for more than 800,000 total hip or knee arthroplasties (28% hip and 72% knee replacements) conducted between 2004 and 2017.
While some 10% of the cohort (mean age 62, 58% women) received a stress test in the 2 months before surgery, the investigators found that the frequency of preoperative stress testing dropped annually starting in late 2006, when it peaked at about 14%, to about 7% in 2017. Older age, male sex and a Revised Cardiac Risk Index score of 1 or greater were all associated with a higher likelihood of being tested.
The overall frequency of myocardial infarction or cardiac arrest was 0.24%, occurring in 1,677 of 686,067 patients. While the rate was higher in patients with at least one RCRI condition, this did not differ significantly between those who received a preoperative stress test and those who did not (0.60%; 221 of 36,554 vs. 0.57%; 694 of 122,466 patients.
The 2007 and 2014 ACC/AHA guidelines make clear that patients with zero RCRI conditions – which comprise a history of ischemic heart disease, heart failure, insulin therapy for diabetes, cerebrovascular disease, or chronic kidney disease – should not receive a stress test before an intermediate-risk surgery such as a hip or knee replacement. But in this study, Dr. Rubin and his colleagues found that almost half of patients who had no RCRI risk factors were stress tested anyway. This means, Dr. Rubin said in an interview, that “there’s still room for improvement” in reducing testing.
“I never want to question how a physician chooses to practice, but I have to applaud physicians for reining in the use of this test. We’re using less of this test and yet the incidence of myocardial infarction and cardiac arrest is also going down, which also calls into question whether we’re getting better at choosing the right patients for the test; or the test doesn’t impact outcomes; or overall health of these patients is improving,” he said.
One surprise finding in the study, Dr. Rubin noted, was a higher rate of complications among people without RCRI conditions who were stress tested, compared with those who were not, with a mean complication rate of 0.27%, compared with 0.14% among those who did not receive a test (P < .001). “The RCRI doesn’t capture certain things,” Dr. Rubin said. “And we know that no risk stratification tool is going to capture everything.”
The RCRI, he noted, is based on a clinical history. “If you haven’t been diagnosed yet, it won’t appear as a risk factor, even if you’re clearly at risk. The question then becomes for a physician, do you do the test or not? On a day-to-day basis it’s hard to make that decision because you want what’s best for the individual patient – and it’s hard to generalize from a study of 800,000 people what’s right for that one patient. That said, it doesn’t appear that stress testing improves outcomes and a decrease in testing appears appropriate.”
Dr. Rubin and his colleagues described as a weakness of their study that it did not capture the full scope of preoperative stress testing among Medicare patients, who are older and therefore more likely to be tested.
That the 2007 and 2014 practice guidelines bore on the drop in testing was not demonstrated by Dr. Rubin and colleagues’ study, which saw declines begin even before the guidelines were published. Nonetheless, the results appear to validate the approach advocated in the guidelines, said guideline coauthor Joshua Beckman, MD, of Vanderbilt University, whose recent research has focused on identifying risk factors for MI after noncardiac surgery.
“I hope that the guidelines have helped in changing the culture for the use of preoperative stress testing as a regular thing,” Dr. Beckman said in an interview. “In fact, the guidelines say you shouldn’t do anything before an operation that you wouldn’t do anyway. So these findings are certainly in agreement with what we’re suggesting and support the idea that unless you have something that is unstable or active, stress testing isn’t likely to help.”
Annemarie Thompson, MD, of Duke University in Durham, N.C., another coauthor on the 2014 guidelines, commented in an interview that Dr. Rubin and colleagues’ findings of a doubled rate of complications among people without RCRI conditions who were stress tested, compared with those who were not might mean something “other than just sheer overuse or overordering of tests inappropriately.”
Rather, she said, physicians might be seeing something in the clinic that cannot be captured by a screening tool reliant on existing diagnoses. “Maybe when they’re sitting in front of you in a clinic, they’re so immobile that you’re left wondering. Or maybe they haven’t been seen by a doctor in a long time,” Dr. Thompson said. “So they don’t have diagnoses if they haven’t been followed. I think what [this finding] shows is that clinicians are detecting something. They may not know what it is. But we have to give a little wiggle room to the clinician who is sitting there looking at a patient who looks like they may not make it through surgery.”
Dr. Thompson said it would be helpful, after a big-data study like this one, to go through the clinical histories of those patients – in this study fewer than 100 – who had no RCRI risk factors and yet were stress tested and ended up having complications. “Until then we’re not going to solve the mystery,” she said. “But it’s a very, very interesting study.”
Dr. Rubin is the president of DRDR Mobile Health, a company that creates mobile applications for health care and from which he has not received compensation. One of his coauthors on the study, Dr. Peter Nagele, reported fee income from Roche Diagnostics. Dr. Beckman disclosed personal fees from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and other pharmaceutical manufacturers. Dr. Thompson has no disclosures.
SOURCE: Rubin et al. JAMA Cardiol. 2020 Sep 30. doi: 10.1001/jamacardio.2020.4311.
Cardiac stress testing before hip and knee replacements has dropped steadily since 2006, according to results from a new study that also showed major cardiac complications to be low in the absence of stress testing – even among people with established risk factors.
Routine stress testing before noncardiac surgeries has come under fire in recent decades as an overuse of resources and a burden on patients. Practice guidelines issued in 2007 and 2014 by the American College of Cardiology and the American Heart Association sought to limit the use of preoperative testing to patients with specific cardiovascular risk factors who might have their management changed by the test results.
For their study, published online in JAMA Cardiology, Daniel S. Rubin, MD, of the University of Chicago and colleagues looked at employee-based insurance data, which included Medicare Advantage claims, for more than 800,000 total hip or knee arthroplasties (28% hip and 72% knee replacements) conducted between 2004 and 2017.
While some 10% of the cohort (mean age 62, 58% women) received a stress test in the 2 months before surgery, the investigators found that the frequency of preoperative stress testing dropped annually starting in late 2006, when it peaked at about 14%, to about 7% in 2017. Older age, male sex and a Revised Cardiac Risk Index score of 1 or greater were all associated with a higher likelihood of being tested.
The overall frequency of myocardial infarction or cardiac arrest was 0.24%, occurring in 1,677 of 686,067 patients. While the rate was higher in patients with at least one RCRI condition, this did not differ significantly between those who received a preoperative stress test and those who did not (0.60%; 221 of 36,554 vs. 0.57%; 694 of 122,466 patients.
The 2007 and 2014 ACC/AHA guidelines make clear that patients with zero RCRI conditions – which comprise a history of ischemic heart disease, heart failure, insulin therapy for diabetes, cerebrovascular disease, or chronic kidney disease – should not receive a stress test before an intermediate-risk surgery such as a hip or knee replacement. But in this study, Dr. Rubin and his colleagues found that almost half of patients who had no RCRI risk factors were stress tested anyway. This means, Dr. Rubin said in an interview, that “there’s still room for improvement” in reducing testing.
“I never want to question how a physician chooses to practice, but I have to applaud physicians for reining in the use of this test. We’re using less of this test and yet the incidence of myocardial infarction and cardiac arrest is also going down, which also calls into question whether we’re getting better at choosing the right patients for the test; or the test doesn’t impact outcomes; or overall health of these patients is improving,” he said.
One surprise finding in the study, Dr. Rubin noted, was a higher rate of complications among people without RCRI conditions who were stress tested, compared with those who were not, with a mean complication rate of 0.27%, compared with 0.14% among those who did not receive a test (P < .001). “The RCRI doesn’t capture certain things,” Dr. Rubin said. “And we know that no risk stratification tool is going to capture everything.”
The RCRI, he noted, is based on a clinical history. “If you haven’t been diagnosed yet, it won’t appear as a risk factor, even if you’re clearly at risk. The question then becomes for a physician, do you do the test or not? On a day-to-day basis it’s hard to make that decision because you want what’s best for the individual patient – and it’s hard to generalize from a study of 800,000 people what’s right for that one patient. That said, it doesn’t appear that stress testing improves outcomes and a decrease in testing appears appropriate.”
Dr. Rubin and his colleagues described as a weakness of their study that it did not capture the full scope of preoperative stress testing among Medicare patients, who are older and therefore more likely to be tested.
That the 2007 and 2014 practice guidelines bore on the drop in testing was not demonstrated by Dr. Rubin and colleagues’ study, which saw declines begin even before the guidelines were published. Nonetheless, the results appear to validate the approach advocated in the guidelines, said guideline coauthor Joshua Beckman, MD, of Vanderbilt University, whose recent research has focused on identifying risk factors for MI after noncardiac surgery.
“I hope that the guidelines have helped in changing the culture for the use of preoperative stress testing as a regular thing,” Dr. Beckman said in an interview. “In fact, the guidelines say you shouldn’t do anything before an operation that you wouldn’t do anyway. So these findings are certainly in agreement with what we’re suggesting and support the idea that unless you have something that is unstable or active, stress testing isn’t likely to help.”
Annemarie Thompson, MD, of Duke University in Durham, N.C., another coauthor on the 2014 guidelines, commented in an interview that Dr. Rubin and colleagues’ findings of a doubled rate of complications among people without RCRI conditions who were stress tested, compared with those who were not might mean something “other than just sheer overuse or overordering of tests inappropriately.”
Rather, she said, physicians might be seeing something in the clinic that cannot be captured by a screening tool reliant on existing diagnoses. “Maybe when they’re sitting in front of you in a clinic, they’re so immobile that you’re left wondering. Or maybe they haven’t been seen by a doctor in a long time,” Dr. Thompson said. “So they don’t have diagnoses if they haven’t been followed. I think what [this finding] shows is that clinicians are detecting something. They may not know what it is. But we have to give a little wiggle room to the clinician who is sitting there looking at a patient who looks like they may not make it through surgery.”
Dr. Thompson said it would be helpful, after a big-data study like this one, to go through the clinical histories of those patients – in this study fewer than 100 – who had no RCRI risk factors and yet were stress tested and ended up having complications. “Until then we’re not going to solve the mystery,” she said. “But it’s a very, very interesting study.”
Dr. Rubin is the president of DRDR Mobile Health, a company that creates mobile applications for health care and from which he has not received compensation. One of his coauthors on the study, Dr. Peter Nagele, reported fee income from Roche Diagnostics. Dr. Beckman disclosed personal fees from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and other pharmaceutical manufacturers. Dr. Thompson has no disclosures.
SOURCE: Rubin et al. JAMA Cardiol. 2020 Sep 30. doi: 10.1001/jamacardio.2020.4311.
FROM JAMA CARDIOLOGY
Standardized protocol guides therapies to reduce VTE after arthroplasty
A simple tool to guide choice of antithrombotic therapy following total joint arthroplasty led to a reduction in pulmonary embolism (PE) after being introduced systemwide, according to a prospectively tracked evaluation of a large patient cohort. The results of the study were reported in an abstract scheduled for release at the annual meeting of the American Academy of Orthopaedic Surgeons. The meeting was canceled because of COVID-19.
“We developed a simplified scoring system for evaluating risk of thromboembolism and guiding prophylaxis that led to a significant reduction in events across a large integrated health care system,” reported James Wylie, MD, associate medical director for hip and knee preservation and orthopedic research at Intermountain Healthcare, Salt Lake City, Utah.
The goal of the methodology was to create a uniform and evidence-based approach to risk assessment in order to guide selection of appropriate venous thromboembolism (VTE) prophylaxis. The tool takes into account the need to individualize antithrombotic drugs for risk of both VTE and for bleeding.
“VTE is a major threat following total joint replacement, but not all patients require anticoagulants. Recent evidence supports a shift to aspirin for low-risk patients,” explained Dr. Wylie in an interview.
The risk tool assigns points for such factors as history of VTE, older age, history of coronary artery disease, history of cancer, and increased body mass index. There are two possible ratings to guide strategies. Those with standard risk are candidates for 81 mg of aspirin twice daily. Those with high risk are candidates for 2.5 mg of apixaban, also administered twice daily. Custom dosing of warfarin is an alternative for the latter group. Regardless of strategy, prophylaxis is administered for 30 days following arthroplasty
“The risk score is calculated automatically, because you have to click a box in the electronic medical record for all of those factors as part of admission orders,” Dr. Wylie said.
The protocol was introduced in July 2017 and adoption was tracked prospectively over 18 months. In an evaluable cohort of 20,284 patients, PE rates in the 71% of patients adherent to the protocol were compared with the 29% who were not.
Over the observation period, the rates of PE were 0.34% and 0.62% (P = .004) for those adherent and nonadherent, respectively. The rate of unplanned readmissions and death, which were secondary outcomes, were both numerically lower in the group treated by adherent surgeons, but the differences did not reach statistical significance.
Adoption of the protocol by surgeons did increase over the course of the observation period, and this correlated with a decrease in unplanned readmissions. Bleeding-related readmission was a rare event in this analysis and did not significantly increase over time, according to Dr. Wylie.
The risk assessment tool, developed by a multispecialty team at Intermountain Healthcare, was based on a review of hundreds of published papers and guidelines, according to Nathan Momberger, MD, who is the associate medical director of total joint replacement at Intermountain and was a coauthor on this study. A member of the team that developed the risk assessment tool, Dr. Momberger noted that new risk score was developed at a time when clinicians have been moving quickly away from warfarin to direct oral anticoagulants.
“None of our surgeons were using the same VTE prophylaxis when we started this project,” Dr. Momberger said. This was a motivation for developing a systemwide approach. In the 22 participating hospitals, there were 50 surgeons performing total knee arthroplasty and 40 surgeons were performing total hip surgery at the time the new protocol was introduced.
Further analyses will provide a more detailed analysis of the effect of the protocol on other thrombotic events, including deep vein thrombosis, and on cost. Since these data were analyzed, protocol adoption has increased and now exceeds 80%, according to Dr. Wylie.
Although a standardized approach to VTE prophylaxis following total joint arthroplasty is attractive, the ideal strategy remains controversial, according to Sunny Parikh, MD, an orthopedic surgeon affiliated with Colchester (England) General Hospital.
As a coauthor of a recent study that quantified symptomatic VTE rates at his and a neighboring hospital over a 3-year period (BMC Musculoskelet Disord. 2020;21:95), Dr. Parikh reported that VTE rates did not reach zero even with a prolonged course of the low-molecular-weight heparin enoxaparin.
At 90 days, the symptomatic VTE rate was only 0.3% for total knee arthroplasty but reached 1.2% for total hip arthroplasty.
“At the time of this study we were using enoxaparin for 28 days following total hip replacements and for 14 days following total knee replacements,” Dr. Parikh reported. Since this study, his institution has switched to a regimen recommended by the U.K.’s National Institute for Health and Clinical Excellence (NICE).
Under the NICE guidelines, VTE prophylaxis for total hip arthroplasty is 40 mg enoxaparin once daily for 14 days followed by 75 mg aspirin for another 14 days, according to Dr. Parikh. For total knee arthroplasty, the standard regimen is 75 mg aspirin for 14 days.
For those who might not be best managed with the standard approach, “there is no clear guideline.” Rather, in patients with renal or liver impairment, “we discuss the case with the hematology team to adjust the doses,” Dr. Parikh reported.
The advantage of a standardized approach applied to all or most patients is that is eliminates disparities, but Dr. Parikh agreed that risk-adjusted prophylaxis might be warranted for optimal outcomes.
Dr. Wylie reported a financial relationship with Arthrex.
A simple tool to guide choice of antithrombotic therapy following total joint arthroplasty led to a reduction in pulmonary embolism (PE) after being introduced systemwide, according to a prospectively tracked evaluation of a large patient cohort. The results of the study were reported in an abstract scheduled for release at the annual meeting of the American Academy of Orthopaedic Surgeons. The meeting was canceled because of COVID-19.
“We developed a simplified scoring system for evaluating risk of thromboembolism and guiding prophylaxis that led to a significant reduction in events across a large integrated health care system,” reported James Wylie, MD, associate medical director for hip and knee preservation and orthopedic research at Intermountain Healthcare, Salt Lake City, Utah.
The goal of the methodology was to create a uniform and evidence-based approach to risk assessment in order to guide selection of appropriate venous thromboembolism (VTE) prophylaxis. The tool takes into account the need to individualize antithrombotic drugs for risk of both VTE and for bleeding.
“VTE is a major threat following total joint replacement, but not all patients require anticoagulants. Recent evidence supports a shift to aspirin for low-risk patients,” explained Dr. Wylie in an interview.
The risk tool assigns points for such factors as history of VTE, older age, history of coronary artery disease, history of cancer, and increased body mass index. There are two possible ratings to guide strategies. Those with standard risk are candidates for 81 mg of aspirin twice daily. Those with high risk are candidates for 2.5 mg of apixaban, also administered twice daily. Custom dosing of warfarin is an alternative for the latter group. Regardless of strategy, prophylaxis is administered for 30 days following arthroplasty
“The risk score is calculated automatically, because you have to click a box in the electronic medical record for all of those factors as part of admission orders,” Dr. Wylie said.
The protocol was introduced in July 2017 and adoption was tracked prospectively over 18 months. In an evaluable cohort of 20,284 patients, PE rates in the 71% of patients adherent to the protocol were compared with the 29% who were not.
Over the observation period, the rates of PE were 0.34% and 0.62% (P = .004) for those adherent and nonadherent, respectively. The rate of unplanned readmissions and death, which were secondary outcomes, were both numerically lower in the group treated by adherent surgeons, but the differences did not reach statistical significance.
Adoption of the protocol by surgeons did increase over the course of the observation period, and this correlated with a decrease in unplanned readmissions. Bleeding-related readmission was a rare event in this analysis and did not significantly increase over time, according to Dr. Wylie.
The risk assessment tool, developed by a multispecialty team at Intermountain Healthcare, was based on a review of hundreds of published papers and guidelines, according to Nathan Momberger, MD, who is the associate medical director of total joint replacement at Intermountain and was a coauthor on this study. A member of the team that developed the risk assessment tool, Dr. Momberger noted that new risk score was developed at a time when clinicians have been moving quickly away from warfarin to direct oral anticoagulants.
“None of our surgeons were using the same VTE prophylaxis when we started this project,” Dr. Momberger said. This was a motivation for developing a systemwide approach. In the 22 participating hospitals, there were 50 surgeons performing total knee arthroplasty and 40 surgeons were performing total hip surgery at the time the new protocol was introduced.
Further analyses will provide a more detailed analysis of the effect of the protocol on other thrombotic events, including deep vein thrombosis, and on cost. Since these data were analyzed, protocol adoption has increased and now exceeds 80%, according to Dr. Wylie.
Although a standardized approach to VTE prophylaxis following total joint arthroplasty is attractive, the ideal strategy remains controversial, according to Sunny Parikh, MD, an orthopedic surgeon affiliated with Colchester (England) General Hospital.
As a coauthor of a recent study that quantified symptomatic VTE rates at his and a neighboring hospital over a 3-year period (BMC Musculoskelet Disord. 2020;21:95), Dr. Parikh reported that VTE rates did not reach zero even with a prolonged course of the low-molecular-weight heparin enoxaparin.
At 90 days, the symptomatic VTE rate was only 0.3% for total knee arthroplasty but reached 1.2% for total hip arthroplasty.
“At the time of this study we were using enoxaparin for 28 days following total hip replacements and for 14 days following total knee replacements,” Dr. Parikh reported. Since this study, his institution has switched to a regimen recommended by the U.K.’s National Institute for Health and Clinical Excellence (NICE).
Under the NICE guidelines, VTE prophylaxis for total hip arthroplasty is 40 mg enoxaparin once daily for 14 days followed by 75 mg aspirin for another 14 days, according to Dr. Parikh. For total knee arthroplasty, the standard regimen is 75 mg aspirin for 14 days.
For those who might not be best managed with the standard approach, “there is no clear guideline.” Rather, in patients with renal or liver impairment, “we discuss the case with the hematology team to adjust the doses,” Dr. Parikh reported.
The advantage of a standardized approach applied to all or most patients is that is eliminates disparities, but Dr. Parikh agreed that risk-adjusted prophylaxis might be warranted for optimal outcomes.
Dr. Wylie reported a financial relationship with Arthrex.
A simple tool to guide choice of antithrombotic therapy following total joint arthroplasty led to a reduction in pulmonary embolism (PE) after being introduced systemwide, according to a prospectively tracked evaluation of a large patient cohort. The results of the study were reported in an abstract scheduled for release at the annual meeting of the American Academy of Orthopaedic Surgeons. The meeting was canceled because of COVID-19.
“We developed a simplified scoring system for evaluating risk of thromboembolism and guiding prophylaxis that led to a significant reduction in events across a large integrated health care system,” reported James Wylie, MD, associate medical director for hip and knee preservation and orthopedic research at Intermountain Healthcare, Salt Lake City, Utah.
The goal of the methodology was to create a uniform and evidence-based approach to risk assessment in order to guide selection of appropriate venous thromboembolism (VTE) prophylaxis. The tool takes into account the need to individualize antithrombotic drugs for risk of both VTE and for bleeding.
“VTE is a major threat following total joint replacement, but not all patients require anticoagulants. Recent evidence supports a shift to aspirin for low-risk patients,” explained Dr. Wylie in an interview.
The risk tool assigns points for such factors as history of VTE, older age, history of coronary artery disease, history of cancer, and increased body mass index. There are two possible ratings to guide strategies. Those with standard risk are candidates for 81 mg of aspirin twice daily. Those with high risk are candidates for 2.5 mg of apixaban, also administered twice daily. Custom dosing of warfarin is an alternative for the latter group. Regardless of strategy, prophylaxis is administered for 30 days following arthroplasty
“The risk score is calculated automatically, because you have to click a box in the electronic medical record for all of those factors as part of admission orders,” Dr. Wylie said.
The protocol was introduced in July 2017 and adoption was tracked prospectively over 18 months. In an evaluable cohort of 20,284 patients, PE rates in the 71% of patients adherent to the protocol were compared with the 29% who were not.
Over the observation period, the rates of PE were 0.34% and 0.62% (P = .004) for those adherent and nonadherent, respectively. The rate of unplanned readmissions and death, which were secondary outcomes, were both numerically lower in the group treated by adherent surgeons, but the differences did not reach statistical significance.
Adoption of the protocol by surgeons did increase over the course of the observation period, and this correlated with a decrease in unplanned readmissions. Bleeding-related readmission was a rare event in this analysis and did not significantly increase over time, according to Dr. Wylie.
The risk assessment tool, developed by a multispecialty team at Intermountain Healthcare, was based on a review of hundreds of published papers and guidelines, according to Nathan Momberger, MD, who is the associate medical director of total joint replacement at Intermountain and was a coauthor on this study. A member of the team that developed the risk assessment tool, Dr. Momberger noted that new risk score was developed at a time when clinicians have been moving quickly away from warfarin to direct oral anticoagulants.
“None of our surgeons were using the same VTE prophylaxis when we started this project,” Dr. Momberger said. This was a motivation for developing a systemwide approach. In the 22 participating hospitals, there were 50 surgeons performing total knee arthroplasty and 40 surgeons were performing total hip surgery at the time the new protocol was introduced.
Further analyses will provide a more detailed analysis of the effect of the protocol on other thrombotic events, including deep vein thrombosis, and on cost. Since these data were analyzed, protocol adoption has increased and now exceeds 80%, according to Dr. Wylie.
Although a standardized approach to VTE prophylaxis following total joint arthroplasty is attractive, the ideal strategy remains controversial, according to Sunny Parikh, MD, an orthopedic surgeon affiliated with Colchester (England) General Hospital.
As a coauthor of a recent study that quantified symptomatic VTE rates at his and a neighboring hospital over a 3-year period (BMC Musculoskelet Disord. 2020;21:95), Dr. Parikh reported that VTE rates did not reach zero even with a prolonged course of the low-molecular-weight heparin enoxaparin.
At 90 days, the symptomatic VTE rate was only 0.3% for total knee arthroplasty but reached 1.2% for total hip arthroplasty.
“At the time of this study we were using enoxaparin for 28 days following total hip replacements and for 14 days following total knee replacements,” Dr. Parikh reported. Since this study, his institution has switched to a regimen recommended by the U.K.’s National Institute for Health and Clinical Excellence (NICE).
Under the NICE guidelines, VTE prophylaxis for total hip arthroplasty is 40 mg enoxaparin once daily for 14 days followed by 75 mg aspirin for another 14 days, according to Dr. Parikh. For total knee arthroplasty, the standard regimen is 75 mg aspirin for 14 days.
For those who might not be best managed with the standard approach, “there is no clear guideline.” Rather, in patients with renal or liver impairment, “we discuss the case with the hematology team to adjust the doses,” Dr. Parikh reported.
The advantage of a standardized approach applied to all or most patients is that is eliminates disparities, but Dr. Parikh agreed that risk-adjusted prophylaxis might be warranted for optimal outcomes.
Dr. Wylie reported a financial relationship with Arthrex.
REPORTING FROM AAOS 2020
Delayed hospital admission after hip fracture raises mortality risk
a retrospective, observational study suggests.
Among 867 elderly patients who underwent hip fracture surgery at a university hospital in China and who were available for follow-up, the proportion hospitalized on the day of injury was 25.4%, and the proportion hospitalized on days 1, 2, and 7 after injury were 54.7%, 66.3%, and 12.6%, respectively, reported Wei He, MD, of the Second Affiliated Hospital of Zhejiang University, Hangzhou, China, and colleagues in the World Journal of Emergency Medicine.
The mean time from admission to surgery was 5.2 days. Mortality rates at 1 year, 3 months, and 1 month after surgery were 10.5%, 5.4%, and 3.3%, respectively. Hospitalization at 7 or more days after injury was an independent risk factor for 1-year mortality (odds ratio, 1.76), the authors found.
Although the influence of surgical delay on mortality and morbidity among hip fracture patients has been widely studied, most data focus on surgery timing among hospitalized patients and fail to consider preadmission waiting time, they noted.
The current study aimed to assess outcomes based on “actual preadmission waiting time” through an analysis of data and surgical outcomes from a hospital electronic medical record system and from postoperative telephone interviews. Study subjects were patients aged over 65 years who underwent hip fracture surgery between Jan. 1, 2014, and Dec. 31, 2017. The mean age was 81.4 years, 74.7% of the patients were women, 67.1% had femoral neck fracture, and 56.1% had hip replacement surgery.
The findings, though limited by the retrospective nature of the study and the single-center design, suggest that, under the current conditions in China, admission delay may increase 1-year mortality, they wrote, concluding that “[i]n addition to early surgery highlighted in the guidelines, we also advocate early admission.”
The authors reported having no disclosures.
SOURCE: He W et al. World J Emerg Med. 2020;11(1):27-32.
a retrospective, observational study suggests.
Among 867 elderly patients who underwent hip fracture surgery at a university hospital in China and who were available for follow-up, the proportion hospitalized on the day of injury was 25.4%, and the proportion hospitalized on days 1, 2, and 7 after injury were 54.7%, 66.3%, and 12.6%, respectively, reported Wei He, MD, of the Second Affiliated Hospital of Zhejiang University, Hangzhou, China, and colleagues in the World Journal of Emergency Medicine.
The mean time from admission to surgery was 5.2 days. Mortality rates at 1 year, 3 months, and 1 month after surgery were 10.5%, 5.4%, and 3.3%, respectively. Hospitalization at 7 or more days after injury was an independent risk factor for 1-year mortality (odds ratio, 1.76), the authors found.
Although the influence of surgical delay on mortality and morbidity among hip fracture patients has been widely studied, most data focus on surgery timing among hospitalized patients and fail to consider preadmission waiting time, they noted.
The current study aimed to assess outcomes based on “actual preadmission waiting time” through an analysis of data and surgical outcomes from a hospital electronic medical record system and from postoperative telephone interviews. Study subjects were patients aged over 65 years who underwent hip fracture surgery between Jan. 1, 2014, and Dec. 31, 2017. The mean age was 81.4 years, 74.7% of the patients were women, 67.1% had femoral neck fracture, and 56.1% had hip replacement surgery.
The findings, though limited by the retrospective nature of the study and the single-center design, suggest that, under the current conditions in China, admission delay may increase 1-year mortality, they wrote, concluding that “[i]n addition to early surgery highlighted in the guidelines, we also advocate early admission.”
The authors reported having no disclosures.
SOURCE: He W et al. World J Emerg Med. 2020;11(1):27-32.
a retrospective, observational study suggests.
Among 867 elderly patients who underwent hip fracture surgery at a university hospital in China and who were available for follow-up, the proportion hospitalized on the day of injury was 25.4%, and the proportion hospitalized on days 1, 2, and 7 after injury were 54.7%, 66.3%, and 12.6%, respectively, reported Wei He, MD, of the Second Affiliated Hospital of Zhejiang University, Hangzhou, China, and colleagues in the World Journal of Emergency Medicine.
The mean time from admission to surgery was 5.2 days. Mortality rates at 1 year, 3 months, and 1 month after surgery were 10.5%, 5.4%, and 3.3%, respectively. Hospitalization at 7 or more days after injury was an independent risk factor for 1-year mortality (odds ratio, 1.76), the authors found.
Although the influence of surgical delay on mortality and morbidity among hip fracture patients has been widely studied, most data focus on surgery timing among hospitalized patients and fail to consider preadmission waiting time, they noted.
The current study aimed to assess outcomes based on “actual preadmission waiting time” through an analysis of data and surgical outcomes from a hospital electronic medical record system and from postoperative telephone interviews. Study subjects were patients aged over 65 years who underwent hip fracture surgery between Jan. 1, 2014, and Dec. 31, 2017. The mean age was 81.4 years, 74.7% of the patients were women, 67.1% had femoral neck fracture, and 56.1% had hip replacement surgery.
The findings, though limited by the retrospective nature of the study and the single-center design, suggest that, under the current conditions in China, admission delay may increase 1-year mortality, they wrote, concluding that “[i]n addition to early surgery highlighted in the guidelines, we also advocate early admission.”
The authors reported having no disclosures.
SOURCE: He W et al. World J Emerg Med. 2020;11(1):27-32.
FROM THE WORLD JOURNAL OF EMERGENCY MEDICINE
Simple prevention strategies can lessen postoperative delirium after orthopedic surgery
A new study has found that
and a prevention program can help improve staff education and outcomes.“In an aging society, it is very important to develop and implement a strategy for POD prevention to ensure that aging patients are treated as safely and effectively as possible,” wrote Jung-Yeon Choi of Seoul (South Korea) National University Bundang Hospital and coauthors. The study was published in BMC Geriatrics.
To determine how to better identify and treat high-risk patients for POD after orthopedic surgery, the researchers led a retrospective cohort study that included an intervention group of participants who were aged at least 65 years (n = 275) and a control group from a year prior (n = 274). Patients in the intervention group had their risk of delirium assessed and categorized using a simple screening tool, and those deemed at risk were entered into a multicomponent delirium prevention program.
Of the 275 patients in the intervention group, 144 required screening for delirium. Ninety-nine were classified as low risk, 29 were classified as high risk, and 16 missed the screening. Fifty-three additional patients were classified as high risk because they were aged 80 years or older. During the study, 17 participants experienced POD, 16 of whom were classified as high risk. In regard to estimating POD risk, the sensitivity and specificity of the delirium screening tool were 94.1% and 72.7%, respectively. Incidence rates of POD were 10.2% in the control group and 6.2% in the intervention group.
The authors noted their study’s limitations, including its design as a retrospective review of medical records rather than a prospective randomized controlled trial. In addition, because it was conducted in just one teaching hospital, they deemed it “not possible to determine the generalizability and long-term effect of our findings.”
The authors reported no conflicts of interest.
SOURCE: Choi JY et al. BMC Geriatr. 2019 Oct 26. doi: 10.1186/s12877-019-1303-z.
A new study has found that
and a prevention program can help improve staff education and outcomes.“In an aging society, it is very important to develop and implement a strategy for POD prevention to ensure that aging patients are treated as safely and effectively as possible,” wrote Jung-Yeon Choi of Seoul (South Korea) National University Bundang Hospital and coauthors. The study was published in BMC Geriatrics.
To determine how to better identify and treat high-risk patients for POD after orthopedic surgery, the researchers led a retrospective cohort study that included an intervention group of participants who were aged at least 65 years (n = 275) and a control group from a year prior (n = 274). Patients in the intervention group had their risk of delirium assessed and categorized using a simple screening tool, and those deemed at risk were entered into a multicomponent delirium prevention program.
Of the 275 patients in the intervention group, 144 required screening for delirium. Ninety-nine were classified as low risk, 29 were classified as high risk, and 16 missed the screening. Fifty-three additional patients were classified as high risk because they were aged 80 years or older. During the study, 17 participants experienced POD, 16 of whom were classified as high risk. In regard to estimating POD risk, the sensitivity and specificity of the delirium screening tool were 94.1% and 72.7%, respectively. Incidence rates of POD were 10.2% in the control group and 6.2% in the intervention group.
The authors noted their study’s limitations, including its design as a retrospective review of medical records rather than a prospective randomized controlled trial. In addition, because it was conducted in just one teaching hospital, they deemed it “not possible to determine the generalizability and long-term effect of our findings.”
The authors reported no conflicts of interest.
SOURCE: Choi JY et al. BMC Geriatr. 2019 Oct 26. doi: 10.1186/s12877-019-1303-z.
A new study has found that
and a prevention program can help improve staff education and outcomes.“In an aging society, it is very important to develop and implement a strategy for POD prevention to ensure that aging patients are treated as safely and effectively as possible,” wrote Jung-Yeon Choi of Seoul (South Korea) National University Bundang Hospital and coauthors. The study was published in BMC Geriatrics.
To determine how to better identify and treat high-risk patients for POD after orthopedic surgery, the researchers led a retrospective cohort study that included an intervention group of participants who were aged at least 65 years (n = 275) and a control group from a year prior (n = 274). Patients in the intervention group had their risk of delirium assessed and categorized using a simple screening tool, and those deemed at risk were entered into a multicomponent delirium prevention program.
Of the 275 patients in the intervention group, 144 required screening for delirium. Ninety-nine were classified as low risk, 29 were classified as high risk, and 16 missed the screening. Fifty-three additional patients were classified as high risk because they were aged 80 years or older. During the study, 17 participants experienced POD, 16 of whom were classified as high risk. In regard to estimating POD risk, the sensitivity and specificity of the delirium screening tool were 94.1% and 72.7%, respectively. Incidence rates of POD were 10.2% in the control group and 6.2% in the intervention group.
The authors noted their study’s limitations, including its design as a retrospective review of medical records rather than a prospective randomized controlled trial. In addition, because it was conducted in just one teaching hospital, they deemed it “not possible to determine the generalizability and long-term effect of our findings.”
The authors reported no conflicts of interest.
SOURCE: Choi JY et al. BMC Geriatr. 2019 Oct 26. doi: 10.1186/s12877-019-1303-z.
FROM BMC GERIATRICS
Scandinavian studies shed light on OA inheritance
TORONTO – Patients with osteoarthritis often want to know if their debilitating disease is likely to be passed on to their children. Karin Magnusson, PhD, believes she can answer that question based upon an analysis of two large Nordic studies.
“OA in the mother, but not in the father, increases the risk of surgical and clinically defined hip, knee, and hand OA in the offspring, and particularly in daughters,” she reported at the OARSI 2019 World Congress.
Dr. Magnusson, an epidemiologist at Lund (Sweden) University, and her coinvestigators, turned to the Musculoskeletal Pain in Ullensaker Study (MUST) of 630 individuals aged 40-79 with rheumatologist-diagnosed hand, hip, or knee OA by American College of Rheumatology clinical criteria and their offspring, as well as the Nor-Twin OA Study of 7,184 twins, aged 30-75, and their children. Linkage with a national registry that records virtually all joint arthroplasties performed in Norway enabled the investigators to identify which subjects in the two studies had joint surgery for OA, she explained at the meeting, sponsored by the Osteoarthritis Research Society International.
The main outcome in this analysis was the relative risk of hip, knee, or hand OA in the sons and daughters of families in which a parent had OA at those sites, compared with the rate when neither parent had OA. The key finding: If the mother had OA, her daughters had a 13% increased risk of OA in MUST and a 44% increased risk in the Nor-Twin OA Study when compared with daughters of women without OA. In contrast, the sons of a mother with OA had no significant increase in risk of OA. And when OA was present in the father, there was no increased risk of OA at any site in his daughters or sons.
“The implication is the heredity of OA is linked to maternal genes and/or maternal-specific factors, such as the fetal environment,” according to Dr. Magnusson.
And for clinical practice, the implication is that it’s important to ask about family history of OA, and in which parent, to better predict future risk of disease transmission to the children, she added.
These Norwegian study results open the door to exploration of the possible role of mitochondrial DNA in familial clustering of OA, since mitochondrial DNA is inherited only from the mother, Dr. Magnusson noted.
David T. Felson, MD, rose from the audience to say, “I’m a little bit worried” about the fact that when he and other Framingham Heart Study investigators looked specifically for possible mother/daughter, mother/son, father/daughter, and father/son associations for knee and hip OA, “we really didn’t find any.
“You can go through all of the explanations that you want about maternal inheritance, but I’m not sure that’s the best explanation. It might just be that what’s going on here is you’re seeing guys who are relatively young and who got their OA through injury or sports, which is fairly common in young men, and not through inheritance,” said Dr. Felson, professor of medicine and epidemiology at Boston University.
So a third observational study in an independent cohort might be needed as a tie breaker regarding the issue of OA inheritance.
Dr. Magnusson reported having no financial conflicts regarding her study, conducted free of commercial support.
SOURCE: Magnusson K et al. Osteoarthritis Cartilage. 2019 Apr;27[suppl 1]:S47, Abstract 33
TORONTO – Patients with osteoarthritis often want to know if their debilitating disease is likely to be passed on to their children. Karin Magnusson, PhD, believes she can answer that question based upon an analysis of two large Nordic studies.
“OA in the mother, but not in the father, increases the risk of surgical and clinically defined hip, knee, and hand OA in the offspring, and particularly in daughters,” she reported at the OARSI 2019 World Congress.
Dr. Magnusson, an epidemiologist at Lund (Sweden) University, and her coinvestigators, turned to the Musculoskeletal Pain in Ullensaker Study (MUST) of 630 individuals aged 40-79 with rheumatologist-diagnosed hand, hip, or knee OA by American College of Rheumatology clinical criteria and their offspring, as well as the Nor-Twin OA Study of 7,184 twins, aged 30-75, and their children. Linkage with a national registry that records virtually all joint arthroplasties performed in Norway enabled the investigators to identify which subjects in the two studies had joint surgery for OA, she explained at the meeting, sponsored by the Osteoarthritis Research Society International.
The main outcome in this analysis was the relative risk of hip, knee, or hand OA in the sons and daughters of families in which a parent had OA at those sites, compared with the rate when neither parent had OA. The key finding: If the mother had OA, her daughters had a 13% increased risk of OA in MUST and a 44% increased risk in the Nor-Twin OA Study when compared with daughters of women without OA. In contrast, the sons of a mother with OA had no significant increase in risk of OA. And when OA was present in the father, there was no increased risk of OA at any site in his daughters or sons.
“The implication is the heredity of OA is linked to maternal genes and/or maternal-specific factors, such as the fetal environment,” according to Dr. Magnusson.
And for clinical practice, the implication is that it’s important to ask about family history of OA, and in which parent, to better predict future risk of disease transmission to the children, she added.
These Norwegian study results open the door to exploration of the possible role of mitochondrial DNA in familial clustering of OA, since mitochondrial DNA is inherited only from the mother, Dr. Magnusson noted.
David T. Felson, MD, rose from the audience to say, “I’m a little bit worried” about the fact that when he and other Framingham Heart Study investigators looked specifically for possible mother/daughter, mother/son, father/daughter, and father/son associations for knee and hip OA, “we really didn’t find any.
“You can go through all of the explanations that you want about maternal inheritance, but I’m not sure that’s the best explanation. It might just be that what’s going on here is you’re seeing guys who are relatively young and who got their OA through injury or sports, which is fairly common in young men, and not through inheritance,” said Dr. Felson, professor of medicine and epidemiology at Boston University.
So a third observational study in an independent cohort might be needed as a tie breaker regarding the issue of OA inheritance.
Dr. Magnusson reported having no financial conflicts regarding her study, conducted free of commercial support.
SOURCE: Magnusson K et al. Osteoarthritis Cartilage. 2019 Apr;27[suppl 1]:S47, Abstract 33
TORONTO – Patients with osteoarthritis often want to know if their debilitating disease is likely to be passed on to their children. Karin Magnusson, PhD, believes she can answer that question based upon an analysis of two large Nordic studies.
“OA in the mother, but not in the father, increases the risk of surgical and clinically defined hip, knee, and hand OA in the offspring, and particularly in daughters,” she reported at the OARSI 2019 World Congress.
Dr. Magnusson, an epidemiologist at Lund (Sweden) University, and her coinvestigators, turned to the Musculoskeletal Pain in Ullensaker Study (MUST) of 630 individuals aged 40-79 with rheumatologist-diagnosed hand, hip, or knee OA by American College of Rheumatology clinical criteria and their offspring, as well as the Nor-Twin OA Study of 7,184 twins, aged 30-75, and their children. Linkage with a national registry that records virtually all joint arthroplasties performed in Norway enabled the investigators to identify which subjects in the two studies had joint surgery for OA, she explained at the meeting, sponsored by the Osteoarthritis Research Society International.
The main outcome in this analysis was the relative risk of hip, knee, or hand OA in the sons and daughters of families in which a parent had OA at those sites, compared with the rate when neither parent had OA. The key finding: If the mother had OA, her daughters had a 13% increased risk of OA in MUST and a 44% increased risk in the Nor-Twin OA Study when compared with daughters of women without OA. In contrast, the sons of a mother with OA had no significant increase in risk of OA. And when OA was present in the father, there was no increased risk of OA at any site in his daughters or sons.
“The implication is the heredity of OA is linked to maternal genes and/or maternal-specific factors, such as the fetal environment,” according to Dr. Magnusson.
And for clinical practice, the implication is that it’s important to ask about family history of OA, and in which parent, to better predict future risk of disease transmission to the children, she added.
These Norwegian study results open the door to exploration of the possible role of mitochondrial DNA in familial clustering of OA, since mitochondrial DNA is inherited only from the mother, Dr. Magnusson noted.
David T. Felson, MD, rose from the audience to say, “I’m a little bit worried” about the fact that when he and other Framingham Heart Study investigators looked specifically for possible mother/daughter, mother/son, father/daughter, and father/son associations for knee and hip OA, “we really didn’t find any.
“You can go through all of the explanations that you want about maternal inheritance, but I’m not sure that’s the best explanation. It might just be that what’s going on here is you’re seeing guys who are relatively young and who got their OA through injury or sports, which is fairly common in young men, and not through inheritance,” said Dr. Felson, professor of medicine and epidemiology at Boston University.
So a third observational study in an independent cohort might be needed as a tie breaker regarding the issue of OA inheritance.
Dr. Magnusson reported having no financial conflicts regarding her study, conducted free of commercial support.
SOURCE: Magnusson K et al. Osteoarthritis Cartilage. 2019 Apr;27[suppl 1]:S47, Abstract 33
REPORTING FROM OARSI 2019
The dangers of dog walking
The estimated number of fractures associated with walking a leashed dog was 4,396 in 2017 among those aged 65 years and older, compared with 1,671 in 2004, which is a significant increase, Kevin Pirruccio of the University of Pennsylvania, Philadelphia, and his associates wrote in JAMA Surgery.
Over the entire study period, 2004-2017, almost 79% of all fractures occurred in women and 67% of all patients were treated in the emergency department and released. The most common injury was hip fracture (17.3%), although upper-extremity fractures were more common (52.1%) than those of the lower extremities (29.4%), trunk (10.1%), or head and neck (7.3%), the investigators reported.
“For older adults – especially those living alone and with decreased bone mineral density – the risks associated with walking leashed dogs merit consideration. Even one such injury could result in a potentially lethal hip fracture, lifelong complications, or loss of independence,” they wrote.
The retrospective, cross-sectional analysis involved the Consumer Product Safety Commission’s National Electronic Injury Surveillance System database, which includes approximately 100 hospital emergency departments. The investigators did not report any conflicts of interest.
SOURCE: Pirruccio K et al. JAMA Surg. 2019 Mar 6. doi: 10.1001/jamasurg.2019.0061.
The estimated number of fractures associated with walking a leashed dog was 4,396 in 2017 among those aged 65 years and older, compared with 1,671 in 2004, which is a significant increase, Kevin Pirruccio of the University of Pennsylvania, Philadelphia, and his associates wrote in JAMA Surgery.
Over the entire study period, 2004-2017, almost 79% of all fractures occurred in women and 67% of all patients were treated in the emergency department and released. The most common injury was hip fracture (17.3%), although upper-extremity fractures were more common (52.1%) than those of the lower extremities (29.4%), trunk (10.1%), or head and neck (7.3%), the investigators reported.
“For older adults – especially those living alone and with decreased bone mineral density – the risks associated with walking leashed dogs merit consideration. Even one such injury could result in a potentially lethal hip fracture, lifelong complications, or loss of independence,” they wrote.
The retrospective, cross-sectional analysis involved the Consumer Product Safety Commission’s National Electronic Injury Surveillance System database, which includes approximately 100 hospital emergency departments. The investigators did not report any conflicts of interest.
SOURCE: Pirruccio K et al. JAMA Surg. 2019 Mar 6. doi: 10.1001/jamasurg.2019.0061.
The estimated number of fractures associated with walking a leashed dog was 4,396 in 2017 among those aged 65 years and older, compared with 1,671 in 2004, which is a significant increase, Kevin Pirruccio of the University of Pennsylvania, Philadelphia, and his associates wrote in JAMA Surgery.
Over the entire study period, 2004-2017, almost 79% of all fractures occurred in women and 67% of all patients were treated in the emergency department and released. The most common injury was hip fracture (17.3%), although upper-extremity fractures were more common (52.1%) than those of the lower extremities (29.4%), trunk (10.1%), or head and neck (7.3%), the investigators reported.
“For older adults – especially those living alone and with decreased bone mineral density – the risks associated with walking leashed dogs merit consideration. Even one such injury could result in a potentially lethal hip fracture, lifelong complications, or loss of independence,” they wrote.
The retrospective, cross-sectional analysis involved the Consumer Product Safety Commission’s National Electronic Injury Surveillance System database, which includes approximately 100 hospital emergency departments. The investigators did not report any conflicts of interest.
SOURCE: Pirruccio K et al. JAMA Surg. 2019 Mar 6. doi: 10.1001/jamasurg.2019.0061.
FROM JAMA SURGERY
Emicizumab performs well in surgical setting
PRAGUE – Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.
Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.
All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.
“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.
The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.
The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.
Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.
Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.
“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.
When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”
Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.
The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.
Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.
SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.
PRAGUE – Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.
Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.
All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.
“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.
The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.
The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.
Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.
Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.
“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.
When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”
Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.
The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.
Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.
SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.
PRAGUE – Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.
Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.
All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.
“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.
The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.
The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.
Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.
Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.
“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.
When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”
Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.
The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.
Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.
SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.
REPORTING FROM EAHAD 2019
Fragility Fractures: Diagnosis and Treatment
ABSTRACT
Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.
Continue to: Fragility fractures are caused by...
Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.
Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.
RISK FACTORS AND CAUSES
The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6
Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10
In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H2 receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.
Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.
An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18
Continue to: DIAGNOSIS...
DIAGNOSIS
Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20
The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.
Table 1. T Score Criteria
T score | Diagnosis |
> -1.0 | Normal |
-1.0 to -2.5 | Osteopenia |
< -2.5 | Osteoporosis |
< -2.5 with fragility fracture | Severe osteoporosis |
Table 2. Z Score Criteria
Z score | Diagnosis |
> -2.0 | Normal BMD for age |
< -2.0 | Low BMD for age |
The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.
In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.
Continue to: TREATMENT...
TREATMENT
NONPHARMACOLOGIC
Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.
Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.
PHARMACOLOGIC
After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28
Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.
Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26
Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30
Continue to: The recommended daily dose for abaloparatide...
The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.
Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.
Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.
Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.
A summary of medications used to treat osteoporosis can be found in Table 3.
Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis
Medication | Indication | Dosing |
Calcium supplementation | Mild osteoporosis | 1200 mg oral/d |
Vitamin D supplementation | Mild osteoporosis | 800 to 1000 IU oral/d |
Alendronate | Postmenopausal osteoporosis
Osteoporosis prevention | 10 mg oral/d 70 mg oral/wk
5 mg/d 35 mg/wk |
Risedronate | Postmenopausal osteoporosis | 5 mg oral/d 35 mg oral/wk 150 mg oral/mo |
Teriparatide (Forteo) | Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis | 600 mcg/2.4 mL subcutaneous/d |
Abaloparatide (Tymlos) | Postmenopausal osteoporosis | 80 mcg subcutaneous/d |
Denosumab (Prolia) | Patients intolerant to bisphosphonates; patients with impaired kidney function. | 60 mg subcutaneous every 6 mo |
Raloxifene | Postmenopausal osteoporosis | 60 mg oral/d |
Tamoxifen | Postmenopausal osteoporosis | 20 mg oral/d |
Calcitonin | Postmenopausal osteoporosis | 100 units intramuscular or subcutaneous/d 200 units (1 spray) intranasal/d |
Strontium ranelate | Postmenopausal osteoporosis Severe osteoporosis in men | 2 g/d dissolved in water, prior to bedtime Not recommended in CrCl <30 mL/min |
Abbreviation: CrCl, creatinine clearance.
CONCLUSION
With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.
- Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
- Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
- Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
- Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
- Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
- Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
- Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
- Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
- Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
- An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
- Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
- Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
- Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
- Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
- Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
- Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
- Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
- Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
- Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
- Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
- MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
- Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
- U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
- Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
- Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
- Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
- Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
- Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
- Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
- Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
- TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
- Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
- Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
- Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
- Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
ABSTRACT
Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.
Continue to: Fragility fractures are caused by...
Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.
Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.
RISK FACTORS AND CAUSES
The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6
Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10
In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H2 receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.
Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.
An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18
Continue to: DIAGNOSIS...
DIAGNOSIS
Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20
The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.
Table 1. T Score Criteria
T score | Diagnosis |
> -1.0 | Normal |
-1.0 to -2.5 | Osteopenia |
< -2.5 | Osteoporosis |
< -2.5 with fragility fracture | Severe osteoporosis |
Table 2. Z Score Criteria
Z score | Diagnosis |
> -2.0 | Normal BMD for age |
< -2.0 | Low BMD for age |
The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.
In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.
Continue to: TREATMENT...
TREATMENT
NONPHARMACOLOGIC
Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.
Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.
PHARMACOLOGIC
After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28
Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.
Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26
Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30
Continue to: The recommended daily dose for abaloparatide...
The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.
Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.
Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.
Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.
A summary of medications used to treat osteoporosis can be found in Table 3.
Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis
Medication | Indication | Dosing |
Calcium supplementation | Mild osteoporosis | 1200 mg oral/d |
Vitamin D supplementation | Mild osteoporosis | 800 to 1000 IU oral/d |
Alendronate | Postmenopausal osteoporosis
Osteoporosis prevention | 10 mg oral/d 70 mg oral/wk
5 mg/d 35 mg/wk |
Risedronate | Postmenopausal osteoporosis | 5 mg oral/d 35 mg oral/wk 150 mg oral/mo |
Teriparatide (Forteo) | Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis | 600 mcg/2.4 mL subcutaneous/d |
Abaloparatide (Tymlos) | Postmenopausal osteoporosis | 80 mcg subcutaneous/d |
Denosumab (Prolia) | Patients intolerant to bisphosphonates; patients with impaired kidney function. | 60 mg subcutaneous every 6 mo |
Raloxifene | Postmenopausal osteoporosis | 60 mg oral/d |
Tamoxifen | Postmenopausal osteoporosis | 20 mg oral/d |
Calcitonin | Postmenopausal osteoporosis | 100 units intramuscular or subcutaneous/d 200 units (1 spray) intranasal/d |
Strontium ranelate | Postmenopausal osteoporosis Severe osteoporosis in men | 2 g/d dissolved in water, prior to bedtime Not recommended in CrCl <30 mL/min |
Abbreviation: CrCl, creatinine clearance.
CONCLUSION
With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.
ABSTRACT
Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.
Continue to: Fragility fractures are caused by...
Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.
Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.
RISK FACTORS AND CAUSES
The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6
Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10
In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H2 receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.
Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.
An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18
Continue to: DIAGNOSIS...
DIAGNOSIS
Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20
The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.
Table 1. T Score Criteria
T score | Diagnosis |
> -1.0 | Normal |
-1.0 to -2.5 | Osteopenia |
< -2.5 | Osteoporosis |
< -2.5 with fragility fracture | Severe osteoporosis |
Table 2. Z Score Criteria
Z score | Diagnosis |
> -2.0 | Normal BMD for age |
< -2.0 | Low BMD for age |
The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.
In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.
Continue to: TREATMENT...
TREATMENT
NONPHARMACOLOGIC
Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.
Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.
PHARMACOLOGIC
After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28
Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.
Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26
Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30
Continue to: The recommended daily dose for abaloparatide...
The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.
Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.
Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.
Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.
A summary of medications used to treat osteoporosis can be found in Table 3.
Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis
Medication | Indication | Dosing |
Calcium supplementation | Mild osteoporosis | 1200 mg oral/d |
Vitamin D supplementation | Mild osteoporosis | 800 to 1000 IU oral/d |
Alendronate | Postmenopausal osteoporosis
Osteoporosis prevention | 10 mg oral/d 70 mg oral/wk
5 mg/d 35 mg/wk |
Risedronate | Postmenopausal osteoporosis | 5 mg oral/d 35 mg oral/wk 150 mg oral/mo |
Teriparatide (Forteo) | Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis | 600 mcg/2.4 mL subcutaneous/d |
Abaloparatide (Tymlos) | Postmenopausal osteoporosis | 80 mcg subcutaneous/d |
Denosumab (Prolia) | Patients intolerant to bisphosphonates; patients with impaired kidney function. | 60 mg subcutaneous every 6 mo |
Raloxifene | Postmenopausal osteoporosis | 60 mg oral/d |
Tamoxifen | Postmenopausal osteoporosis | 20 mg oral/d |
Calcitonin | Postmenopausal osteoporosis | 100 units intramuscular or subcutaneous/d 200 units (1 spray) intranasal/d |
Strontium ranelate | Postmenopausal osteoporosis Severe osteoporosis in men | 2 g/d dissolved in water, prior to bedtime Not recommended in CrCl <30 mL/min |
Abbreviation: CrCl, creatinine clearance.
CONCLUSION
With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.
- Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
- Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
- Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
- Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
- Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
- Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
- Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
- Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
- Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
- An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
- Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
- Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
- Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
- Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
- Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
- Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
- Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
- Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
- Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
- Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
- MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
- Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
- U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
- Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
- Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
- Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
- Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
- Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
- Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
- Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
- TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
- Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
- Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
- Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
- Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
- Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
- Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
- Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
- Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
- Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
- Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
- Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
- Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
- Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
- An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
- Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
- Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
- Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
- Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
- Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
- Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
- Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
- Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
- Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
- Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
- MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
- Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
- U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
- Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
- Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
- Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
- Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
- Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
- Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
- Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
- TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
- Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
- Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
- Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
- Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
TAKE-HOME POINTS
- 3 million people sustain fragility fractures annually, and nearly 30% die within a year of the fracture.
- The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.
- The World Health Organization has developed a set of T-core criteria to diagnose osteoporosis in postmenopausal women: a score >–1 is normal; <–1 but >–2.5 signifies osteopenia; <–2.5 denotes osteoporosis; and <–2.5 with fragility fracture indicates severe osteoporosis.
- The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children. The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender. Z scores <–2.0 indicate low BMD for chronological age. A Z score > –2.0 is considered within the expected range for age.
- After an initial fragility fracture, the risk for additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture.26
Preoperative Corticosteroid Use for Medical Conditions is Associated with Increased Postoperative Infectious Complications and Readmissions After Total Hip Arthroplasty: A Propensity-Matched Study
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
28. Shrader MW, Schall D, Parvizi J, McCarthy JT, Lewallen DG. Total hip arthroplasty in patients with renal failure: a comparison between transplant and dialysis patients. J Arthroplasty. 2006;21(3):324-329. doi: 10.1016/j.arth.2005.07.008.
29. Nowicki P, Chaudhary H. Total hip replacement in renal transplant patients. J Bone Joint Surg Br. 2007;89(12):1561-1566.
30. Johannesdottir SA, Horváth-Puhó E, Dekkers OM, Cannegieter SC, Jørgensen JO, Ehrenstein V, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. doi: 10.1001/jamainternmed.2013.122.
31. Hartman J, Khanna V, Habib A, Farrokhyar F, Memon M, Adili A. Perioperative systemic glucocorticoids in total hip and knee arthroplasty: a systematic review of outcomes. J Orthop. 2017;14(2):294-301. doi: 10.1016/j.jor.2017.03.012.
32. Sculco PK, McLawhorn AS, Desai N, Su EP, Padgett DE, Jules-Elysee K. The effect of perioperative corticosteroids in total hip arthroplasty: a prospective double-blind placebo controlled pilot study. J Arthroplasty. 2016;31(6):1208-1212. doi: 10.1016/j.arth.2015.11.011.
33. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470. doi: 10.1007/s11999-013-3121-5.
34. US Department of Health and Human Services. Comprehensive Care for Joint Replacement Model. Centers for Medicare & Medicaid Services. https://innovation.cms.gov/initiatives/cjr. Accessed June 15, 2017.
35. Bozic KJ, Ward L, Vail TP, Maze M. Bundled payments in total joint arthroplasty: targeting opportunities for quality improvement and cost reduction. Clin Orthop Relat Res. 2014;472(1):188-193. doi: 10.1007/s11999-013-3034-3.
36. Bosco JA, 3rd, Karkenny AJ, Hutzler LH, Slover JD, Iorio R. Cost burden of 30-day readmissions following Medicare total hip and knee arthroplasty. J Arthroplasty. 2014;29(5): 903-905. doi: 10.1016/j.arth.2013.11.006.
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
ABSTRACT
Systemic corticosteroids are used to treat a number of medical conditions; however, they are associated with numerous adverse effects. The impact of preoperative chronic corticosteroid use on postoperative outcomes following total hip arthroplasty (THA) is unclear. The purpose of this study was to assess the independent effect of chronic systemic preoperative steroid use on short-term perioperative complications and readmissions after THA.
All patients undergoing primary THA in the American College of Surgeons National Surgical Quality Improvement Program registry from 2005 to -–2015 were identified. Patients were considered chronic steroid users if they used any dosage of oral or parenteral steroids for >10 of the preceding 30 days before THA. Two equally sized propensity-matched groups based on preoperative steroid use were generated to account for differences in operative and baseline characteristics between the groups. Thirty-day complications and hospital readmissions rates were compared using bivariate analysis.
Of 101,532 THA patients who underwent primary THA, 3714 (3.7%) were identified as chronic corticosteroid users. Comparison of propensity-matched cohorts identified an increased rate of any complication (odds ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), urinary tract infection (OR 1.61, P = .020), superficial surgical site infection (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001) in patients who used systemic steroids preoperatively. Readmissions in preoperative steroid users were most commonly for infectious reasons.
Patients prescribed chronic corticosteroids are at a significantly increased risk of both 30-day periopative complications and hospital readmissions. This finding has important implications for pre- and postoperative patient counseling as well as preoperative risk stratification.
Continue to: Corticosteroids are powerful...
Corticosteroids are powerful anti-inflammatory steroid hormones that have many indications in the treatment of medical diseases, including advanced or poorly controlled asthma, chronic obstructive pulmonary disease (COPD), inflammatory bowel disease, allergic conditions, among other indications.1-4 In orthopedics and rheumatology, systemic steroids are, at times, used in patients with rheumatoid arthritis, systemic lupus erythematosus, and vasculitides.5-7 Overman and colleagues,8 using data from the National Health and Nutrition Examination Survey between 1999 and 2008 identified both a 1.2% prevalence of chronic corticosteroid usage in the United States across all age groups and a positive correlation between steroid use prevalence and increasing age. In that study, nearly two-thirds of survey respondents reported using corticosteroids chronically for >90 days. Another observational study in the United Kingdom found that long-term steroid prescriptions increased between 1989 to 2008 and that 13.6% of patients with rheumatoid arthritis and 66.5% of patients with polymyalgia rheumatica or giant cell arteritis used long-term steroids.9
Enterally- or parenterally-administered corticosteroids have numerous systemic effects that are of particular relevance to orthopedic surgeons. Corticosteroids induce osteoporosis by preferentially inducing osteoclastic activity while inhibiting the differentiation of osteoblasts, ultimately leading to decreased bone quality and mass.10 As a consequence, patients who have previously used corticosteroids are more than twice as likely to have a hip fracture.11 Steroids also increase the risk of both osteonecrosis and myopathy, among other musculoskeletal effects.12 In addition to orthopedic complications, steroids have broad inhibitory effects on both acquired and innate immunity, which significantly increases the risk of infections.13 This increased risk of infection is dose-dependent14 and synergistic with other immunosuppressive drugs.15
Patients with hip pain may receive localized corticosteroid hip joint injections during the nonoperative management of various hip pathologies, including arthritis, bursitis, and labral tears.16,17 Outcomes of patients who received intra-articular corticosteroid injections before total hip arthroplasty (THA) were evaluated in a systematic review of 9 studies by Pereira and colleagues.17 These authors found that the infection rate (both superficial and deep surgical site infections [SSI]) after THA in patients who received local steroid injection into the hip before surgery was between 0% and 30%.17 However, similar studies assessing the impact that systemic steroids have on outcomes after THA are lacking. Patients who undergo THA for conditions associated with higher lifetime steroid usage have worse outcomes than those who do not. For instance, in patients undergoing THA for rheumatoid arthritis, the rates of both postoperative periprosthetic joint infection and hip dislocation are higher, when compared with osteoarthritis.18,19 However, it is unclear how much of this difference in outcomes is due to the underlying disease, adverse effects of steroids, or both. Given the high prevalence of chronic systemic steroid use, it is essential to elucidate more clearly the impact that these medications have on perioperative outcomes after THA.
Therefore, the purpose of this study was to characterize short-term perioperative outcomes, including complication and readmission rates in patients undergoing THA while taking chronic preoperative corticosteroids. We also sought to identify the most common reasons for hospital readmission in patients who did and did not use long-term steroids.
MATERIALS AND METHODS
STUDY DESIGN AND SETTING
This investigation was a retrospective cohort study that utilized the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) registry.20 The ACS-NSQIP is a prospectively collected, multi-institutional database that collects demographical information, operative variables, and both postoperative complications and hospital readmission data. Data is collected for up to 30 days after the index procedure, and patients are contacted by telephone if they are discharged before 30 days. Patient data is entered by specially trained surgical clinical reviewers and is routinely audited by the ACS-NSQIP, leading to more accurate data when compared with administrative research databases.21,22 The ACS-NSQIP has been used in orthopedic surgery outcomes-based studies.23-25
Continue to: All patients undergoing...
All patients undergoing THA between 2005 and 2015 were identified in the registry using primary Current Procedural Terminology code 27130. Patients were split into 2 groups based on whether or not they chronically used corticosteroids preoperatively for a medical condition. A patient was considered a chronic corticosteroid user if he/she used oral or parenteral corticosteroids within 30 days before the index procedure for >10 of the preceding 30 days. Those who received a 1-time steroid pulse or those who used topical or inhaled steroids were not considered as steroid users in this study.
BASELINE CHARACTERISTICS AND PERIOPERATIVE OUTCOMES
Baseline patient and operative characteristics, including patient age, gender, body mass index (BMI), functional status, American Society of Anesthesiologists (ASA) class, anesthesia type, operative duration, and medical comorbidities including hypertension, COPD, diabetes mellitus, and smoking history, were compared between both groups. Perioperative outcomes that were assessed in this study include death, renal, respiratory, and cardiac complications, deep vein thrombosis or pulmonary embolism, stroke, sepsis, return to the operating room, urinary tract infection (UTI), wound dehiscence, superficial and deep SSI, need for a blood transfusion within 72 hours of index surgical procedure, and hospital readmissions. Renal complications were defined as acute or progressive renal insufficiency; respiratory complications were defined as failure to wean from the ventilator, need for intubation after the index procedure, and the occurrence of pneumonia; and cardiac complications were defined as myocardial infarction or cardiac arrest requiring cardiopulmonary resuscitation. Patients were excluded if they had missing baseline or operative characteristic data, an unclean wound classification at the time of admission, or if their THA was considered emergent.
STATISTICAL ANALYSIS
A propensity score-matched comparison was performed to adjust for differences in baseline and operative characteristics between the 2 cohorts in this study. In the current study, the propensity score was defined as the conditional probability that a patient chronically used preoperative corticosteroids for a medical condition, as a function of age, BMI, gender, ASA class, functional status, medical comorbidities, anesthesia type, and operative duration. A 1:1 matching with tight calipers (0.0001), and nearest-neighbor matching was used to generate 2 equally-sized, propensity-matched cohorts based on steroid status.26 Nearest-neighbor matching identifies patients in both cohorts with the closest propensity scores for inclusion in propensity-matched cohorts. This matching is continued until 1 group runs out of patients to match. Baseline patient and operative characteristics for the unadjusted and propensity-matched groups were compared using Pearson’s χ2 analysis. Outcomes after THA by steroid status were also compared in both unadjusted and propensity-matched groups. Finally, all patients who were readmitted were identified, and the reason for readmission was determined using the International Classification of Disease Ninth (ICD-9) and Tenth (ICD-10) edition codes. Patients were classified as having an infectious readmission only if the ICD code clearly stated an infectious etiology. For instance, a patient with an intestinal infection due to Clostridium difficile (ICD-9 008.45) was counted as a gastrointestinal infection, whereas diarrhea without a distinctly specified etiology (ICD-9 787.91, ICD-10 R19.7) was counted as a gastrointestinal medical complication. Readmission data was only available in ACS-NSQIP from 2011 to 2015, constituting 92.5% of all patients included in this study. We used SPSS version 23 (IBM Corporation) for all statistical analyses, and defined a significant P value as <.05.
RESULTS
BASELINE PATIENTS AND OPERATIVE CHARACTERISTICS
In total, we identified 101,532 patients who underwent THA (Table 1). O these, 3714 (3.7%) chronically used corticosteroids preoperatively, whereas 97,818 (96.3%) did not.
When the unadjusted cohorts were compared, patients using corticosteroids were more likely to be female, less likely to obese, more likely to have hypertension, diabetes mellitus, COPD, higher ASA class, undergone THA with general anesthesia, and have a dependent functional status (P < .001 for all comparisons). After propensity matching, 2 equally sized cohorts of 3618 patients each were generated based on steroid status and no differences in baseline and operative characteristics were identified between the 2 groups.
Continue to: CLINICAL OUTCOMES BY STEROID STATUS
CLINCIAL OUTCOMES BY STEROID STATUS
A comparison of unadjusted cohorts showed that patients who used preoperative steroids had an increased rate of any complication (7.89%) when compared with those who did not (4.87%) (Table 2).
Similarly, those who used corticosteroids preoperatively had an increased rate of renal complications, respiratory complications, return to the operating room, sepsis, UTI, superficial and deep SSI, and perioperative blood transfusions. They also were more likely to have a 30-day hospital readmission (P < .05 for all comparisons).
When propensity-matched cohorts were compared, patients who used steroids preoperatively were found to have higher rates of any complication (odds Ratio [OR] 1.30, P = .003), sepsis (OR 2.07, P = .022), UTI (OR 1.61, P = .020), superficial SSI (OR 1.73, P = .038), and hospital readmission (OR 1.50, P < .001; Table 3).
REASONS FOR HOSPITAL READMISSION
In total, 3397 patients were readmitted to the hospital within thirty days. Of these, 226 used steroids preoperatively, and 3171 did not (Table 4).
The most common reason for hospital readmission in patients who used preoperative corticosteroids was infectious complications (72 patients, 31.9% of all readmitted patients in this cohort), followed by medical complications (59 patients, 26.1%), and hip-related complications (48 patients, 21.2%). In those who did not use steroids preoperatively, the most common reason for hospital readmission was medical complications (932 patients, 29.4% of all readmitted patients in this cohort), followed by infectious complications (792 patients, 25.0%), and hip-related complications (763 patients, 24.1%).
Continue to: DISCUSSION
DISCUSSION
Nearly 3% of individuals >80 years in the US population chronically use corticosteroids for a medical condition,8 and this rate is likely higher in specific subsets of patients, such as those with rheumatoid arthritis.9 While some studies have assessed the impact of intra-articular corticosteroid hip injections on perioperative outcomes in THA,17 similar studies assessing systemic corticosteroid usage are lacking. The purpose of this study was to characterize short-term perioperative outcomes in patients undergoing THA who chronically use systemic steroids when compared with those who do not. We found that the prevalence of preoperative chronic steroid use in this cohort of THA patients was 3.7%. We also identified increased rates of infectious complications, including sepsis, UTI, and superficial SSI, in patients who used preoperative corticosteroids. Furthermore, we found an increased rate of hospital readmissions in corticosteroid users and identified the most common reason for hospital readmission as infectious complications in this cohort.
The primary finding of this study was an increase in postoperative infections in patients who use preoperative steroids chronically for medical conditions. Immunosuppression has previously been identified as a risk factor for developing periprosthetic joint infections. Tannenbaum and colleagues27 performed a retrospective study of 19 patients who underwent either a kidney or liver transplant and were maintained on an induction regimen of either prednisone and azathioprine or cyclosporine. These 19 patients also underwent either a THA or total knee arthroplasty, and 5 of these patients (26.3%) developed a periprosthetic joint infection after an average of 3.4 years following the arthroplasty procedure. In another study of 37 renal transplant and dialysis patients who underwent a total of 45 THA procedures, there were 3 instances of superficial SSI and 2 instances of deep SSI.28 However, reported infection rates in transplant patients undergoing THA vary significantly, and studies have been unable to assess the true impact that chronic immunosuppression has on perioperative infection rates.29 In this study, patients who used preoperative corticosteroids chronically were at increased risk of perioperative infections, including sepsis, UTI, and superficial SSI.
Deep vein thrombosis is another postoperative complication that has been associated with chronic steroid use.30 In a case-control study of 38,765 patients who developed a venous thromboembolism and 387,650 control patients who did not, Johannesdottir and colleagues30 found an increased thromboembolic risk in current users of systemic glucocorticoids, but not former users, as well as an increased risk as the dose of glucocorticoids increased. We were not able to identify a similar increase in DVT/PE in chronic corticosteroid users, perhaps due to our sample size, or because we could not do subgroup analyses based on the type or dosage of steroid that a patient was taking. Future studies that identify the highest risk patients among those using systemic corticosteroids are important because parenteral corticosteroids are being increasingly used in THA to alleviate postoperative pain as an opioid-sparing measure.31,32
Finally, we also found that patients who use chronic, systemic corticosteroids are at an increased risk for hospital readmission, when compared with those patients who are not using steroids and are most likely to be readmitted for an infectious complication. Schairer and colleagues33 assessed readmission rates after THA and found 30- and 90-day readmission rate of 4% and 7%, respectively. These authors also found that medical complications accounted for approximately 25% of readmissions, and hip-related complications (eg, dislocation, SSI) accounted for >50%. In our study, we found a 30-day readmission rate in non-steroid users of 3.53% and a rate of 6.52% in chronic steroid users. More than 30% of patients using a steroid were readmitted for infectious complications. As THA is becoming increasingly reimbursed under a bundled payments model by Medicare and Medicaid,34-36 reducing short-term readmissions is imperative. Therefore, discharge counseling that emphasizes how to recognize both the signs and symptoms of infection as well as how to prevent infections, such as reducing SSIs through appropriate wound care, may be warranted in higher risk chronic steroid users.
This study has a number of limitations that are inherent to ACS-NSQIP. First, we lacked specific information on a patient’s steroid history, including which corticosteroid they were using, dosage, frequency, and the indication for corticosteroid therapy. Therefore, we were unable to establish a dose-dependent relationship between steroid exposure and postoperative complications after THA. Second, we were able to assess only 30-day rates of complications and readmissions, and therefore, we were unable to identify intermediate- and long-term effects of systemic corticosteroid use on THA. Finally, we could not determine orthopedic- or hip-specific postoperative outcomes, such as functional scores and range of motion.
Continue to: CONCLUSION
CONCLUSION
In conclusion, this study quantified the increased risk for perioperative complications and hospital readmissions in patients who chronically use corticosteroids and are undergoing THA, when compared with those who do not use corticosteroids. These results suggest that patients who are on long-term steroids are at an increased risk for complications, primarily infectious complications. This finding has important implications for patient counseling, preoperative risk stratification, and suggests that higher risk patients, such as chronic steroid users, may benefit from improved discharge care to decrease complication rates.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
28. Shrader MW, Schall D, Parvizi J, McCarthy JT, Lewallen DG. Total hip arthroplasty in patients with renal failure: a comparison between transplant and dialysis patients. J Arthroplasty. 2006;21(3):324-329. doi: 10.1016/j.arth.2005.07.008.
29. Nowicki P, Chaudhary H. Total hip replacement in renal transplant patients. J Bone Joint Surg Br. 2007;89(12):1561-1566.
30. Johannesdottir SA, Horváth-Puhó E, Dekkers OM, Cannegieter SC, Jørgensen JO, Ehrenstein V, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. doi: 10.1001/jamainternmed.2013.122.
31. Hartman J, Khanna V, Habib A, Farrokhyar F, Memon M, Adili A. Perioperative systemic glucocorticoids in total hip and knee arthroplasty: a systematic review of outcomes. J Orthop. 2017;14(2):294-301. doi: 10.1016/j.jor.2017.03.012.
32. Sculco PK, McLawhorn AS, Desai N, Su EP, Padgett DE, Jules-Elysee K. The effect of perioperative corticosteroids in total hip arthroplasty: a prospective double-blind placebo controlled pilot study. J Arthroplasty. 2016;31(6):1208-1212. doi: 10.1016/j.arth.2015.11.011.
33. Schairer WW, Sing DC, Vail TP, Bozic KJ. Causes and frequency of unplanned hospital readmission after total hip arthroplasty. Clin Orthop Relat Res. 2014;472(2):464-470. doi: 10.1007/s11999-013-3121-5.
34. US Department of Health and Human Services. Comprehensive Care for Joint Replacement Model. Centers for Medicare & Medicaid Services. https://innovation.cms.gov/initiatives/cjr. Accessed June 15, 2017.
35. Bozic KJ, Ward L, Vail TP, Maze M. Bundled payments in total joint arthroplasty: targeting opportunities for quality improvement and cost reduction. Clin Orthop Relat Res. 2014;472(1):188-193. doi: 10.1007/s11999-013-3034-3.
36. Bosco JA, 3rd, Karkenny AJ, Hutzler LH, Slover JD, Iorio R. Cost burden of 30-day readmissions following Medicare total hip and knee arthroplasty. J Arthroplasty. 2014;29(5): 903-905. doi: 10.1016/j.arth.2013.11.006.
1. Normansell R, Kew KM, Mansour G. Different oral corticosteroid regimens for acute asthma. Cochrane Database Syst Rev. 2016;13(5):CD011801. doi: 10.1002/14651858.CD011801.pub2.
2. Walters JA, Tan DJ, White CJ, Wood-Baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2014;(12):CD006897.
3. Nunes T, Barreiro-de Acosta M, Marin-Jimenez I, Nos P, Sans M. Oral locally active steroids in inflammatory bowel disease. J Crohns Colitis. 2013;7(3):183-191. doi: 10.1016/j.crohns.2012.06.010.
4. Karatzanis A, Chatzidakis A, Milioni A, Vlaminck S, Kawauchi H, Velegrakis S, et al. Contemporary use of corticosteroids in rhinology. Curr Allergy Asthm R. 2017;17(2). doi: 10.1007/s11882-017-0679-0.
5. Parker BJ, Bruce IN. High dose methylprednisolone therapy for the treatment of severe systemic lupus erythematosus. Lupus. 2007;16(6):387-393. doi: 10.1177/0961203307079502.
6. Ferreira JF, Ahmed Mohamed AA, Emery P. Glucocorticoids and rheumatoid arthritis. Rheum Dis Clin North Am. 2016;42(1):33-46. doi: 10.1016/j.rdc.2015.08.006.
7. Buttgereit F, Dejaco C, Matteson EL, Dasgupta B. Polymyalgia rheumatica and giant cell arteritis: a systematic review. JAMA. 2016;315(22):2442-2458. doi: 10.1001/jama.2016.5444.
8. Overman RA, Yeh JY, Deal CL. Prevalence of oral glucocorticoid usage in the United States: a general population perspective. Arthritis Care Res. 2013;65(2):294-298. doi: 10.1002/acr.21796.
9. Fardet L, Petersen I, Nazareth I. Prevalence of long-term oral glucocorticoid prescriptions in the UK over the past 20 years. Rheumatology. 2011;50(11):1982-1990. doi: 10.1093/rheumatology/ker017.
10. Canalis E, Mazziotti G, Giustina A, Bilezikian JP. Glucocorticoid-induced osteoporosis: pathophysiology and therapy.Osteoporos Int. 2007;18(10):1319-1328. doi: 10.1007/s00198-007-0394-0.
11. Kanis JA, Johansson H, Oden A, Johnell O, de Laet C, Melton LJ, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19(6):893-899. doi: /10.1359/JBMR.040134.
12. Caplan A, Fett N, Rosenbach M, Werth VP, Micheletti RG. Prevention and management of glucocorticoid-induced side effects: a comprehensive review: a review of glucocorticoid pharmacology and bone health. J Am Acad Dermatol. 2017;76(1):1-9. doi: 10.1016/j.jaad.2016.01.062.
13. Cutolo M, Seriolo B, Pizzorni C, Secchi ME, Soldano S, Paolino S, et al. Use of glucocorticoids and risk of infections. Autoimmun Rev. 2008;8(2):153-155. doi: 10.1016/j.autrev.2008.07.010.
14. Blackwood LL, Pennington JE. Dose-dependent effect of glucocorticosteroids on pulmonary defenses in a steroid-resistant host. Am Rev Respir Dis. 1982;126(6):1045-1049.
15. Toruner M, Loftus EV, Jr., Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, et al. Risk factors for opportunistic infections in patients with inflammatory bowel disease. Gastroenterology. 2008;134(4):929-936. doi: 10.1053/j.gastro.2008.01.012.
16. Barratt PA, Brookes N, Newson A. Conservative treatments for greater trochanteric pain syndrome: a systematic review. Br J Sports Med. 2017;51(2):97-104. doi: 10.1136/bjsports-2015-095858.
17. Pereira LC, Kerr J, Jolles BM. Intra-articular steroid injection for osteoarthritis of the hip prior to total hip arthroplasty: is it safe? a systematic review. Bone Joint J. 2016;98-B(8):1027-1035. doi: 10.1302/0301-620X.98B8.37420.
18. Ravi B, Escott B, Shah PS, Jenkinson R, Chahal J, Bogoch E, et al. A systematic review and meta-analysis comparing complications following total joint arthroplasty for rheumatoid arthritis versus for osteoarthritis. Arthritis Rheum. 2012;64(12):3839-3849. doi: 10.1002/art.37690.
19. Ravi B, Croxford R, Hollands S, Paterson JM, Bogoch E, Kreder H, et al. Increased risk of complications following total joint arthroplasty in patients with rheumatoid arthritis. Arthritis Rheumatol. 2014;66(2):254-263. doi: 10.1002/art.38231.
20. ACS NSQIP Participant Use Data Files. https://www.facs.org/quality-programs/acs-nsqip/program-specifics/participant-use. Accessed December 6, 2018.
21. Lawson EH, Louie R, Zingmond DS, Brook RH, Hall BL, Han L, et al. A comparison of clinical registry versus administrative claims data for reporting of 30-day surgical complications. Ann Surg. 2012;256(6):973-981. doi: 10.1097/SLA.0b013e31826b4c4f.
22. Weiss A, Anderson JE, Chang DC. Comparing the national surgical quality improvement program with the nationwide inpatient sample database. JAMA Surg. 2015;150(8):815-816. doi: 10.1001/jamasurg.2015.0962.
23. Boddapati V, Fu MC, Mayman DJ, Su EP, Sculco PK, McLawhorn AS. Revision total knee arthroplasty for periprosthetic joint infection is associated with increased postoperative morbidity and mortality relative to noninfectious revisions. J Arthroplasty. 2018;33(2):521-526. doi: 10.1016/j.arth.2017.09.021.
24. Boddapati V, Fu MC, Schairer WW, Gulotta LV, Dines DM, Dines JS. Revision total shoulder arthroplasty is associated with increased thirty-day postoperative complications and wound infections relative to primary total shoulder arthroplasty. HSS J. 2018;14(1):23-28. doi: 10.1007/s11420-017-9573-5.
25. Boddapati V, Fu MC, Schiarer WW, Ranawat AS, Dines DM, Taylor SA, Dines DM. Increased shoulder arthroscopy time is associated with overnight hospital stay and surgical site infection. Arthroscopy. 2018;34(2):363-368. doi: 10.1016/j.arthro.2017.08.243.
26. Lunt M. Selecting an appropriate caliper can be essential for achieving good balance with propensity score matching. Am J Epidemiol. 2014 Jan 15;179(2):226-235. doi: 10.1093/aje/kwt212.
27. Tannenbaum DA, Matthews LS, Grady-Benson JC. Infection around joint replacements in patients who have a renal or liver transplantation. J Bone Joint Surg Am. 1997;79(1):36-43.
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TAKE-HOME POINTS
- The rate of preoperative corticosteroid usage is low (3.7%).
- Patients using preoperative corticosteroids had increased rates of total 30-day complications.
- Adverse outcomes that are increased include infectious complications (eg, sepsis, urinary tract infection, surgical site infection).
- Hospital readmissions are also increased in patients taking preoperative corticosteroids, with the most common reason being infection.
- Increased postoperative counseling and surveillance may be warranted in this patient population.