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Supportive care alone linked to worse outcomes in mucocutaneous reactions
CHICAGO –
, compared with other treatment modalities, a systematic review suggested.Although rare in the pediatric population – with an incidence of approximately 1 case in 2 million – Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are both life-threatening mucocutaneous reactions.
Because reliable and validated data in the management of these conditions are lacking, he and his associates performed a systematic review to evaluate the effectiveness of reported treatment modalities using specific outcome measures.
“This study is unique in that it aims to not only capture more commonly employed interventions such as supportive care, surgical debridement, intravenous immunoglobulin [IVIG], and corticosteroids but also newer modalities that coincide with our improved understanding of the pathogenesis of the disease, such as the use of cyclosporine and biologics,” said Mr. Mansour, a third-year medical student at the University of Toronto.
The researchers systematically reviewed English and non-English articles using EMBASE, MEDLINE, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, the NHS Economic Evaluation Database, and the Health Technology Assessment Database. They excluded nonpediatric cases and those in which specific treatment modalities and outcome measures of interest were missing. In all, 302 articles were included in the study – 197 that examined mortality and 105 that examined time for arrest of progression of blistering, re-epithelialization, and length of hospital stay.
The main treatment modalities included supportive care alone, IVIG, corticosteroids, cyclosporine, surgical debridement, and biologics. The average time for arrest of progression of blistering was 8.4 days for supportive care, 4 days for IVIG, 6 days for corticosteroids, 2.5 days for cyclosporine, and 1 for infliximab. No data were available for time to arrest of progression for surgical debridement alone.
The average time for re-epithelialization was 24 days for supportive care, 18 days for surgical debridement, 8.7 days for IVIG, 12.2 days for corticosteroids, 10.6 days for cyclosporine, and 13 days for infliximab. Average length of hospital stay varied from 15.6 days for supportive care, 24.3 days for surgical debridement, 17.4 days for IVIG, 11.5 for corticosteroids, 15.5 for cyclosporine, and 26.3 for biologics.
The overall mortality was 4.6% among those who received supportive care alone, 8.3% among those who received IVIG, 4.5% among those who received corticosteroids, and 0.9% among those who received IVIG plus corticosteroids. Specifically, the rates of mortality for SJS and TEN cases treated with supportive care alone were 2% for SJS cases and 15.3% for TEN cases, respectively. The rates for other treatment modalities were 3.1% and 11% for IVIG, 1.7% and 9.3% for corticosteroids, and 0% and 2.1% for IVIG plus corticosteroids.
“While it was not surprising that mortality rates in pediatric SJS and TEN are low, the rates were slightly higher than anticipated,” Mr. Mansour said. “In addition, our data show that, although mortality is not influenced by certain therapeutic interventions in SJS patients, it may play a role in the management of the more severe disease, TEN.”
He acknowledged certain limitations of the study, including the fact that many of the data were derived from small-cohort retrospective studies and isolated case reports, giving rise to data heterogeneity and publication bias. “In addition, the mortality data we gathered may not necessarily represent patient survival, as many studies had variable follow-up duration,” he said. “Lastly, the additive effect of combination treatment and variable dosing was not captured in the present analysis, and further statistical analysis is required for re-epithelialization–based outcome measures and length of stay to ascertain significance.”
Mr. Mansour reported having no financial disclosures.
CHICAGO –
, compared with other treatment modalities, a systematic review suggested.Although rare in the pediatric population – with an incidence of approximately 1 case in 2 million – Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are both life-threatening mucocutaneous reactions.
Because reliable and validated data in the management of these conditions are lacking, he and his associates performed a systematic review to evaluate the effectiveness of reported treatment modalities using specific outcome measures.
“This study is unique in that it aims to not only capture more commonly employed interventions such as supportive care, surgical debridement, intravenous immunoglobulin [IVIG], and corticosteroids but also newer modalities that coincide with our improved understanding of the pathogenesis of the disease, such as the use of cyclosporine and biologics,” said Mr. Mansour, a third-year medical student at the University of Toronto.
The researchers systematically reviewed English and non-English articles using EMBASE, MEDLINE, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, the NHS Economic Evaluation Database, and the Health Technology Assessment Database. They excluded nonpediatric cases and those in which specific treatment modalities and outcome measures of interest were missing. In all, 302 articles were included in the study – 197 that examined mortality and 105 that examined time for arrest of progression of blistering, re-epithelialization, and length of hospital stay.
The main treatment modalities included supportive care alone, IVIG, corticosteroids, cyclosporine, surgical debridement, and biologics. The average time for arrest of progression of blistering was 8.4 days for supportive care, 4 days for IVIG, 6 days for corticosteroids, 2.5 days for cyclosporine, and 1 for infliximab. No data were available for time to arrest of progression for surgical debridement alone.
The average time for re-epithelialization was 24 days for supportive care, 18 days for surgical debridement, 8.7 days for IVIG, 12.2 days for corticosteroids, 10.6 days for cyclosporine, and 13 days for infliximab. Average length of hospital stay varied from 15.6 days for supportive care, 24.3 days for surgical debridement, 17.4 days for IVIG, 11.5 for corticosteroids, 15.5 for cyclosporine, and 26.3 for biologics.
The overall mortality was 4.6% among those who received supportive care alone, 8.3% among those who received IVIG, 4.5% among those who received corticosteroids, and 0.9% among those who received IVIG plus corticosteroids. Specifically, the rates of mortality for SJS and TEN cases treated with supportive care alone were 2% for SJS cases and 15.3% for TEN cases, respectively. The rates for other treatment modalities were 3.1% and 11% for IVIG, 1.7% and 9.3% for corticosteroids, and 0% and 2.1% for IVIG plus corticosteroids.
“While it was not surprising that mortality rates in pediatric SJS and TEN are low, the rates were slightly higher than anticipated,” Mr. Mansour said. “In addition, our data show that, although mortality is not influenced by certain therapeutic interventions in SJS patients, it may play a role in the management of the more severe disease, TEN.”
He acknowledged certain limitations of the study, including the fact that many of the data were derived from small-cohort retrospective studies and isolated case reports, giving rise to data heterogeneity and publication bias. “In addition, the mortality data we gathered may not necessarily represent patient survival, as many studies had variable follow-up duration,” he said. “Lastly, the additive effect of combination treatment and variable dosing was not captured in the present analysis, and further statistical analysis is required for re-epithelialization–based outcome measures and length of stay to ascertain significance.”
Mr. Mansour reported having no financial disclosures.
CHICAGO –
, compared with other treatment modalities, a systematic review suggested.Although rare in the pediatric population – with an incidence of approximately 1 case in 2 million – Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are both life-threatening mucocutaneous reactions.
Because reliable and validated data in the management of these conditions are lacking, he and his associates performed a systematic review to evaluate the effectiveness of reported treatment modalities using specific outcome measures.
“This study is unique in that it aims to not only capture more commonly employed interventions such as supportive care, surgical debridement, intravenous immunoglobulin [IVIG], and corticosteroids but also newer modalities that coincide with our improved understanding of the pathogenesis of the disease, such as the use of cyclosporine and biologics,” said Mr. Mansour, a third-year medical student at the University of Toronto.
The researchers systematically reviewed English and non-English articles using EMBASE, MEDLINE, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, the NHS Economic Evaluation Database, and the Health Technology Assessment Database. They excluded nonpediatric cases and those in which specific treatment modalities and outcome measures of interest were missing. In all, 302 articles were included in the study – 197 that examined mortality and 105 that examined time for arrest of progression of blistering, re-epithelialization, and length of hospital stay.
The main treatment modalities included supportive care alone, IVIG, corticosteroids, cyclosporine, surgical debridement, and biologics. The average time for arrest of progression of blistering was 8.4 days for supportive care, 4 days for IVIG, 6 days for corticosteroids, 2.5 days for cyclosporine, and 1 for infliximab. No data were available for time to arrest of progression for surgical debridement alone.
The average time for re-epithelialization was 24 days for supportive care, 18 days for surgical debridement, 8.7 days for IVIG, 12.2 days for corticosteroids, 10.6 days for cyclosporine, and 13 days for infliximab. Average length of hospital stay varied from 15.6 days for supportive care, 24.3 days for surgical debridement, 17.4 days for IVIG, 11.5 for corticosteroids, 15.5 for cyclosporine, and 26.3 for biologics.
The overall mortality was 4.6% among those who received supportive care alone, 8.3% among those who received IVIG, 4.5% among those who received corticosteroids, and 0.9% among those who received IVIG plus corticosteroids. Specifically, the rates of mortality for SJS and TEN cases treated with supportive care alone were 2% for SJS cases and 15.3% for TEN cases, respectively. The rates for other treatment modalities were 3.1% and 11% for IVIG, 1.7% and 9.3% for corticosteroids, and 0% and 2.1% for IVIG plus corticosteroids.
“While it was not surprising that mortality rates in pediatric SJS and TEN are low, the rates were slightly higher than anticipated,” Mr. Mansour said. “In addition, our data show that, although mortality is not influenced by certain therapeutic interventions in SJS patients, it may play a role in the management of the more severe disease, TEN.”
He acknowledged certain limitations of the study, including the fact that many of the data were derived from small-cohort retrospective studies and isolated case reports, giving rise to data heterogeneity and publication bias. “In addition, the mortality data we gathered may not necessarily represent patient survival, as many studies had variable follow-up duration,” he said. “Lastly, the additive effect of combination treatment and variable dosing was not captured in the present analysis, and further statistical analysis is required for re-epithelialization–based outcome measures and length of stay to ascertain significance.”
Mr. Mansour reported having no financial disclosures.
AT WCPD 2017
Key clinical point: Reliable and validated data informing the best treatment intervention for Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are lacking.
Major finding: The overall mortality was 4.6% among those who received supportive care alone, 8.3% among those who received IVIG, 4.5% among those who received corticosteroids, and 0.9% among those who received IVIG plus corticosteroids.
Data source: A systematic review of 302 studies that evaluated the effectiveness of reported treatment modalities for SJS/TEN using specific outcome measures.
Disclosures: Mr. Mansour reported having no financial disclosures.
Pediatric hospital medicine marches toward subspecialty recognition
Pediatric hospital medicine is moving quickly toward recognition as a board-certified, fellowship-trained medical subspecialty, joining 14 other pediatric subspecialties now certified by the American Board of Pediatrics (ABP).
It was approved as a subspecialty by the American Board of Medical Specialties (ABMS) at its October 2016 board meeting in Chicago in response to a petition from the ABP. Following years of discussion within the field,1 it will take 2 more years to describe pediatric hospital medicine’s specialized knowledge base and write test questions for biannual board exams that are projected to commence in the fall of 2019.
Eventually, starting in 2025, pediatric hospitalists will need to complete a fellowship of 2 years or more if they wish to sit for the exam and become board-certified in the field. But for the next 7 years, hospitalists in current practice will be able to qualify based on their work experience. Maintenance of certification requirements likely will be similar to those in other subspecialties, and doctors certified in pediatric hospital medicine won’t be required to maintain general pediatric certification, Dr. Rauch said.
Formal eligibility criteria have not been set, but likely will include working half-time overall in pediatric-related activities, and quarter-time in clinical practice in pediatric hospital medicine for 4 years prior to qualifying for the exam. How the hours might break down between clinical and other hospital responsibilities, and between pediatric or adult patients, still needs to be determined, Dr. Rauch said. He added that the experiential pathway is likely to be defined broadly, with latitude for determinations based on percentages of time worked, rather than absolute number of hours worked. Local pediatric institutions will be granted latitude to determine how that “plays out” in real world situations, he said, “and an ABP credentialing committee will be available to hear appeals for people who have complicated life circumstances.”
“I was part of a committee that explored these issues. We were an independent group of hospitalists who decided that board certification was a good way to advance the field,” Dr. Quinonez said. “We’ve seen what subspecialty certification has done, for example, for pediatric emergency medicine and pediatric critical care medicine – advancing them tremendously from a research standpoint and helping to develop a distinct body of knowledge reflecting increased severity of illness in hospitalized children.”
Discrepancy between practicing hospitalists, fellowships
An estimated 4,000 pediatric hospitalists now practice in the United States, and 2,100 of those belong to the American Academy of Pediatrics’ Section on Hospital Medicine. There are 40 pediatric hospital medicine fellowship programs listed on the website of AAP’s Section on Hospital Medicine (http://phmfellows.org/phm-programs/), although formal training assessment criteria will be needed for the American College of Graduate Medical Education to recognize programs that qualify their fellows to sit for the PHM exam. A wide gap is anticipated between the demand for pediatric hospitalists and currently available fellowship training slots to generate new candidates for board certification, although Dr. Rauch projects that fellowship slots will double in coming years.
“My message to the field is that historically, board certification has been the launching point for further development of the field,” Dr. Rauch said. “It leads to standardization of who is a subspecialist. Right now, who is a pediatric hospitalist is subject to wide variation. We need to standardize training and to create for this field the same distinction and stature as other medical subspecialties,” he said, noting that subspecialty status also has ramifications for academic settings, and for career advancement and career satisfaction for the individuals who choose to pursue it.
“I know there has been some hue and cry about this in the field, but in most cases certification will not change a pediatric hospitalist’s ability to obtain a job,” he said. “Already, you can’t become a division leader at a children’s hospital without additional training. This isn’t going to change that reality. But for people who don’t want to follow an academic career path, there will never be enough board-certified or fellowship-trained pediatric hospitalists to fill all of the pediatric positions in all the hospitals in the country. Community hospitals aren’t going to say: We won’t hire you unless you are board certified.”
Is the fellowship good for the field?
The subspecialty development process clearly is moving forward. Those in favor believe it will increase scholarship, research, and recognition for the subspecialty by the public for its specialized body of knowledge. But not everyone in the field agrees. Last fall The Hospitalist published3 an opinion piece questioning the need for fellowship-based board certification in pediatric hospital medicine. The author recommended instead retaining the current voluntary approach to fellowships and establishing a pediatric “focused practice” incorporated into residency training, much as the American Board of Internal Medicine and the American Board of Family Medicine have done for hospitalists in adult medicine.
“Will it lead to uncertainty among those currently in residency programs? If you are a pediatric resident and you want to become a board-certified pediatric hospitalist, you’ll need at least 2 years more of training. Is that going to deter qualified individuals?” Dr. Chang said. “The people this decision will impact the most are med-peds doctors – who complete a combined internal medicine and pediatrics residency – and part-timers. They may find themselves in a difficult position if the number of hours don’t add up for them to sit for the boards. For the most part, we’ll have to wait and see for answers to these questions.”
Brian Alverson, MD, FAAP, current chair of the AAP’s Section on Hospital Medicine and associate professor of pediatrics at Brown University, Providence, R.I., says he can see both sides of the debate.
But at the same time, there is a significant opportunity cost for doing 2 more years of fellowship training, Dr. Alverson said.
“We don’t know how much the board certification test will improve actual care,” he noted. “Does it truly identify higher quality doctors, or just doctors who are good at taking multiple choice exams? There are a number of people in pediatrics who do a lot of different things in their jobs, and it’s important that they not lose their ability to practice in the field. Two-thirds of our work force is in community hospitals, not academic medical centers. They work hard to provide the backbone of hospital care for young patients, and many of them are unlikely to ever do a fellowship.”
Nonetheless, Dr. Alverson believes pediatric hospitalists needn’t worry. “You still have plenty of time to figure out what’s going to happen in your hospital,” he said.
References
1. Section on Hospital Medicine. Guiding principles for pediatric hospital medicine program. Pediatrics; 2013; 132:782-786.
2. Stucky E. The Pediatric Hospital Medicine Core Competencies. Wiley-Blackwell; 2010.
3. Feldman LS, Monash B, Eniasivam A. Why required pediatric hospital medicine fellowships are unnecessary. The Hospitalist Magazine, October 8, 2016.
Pediatric hospital medicine is moving quickly toward recognition as a board-certified, fellowship-trained medical subspecialty, joining 14 other pediatric subspecialties now certified by the American Board of Pediatrics (ABP).
It was approved as a subspecialty by the American Board of Medical Specialties (ABMS) at its October 2016 board meeting in Chicago in response to a petition from the ABP. Following years of discussion within the field,1 it will take 2 more years to describe pediatric hospital medicine’s specialized knowledge base and write test questions for biannual board exams that are projected to commence in the fall of 2019.
Eventually, starting in 2025, pediatric hospitalists will need to complete a fellowship of 2 years or more if they wish to sit for the exam and become board-certified in the field. But for the next 7 years, hospitalists in current practice will be able to qualify based on their work experience. Maintenance of certification requirements likely will be similar to those in other subspecialties, and doctors certified in pediatric hospital medicine won’t be required to maintain general pediatric certification, Dr. Rauch said.
Formal eligibility criteria have not been set, but likely will include working half-time overall in pediatric-related activities, and quarter-time in clinical practice in pediatric hospital medicine for 4 years prior to qualifying for the exam. How the hours might break down between clinical and other hospital responsibilities, and between pediatric or adult patients, still needs to be determined, Dr. Rauch said. He added that the experiential pathway is likely to be defined broadly, with latitude for determinations based on percentages of time worked, rather than absolute number of hours worked. Local pediatric institutions will be granted latitude to determine how that “plays out” in real world situations, he said, “and an ABP credentialing committee will be available to hear appeals for people who have complicated life circumstances.”
“I was part of a committee that explored these issues. We were an independent group of hospitalists who decided that board certification was a good way to advance the field,” Dr. Quinonez said. “We’ve seen what subspecialty certification has done, for example, for pediatric emergency medicine and pediatric critical care medicine – advancing them tremendously from a research standpoint and helping to develop a distinct body of knowledge reflecting increased severity of illness in hospitalized children.”
Discrepancy between practicing hospitalists, fellowships
An estimated 4,000 pediatric hospitalists now practice in the United States, and 2,100 of those belong to the American Academy of Pediatrics’ Section on Hospital Medicine. There are 40 pediatric hospital medicine fellowship programs listed on the website of AAP’s Section on Hospital Medicine (http://phmfellows.org/phm-programs/), although formal training assessment criteria will be needed for the American College of Graduate Medical Education to recognize programs that qualify their fellows to sit for the PHM exam. A wide gap is anticipated between the demand for pediatric hospitalists and currently available fellowship training slots to generate new candidates for board certification, although Dr. Rauch projects that fellowship slots will double in coming years.
“My message to the field is that historically, board certification has been the launching point for further development of the field,” Dr. Rauch said. “It leads to standardization of who is a subspecialist. Right now, who is a pediatric hospitalist is subject to wide variation. We need to standardize training and to create for this field the same distinction and stature as other medical subspecialties,” he said, noting that subspecialty status also has ramifications for academic settings, and for career advancement and career satisfaction for the individuals who choose to pursue it.
“I know there has been some hue and cry about this in the field, but in most cases certification will not change a pediatric hospitalist’s ability to obtain a job,” he said. “Already, you can’t become a division leader at a children’s hospital without additional training. This isn’t going to change that reality. But for people who don’t want to follow an academic career path, there will never be enough board-certified or fellowship-trained pediatric hospitalists to fill all of the pediatric positions in all the hospitals in the country. Community hospitals aren’t going to say: We won’t hire you unless you are board certified.”
Is the fellowship good for the field?
The subspecialty development process clearly is moving forward. Those in favor believe it will increase scholarship, research, and recognition for the subspecialty by the public for its specialized body of knowledge. But not everyone in the field agrees. Last fall The Hospitalist published3 an opinion piece questioning the need for fellowship-based board certification in pediatric hospital medicine. The author recommended instead retaining the current voluntary approach to fellowships and establishing a pediatric “focused practice” incorporated into residency training, much as the American Board of Internal Medicine and the American Board of Family Medicine have done for hospitalists in adult medicine.
“Will it lead to uncertainty among those currently in residency programs? If you are a pediatric resident and you want to become a board-certified pediatric hospitalist, you’ll need at least 2 years more of training. Is that going to deter qualified individuals?” Dr. Chang said. “The people this decision will impact the most are med-peds doctors – who complete a combined internal medicine and pediatrics residency – and part-timers. They may find themselves in a difficult position if the number of hours don’t add up for them to sit for the boards. For the most part, we’ll have to wait and see for answers to these questions.”
Brian Alverson, MD, FAAP, current chair of the AAP’s Section on Hospital Medicine and associate professor of pediatrics at Brown University, Providence, R.I., says he can see both sides of the debate.
But at the same time, there is a significant opportunity cost for doing 2 more years of fellowship training, Dr. Alverson said.
“We don’t know how much the board certification test will improve actual care,” he noted. “Does it truly identify higher quality doctors, or just doctors who are good at taking multiple choice exams? There are a number of people in pediatrics who do a lot of different things in their jobs, and it’s important that they not lose their ability to practice in the field. Two-thirds of our work force is in community hospitals, not academic medical centers. They work hard to provide the backbone of hospital care for young patients, and many of them are unlikely to ever do a fellowship.”
Nonetheless, Dr. Alverson believes pediatric hospitalists needn’t worry. “You still have plenty of time to figure out what’s going to happen in your hospital,” he said.
References
1. Section on Hospital Medicine. Guiding principles for pediatric hospital medicine program. Pediatrics; 2013; 132:782-786.
2. Stucky E. The Pediatric Hospital Medicine Core Competencies. Wiley-Blackwell; 2010.
3. Feldman LS, Monash B, Eniasivam A. Why required pediatric hospital medicine fellowships are unnecessary. The Hospitalist Magazine, October 8, 2016.
Pediatric hospital medicine is moving quickly toward recognition as a board-certified, fellowship-trained medical subspecialty, joining 14 other pediatric subspecialties now certified by the American Board of Pediatrics (ABP).
It was approved as a subspecialty by the American Board of Medical Specialties (ABMS) at its October 2016 board meeting in Chicago in response to a petition from the ABP. Following years of discussion within the field,1 it will take 2 more years to describe pediatric hospital medicine’s specialized knowledge base and write test questions for biannual board exams that are projected to commence in the fall of 2019.
Eventually, starting in 2025, pediatric hospitalists will need to complete a fellowship of 2 years or more if they wish to sit for the exam and become board-certified in the field. But for the next 7 years, hospitalists in current practice will be able to qualify based on their work experience. Maintenance of certification requirements likely will be similar to those in other subspecialties, and doctors certified in pediatric hospital medicine won’t be required to maintain general pediatric certification, Dr. Rauch said.
Formal eligibility criteria have not been set, but likely will include working half-time overall in pediatric-related activities, and quarter-time in clinical practice in pediatric hospital medicine for 4 years prior to qualifying for the exam. How the hours might break down between clinical and other hospital responsibilities, and between pediatric or adult patients, still needs to be determined, Dr. Rauch said. He added that the experiential pathway is likely to be defined broadly, with latitude for determinations based on percentages of time worked, rather than absolute number of hours worked. Local pediatric institutions will be granted latitude to determine how that “plays out” in real world situations, he said, “and an ABP credentialing committee will be available to hear appeals for people who have complicated life circumstances.”
“I was part of a committee that explored these issues. We were an independent group of hospitalists who decided that board certification was a good way to advance the field,” Dr. Quinonez said. “We’ve seen what subspecialty certification has done, for example, for pediatric emergency medicine and pediatric critical care medicine – advancing them tremendously from a research standpoint and helping to develop a distinct body of knowledge reflecting increased severity of illness in hospitalized children.”
Discrepancy between practicing hospitalists, fellowships
An estimated 4,000 pediatric hospitalists now practice in the United States, and 2,100 of those belong to the American Academy of Pediatrics’ Section on Hospital Medicine. There are 40 pediatric hospital medicine fellowship programs listed on the website of AAP’s Section on Hospital Medicine (http://phmfellows.org/phm-programs/), although formal training assessment criteria will be needed for the American College of Graduate Medical Education to recognize programs that qualify their fellows to sit for the PHM exam. A wide gap is anticipated between the demand for pediatric hospitalists and currently available fellowship training slots to generate new candidates for board certification, although Dr. Rauch projects that fellowship slots will double in coming years.
“My message to the field is that historically, board certification has been the launching point for further development of the field,” Dr. Rauch said. “It leads to standardization of who is a subspecialist. Right now, who is a pediatric hospitalist is subject to wide variation. We need to standardize training and to create for this field the same distinction and stature as other medical subspecialties,” he said, noting that subspecialty status also has ramifications for academic settings, and for career advancement and career satisfaction for the individuals who choose to pursue it.
“I know there has been some hue and cry about this in the field, but in most cases certification will not change a pediatric hospitalist’s ability to obtain a job,” he said. “Already, you can’t become a division leader at a children’s hospital without additional training. This isn’t going to change that reality. But for people who don’t want to follow an academic career path, there will never be enough board-certified or fellowship-trained pediatric hospitalists to fill all of the pediatric positions in all the hospitals in the country. Community hospitals aren’t going to say: We won’t hire you unless you are board certified.”
Is the fellowship good for the field?
The subspecialty development process clearly is moving forward. Those in favor believe it will increase scholarship, research, and recognition for the subspecialty by the public for its specialized body of knowledge. But not everyone in the field agrees. Last fall The Hospitalist published3 an opinion piece questioning the need for fellowship-based board certification in pediatric hospital medicine. The author recommended instead retaining the current voluntary approach to fellowships and establishing a pediatric “focused practice” incorporated into residency training, much as the American Board of Internal Medicine and the American Board of Family Medicine have done for hospitalists in adult medicine.
“Will it lead to uncertainty among those currently in residency programs? If you are a pediatric resident and you want to become a board-certified pediatric hospitalist, you’ll need at least 2 years more of training. Is that going to deter qualified individuals?” Dr. Chang said. “The people this decision will impact the most are med-peds doctors – who complete a combined internal medicine and pediatrics residency – and part-timers. They may find themselves in a difficult position if the number of hours don’t add up for them to sit for the boards. For the most part, we’ll have to wait and see for answers to these questions.”
Brian Alverson, MD, FAAP, current chair of the AAP’s Section on Hospital Medicine and associate professor of pediatrics at Brown University, Providence, R.I., says he can see both sides of the debate.
But at the same time, there is a significant opportunity cost for doing 2 more years of fellowship training, Dr. Alverson said.
“We don’t know how much the board certification test will improve actual care,” he noted. “Does it truly identify higher quality doctors, or just doctors who are good at taking multiple choice exams? There are a number of people in pediatrics who do a lot of different things in their jobs, and it’s important that they not lose their ability to practice in the field. Two-thirds of our work force is in community hospitals, not academic medical centers. They work hard to provide the backbone of hospital care for young patients, and many of them are unlikely to ever do a fellowship.”
Nonetheless, Dr. Alverson believes pediatric hospitalists needn’t worry. “You still have plenty of time to figure out what’s going to happen in your hospital,” he said.
References
1. Section on Hospital Medicine. Guiding principles for pediatric hospital medicine program. Pediatrics; 2013; 132:782-786.
2. Stucky E. The Pediatric Hospital Medicine Core Competencies. Wiley-Blackwell; 2010.
3. Feldman LS, Monash B, Eniasivam A. Why required pediatric hospital medicine fellowships are unnecessary. The Hospitalist Magazine, October 8, 2016.
IMiD/Anti-CD20 combo induces complete responses in r/r NHL
Lugano, Switzerland – A combination of obinutuzumab (Gazyva) and the experimental immunomodulatory agent CC-122 showed “clinically meaningful” activity against relapsed/refractory diffuse large B cell lymphoma (DLBCL) and indolent non-Hodgkin lymphoma (NHL) in a phase 1b study.
Among 38 patients with heavily pretreated, relapsed/refractory DLBCL, follicular lymphoma (FL), or marginal zone lymphoma (MZL), the overall response rate was 66%, including 12 patients (32%) with a complete response (CR), reported Jean-Marie Michot, MD, from the Goustave-Roussy Cancer Center in Villejuif, France.
CC-122 is a thalidomide analog that shares a molecular target with its cousin lenalidomide (Revlimid). Both molecules bind to the protein cereblon to cause degradation of the lymphoid transcription factors Aiolos and Ikaros.
As a single agent, CC-122 has been shown to have immunomodulatory effects on T-cell and natural killer (NK)–cell functions and has shown clinical activity in heavily pretreated patients with relapsed refractory NHL, including various cell-of-origin–based DLBCL subtypes, Dr, Michot said.
In preclinical studies, the combination of CC-122 and obinutuzumab, an anti-CD20 monoclonal antibody, has shown synergistic effects against FL and greater antilymphoma effects against DLBCL than either agent alone, he added.
In a multicenter, open-label, phase 1b dose-escalation and expansion study, investigators enrolled 19 patients with FL or MZL for whom at least one prior regimen had failed and 19 patients with relapsed/refractory DLBCL following at least two prior regimens and failed autologous stem cell transplant.
The patients received oral CC-122 at different dose levels for 5 of 7 days in each 28 day treatment cycle, plus intravenous obinutuzumab 1000 mg on days 2, 8, and 15 of cycle 1 and day 1 of cycles 2 through 8.
Responses were assessed according to International Working Group 2007 revised response criteria for malignant lymphoma.
Among all 38 patients, 25 (66%) had a response. Responses consisted of 12 CR (3 in patients with DLBCL, and 9 in patients with FL/MZL) and 13 partial responses (six and seven patients, respectively),
The median time to best response was 57 days. Responses were seen in 23 of the 30 patients who received CC-122 at dose level of 3 mg or higher.
“To date, patients receiving CC-122 at a dose of 3 mg and higher have the best and more durable responses to CC-122 plus obinutuzumab,” Dr. Michot said.
Patients generally tolerated the combination well. The most common grade 3 or 4 adverse events were hematologic and included grade 4 febrile neutropenia in two patients. Two patients discontinued treatment because of adverse events.
There was a dose-limiting toxicity, grade 4 neutropenia in one patient who received CC-122 at the 3 mg dose level, and one death from a tumor flare reaction in a patient treated at the 4 mg dose level.
The dose-escalation arm of the study has completed, and investigators are enrolling patients in a dose expansion phase at the 3 mg level.
The study was sponsored by Celgene. Hoffman La-Roche contributed obinutuzumab for the study. Dr. Michot reported serving as an advisor to Bristol-Myers Squibb and receiving travel grants from BMS, Pfizer, and Roche. Seven coauthors are Celgene employees and stockholders.
Lugano, Switzerland – A combination of obinutuzumab (Gazyva) and the experimental immunomodulatory agent CC-122 showed “clinically meaningful” activity against relapsed/refractory diffuse large B cell lymphoma (DLBCL) and indolent non-Hodgkin lymphoma (NHL) in a phase 1b study.
Among 38 patients with heavily pretreated, relapsed/refractory DLBCL, follicular lymphoma (FL), or marginal zone lymphoma (MZL), the overall response rate was 66%, including 12 patients (32%) with a complete response (CR), reported Jean-Marie Michot, MD, from the Goustave-Roussy Cancer Center in Villejuif, France.
CC-122 is a thalidomide analog that shares a molecular target with its cousin lenalidomide (Revlimid). Both molecules bind to the protein cereblon to cause degradation of the lymphoid transcription factors Aiolos and Ikaros.
As a single agent, CC-122 has been shown to have immunomodulatory effects on T-cell and natural killer (NK)–cell functions and has shown clinical activity in heavily pretreated patients with relapsed refractory NHL, including various cell-of-origin–based DLBCL subtypes, Dr, Michot said.
In preclinical studies, the combination of CC-122 and obinutuzumab, an anti-CD20 monoclonal antibody, has shown synergistic effects against FL and greater antilymphoma effects against DLBCL than either agent alone, he added.
In a multicenter, open-label, phase 1b dose-escalation and expansion study, investigators enrolled 19 patients with FL or MZL for whom at least one prior regimen had failed and 19 patients with relapsed/refractory DLBCL following at least two prior regimens and failed autologous stem cell transplant.
The patients received oral CC-122 at different dose levels for 5 of 7 days in each 28 day treatment cycle, plus intravenous obinutuzumab 1000 mg on days 2, 8, and 15 of cycle 1 and day 1 of cycles 2 through 8.
Responses were assessed according to International Working Group 2007 revised response criteria for malignant lymphoma.
Among all 38 patients, 25 (66%) had a response. Responses consisted of 12 CR (3 in patients with DLBCL, and 9 in patients with FL/MZL) and 13 partial responses (six and seven patients, respectively),
The median time to best response was 57 days. Responses were seen in 23 of the 30 patients who received CC-122 at dose level of 3 mg or higher.
“To date, patients receiving CC-122 at a dose of 3 mg and higher have the best and more durable responses to CC-122 plus obinutuzumab,” Dr. Michot said.
Patients generally tolerated the combination well. The most common grade 3 or 4 adverse events were hematologic and included grade 4 febrile neutropenia in two patients. Two patients discontinued treatment because of adverse events.
There was a dose-limiting toxicity, grade 4 neutropenia in one patient who received CC-122 at the 3 mg dose level, and one death from a tumor flare reaction in a patient treated at the 4 mg dose level.
The dose-escalation arm of the study has completed, and investigators are enrolling patients in a dose expansion phase at the 3 mg level.
The study was sponsored by Celgene. Hoffman La-Roche contributed obinutuzumab for the study. Dr. Michot reported serving as an advisor to Bristol-Myers Squibb and receiving travel grants from BMS, Pfizer, and Roche. Seven coauthors are Celgene employees and stockholders.
Lugano, Switzerland – A combination of obinutuzumab (Gazyva) and the experimental immunomodulatory agent CC-122 showed “clinically meaningful” activity against relapsed/refractory diffuse large B cell lymphoma (DLBCL) and indolent non-Hodgkin lymphoma (NHL) in a phase 1b study.
Among 38 patients with heavily pretreated, relapsed/refractory DLBCL, follicular lymphoma (FL), or marginal zone lymphoma (MZL), the overall response rate was 66%, including 12 patients (32%) with a complete response (CR), reported Jean-Marie Michot, MD, from the Goustave-Roussy Cancer Center in Villejuif, France.
CC-122 is a thalidomide analog that shares a molecular target with its cousin lenalidomide (Revlimid). Both molecules bind to the protein cereblon to cause degradation of the lymphoid transcription factors Aiolos and Ikaros.
As a single agent, CC-122 has been shown to have immunomodulatory effects on T-cell and natural killer (NK)–cell functions and has shown clinical activity in heavily pretreated patients with relapsed refractory NHL, including various cell-of-origin–based DLBCL subtypes, Dr, Michot said.
In preclinical studies, the combination of CC-122 and obinutuzumab, an anti-CD20 monoclonal antibody, has shown synergistic effects against FL and greater antilymphoma effects against DLBCL than either agent alone, he added.
In a multicenter, open-label, phase 1b dose-escalation and expansion study, investigators enrolled 19 patients with FL or MZL for whom at least one prior regimen had failed and 19 patients with relapsed/refractory DLBCL following at least two prior regimens and failed autologous stem cell transplant.
The patients received oral CC-122 at different dose levels for 5 of 7 days in each 28 day treatment cycle, plus intravenous obinutuzumab 1000 mg on days 2, 8, and 15 of cycle 1 and day 1 of cycles 2 through 8.
Responses were assessed according to International Working Group 2007 revised response criteria for malignant lymphoma.
Among all 38 patients, 25 (66%) had a response. Responses consisted of 12 CR (3 in patients with DLBCL, and 9 in patients with FL/MZL) and 13 partial responses (six and seven patients, respectively),
The median time to best response was 57 days. Responses were seen in 23 of the 30 patients who received CC-122 at dose level of 3 mg or higher.
“To date, patients receiving CC-122 at a dose of 3 mg and higher have the best and more durable responses to CC-122 plus obinutuzumab,” Dr. Michot said.
Patients generally tolerated the combination well. The most common grade 3 or 4 adverse events were hematologic and included grade 4 febrile neutropenia in two patients. Two patients discontinued treatment because of adverse events.
There was a dose-limiting toxicity, grade 4 neutropenia in one patient who received CC-122 at the 3 mg dose level, and one death from a tumor flare reaction in a patient treated at the 4 mg dose level.
The dose-escalation arm of the study has completed, and investigators are enrolling patients in a dose expansion phase at the 3 mg level.
The study was sponsored by Celgene. Hoffman La-Roche contributed obinutuzumab for the study. Dr. Michot reported serving as an advisor to Bristol-Myers Squibb and receiving travel grants from BMS, Pfizer, and Roche. Seven coauthors are Celgene employees and stockholders.
AT 14-ICML
Key clinical point: A combination of the experimental immunomodulator CC-122 and obinutuzumab showed significant activity against relapsed/refractory non-Hodgkin lymphoma.
Major finding: The overall response rate was 66%, including 32% complete responses.
Data source: A multicenter open-label phase 1b dose-escalation study in 19 patients with DLBCL and 19 with follicular lymphoma or marginal zone lymphoma.
Disclosures: The study was sponsored by Celgene. Hoffman La-Roche contributed obinutuzumab for the study. Dr. Michot reported serving as an advisor to Bristol-Myers Squibb and receiving travel grants from BMS, Pfizer, and Roche. Seven coauthors are Celgene employees and stockholders.
Hospitalizations may speed up cognitive decline in older adults
LONDON – Older adult patients who already had cognitive decline when they were admitted to a hospital often left with a significantly accelerated rate of decline, according to findings from a large longitudinal cohort study.
The study found up to a 62% acceleration of prehospital cognitive decline after any hospitalization. Urgent or emergency hospitalizations exacted the biggest toll on cognitive health, Bryan James, PhD, said at the Alzheimer’s Association International Conference.
Cognitive decline after hospitalization in older patients is a common occurrence but still poorly understood, he said. “Some data suggest this could actually be seen as a public health crisis since 40% of all hospitalized patients in the U.S. are older than 65, and the risk of past-hospitalization cognitive impairment rises with age.
“Given the risk to cognitive health, older patients, families, and physicians require information on when to admit to the hospital,” Dr. James said. “We wondered if those who decline rapidly after the hospital admission were already declining before. Our second question was whether elective hospital admissions are associated with the same negative cognitive outcomes as nonelective (emergent or urgent) admissions.”
To examine this, Dr. James and his colleagues used patient data from the Rush Memory and Aging Project, which provides each participant with an annual cognitive assessment consisting of 19 neuropsychological tests. They linked these data to each patient’s Medicare claims record, allowing them to assess cognitive function both before and after the index hospitalization.
The cohort comprised 930 patients who were followed for a mean of 5 years. Hospitalized patients were older (81 vs. 79 years). Most patients in both groups had at least one medical condition, such as hypertension, heart disease, diabetes, cancer, thyroid disease, head injury, or stroke. Cognition was already impaired in many of the hospitalized patients; 62% had mild cognitive impairment (MCI) and 35% had dementia. Among the nonhospitalized subjects, 49% had MCI and 24% had dementia.
Of the cohort, 66% experienced a hospitalization during follow-up. Most hospitalizations (57%) were either for urgent or emergency problems. The rest were elective admissions. The main outcome was change in global cognition – an averaged z-score of all 19 tests of working memory, episodic memory, semantic memory, visuospatial processing, and perceptual speed.
Elective admissions were mostly planned surgeries (94%), and unplanned surgeries occurred in 64% of the nonelective admissions. Most of the elective admissions (81%) involved anesthesia, compared with 32% of the nonelective admissions. About 40% of each group required a stay in the intensive care unit. Around 11% in each group had a critical illness – a stroke, hemorrhage, or brain trauma in about 6% of each group.
A multivariate analysis looked at the change in cognition during two time points: 2 years before the index hospitalization and up to 8 years after it. As could be expected of aged subjects in a memory study cohort, most patients experienced a decline in cognition over the study period. However, nonhospitalized patients continued on a smooth linear slope of decline. Hospitalized patients experienced a significant 62% increased rate of decline, even after controlling for age, education, comorbidities, depression, Activities of Daily Living disability, and physical activity.
Visuospatial processing was the only domain not significantly affected by a hospital admission. All of the memory domains, as well as perceptual speed, declined significantly faster after hospitalization than before.
The second analysis examined which type of admission was most dangerous for cognitive health. This controlled for even more potential confounding factors, including length of stay, surgery and anesthesia, Charlson comorbidity index, critical illness, brain injury, and number of hospitalizations during the follow-up period.
Urgent and emergency admissions drove virtually all of the increase in decline, Dr. James said, with a 60% increase in the rate of decline, compared with the prehospitalization rate. Patients who had elective admissions showed no variance from their baseline rate of decline, and, in fact, followed the same slope as nonhospitalized patients. Again, change was seen in the global score and in all the memory domains and perceptual speed. Only visuospatial processing was unaffected.
“It’s unclear why the urgent and emergent admissions drove this finding, even after we controlled for illness and injury severity and other factors,” Dr. James said. “Obviously, we need more research in this area.”
He had no financial disclosures.
[email protected]
On Twitter @alz_gal
LONDON – Older adult patients who already had cognitive decline when they were admitted to a hospital often left with a significantly accelerated rate of decline, according to findings from a large longitudinal cohort study.
The study found up to a 62% acceleration of prehospital cognitive decline after any hospitalization. Urgent or emergency hospitalizations exacted the biggest toll on cognitive health, Bryan James, PhD, said at the Alzheimer’s Association International Conference.
Cognitive decline after hospitalization in older patients is a common occurrence but still poorly understood, he said. “Some data suggest this could actually be seen as a public health crisis since 40% of all hospitalized patients in the U.S. are older than 65, and the risk of past-hospitalization cognitive impairment rises with age.
“Given the risk to cognitive health, older patients, families, and physicians require information on when to admit to the hospital,” Dr. James said. “We wondered if those who decline rapidly after the hospital admission were already declining before. Our second question was whether elective hospital admissions are associated with the same negative cognitive outcomes as nonelective (emergent or urgent) admissions.”
To examine this, Dr. James and his colleagues used patient data from the Rush Memory and Aging Project, which provides each participant with an annual cognitive assessment consisting of 19 neuropsychological tests. They linked these data to each patient’s Medicare claims record, allowing them to assess cognitive function both before and after the index hospitalization.
The cohort comprised 930 patients who were followed for a mean of 5 years. Hospitalized patients were older (81 vs. 79 years). Most patients in both groups had at least one medical condition, such as hypertension, heart disease, diabetes, cancer, thyroid disease, head injury, or stroke. Cognition was already impaired in many of the hospitalized patients; 62% had mild cognitive impairment (MCI) and 35% had dementia. Among the nonhospitalized subjects, 49% had MCI and 24% had dementia.
Of the cohort, 66% experienced a hospitalization during follow-up. Most hospitalizations (57%) were either for urgent or emergency problems. The rest were elective admissions. The main outcome was change in global cognition – an averaged z-score of all 19 tests of working memory, episodic memory, semantic memory, visuospatial processing, and perceptual speed.
Elective admissions were mostly planned surgeries (94%), and unplanned surgeries occurred in 64% of the nonelective admissions. Most of the elective admissions (81%) involved anesthesia, compared with 32% of the nonelective admissions. About 40% of each group required a stay in the intensive care unit. Around 11% in each group had a critical illness – a stroke, hemorrhage, or brain trauma in about 6% of each group.
A multivariate analysis looked at the change in cognition during two time points: 2 years before the index hospitalization and up to 8 years after it. As could be expected of aged subjects in a memory study cohort, most patients experienced a decline in cognition over the study period. However, nonhospitalized patients continued on a smooth linear slope of decline. Hospitalized patients experienced a significant 62% increased rate of decline, even after controlling for age, education, comorbidities, depression, Activities of Daily Living disability, and physical activity.
Visuospatial processing was the only domain not significantly affected by a hospital admission. All of the memory domains, as well as perceptual speed, declined significantly faster after hospitalization than before.
The second analysis examined which type of admission was most dangerous for cognitive health. This controlled for even more potential confounding factors, including length of stay, surgery and anesthesia, Charlson comorbidity index, critical illness, brain injury, and number of hospitalizations during the follow-up period.
Urgent and emergency admissions drove virtually all of the increase in decline, Dr. James said, with a 60% increase in the rate of decline, compared with the prehospitalization rate. Patients who had elective admissions showed no variance from their baseline rate of decline, and, in fact, followed the same slope as nonhospitalized patients. Again, change was seen in the global score and in all the memory domains and perceptual speed. Only visuospatial processing was unaffected.
“It’s unclear why the urgent and emergent admissions drove this finding, even after we controlled for illness and injury severity and other factors,” Dr. James said. “Obviously, we need more research in this area.”
He had no financial disclosures.
[email protected]
On Twitter @alz_gal
LONDON – Older adult patients who already had cognitive decline when they were admitted to a hospital often left with a significantly accelerated rate of decline, according to findings from a large longitudinal cohort study.
The study found up to a 62% acceleration of prehospital cognitive decline after any hospitalization. Urgent or emergency hospitalizations exacted the biggest toll on cognitive health, Bryan James, PhD, said at the Alzheimer’s Association International Conference.
Cognitive decline after hospitalization in older patients is a common occurrence but still poorly understood, he said. “Some data suggest this could actually be seen as a public health crisis since 40% of all hospitalized patients in the U.S. are older than 65, and the risk of past-hospitalization cognitive impairment rises with age.
“Given the risk to cognitive health, older patients, families, and physicians require information on when to admit to the hospital,” Dr. James said. “We wondered if those who decline rapidly after the hospital admission were already declining before. Our second question was whether elective hospital admissions are associated with the same negative cognitive outcomes as nonelective (emergent or urgent) admissions.”
To examine this, Dr. James and his colleagues used patient data from the Rush Memory and Aging Project, which provides each participant with an annual cognitive assessment consisting of 19 neuropsychological tests. They linked these data to each patient’s Medicare claims record, allowing them to assess cognitive function both before and after the index hospitalization.
The cohort comprised 930 patients who were followed for a mean of 5 years. Hospitalized patients were older (81 vs. 79 years). Most patients in both groups had at least one medical condition, such as hypertension, heart disease, diabetes, cancer, thyroid disease, head injury, or stroke. Cognition was already impaired in many of the hospitalized patients; 62% had mild cognitive impairment (MCI) and 35% had dementia. Among the nonhospitalized subjects, 49% had MCI and 24% had dementia.
Of the cohort, 66% experienced a hospitalization during follow-up. Most hospitalizations (57%) were either for urgent or emergency problems. The rest were elective admissions. The main outcome was change in global cognition – an averaged z-score of all 19 tests of working memory, episodic memory, semantic memory, visuospatial processing, and perceptual speed.
Elective admissions were mostly planned surgeries (94%), and unplanned surgeries occurred in 64% of the nonelective admissions. Most of the elective admissions (81%) involved anesthesia, compared with 32% of the nonelective admissions. About 40% of each group required a stay in the intensive care unit. Around 11% in each group had a critical illness – a stroke, hemorrhage, or brain trauma in about 6% of each group.
A multivariate analysis looked at the change in cognition during two time points: 2 years before the index hospitalization and up to 8 years after it. As could be expected of aged subjects in a memory study cohort, most patients experienced a decline in cognition over the study period. However, nonhospitalized patients continued on a smooth linear slope of decline. Hospitalized patients experienced a significant 62% increased rate of decline, even after controlling for age, education, comorbidities, depression, Activities of Daily Living disability, and physical activity.
Visuospatial processing was the only domain not significantly affected by a hospital admission. All of the memory domains, as well as perceptual speed, declined significantly faster after hospitalization than before.
The second analysis examined which type of admission was most dangerous for cognitive health. This controlled for even more potential confounding factors, including length of stay, surgery and anesthesia, Charlson comorbidity index, critical illness, brain injury, and number of hospitalizations during the follow-up period.
Urgent and emergency admissions drove virtually all of the increase in decline, Dr. James said, with a 60% increase in the rate of decline, compared with the prehospitalization rate. Patients who had elective admissions showed no variance from their baseline rate of decline, and, in fact, followed the same slope as nonhospitalized patients. Again, change was seen in the global score and in all the memory domains and perceptual speed. Only visuospatial processing was unaffected.
“It’s unclear why the urgent and emergent admissions drove this finding, even after we controlled for illness and injury severity and other factors,” Dr. James said. “Obviously, we need more research in this area.”
He had no financial disclosures.
[email protected]
On Twitter @alz_gal
AT AAIC 2017
Key clinical point:
Major finding: Urgent or emergency admissions accelerated the rate of cognitive decline by 60%, compared with the prehospitalization rate. Elective admissions did not change the rate of cognitive decline.
Data source: The 930 patients were drawn from the Rush Memory and Aging Project.
Disclosures: The presenter had no financial disclosures.
Bowel prep score helps predict missed polyps
“Several recent prospective studies of one-time colonoscopies have demonstrated an association between higher BBPS (Boston Bowel Preparation Scale) scores and higher polyp and adenoma detection rates,” wrote Matthew A. Kluge, MD, of Boston University Medical Center, and his colleagues.
“We hypothesized that the BBPS could predict the likelihood of missed polyps based on initial BBPS segment scores among a large consortium of gastroenterology practices throughout the United States, thereby providing evidence to inform recommendations for repeat colonoscopy after less-than-perfect bowel preparation,” they said.
The researchers reviewed data from 335 pairs of colonoscopy exams in which the second exam (C2) was performed within 3 years of the first exam (C1). The primary endpoint was the detection of polyps and advanced polyps among colon segments at C2 stratified by BBPS scores at C1 (Gastrointest Endosc. 2017 Jun 22. doi: 10.1016/j.gie.2017.06.012).
Overall, patients with inadequate bowel prep were significantly more likely than those with adequate prep to be male (71% vs. 60%) and younger (average age, 59 years vs. 61 years). *
In a multivariate model, the risk of advanced polyps at C2 was significantly higher for patients who had advanced polyps at C1 (odds ratio, 3.5), but inadequate BBPS scores at C1 had no significant impact on advanced polyp risk at C2. The risk of advanced polyps at C2 increased slightly with each year of age (OR, 1.1), but was not impacted by sex or time between C1 and C2 visits.
In addition, polyps at C2 were significantly more likely in patients with inadequate examinations at C1 vs. adequate C1 exams (18% vs. 7%).
The study’s strengths include the use of a large database, but limitations include lack of information about pathology and the use of surrogate measures of polyp size, the researchers noted. However, the results highlight the importance of proper bowel prep and support previous observations that “individuals with a BBPS segment score of 0 and 1 may be at increased risk for missed polyps, especially if advanced polyps are detected,” they said.
The study was supported in part by the Clinical Outcomes Research Initiative (CORI) and by the National Institutes of Health, and CORI has received infrastructure support from companies including AstraZeneca, Bard International, Endosoft, Ethicon, GIVEN Imaging, Pentax USA, and ProVation. Lead author Dr. Kluge had no financial conflicts to disclose.
* This story was updated on 7/26/2017
“Several recent prospective studies of one-time colonoscopies have demonstrated an association between higher BBPS (Boston Bowel Preparation Scale) scores and higher polyp and adenoma detection rates,” wrote Matthew A. Kluge, MD, of Boston University Medical Center, and his colleagues.
“We hypothesized that the BBPS could predict the likelihood of missed polyps based on initial BBPS segment scores among a large consortium of gastroenterology practices throughout the United States, thereby providing evidence to inform recommendations for repeat colonoscopy after less-than-perfect bowel preparation,” they said.
The researchers reviewed data from 335 pairs of colonoscopy exams in which the second exam (C2) was performed within 3 years of the first exam (C1). The primary endpoint was the detection of polyps and advanced polyps among colon segments at C2 stratified by BBPS scores at C1 (Gastrointest Endosc. 2017 Jun 22. doi: 10.1016/j.gie.2017.06.012).
Overall, patients with inadequate bowel prep were significantly more likely than those with adequate prep to be male (71% vs. 60%) and younger (average age, 59 years vs. 61 years). *
In a multivariate model, the risk of advanced polyps at C2 was significantly higher for patients who had advanced polyps at C1 (odds ratio, 3.5), but inadequate BBPS scores at C1 had no significant impact on advanced polyp risk at C2. The risk of advanced polyps at C2 increased slightly with each year of age (OR, 1.1), but was not impacted by sex or time between C1 and C2 visits.
In addition, polyps at C2 were significantly more likely in patients with inadequate examinations at C1 vs. adequate C1 exams (18% vs. 7%).
The study’s strengths include the use of a large database, but limitations include lack of information about pathology and the use of surrogate measures of polyp size, the researchers noted. However, the results highlight the importance of proper bowel prep and support previous observations that “individuals with a BBPS segment score of 0 and 1 may be at increased risk for missed polyps, especially if advanced polyps are detected,” they said.
The study was supported in part by the Clinical Outcomes Research Initiative (CORI) and by the National Institutes of Health, and CORI has received infrastructure support from companies including AstraZeneca, Bard International, Endosoft, Ethicon, GIVEN Imaging, Pentax USA, and ProVation. Lead author Dr. Kluge had no financial conflicts to disclose.
* This story was updated on 7/26/2017
“Several recent prospective studies of one-time colonoscopies have demonstrated an association between higher BBPS (Boston Bowel Preparation Scale) scores and higher polyp and adenoma detection rates,” wrote Matthew A. Kluge, MD, of Boston University Medical Center, and his colleagues.
“We hypothesized that the BBPS could predict the likelihood of missed polyps based on initial BBPS segment scores among a large consortium of gastroenterology practices throughout the United States, thereby providing evidence to inform recommendations for repeat colonoscopy after less-than-perfect bowel preparation,” they said.
The researchers reviewed data from 335 pairs of colonoscopy exams in which the second exam (C2) was performed within 3 years of the first exam (C1). The primary endpoint was the detection of polyps and advanced polyps among colon segments at C2 stratified by BBPS scores at C1 (Gastrointest Endosc. 2017 Jun 22. doi: 10.1016/j.gie.2017.06.012).
Overall, patients with inadequate bowel prep were significantly more likely than those with adequate prep to be male (71% vs. 60%) and younger (average age, 59 years vs. 61 years). *
In a multivariate model, the risk of advanced polyps at C2 was significantly higher for patients who had advanced polyps at C1 (odds ratio, 3.5), but inadequate BBPS scores at C1 had no significant impact on advanced polyp risk at C2. The risk of advanced polyps at C2 increased slightly with each year of age (OR, 1.1), but was not impacted by sex or time between C1 and C2 visits.
In addition, polyps at C2 were significantly more likely in patients with inadequate examinations at C1 vs. adequate C1 exams (18% vs. 7%).
The study’s strengths include the use of a large database, but limitations include lack of information about pathology and the use of surrogate measures of polyp size, the researchers noted. However, the results highlight the importance of proper bowel prep and support previous observations that “individuals with a BBPS segment score of 0 and 1 may be at increased risk for missed polyps, especially if advanced polyps are detected,” they said.
The study was supported in part by the Clinical Outcomes Research Initiative (CORI) and by the National Institutes of Health, and CORI has received infrastructure support from companies including AstraZeneca, Bard International, Endosoft, Ethicon, GIVEN Imaging, Pentax USA, and ProVation. Lead author Dr. Kluge had no financial conflicts to disclose.
* This story was updated on 7/26/2017
FROM GASTROINTESTINAL ENDOSCOPY
Key clinical point: Individuals with a score of 0 or 1 on the Boston Bowel Preparation Scale may be at increased risk for missed polyps.
Major finding: Polyps at a second colonoscopy were significantly more likely in patients who had advanced polyps at an initial visit (odds ratio, 3.5).
Data source: The data come from a prospective, observational study of adults aged 50-75 years who had average risk screening colonoscopies.
Disclosures: The study was supported in part by the Clinical Outcomes Research Initiative (CORI) and by the National Institutes of Health, and CORI has received infrastructure support from companies including AstraZeneca, Bard International, Endosoft, Ethicon, GIVEN Imaging, Pentax USA, and ProVation. Dr. Kluge had no financial conflicts to disclose.
Early neuroimaging essential for Zika-exposed neonates
DENVER – The experience gleaned at ground zero of the Brazilian Zika virus epidemic drives home a clinical imperative: every neonate whose pregnant mother has presumed or confirmed Zika infection needs to undergo prompt neuroimaging, even if head circumference at birth is normal, Vanessa van der Linden, MD, said at the annual meeting of the Teratology Society.
Dr. van der Linden, a pediatric neurologist at the Association for Assistance of Disabled Children in Recife, Brazil, has done pioneering work in characterizing the recently recognized congenital Zika syndrome. She was the lead author of the first report of infants who had laboratory evidence of congenital Zika infection and normal head circumference at birth but who developed poor head growth and microcephaly later in infancy.
Comprehensive multispecialty medical and developmental follow-up documented that 10 of 13 infants had dysphagia, 7 had epilepsy, 3 had chorioretinal abnormalities, all 13 had hypertonia, and 12 had pyramidal and extrapyramidal signs with dystonia (MMWR. 2016 Dec 2;65[47]:1343-8).
In another recent publication, Dr. van der Linden and her coinvestigators described classic congenital Zika syndrome with microcephaly at birth as simply the tip of the Zika virus iceberg. In their retrospective review of 77 infants exposed to Zika in utero, 9 had microcephaly at birth, 7 developed microcephaly postnatally, and 3 didn’t have microcephaly at all. Those with microcephaly at birth showed the traditional neuroimaging findings of congenital Zika syndrome, including reduced brain volume, ventriculomegaly, subcortical calcifications, corpus callosum abnormalities, and an enlarged extra-axial space.
Those who subsequently developed microcephaly later in infancy showed most of the same neuroimaging abnormalities. The three infants who remained normocephalic displayed calcifications in the cortico-subcortical junction, asymmetric frontal polymicrogyria, delayed myelination, and milder ventriculomegaly than in the other two groups (AJNR Am J Neuroradiol. 2017 Jul;38[7]:1427-34).
The rehabilitation center where Dr. van der Linden and her colleagues are currently following roughly 200 children with congenital Zika syndrome is in the state of Pernambuco, which was particularly hard hit by the Zika epidemic.
She reported having no relevant financial disclosures.
DENVER – The experience gleaned at ground zero of the Brazilian Zika virus epidemic drives home a clinical imperative: every neonate whose pregnant mother has presumed or confirmed Zika infection needs to undergo prompt neuroimaging, even if head circumference at birth is normal, Vanessa van der Linden, MD, said at the annual meeting of the Teratology Society.
Dr. van der Linden, a pediatric neurologist at the Association for Assistance of Disabled Children in Recife, Brazil, has done pioneering work in characterizing the recently recognized congenital Zika syndrome. She was the lead author of the first report of infants who had laboratory evidence of congenital Zika infection and normal head circumference at birth but who developed poor head growth and microcephaly later in infancy.
Comprehensive multispecialty medical and developmental follow-up documented that 10 of 13 infants had dysphagia, 7 had epilepsy, 3 had chorioretinal abnormalities, all 13 had hypertonia, and 12 had pyramidal and extrapyramidal signs with dystonia (MMWR. 2016 Dec 2;65[47]:1343-8).
In another recent publication, Dr. van der Linden and her coinvestigators described classic congenital Zika syndrome with microcephaly at birth as simply the tip of the Zika virus iceberg. In their retrospective review of 77 infants exposed to Zika in utero, 9 had microcephaly at birth, 7 developed microcephaly postnatally, and 3 didn’t have microcephaly at all. Those with microcephaly at birth showed the traditional neuroimaging findings of congenital Zika syndrome, including reduced brain volume, ventriculomegaly, subcortical calcifications, corpus callosum abnormalities, and an enlarged extra-axial space.
Those who subsequently developed microcephaly later in infancy showed most of the same neuroimaging abnormalities. The three infants who remained normocephalic displayed calcifications in the cortico-subcortical junction, asymmetric frontal polymicrogyria, delayed myelination, and milder ventriculomegaly than in the other two groups (AJNR Am J Neuroradiol. 2017 Jul;38[7]:1427-34).
The rehabilitation center where Dr. van der Linden and her colleagues are currently following roughly 200 children with congenital Zika syndrome is in the state of Pernambuco, which was particularly hard hit by the Zika epidemic.
She reported having no relevant financial disclosures.
DENVER – The experience gleaned at ground zero of the Brazilian Zika virus epidemic drives home a clinical imperative: every neonate whose pregnant mother has presumed or confirmed Zika infection needs to undergo prompt neuroimaging, even if head circumference at birth is normal, Vanessa van der Linden, MD, said at the annual meeting of the Teratology Society.
Dr. van der Linden, a pediatric neurologist at the Association for Assistance of Disabled Children in Recife, Brazil, has done pioneering work in characterizing the recently recognized congenital Zika syndrome. She was the lead author of the first report of infants who had laboratory evidence of congenital Zika infection and normal head circumference at birth but who developed poor head growth and microcephaly later in infancy.
Comprehensive multispecialty medical and developmental follow-up documented that 10 of 13 infants had dysphagia, 7 had epilepsy, 3 had chorioretinal abnormalities, all 13 had hypertonia, and 12 had pyramidal and extrapyramidal signs with dystonia (MMWR. 2016 Dec 2;65[47]:1343-8).
In another recent publication, Dr. van der Linden and her coinvestigators described classic congenital Zika syndrome with microcephaly at birth as simply the tip of the Zika virus iceberg. In their retrospective review of 77 infants exposed to Zika in utero, 9 had microcephaly at birth, 7 developed microcephaly postnatally, and 3 didn’t have microcephaly at all. Those with microcephaly at birth showed the traditional neuroimaging findings of congenital Zika syndrome, including reduced brain volume, ventriculomegaly, subcortical calcifications, corpus callosum abnormalities, and an enlarged extra-axial space.
Those who subsequently developed microcephaly later in infancy showed most of the same neuroimaging abnormalities. The three infants who remained normocephalic displayed calcifications in the cortico-subcortical junction, asymmetric frontal polymicrogyria, delayed myelination, and milder ventriculomegaly than in the other two groups (AJNR Am J Neuroradiol. 2017 Jul;38[7]:1427-34).
The rehabilitation center where Dr. van der Linden and her colleagues are currently following roughly 200 children with congenital Zika syndrome is in the state of Pernambuco, which was particularly hard hit by the Zika epidemic.
She reported having no relevant financial disclosures.
EXPERT ANALYSIS FROM TERATOLOGY SOCIETY 2017
FDA approves new treatment for adults with HCV
The Food and Drug Administration announced on July 18 the approval of Vosevi to treat adults with chronic hepatitis C virus (HCV) genotypes 1-6 without cirrhosis or with mild cirrhosis.
Vosevi is now the first treatment for patients who have been previously treated with the direct-acting antiviral drug sofosbuvir or other drugs for HCV that inhibit a protein called NS5A. The new drug is a fixed-dose, combination tablet containing sofosbuvir and velpatasvir (both approved before) and a new drug – voxilaprevir.
It is noted that treatment recommendations for Vosevi are different depending on viral genotype and prior treatment history. Vosevi is contraindicated in patients taking the drug rifampin.
“Direct-acting antiviral drugs prevent the virus from multiplying and often cure HCV. Vosevi provides a treatment option for some patients who were not successfully treated with other HCV drugs in the past,” Edward Cox, MD, director of the Office of Antimicrobial Products in the FDA’s Center for Drug Evaluation and Research, said in a press release.
Read the full press release on the FDA’s website.
The Food and Drug Administration announced on July 18 the approval of Vosevi to treat adults with chronic hepatitis C virus (HCV) genotypes 1-6 without cirrhosis or with mild cirrhosis.
Vosevi is now the first treatment for patients who have been previously treated with the direct-acting antiviral drug sofosbuvir or other drugs for HCV that inhibit a protein called NS5A. The new drug is a fixed-dose, combination tablet containing sofosbuvir and velpatasvir (both approved before) and a new drug – voxilaprevir.
It is noted that treatment recommendations for Vosevi are different depending on viral genotype and prior treatment history. Vosevi is contraindicated in patients taking the drug rifampin.
“Direct-acting antiviral drugs prevent the virus from multiplying and often cure HCV. Vosevi provides a treatment option for some patients who were not successfully treated with other HCV drugs in the past,” Edward Cox, MD, director of the Office of Antimicrobial Products in the FDA’s Center for Drug Evaluation and Research, said in a press release.
Read the full press release on the FDA’s website.
The Food and Drug Administration announced on July 18 the approval of Vosevi to treat adults with chronic hepatitis C virus (HCV) genotypes 1-6 without cirrhosis or with mild cirrhosis.
Vosevi is now the first treatment for patients who have been previously treated with the direct-acting antiviral drug sofosbuvir or other drugs for HCV that inhibit a protein called NS5A. The new drug is a fixed-dose, combination tablet containing sofosbuvir and velpatasvir (both approved before) and a new drug – voxilaprevir.
It is noted that treatment recommendations for Vosevi are different depending on viral genotype and prior treatment history. Vosevi is contraindicated in patients taking the drug rifampin.
“Direct-acting antiviral drugs prevent the virus from multiplying and often cure HCV. Vosevi provides a treatment option for some patients who were not successfully treated with other HCV drugs in the past,” Edward Cox, MD, director of the Office of Antimicrobial Products in the FDA’s Center for Drug Evaluation and Research, said in a press release.
Read the full press release on the FDA’s website.
Biceps Tenodesis: An Evolution of Treatment
Take-Home Points
- The LHB tendon has been shown to be a significant pain generator in the shoulder.
- At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
- The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
- Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
- Biceps tenodesis has become a more common procedure to treat shoulder pathology.
Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9
Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.
Methods
Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.
The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).
For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)
Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.
Results
Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).
Discussion
Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.
Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15
Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.
One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.
Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.
3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.
4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.
5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.
6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.
7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.
8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.
9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.
10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.
12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.
13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.
16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.
17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.
18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.
21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.
23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.
24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.
Take-Home Points
- The LHB tendon has been shown to be a significant pain generator in the shoulder.
- At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
- The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
- Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
- Biceps tenodesis has become a more common procedure to treat shoulder pathology.
Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9
Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.
Methods
Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.
The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).
For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)
Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.
Results
Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).
Discussion
Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.
Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15
Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.
One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.
Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- The LHB tendon has been shown to be a significant pain generator in the shoulder.
- At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
- The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
- Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
- Biceps tenodesis has become a more common procedure to treat shoulder pathology.
Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9
Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.
Methods
Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.
The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).
For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)
Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.
Results
Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).
Discussion
Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.
Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15
Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.
One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.
Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.
3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.
4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.
5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.
6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.
7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.
8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.
9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.
10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.
12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.
13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.
16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.
17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.
18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.
21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.
23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.
24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.
1. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length–tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.
3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.
4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.
5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.
6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.
7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.
8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.
9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.
10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.
12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.
13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.
16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.
17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.
18. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.
20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.
21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.
23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.
24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.
No survival benefit with adjuvant girentuximab in high-risk RCC
The monoclonal antibody girentuximab does not appear to have a clinical benefit in patients with high-risk clear cell renal cell carcinoma (ccRCC).
Adjuvant therapy with girentuximab failed to improve either disease-free or overall survival, compared with placebo, in a cohort of patients who had undergone full surgical resection, according to phase 3 results of the ARISER trial.
In a subset of patients with CAIX scores of 200 or greater, however, there was disease-free survival benefit although it did not reach significance, reported lead author Karim Chamie, MD, of the David Geffen School of Medicine at UCLA, and his colleagues (JAMA Oncol. 2017;3[7]:913-20).
The drug was well tolerated, with an excellent safety profile, and there were no reported drug-related serious adverse events.
“Our finding that girentuximab was more effective in the subgroup of patients younger than 65 years is consistent with these observations and, while requiring prospective confirmation, suggests that an insufficient activation of [antibody-dependent cellular cytotoxicity] could explain the failure of its efficacy,” wrote Dr. Chamie and his colleagues.
The authors also point out that “virtually all trials of adjuvant therapy in high-risk RCC have failed to show a treatment benefit,” and thus illustrates the difficulty in identifying successful adjuvant therapies.
“The success of future adjuvant trials will require use of inclusion criteria sufficiently broad to meet accrual goals while limiting inclusion to patients who are most likely to benefit from therapy,” they write.
Girentuximab is a chimeric monoclonal antibody that binds carbonic anhydrase IX, a cell surface glycoprotein that is ubiquitously expressed in ccRCC. Phase 2 studies showed the agent to be safe and active in this setting, and served as the basis for conducting the current phase 3 ARISER trial (Adjuvant Rencarex Immunotherapy Phase 3 Trial to Study Efficacy in Nonmetastatic RCC).
The randomized, double-blind, placebo-controlled trial was conducted at 142 academic medical centers in 15 countries in North and South America and Europe and included a cohort of 864 patients who had undergone partial or radical nephrectomy for ccRCC and fell into one of the following high-risk groups: pT3/pT4Nx/N0M0 or pTanyN+M0 or pT1b/pT2Nx/N0M0 with nuclear grade 3 or greater.
The cohort was randomly assigned to either a single loading dose of girentuximab, 50 mg (week 1), followed by weekly intravenous infusions of girentuximab, 20 mg (weeks 2-24), or placebo, stratified by risk group and region.
The overall disease-free survival was comparable for the two groups: at 5 years it was 53.9% and 51.6% for the girentuximab and placebo groups, respectively, while the median disease-free survival was 71.4 months (interquartile range, 3 months to not reached) for patients who received girentuximab and was not reached for those receiving placebo (P = .74).
Median overall survival was not reached for either of the two groups, and there was no difference in overall survival between arms (hazard ratio, 0.99; 95% confidence interval, 0.74-1.32).
Adverse events were reported in 185 patients (21.6%), and were comparable between groups, and serious events occurred in 72 patients (8.4%), and were also comparable between the two arms.
The study was funded by Wilex, AG. Dr. Chamie receives research support from and serves as a consultant for UroGen Pharma, receives grant support from Phase One Foundation and Stop Cancer, and is a consultant for Cold Genesys and a scientific advisory board member of Altor. Several coauthors reported relationships with industry.
The monoclonal antibody girentuximab does not appear to have a clinical benefit in patients with high-risk clear cell renal cell carcinoma (ccRCC).
Adjuvant therapy with girentuximab failed to improve either disease-free or overall survival, compared with placebo, in a cohort of patients who had undergone full surgical resection, according to phase 3 results of the ARISER trial.
In a subset of patients with CAIX scores of 200 or greater, however, there was disease-free survival benefit although it did not reach significance, reported lead author Karim Chamie, MD, of the David Geffen School of Medicine at UCLA, and his colleagues (JAMA Oncol. 2017;3[7]:913-20).
The drug was well tolerated, with an excellent safety profile, and there were no reported drug-related serious adverse events.
“Our finding that girentuximab was more effective in the subgroup of patients younger than 65 years is consistent with these observations and, while requiring prospective confirmation, suggests that an insufficient activation of [antibody-dependent cellular cytotoxicity] could explain the failure of its efficacy,” wrote Dr. Chamie and his colleagues.
The authors also point out that “virtually all trials of adjuvant therapy in high-risk RCC have failed to show a treatment benefit,” and thus illustrates the difficulty in identifying successful adjuvant therapies.
“The success of future adjuvant trials will require use of inclusion criteria sufficiently broad to meet accrual goals while limiting inclusion to patients who are most likely to benefit from therapy,” they write.
Girentuximab is a chimeric monoclonal antibody that binds carbonic anhydrase IX, a cell surface glycoprotein that is ubiquitously expressed in ccRCC. Phase 2 studies showed the agent to be safe and active in this setting, and served as the basis for conducting the current phase 3 ARISER trial (Adjuvant Rencarex Immunotherapy Phase 3 Trial to Study Efficacy in Nonmetastatic RCC).
The randomized, double-blind, placebo-controlled trial was conducted at 142 academic medical centers in 15 countries in North and South America and Europe and included a cohort of 864 patients who had undergone partial or radical nephrectomy for ccRCC and fell into one of the following high-risk groups: pT3/pT4Nx/N0M0 or pTanyN+M0 or pT1b/pT2Nx/N0M0 with nuclear grade 3 or greater.
The cohort was randomly assigned to either a single loading dose of girentuximab, 50 mg (week 1), followed by weekly intravenous infusions of girentuximab, 20 mg (weeks 2-24), or placebo, stratified by risk group and region.
The overall disease-free survival was comparable for the two groups: at 5 years it was 53.9% and 51.6% for the girentuximab and placebo groups, respectively, while the median disease-free survival was 71.4 months (interquartile range, 3 months to not reached) for patients who received girentuximab and was not reached for those receiving placebo (P = .74).
Median overall survival was not reached for either of the two groups, and there was no difference in overall survival between arms (hazard ratio, 0.99; 95% confidence interval, 0.74-1.32).
Adverse events were reported in 185 patients (21.6%), and were comparable between groups, and serious events occurred in 72 patients (8.4%), and were also comparable between the two arms.
The study was funded by Wilex, AG. Dr. Chamie receives research support from and serves as a consultant for UroGen Pharma, receives grant support from Phase One Foundation and Stop Cancer, and is a consultant for Cold Genesys and a scientific advisory board member of Altor. Several coauthors reported relationships with industry.
The monoclonal antibody girentuximab does not appear to have a clinical benefit in patients with high-risk clear cell renal cell carcinoma (ccRCC).
Adjuvant therapy with girentuximab failed to improve either disease-free or overall survival, compared with placebo, in a cohort of patients who had undergone full surgical resection, according to phase 3 results of the ARISER trial.
In a subset of patients with CAIX scores of 200 or greater, however, there was disease-free survival benefit although it did not reach significance, reported lead author Karim Chamie, MD, of the David Geffen School of Medicine at UCLA, and his colleagues (JAMA Oncol. 2017;3[7]:913-20).
The drug was well tolerated, with an excellent safety profile, and there were no reported drug-related serious adverse events.
“Our finding that girentuximab was more effective in the subgroup of patients younger than 65 years is consistent with these observations and, while requiring prospective confirmation, suggests that an insufficient activation of [antibody-dependent cellular cytotoxicity] could explain the failure of its efficacy,” wrote Dr. Chamie and his colleagues.
The authors also point out that “virtually all trials of adjuvant therapy in high-risk RCC have failed to show a treatment benefit,” and thus illustrates the difficulty in identifying successful adjuvant therapies.
“The success of future adjuvant trials will require use of inclusion criteria sufficiently broad to meet accrual goals while limiting inclusion to patients who are most likely to benefit from therapy,” they write.
Girentuximab is a chimeric monoclonal antibody that binds carbonic anhydrase IX, a cell surface glycoprotein that is ubiquitously expressed in ccRCC. Phase 2 studies showed the agent to be safe and active in this setting, and served as the basis for conducting the current phase 3 ARISER trial (Adjuvant Rencarex Immunotherapy Phase 3 Trial to Study Efficacy in Nonmetastatic RCC).
The randomized, double-blind, placebo-controlled trial was conducted at 142 academic medical centers in 15 countries in North and South America and Europe and included a cohort of 864 patients who had undergone partial or radical nephrectomy for ccRCC and fell into one of the following high-risk groups: pT3/pT4Nx/N0M0 or pTanyN+M0 or pT1b/pT2Nx/N0M0 with nuclear grade 3 or greater.
The cohort was randomly assigned to either a single loading dose of girentuximab, 50 mg (week 1), followed by weekly intravenous infusions of girentuximab, 20 mg (weeks 2-24), or placebo, stratified by risk group and region.
The overall disease-free survival was comparable for the two groups: at 5 years it was 53.9% and 51.6% for the girentuximab and placebo groups, respectively, while the median disease-free survival was 71.4 months (interquartile range, 3 months to not reached) for patients who received girentuximab and was not reached for those receiving placebo (P = .74).
Median overall survival was not reached for either of the two groups, and there was no difference in overall survival between arms (hazard ratio, 0.99; 95% confidence interval, 0.74-1.32).
Adverse events were reported in 185 patients (21.6%), and were comparable between groups, and serious events occurred in 72 patients (8.4%), and were also comparable between the two arms.
The study was funded by Wilex, AG. Dr. Chamie receives research support from and serves as a consultant for UroGen Pharma, receives grant support from Phase One Foundation and Stop Cancer, and is a consultant for Cold Genesys and a scientific advisory board member of Altor. Several coauthors reported relationships with industry.
FROM JAMA ONCOLOGY
Key clinical point: Adjuvant girentuximab did not confer a survival benefit in patients with high-risk clear cell renal cell carcinoma.
Major finding: Five-year disease-free survival was 53.9% and 51.6% for the girentuximab and placebo groups, respectively.
Data source: A phase 3 placebo controlled multicenter clinical trial that included 864 patients with high-risk clear cell renal cell carcinoma.
Disclosures: The study was funded by Wilex, AG. Dr. Chamie receives research support from and serves as a consultant for UroGen Pharma, receives grant support from Phase One Foundation and Stop Cancer, and is a consultant for Cold Genesys and a scientific advisory board member of Altor. Several coauthors reported relationships with industry.
New tool predicts antimicrobial resistance in sepsis
Use of a clinical decision tree predicted antibiotic resistance in sepsis patients infected with gram-negative bacteria, based on data from 1,618 patients.
Increasing rates of bacterial resistance have “contributed to the unwarranted empiric administration of broad-spectrum antibiotics, further promoting resistance emergence across microbial species,” said M. Cristina Vazquez Guillamet, MD, of the University of New Mexico, Albuquerque, and her colleagues (Clin Infect Dis. cix612. 2017 Jul 10. doi: 10.1093/cid/cix612).
The researchers identified adults with sepsis or septic shock caused by bloodstream infections who were treated at a single center between 2008 and 2015. They developed clinical decision trees using the CHAID algorithm (Chi squared Automatic Interaction Detection) to analyze risk factors for resistance associated with three antibiotics: piperacillin-tazobactam (PT), cefepime (CE), and meropenem (ME).
Overall, resistance rates to PT, CE, and ME were 29%, 22%, and 9%, respectively, and 6.6% of the isolates were resistant to all three antibiotics.
Factors associated with increased resistance risk included residence in a nursing home, transfer from an outside hospital, and prior antibiotics use. Resistance to ME was associated with infection with Pseudomonas or Acinetobacter spp, the researchers noted, and resistance to PT was associated with central nervous system and central venous catheter infections.
Clinical decision trees were able to separate patients at low risk for resistance to PT and CE, as well as those with a risk greater than 30% of resistance to PT, CE, or ME. “We also found good overall agreement between the accuracies of the [multivariable logistic regression] models and the decision tree analyses for predicting antibiotic resistance,” the researchers said.
The findings were limited by several factors, including the use of data from a single center and incomplete reporting of previous antibiotic exposure, the researchers noted. However, the results “provide a framework for how empiric antibiotics can be tailored according to decision tree patient clusters,” they said.
Combining user-friendly clinical decision trees and multivariable logistic regression models may offer the best opportunities for hospitals to derive local models to help with antimicrobial prescription.
The researchers had no financial conflicts to disclose.
Use of a clinical decision tree predicted antibiotic resistance in sepsis patients infected with gram-negative bacteria, based on data from 1,618 patients.
Increasing rates of bacterial resistance have “contributed to the unwarranted empiric administration of broad-spectrum antibiotics, further promoting resistance emergence across microbial species,” said M. Cristina Vazquez Guillamet, MD, of the University of New Mexico, Albuquerque, and her colleagues (Clin Infect Dis. cix612. 2017 Jul 10. doi: 10.1093/cid/cix612).
The researchers identified adults with sepsis or septic shock caused by bloodstream infections who were treated at a single center between 2008 and 2015. They developed clinical decision trees using the CHAID algorithm (Chi squared Automatic Interaction Detection) to analyze risk factors for resistance associated with three antibiotics: piperacillin-tazobactam (PT), cefepime (CE), and meropenem (ME).
Overall, resistance rates to PT, CE, and ME were 29%, 22%, and 9%, respectively, and 6.6% of the isolates were resistant to all three antibiotics.
Factors associated with increased resistance risk included residence in a nursing home, transfer from an outside hospital, and prior antibiotics use. Resistance to ME was associated with infection with Pseudomonas or Acinetobacter spp, the researchers noted, and resistance to PT was associated with central nervous system and central venous catheter infections.
Clinical decision trees were able to separate patients at low risk for resistance to PT and CE, as well as those with a risk greater than 30% of resistance to PT, CE, or ME. “We also found good overall agreement between the accuracies of the [multivariable logistic regression] models and the decision tree analyses for predicting antibiotic resistance,” the researchers said.
The findings were limited by several factors, including the use of data from a single center and incomplete reporting of previous antibiotic exposure, the researchers noted. However, the results “provide a framework for how empiric antibiotics can be tailored according to decision tree patient clusters,” they said.
Combining user-friendly clinical decision trees and multivariable logistic regression models may offer the best opportunities for hospitals to derive local models to help with antimicrobial prescription.
The researchers had no financial conflicts to disclose.
Use of a clinical decision tree predicted antibiotic resistance in sepsis patients infected with gram-negative bacteria, based on data from 1,618 patients.
Increasing rates of bacterial resistance have “contributed to the unwarranted empiric administration of broad-spectrum antibiotics, further promoting resistance emergence across microbial species,” said M. Cristina Vazquez Guillamet, MD, of the University of New Mexico, Albuquerque, and her colleagues (Clin Infect Dis. cix612. 2017 Jul 10. doi: 10.1093/cid/cix612).
The researchers identified adults with sepsis or septic shock caused by bloodstream infections who were treated at a single center between 2008 and 2015. They developed clinical decision trees using the CHAID algorithm (Chi squared Automatic Interaction Detection) to analyze risk factors for resistance associated with three antibiotics: piperacillin-tazobactam (PT), cefepime (CE), and meropenem (ME).
Overall, resistance rates to PT, CE, and ME were 29%, 22%, and 9%, respectively, and 6.6% of the isolates were resistant to all three antibiotics.
Factors associated with increased resistance risk included residence in a nursing home, transfer from an outside hospital, and prior antibiotics use. Resistance to ME was associated with infection with Pseudomonas or Acinetobacter spp, the researchers noted, and resistance to PT was associated with central nervous system and central venous catheter infections.
Clinical decision trees were able to separate patients at low risk for resistance to PT and CE, as well as those with a risk greater than 30% of resistance to PT, CE, or ME. “We also found good overall agreement between the accuracies of the [multivariable logistic regression] models and the decision tree analyses for predicting antibiotic resistance,” the researchers said.
The findings were limited by several factors, including the use of data from a single center and incomplete reporting of previous antibiotic exposure, the researchers noted. However, the results “provide a framework for how empiric antibiotics can be tailored according to decision tree patient clusters,” they said.
Combining user-friendly clinical decision trees and multivariable logistic regression models may offer the best opportunities for hospitals to derive local models to help with antimicrobial prescription.
The researchers had no financial conflicts to disclose.
FROM CLINICAL INFECTIOUS DISEASES
Key clinical point:
Major finding: The model found prevalence rates for resistance to piperacillin-tazobactam, cefepime, and meropenem of 28.6%, 21.8%, and 8.5%, respectively.
Data source: A review of 1,618 adults with sepsis.
Disclosures: The researchers had no financial conflicts to disclose.