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Prophylactic rudeness, surgical barbecue, and MRI-ectomy
Stay rude, stay alive
Middle fingers up! Did you know there’s a biological theory that proposes rudeness as a mechanism for health?
The theory proposes that the single most important factor of determining human behavior is disease. Where disease flourishes, humans are meaner to strangers. This is a self-preservation tactic – strangers could carry sickness, so it’s best to steer clear. As people continue to avoid strangers (and potential new diseases), larger divides develop between language and culture.
Researchers looked at countries and cultures around the world and found that their theory held true: Locations that had less disease tended to have less diversity in language and culture, while higher disease rates coincided with more cultural diversity.
Can disease really be the sole factor for all human behavior, however? Tough to say, but in the meantime we’ll endorse never talking to strangers – just in case.
Facebook fires
If you’re a health care provider, you’ve probably had a difficult patient experience or two … or 7,000. In the olden days before the Internet, perhaps you turned to a trusted friend to vent your frustrations. Maybe you were an avid journaler, furiously sharing your problems with the page. With the advent of social media, however, you can publicly exorcise your doctor demons for your whole network to share!
In case you weren’t sure, this is a terrible idea – and now there are the data to prove it.
Participants in a recent study rated (fake) Facebook profiles of medical professionals who posted comments about their workday. Some comments were ambiguous, such as, “Started with new electronic patient charts today ... interesting experience for sure.” Other comments were blatantly frustrated, saying things like “What is it with some people?? I know I only went through 9 years of university ... but really, I know what I’m talking about ... yeesh!!!”
Unsurprisingly, the Facebook profiles with the obviously frustrated comments were rated “significantly less credible” than profiles with ambiguous comments, and they negatively affected willingness to become a patient of the fake doctor.
All this to say, when you get the urge to angrily post on Facebook about that overprotective parent in your office, perhaps turn to your diary instead.
Saying goodbye to a 12,000-lb friend
Lots of physicians have ordered MRI scans for their patients, but how many have performed an MRI-ectomy?
What? No, no, NO! We’re not talking about removing one from a patient! How would that even work? You do know that the patient goes inside the machine, right?
Okay, let’s try again.
How do you remove an MRI machine from a medical center? Verrrry carefully … with a forklift … after you’ve cut a big hole in the side of the building. That’s what they did at OSF HealthCare’s Center for Health – Glen Park in Peoria, Ill., on June 10. They had a party first, though, and someone brought one of those giant cookies, which said, “We will miss you, Open MRI,” the Pekin Daily Times reported.
Photos were taken, cookie was eaten, and tears were shed. “It’s definitely kind of bittersweet that it’s going away,” said Jamie White, manager of CT and MRI outpatient diagnostics.
On the day of the actual removal, a small crowd gathered outside to watch the experts who were brought in to extract the 6-ton machine. “I just took it off life support,” said Eddie Rivera, an engineer with ATI-Advanced Technologies, Miami, when he disconnected the electricity.
We’re tearing up a bit ourselves, actually, but there is some good news. The machine is not headed to that big imaging center in the sky just yet. Like the saying goes: Old MRIs never die, they just get hauled off to Arizona for refurbishment.
A bad case of heartburn
You would think that your day couldn’t get much worse than having to undergo emergency surgery. That’s a pretty rough time, no matter what. But for a 60-year-old man receiving a repair of an ascending aortic dissection, his doctors managed to add insult to a very serious injury: They lit a fire inside their patient.
According to a case study presented at the 2019 Euroanaesthesia Congress in Vienna, it all started with the patient’s history of chronic obstructive pulmonary disease. Bullae in the lungs caused by the disease were stuck to the sternum, and during an attempt to separate the lung from the sternum, a bulla was punctured, causing an air leak. To compensate, the surgeons boosted the proportion of oxygen to 100%.
In retrospect, what happened next almost seems predictable. A spark from the electrocautery device ignited a dry surgical pack, and with the assist of that extra oxygen, the doctors immediately had a fire on their hands, localized within their patient’s chest cavity. We believe this is what the medical community calls a “complication.”
To the surgeons’ credit, the fire was extinguished immediately, and after they presumably took a break to change into clean underwear, the rest of the operation went without incident. Though we imagine the patient was a bit confused when he woke up to the smell of barbecue.
Stay rude, stay alive
Middle fingers up! Did you know there’s a biological theory that proposes rudeness as a mechanism for health?
The theory proposes that the single most important factor of determining human behavior is disease. Where disease flourishes, humans are meaner to strangers. This is a self-preservation tactic – strangers could carry sickness, so it’s best to steer clear. As people continue to avoid strangers (and potential new diseases), larger divides develop between language and culture.
Researchers looked at countries and cultures around the world and found that their theory held true: Locations that had less disease tended to have less diversity in language and culture, while higher disease rates coincided with more cultural diversity.
Can disease really be the sole factor for all human behavior, however? Tough to say, but in the meantime we’ll endorse never talking to strangers – just in case.
Facebook fires
If you’re a health care provider, you’ve probably had a difficult patient experience or two … or 7,000. In the olden days before the Internet, perhaps you turned to a trusted friend to vent your frustrations. Maybe you were an avid journaler, furiously sharing your problems with the page. With the advent of social media, however, you can publicly exorcise your doctor demons for your whole network to share!
In case you weren’t sure, this is a terrible idea – and now there are the data to prove it.
Participants in a recent study rated (fake) Facebook profiles of medical professionals who posted comments about their workday. Some comments were ambiguous, such as, “Started with new electronic patient charts today ... interesting experience for sure.” Other comments were blatantly frustrated, saying things like “What is it with some people?? I know I only went through 9 years of university ... but really, I know what I’m talking about ... yeesh!!!”
Unsurprisingly, the Facebook profiles with the obviously frustrated comments were rated “significantly less credible” than profiles with ambiguous comments, and they negatively affected willingness to become a patient of the fake doctor.
All this to say, when you get the urge to angrily post on Facebook about that overprotective parent in your office, perhaps turn to your diary instead.
Saying goodbye to a 12,000-lb friend
Lots of physicians have ordered MRI scans for their patients, but how many have performed an MRI-ectomy?
What? No, no, NO! We’re not talking about removing one from a patient! How would that even work? You do know that the patient goes inside the machine, right?
Okay, let’s try again.
How do you remove an MRI machine from a medical center? Verrrry carefully … with a forklift … after you’ve cut a big hole in the side of the building. That’s what they did at OSF HealthCare’s Center for Health – Glen Park in Peoria, Ill., on June 10. They had a party first, though, and someone brought one of those giant cookies, which said, “We will miss you, Open MRI,” the Pekin Daily Times reported.
Photos were taken, cookie was eaten, and tears were shed. “It’s definitely kind of bittersweet that it’s going away,” said Jamie White, manager of CT and MRI outpatient diagnostics.
On the day of the actual removal, a small crowd gathered outside to watch the experts who were brought in to extract the 6-ton machine. “I just took it off life support,” said Eddie Rivera, an engineer with ATI-Advanced Technologies, Miami, when he disconnected the electricity.
We’re tearing up a bit ourselves, actually, but there is some good news. The machine is not headed to that big imaging center in the sky just yet. Like the saying goes: Old MRIs never die, they just get hauled off to Arizona for refurbishment.
A bad case of heartburn
You would think that your day couldn’t get much worse than having to undergo emergency surgery. That’s a pretty rough time, no matter what. But for a 60-year-old man receiving a repair of an ascending aortic dissection, his doctors managed to add insult to a very serious injury: They lit a fire inside their patient.
According to a case study presented at the 2019 Euroanaesthesia Congress in Vienna, it all started with the patient’s history of chronic obstructive pulmonary disease. Bullae in the lungs caused by the disease were stuck to the sternum, and during an attempt to separate the lung from the sternum, a bulla was punctured, causing an air leak. To compensate, the surgeons boosted the proportion of oxygen to 100%.
In retrospect, what happened next almost seems predictable. A spark from the electrocautery device ignited a dry surgical pack, and with the assist of that extra oxygen, the doctors immediately had a fire on their hands, localized within their patient’s chest cavity. We believe this is what the medical community calls a “complication.”
To the surgeons’ credit, the fire was extinguished immediately, and after they presumably took a break to change into clean underwear, the rest of the operation went without incident. Though we imagine the patient was a bit confused when he woke up to the smell of barbecue.
Stay rude, stay alive
Middle fingers up! Did you know there’s a biological theory that proposes rudeness as a mechanism for health?
The theory proposes that the single most important factor of determining human behavior is disease. Where disease flourishes, humans are meaner to strangers. This is a self-preservation tactic – strangers could carry sickness, so it’s best to steer clear. As people continue to avoid strangers (and potential new diseases), larger divides develop between language and culture.
Researchers looked at countries and cultures around the world and found that their theory held true: Locations that had less disease tended to have less diversity in language and culture, while higher disease rates coincided with more cultural diversity.
Can disease really be the sole factor for all human behavior, however? Tough to say, but in the meantime we’ll endorse never talking to strangers – just in case.
Facebook fires
If you’re a health care provider, you’ve probably had a difficult patient experience or two … or 7,000. In the olden days before the Internet, perhaps you turned to a trusted friend to vent your frustrations. Maybe you were an avid journaler, furiously sharing your problems with the page. With the advent of social media, however, you can publicly exorcise your doctor demons for your whole network to share!
In case you weren’t sure, this is a terrible idea – and now there are the data to prove it.
Participants in a recent study rated (fake) Facebook profiles of medical professionals who posted comments about their workday. Some comments were ambiguous, such as, “Started with new electronic patient charts today ... interesting experience for sure.” Other comments were blatantly frustrated, saying things like “What is it with some people?? I know I only went through 9 years of university ... but really, I know what I’m talking about ... yeesh!!!”
Unsurprisingly, the Facebook profiles with the obviously frustrated comments were rated “significantly less credible” than profiles with ambiguous comments, and they negatively affected willingness to become a patient of the fake doctor.
All this to say, when you get the urge to angrily post on Facebook about that overprotective parent in your office, perhaps turn to your diary instead.
Saying goodbye to a 12,000-lb friend
Lots of physicians have ordered MRI scans for their patients, but how many have performed an MRI-ectomy?
What? No, no, NO! We’re not talking about removing one from a patient! How would that even work? You do know that the patient goes inside the machine, right?
Okay, let’s try again.
How do you remove an MRI machine from a medical center? Verrrry carefully … with a forklift … after you’ve cut a big hole in the side of the building. That’s what they did at OSF HealthCare’s Center for Health – Glen Park in Peoria, Ill., on June 10. They had a party first, though, and someone brought one of those giant cookies, which said, “We will miss you, Open MRI,” the Pekin Daily Times reported.
Photos were taken, cookie was eaten, and tears were shed. “It’s definitely kind of bittersweet that it’s going away,” said Jamie White, manager of CT and MRI outpatient diagnostics.
On the day of the actual removal, a small crowd gathered outside to watch the experts who were brought in to extract the 6-ton machine. “I just took it off life support,” said Eddie Rivera, an engineer with ATI-Advanced Technologies, Miami, when he disconnected the electricity.
We’re tearing up a bit ourselves, actually, but there is some good news. The machine is not headed to that big imaging center in the sky just yet. Like the saying goes: Old MRIs never die, they just get hauled off to Arizona for refurbishment.
A bad case of heartburn
You would think that your day couldn’t get much worse than having to undergo emergency surgery. That’s a pretty rough time, no matter what. But for a 60-year-old man receiving a repair of an ascending aortic dissection, his doctors managed to add insult to a very serious injury: They lit a fire inside their patient.
According to a case study presented at the 2019 Euroanaesthesia Congress in Vienna, it all started with the patient’s history of chronic obstructive pulmonary disease. Bullae in the lungs caused by the disease were stuck to the sternum, and during an attempt to separate the lung from the sternum, a bulla was punctured, causing an air leak. To compensate, the surgeons boosted the proportion of oxygen to 100%.
In retrospect, what happened next almost seems predictable. A spark from the electrocautery device ignited a dry surgical pack, and with the assist of that extra oxygen, the doctors immediately had a fire on their hands, localized within their patient’s chest cavity. We believe this is what the medical community calls a “complication.”
To the surgeons’ credit, the fire was extinguished immediately, and after they presumably took a break to change into clean underwear, the rest of the operation went without incident. Though we imagine the patient was a bit confused when he woke up to the smell of barbecue.
Novel chip system could improve preclinical drug studies
A novel multiorgan body-on-a-chip system shows promise to improve the preclinical evaluation of various anticancer therapies, investigators report.
“Initially, organ-on-a-chip systems were designed for specific applications with limited ability for reconfiguration and typically with cells from a single organ,” wrote Christopher W. McAleer, PhD, of Hesperos Inc., Orlando, and colleagues. Their report is in Science Translational Medicine.
“To address these issues, a reconfigurable body-on-a-chip system was developed with the capacity to house multiple organ-like tissue constructs,” the authors explained.
The researchers used two different system configurations to evaluate the off-target organ toxicities, metabolism, and efficacy of diclofenac and imatinib (system 1), in addition to tamoxifen (system 2). Both therapies were combined with verapamil in the study.
In system 1, cancer-derived bone marrow cells were cultured with primary hepatocytes, and were analyzed for anti-leukemic activity. In this configuration, both imatinib and diclofenac showed cytostatic activity on cancer progression in the bone marrow cells.
“Liver viability was not affected by imatinib; however, diclofenac reduced liver viability by 30%,” the researchers wrote.
System 2 included a wide variety of cell-lines, including primary hepatocytes, induced pluripotent stem cell-derived cardiomyocytes, a multidrug-resistant vulva cancer line, and a non-multidrug-resistant breast cancer line.
In this configuration, tamoxifen monotherapy and tamoxifen coadministered with verapamil resulted in off-target cardiac toxicities, but did not alter cell viability.
“These systems demonstrate the utility of a human cell–based in vitro culture system to evaluate both on-target efficacy and off-target toxicity for parent drugs and their metabolites,” Dr. McAleer and colleagues wrote.
The researchers acknowledged that the dosing parameters used in the model were acute. As a result, chronic, low-dose treatment strategies may reflect clinical conditions more accurately.
“These systems can augment and reduce the use of animals and increase the efficiency of drug evaluations in preclinical studies,” they concluded.
The study was supported by Hesperos Internal Development funds, the NIH, and Roche. The authors reported financial affiliations with Hesperos and Roche.
SOURCE: McAleer CW et al. Sci Transl Med. 2019 Jun 19. doi: 10.1126/scitranslmed.aav1386.
A novel multiorgan body-on-a-chip system shows promise to improve the preclinical evaluation of various anticancer therapies, investigators report.
“Initially, organ-on-a-chip systems were designed for specific applications with limited ability for reconfiguration and typically with cells from a single organ,” wrote Christopher W. McAleer, PhD, of Hesperos Inc., Orlando, and colleagues. Their report is in Science Translational Medicine.
“To address these issues, a reconfigurable body-on-a-chip system was developed with the capacity to house multiple organ-like tissue constructs,” the authors explained.
The researchers used two different system configurations to evaluate the off-target organ toxicities, metabolism, and efficacy of diclofenac and imatinib (system 1), in addition to tamoxifen (system 2). Both therapies were combined with verapamil in the study.
In system 1, cancer-derived bone marrow cells were cultured with primary hepatocytes, and were analyzed for anti-leukemic activity. In this configuration, both imatinib and diclofenac showed cytostatic activity on cancer progression in the bone marrow cells.
“Liver viability was not affected by imatinib; however, diclofenac reduced liver viability by 30%,” the researchers wrote.
System 2 included a wide variety of cell-lines, including primary hepatocytes, induced pluripotent stem cell-derived cardiomyocytes, a multidrug-resistant vulva cancer line, and a non-multidrug-resistant breast cancer line.
In this configuration, tamoxifen monotherapy and tamoxifen coadministered with verapamil resulted in off-target cardiac toxicities, but did not alter cell viability.
“These systems demonstrate the utility of a human cell–based in vitro culture system to evaluate both on-target efficacy and off-target toxicity for parent drugs and their metabolites,” Dr. McAleer and colleagues wrote.
The researchers acknowledged that the dosing parameters used in the model were acute. As a result, chronic, low-dose treatment strategies may reflect clinical conditions more accurately.
“These systems can augment and reduce the use of animals and increase the efficiency of drug evaluations in preclinical studies,” they concluded.
The study was supported by Hesperos Internal Development funds, the NIH, and Roche. The authors reported financial affiliations with Hesperos and Roche.
SOURCE: McAleer CW et al. Sci Transl Med. 2019 Jun 19. doi: 10.1126/scitranslmed.aav1386.
A novel multiorgan body-on-a-chip system shows promise to improve the preclinical evaluation of various anticancer therapies, investigators report.
“Initially, organ-on-a-chip systems were designed for specific applications with limited ability for reconfiguration and typically with cells from a single organ,” wrote Christopher W. McAleer, PhD, of Hesperos Inc., Orlando, and colleagues. Their report is in Science Translational Medicine.
“To address these issues, a reconfigurable body-on-a-chip system was developed with the capacity to house multiple organ-like tissue constructs,” the authors explained.
The researchers used two different system configurations to evaluate the off-target organ toxicities, metabolism, and efficacy of diclofenac and imatinib (system 1), in addition to tamoxifen (system 2). Both therapies were combined with verapamil in the study.
In system 1, cancer-derived bone marrow cells were cultured with primary hepatocytes, and were analyzed for anti-leukemic activity. In this configuration, both imatinib and diclofenac showed cytostatic activity on cancer progression in the bone marrow cells.
“Liver viability was not affected by imatinib; however, diclofenac reduced liver viability by 30%,” the researchers wrote.
System 2 included a wide variety of cell-lines, including primary hepatocytes, induced pluripotent stem cell-derived cardiomyocytes, a multidrug-resistant vulva cancer line, and a non-multidrug-resistant breast cancer line.
In this configuration, tamoxifen monotherapy and tamoxifen coadministered with verapamil resulted in off-target cardiac toxicities, but did not alter cell viability.
“These systems demonstrate the utility of a human cell–based in vitro culture system to evaluate both on-target efficacy and off-target toxicity for parent drugs and their metabolites,” Dr. McAleer and colleagues wrote.
The researchers acknowledged that the dosing parameters used in the model were acute. As a result, chronic, low-dose treatment strategies may reflect clinical conditions more accurately.
“These systems can augment and reduce the use of animals and increase the efficiency of drug evaluations in preclinical studies,” they concluded.
The study was supported by Hesperos Internal Development funds, the NIH, and Roche. The authors reported financial affiliations with Hesperos and Roche.
SOURCE: McAleer CW et al. Sci Transl Med. 2019 Jun 19. doi: 10.1126/scitranslmed.aav1386.
FROM SCIENCE TRANSLATIONAL MEDICINE
Key clinical point: A novel multiorgan body-on-a-chip system shows promise to improve the preclinical evaluation of anticancer therapies.
Major finding: Overall, results support the utility of the system to assess both off-target toxicity and on-target efficacy for various anticancer drugs.
Study details: A study exploring the utility of a multi-organ-on-a-chip system to assess safety and effectiveness of anticancer therapies in the preclinical setting.
Disclosures: The study was supported by Hesperos Internal Development funds, the NIH, and Roche. The authors reported financial affiliations with Hesperos and Roche.
Source: McAleer CW et al. Sci Transl Med. 2019 Jun 19. doi: 10.1126/scitranslmed.aav1386.
Senators agree surprise medical bills must go. But how?
Two years, 16 hearings, and one massive bipartisan package of legislation later, a key Senate committee says it is ready to start marking up a bill the week of June 24 designed to contain health care costs. But it might not be easy since lawmakers and stakeholders at a final hearing June 18 showed they are still far apart on one simple aspect of the proposal.
That sticking point: a formula for paying for surprise medical bills, those unexpected and often high charges patients face when they get care from a doctor or hospital that isn’t in their insurance network.
“People get health insurance precisely so they won’t be surprised by health care bills,” said Sen. Maggie Hassan (D-N.H.), the coauthor of a separate proposal to tamp down surprise bills. “So it is completely unacceptable that people do everything that they’re supposed to do to ensure that their care is in their insurance network and then still end up with large, unexpected bills from an out-of-network provider.”
It’s a cause that has been taken up by President Donald Trump and various bipartisan groups of lawmakers on Capitol Hill.
The wide-ranging legislative package on curbing health care costs is sponsored by Sen. Lamar Alexander (R-Tenn.) and Sen. Patty Murray (D-Wash.), the chairman and ranking member, respectively, of the Health, Education, Labor and Pensions (HELP) Committee. Given the committee’s influence, and because this legislation has bipartisan support in the Senate where not many bills are moving, industry observers are taking the HELP panel’s proposal very seriously.
The Alexander/Murray bill lays out three options for paying surprise medical bills but does not specify which path the final legislation should take. Advocates for each of the choices were among the five witnesses June 18.
Their positions fell along familiar fault lines. Everyone acknowledged that patients who stumble into a surprise bill because their emergency care was handled at a facility not in their insurance network or because a doctor at their in-network hospital doesn’t take the patient’s plan should not have to pay more than they would for an inpatient service. But they differ on how much doctors, hospitals, and other providers should be compensated and how the disputes should be resolved.
Tom Nickels, an executive vice president of the American Hospital Association, cautioned against using benchmarks to set pay levels, such as local customary averages or a price set in relation to Medicare. He said such a plan might underpay providers and hospitals could lose their leverage to negotiate with insurers.
Elizabeth Mitchell, president and CEO of the Pacific Business Group on Health – a group that represents employers, including some who are self-insured who pay their workers’ health costs – said doctors should be paid 125% of what Medicare pays. She told senators that an independent arbitration process like the one Nickels advocates would add unnecessary costs to the system.
Benedic Ippolito, a researcher with the American Enterprise Institute, said requiring all providers in a hospital to be in-network was the cleanest solution.
“On surprise billing, all three approaches are equal in that first and foremost they protect the consumer,” said Sean Cavanaugh, chief administrative officer for Aledade, a company that matches primary care physicians with accountable care organizations.
There was also broad support among the witnesses for some of the legislation’s transparency measures, especially the creation of a nongovernmental nonprofit organization to collect claims data from private health plans, Medicare, and some states to create what’s called an all-payer claims database. That could help policymakers better understand the true cost of care, these experts told the committee.
Sen. Susan Collins (R-Maine) expressed trepidation about the all-payer claims database, noting that increased transparency could hurt rural hospitals, which typically charge higher prices than those in cities because their patient base is small and they need to bring in enough revenue to cover fixed costs.
The witnesses also offered support for eliminating “gag clauses” between doctors and health plans. These stipulations often prevent providers from telling patients the cost of a procedure or service.
“Patients and families absolutely have skin in the game ... but they are in a completely untenable and unfair situation. They have no information,” said Ms. Mitchell, from the Pacific Business Group on Health. “We’re talking about providers not being allowed to share information. ... Transparency is necessary so people can have active involvement.”
If one thing is clear, it’s that Sen. Alexander doesn’t want this summer to be a rehash of last year, when it appeared he had a bipartisan deal to address problems in the federal health law’s marketplaces before the effort fell apart.
“For the last decade, Congress had been locked in an argument about the individual health care market,” said Sen. Alexander at the hearing. “That is not this discussion. This is a different discussion. We’ll never lower the cost of health insurance until we lower the cost of health care.”
Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
Two years, 16 hearings, and one massive bipartisan package of legislation later, a key Senate committee says it is ready to start marking up a bill the week of June 24 designed to contain health care costs. But it might not be easy since lawmakers and stakeholders at a final hearing June 18 showed they are still far apart on one simple aspect of the proposal.
That sticking point: a formula for paying for surprise medical bills, those unexpected and often high charges patients face when they get care from a doctor or hospital that isn’t in their insurance network.
“People get health insurance precisely so they won’t be surprised by health care bills,” said Sen. Maggie Hassan (D-N.H.), the coauthor of a separate proposal to tamp down surprise bills. “So it is completely unacceptable that people do everything that they’re supposed to do to ensure that their care is in their insurance network and then still end up with large, unexpected bills from an out-of-network provider.”
It’s a cause that has been taken up by President Donald Trump and various bipartisan groups of lawmakers on Capitol Hill.
The wide-ranging legislative package on curbing health care costs is sponsored by Sen. Lamar Alexander (R-Tenn.) and Sen. Patty Murray (D-Wash.), the chairman and ranking member, respectively, of the Health, Education, Labor and Pensions (HELP) Committee. Given the committee’s influence, and because this legislation has bipartisan support in the Senate where not many bills are moving, industry observers are taking the HELP panel’s proposal very seriously.
The Alexander/Murray bill lays out three options for paying surprise medical bills but does not specify which path the final legislation should take. Advocates for each of the choices were among the five witnesses June 18.
Their positions fell along familiar fault lines. Everyone acknowledged that patients who stumble into a surprise bill because their emergency care was handled at a facility not in their insurance network or because a doctor at their in-network hospital doesn’t take the patient’s plan should not have to pay more than they would for an inpatient service. But they differ on how much doctors, hospitals, and other providers should be compensated and how the disputes should be resolved.
Tom Nickels, an executive vice president of the American Hospital Association, cautioned against using benchmarks to set pay levels, such as local customary averages or a price set in relation to Medicare. He said such a plan might underpay providers and hospitals could lose their leverage to negotiate with insurers.
Elizabeth Mitchell, president and CEO of the Pacific Business Group on Health – a group that represents employers, including some who are self-insured who pay their workers’ health costs – said doctors should be paid 125% of what Medicare pays. She told senators that an independent arbitration process like the one Nickels advocates would add unnecessary costs to the system.
Benedic Ippolito, a researcher with the American Enterprise Institute, said requiring all providers in a hospital to be in-network was the cleanest solution.
“On surprise billing, all three approaches are equal in that first and foremost they protect the consumer,” said Sean Cavanaugh, chief administrative officer for Aledade, a company that matches primary care physicians with accountable care organizations.
There was also broad support among the witnesses for some of the legislation’s transparency measures, especially the creation of a nongovernmental nonprofit organization to collect claims data from private health plans, Medicare, and some states to create what’s called an all-payer claims database. That could help policymakers better understand the true cost of care, these experts told the committee.
Sen. Susan Collins (R-Maine) expressed trepidation about the all-payer claims database, noting that increased transparency could hurt rural hospitals, which typically charge higher prices than those in cities because their patient base is small and they need to bring in enough revenue to cover fixed costs.
The witnesses also offered support for eliminating “gag clauses” between doctors and health plans. These stipulations often prevent providers from telling patients the cost of a procedure or service.
“Patients and families absolutely have skin in the game ... but they are in a completely untenable and unfair situation. They have no information,” said Ms. Mitchell, from the Pacific Business Group on Health. “We’re talking about providers not being allowed to share information. ... Transparency is necessary so people can have active involvement.”
If one thing is clear, it’s that Sen. Alexander doesn’t want this summer to be a rehash of last year, when it appeared he had a bipartisan deal to address problems in the federal health law’s marketplaces before the effort fell apart.
“For the last decade, Congress had been locked in an argument about the individual health care market,” said Sen. Alexander at the hearing. “That is not this discussion. This is a different discussion. We’ll never lower the cost of health insurance until we lower the cost of health care.”
Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
Two years, 16 hearings, and one massive bipartisan package of legislation later, a key Senate committee says it is ready to start marking up a bill the week of June 24 designed to contain health care costs. But it might not be easy since lawmakers and stakeholders at a final hearing June 18 showed they are still far apart on one simple aspect of the proposal.
That sticking point: a formula for paying for surprise medical bills, those unexpected and often high charges patients face when they get care from a doctor or hospital that isn’t in their insurance network.
“People get health insurance precisely so they won’t be surprised by health care bills,” said Sen. Maggie Hassan (D-N.H.), the coauthor of a separate proposal to tamp down surprise bills. “So it is completely unacceptable that people do everything that they’re supposed to do to ensure that their care is in their insurance network and then still end up with large, unexpected bills from an out-of-network provider.”
It’s a cause that has been taken up by President Donald Trump and various bipartisan groups of lawmakers on Capitol Hill.
The wide-ranging legislative package on curbing health care costs is sponsored by Sen. Lamar Alexander (R-Tenn.) and Sen. Patty Murray (D-Wash.), the chairman and ranking member, respectively, of the Health, Education, Labor and Pensions (HELP) Committee. Given the committee’s influence, and because this legislation has bipartisan support in the Senate where not many bills are moving, industry observers are taking the HELP panel’s proposal very seriously.
The Alexander/Murray bill lays out three options for paying surprise medical bills but does not specify which path the final legislation should take. Advocates for each of the choices were among the five witnesses June 18.
Their positions fell along familiar fault lines. Everyone acknowledged that patients who stumble into a surprise bill because their emergency care was handled at a facility not in their insurance network or because a doctor at their in-network hospital doesn’t take the patient’s plan should not have to pay more than they would for an inpatient service. But they differ on how much doctors, hospitals, and other providers should be compensated and how the disputes should be resolved.
Tom Nickels, an executive vice president of the American Hospital Association, cautioned against using benchmarks to set pay levels, such as local customary averages or a price set in relation to Medicare. He said such a plan might underpay providers and hospitals could lose their leverage to negotiate with insurers.
Elizabeth Mitchell, president and CEO of the Pacific Business Group on Health – a group that represents employers, including some who are self-insured who pay their workers’ health costs – said doctors should be paid 125% of what Medicare pays. She told senators that an independent arbitration process like the one Nickels advocates would add unnecessary costs to the system.
Benedic Ippolito, a researcher with the American Enterprise Institute, said requiring all providers in a hospital to be in-network was the cleanest solution.
“On surprise billing, all three approaches are equal in that first and foremost they protect the consumer,” said Sean Cavanaugh, chief administrative officer for Aledade, a company that matches primary care physicians with accountable care organizations.
There was also broad support among the witnesses for some of the legislation’s transparency measures, especially the creation of a nongovernmental nonprofit organization to collect claims data from private health plans, Medicare, and some states to create what’s called an all-payer claims database. That could help policymakers better understand the true cost of care, these experts told the committee.
Sen. Susan Collins (R-Maine) expressed trepidation about the all-payer claims database, noting that increased transparency could hurt rural hospitals, which typically charge higher prices than those in cities because their patient base is small and they need to bring in enough revenue to cover fixed costs.
The witnesses also offered support for eliminating “gag clauses” between doctors and health plans. These stipulations often prevent providers from telling patients the cost of a procedure or service.
“Patients and families absolutely have skin in the game ... but they are in a completely untenable and unfair situation. They have no information,” said Ms. Mitchell, from the Pacific Business Group on Health. “We’re talking about providers not being allowed to share information. ... Transparency is necessary so people can have active involvement.”
If one thing is clear, it’s that Sen. Alexander doesn’t want this summer to be a rehash of last year, when it appeared he had a bipartisan deal to address problems in the federal health law’s marketplaces before the effort fell apart.
“For the last decade, Congress had been locked in an argument about the individual health care market,” said Sen. Alexander at the hearing. “That is not this discussion. This is a different discussion. We’ll never lower the cost of health insurance until we lower the cost of health care.”
Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
Benefits of Medicare Shared Savings Program ACOs lacking
or improving quality, according to new research.
“Our conclusion that the MSSP was not associated with improvements in spending, quality, or most measures of hospital use differ from that of previous evaluations of Medicare ACOs,” Adam Markovitz, of the University of Michigan, Ann Arbor, and colleagues wrote in a new research report published in Annals of Internal Medicine.
“Our instrumental variable model addresses selection effects not directly captured in previous evaluations,” the researchers continued.
To illustrate the point, the researchers found an association between MSSP and spending when using an adjusted longitudinal model (change, –$118; 95% confidence interval, –$151 to –$85 per beneficiary per quarter), with savings coming from reductions in inpatient services, outpatient services, and skilled nursing facility charges.
However, when employing an instrumental variable model, there was not an association with changes in total spending (change, $5; 95%CI, –$51 to $62 per beneficiary per quarter.
“The instrumental variable estimate for spending differed significantly from the adjusted estimate,” Mr. Markovitz and colleagues noted. “Estimated savings were smaller in instrumental variable models than in adjusted models across each ACO cohort.”
Similar patterns were observed in quality observations.
“The MSSP was associated with improvements in all four clinical quality indicators in the adjusted longitudinal model but not in the instrumental variable model,” the authors wrote. “The MSSP was associated with modest decreases in all-cause hospitalizations and preventable hospitalizations in the longitudinal model but not in the instrumental variable model.”
Overall, the authors noted that the results “challenge the view that MSSP ACOs have lowered spending and improved quality; they indicate that savings by MSSP ACOs may be driven by nonrandom exit of high-cost clinicians and their patient panels from this voluntary program.”
Indeed, the report states that removing “high-cost clinicians from ACO contracts could have large effects on spending estimates and may contribute to reported findings that MSSP savings grow over time.”
Primary sources of funding for the research included the Horowitz Foundation for Social Policy, Agency for Healthcare Research and Quality, and the National Institute on Aging. No relevant disclosures were made by the authors.
SOURCE: Markovitz A et al. Ann Intern Med. 2019 Jun 18. doi: 10.7326/M18-2539.
or improving quality, according to new research.
“Our conclusion that the MSSP was not associated with improvements in spending, quality, or most measures of hospital use differ from that of previous evaluations of Medicare ACOs,” Adam Markovitz, of the University of Michigan, Ann Arbor, and colleagues wrote in a new research report published in Annals of Internal Medicine.
“Our instrumental variable model addresses selection effects not directly captured in previous evaluations,” the researchers continued.
To illustrate the point, the researchers found an association between MSSP and spending when using an adjusted longitudinal model (change, –$118; 95% confidence interval, –$151 to –$85 per beneficiary per quarter), with savings coming from reductions in inpatient services, outpatient services, and skilled nursing facility charges.
However, when employing an instrumental variable model, there was not an association with changes in total spending (change, $5; 95%CI, –$51 to $62 per beneficiary per quarter.
“The instrumental variable estimate for spending differed significantly from the adjusted estimate,” Mr. Markovitz and colleagues noted. “Estimated savings were smaller in instrumental variable models than in adjusted models across each ACO cohort.”
Similar patterns were observed in quality observations.
“The MSSP was associated with improvements in all four clinical quality indicators in the adjusted longitudinal model but not in the instrumental variable model,” the authors wrote. “The MSSP was associated with modest decreases in all-cause hospitalizations and preventable hospitalizations in the longitudinal model but not in the instrumental variable model.”
Overall, the authors noted that the results “challenge the view that MSSP ACOs have lowered spending and improved quality; they indicate that savings by MSSP ACOs may be driven by nonrandom exit of high-cost clinicians and their patient panels from this voluntary program.”
Indeed, the report states that removing “high-cost clinicians from ACO contracts could have large effects on spending estimates and may contribute to reported findings that MSSP savings grow over time.”
Primary sources of funding for the research included the Horowitz Foundation for Social Policy, Agency for Healthcare Research and Quality, and the National Institute on Aging. No relevant disclosures were made by the authors.
SOURCE: Markovitz A et al. Ann Intern Med. 2019 Jun 18. doi: 10.7326/M18-2539.
or improving quality, according to new research.
“Our conclusion that the MSSP was not associated with improvements in spending, quality, or most measures of hospital use differ from that of previous evaluations of Medicare ACOs,” Adam Markovitz, of the University of Michigan, Ann Arbor, and colleagues wrote in a new research report published in Annals of Internal Medicine.
“Our instrumental variable model addresses selection effects not directly captured in previous evaluations,” the researchers continued.
To illustrate the point, the researchers found an association between MSSP and spending when using an adjusted longitudinal model (change, –$118; 95% confidence interval, –$151 to –$85 per beneficiary per quarter), with savings coming from reductions in inpatient services, outpatient services, and skilled nursing facility charges.
However, when employing an instrumental variable model, there was not an association with changes in total spending (change, $5; 95%CI, –$51 to $62 per beneficiary per quarter.
“The instrumental variable estimate for spending differed significantly from the adjusted estimate,” Mr. Markovitz and colleagues noted. “Estimated savings were smaller in instrumental variable models than in adjusted models across each ACO cohort.”
Similar patterns were observed in quality observations.
“The MSSP was associated with improvements in all four clinical quality indicators in the adjusted longitudinal model but not in the instrumental variable model,” the authors wrote. “The MSSP was associated with modest decreases in all-cause hospitalizations and preventable hospitalizations in the longitudinal model but not in the instrumental variable model.”
Overall, the authors noted that the results “challenge the view that MSSP ACOs have lowered spending and improved quality; they indicate that savings by MSSP ACOs may be driven by nonrandom exit of high-cost clinicians and their patient panels from this voluntary program.”
Indeed, the report states that removing “high-cost clinicians from ACO contracts could have large effects on spending estimates and may contribute to reported findings that MSSP savings grow over time.”
Primary sources of funding for the research included the Horowitz Foundation for Social Policy, Agency for Healthcare Research and Quality, and the National Institute on Aging. No relevant disclosures were made by the authors.
SOURCE: Markovitz A et al. Ann Intern Med. 2019 Jun 18. doi: 10.7326/M18-2539.
FROM ANNALS OF INTERNAL MEDICINE
A healthy 8-year-old boy presents with several skin-colored, round 1-3 mm papules on the nose, forehead, and cheeks
A shave biopsy of one of the lesions was performed that showed a proliferation of nests of basaloid cells on the dermis with palisading and rare vacuolated clear cell change. A rare ductal structure with luminal proteinaceous contents was noted. The findings were consistent with a trichoepithelioma.
Trichoepitheliomas are rare, benign, adnexal skin tumors that can start in early childhood or during puberty. The lesions are most commonly seen in girls as skin color papules on the face, and sometimes on the trunk and the neck. Trichoepitheliomas can appear as a benign single lesion nonfamilial form or as a familial form with multiple lesions.1 Brooke-Spiegler syndrome (BSS) is a rare autosomal dominant condition where affected individuals have multiple trichoepitheliomas, cylindromas, and spiradenomas. Depending on the predominant type of lesion, phenotypic variants include multiple familial trichoepithelioma type 1 and familial cylindromatosis.2 BSS is caused by mutations within CYLD, a tumor-suppressor gene located on chromosome 16q12-q13.3 Our patient presented only with trichoepitheliomas with no other lesions on the scalp, neck, or torso.
Multiple trichoepitheliomas also can be seen in other syndromes including Rombo syndrome, which is characterized by basal cell carcinomas, milia, hypotrichosis, distal vasodilation, and atrophoderma vermiculata; none seen in our patient. Bazex-Dupré-Christol syndrome is an X-linked dominant condition in which affected individuals can present with multiple trichoepitheliomas, as well as milia, hypotrichosis, follicular atrophoderma, and basal cell carcinomas.
The differential diagnosis of skin color papules on the central face on a child should include acne, flat warts, and angiofibromas seen in tuberous sclerosis. Our patient’s lesions were monomorphous, and there were no comedones, pustules, or inflammatory papules characteristic of acne.
He had warts on his hands which could make it suspicious for the face lesions to be verrucous in nature. Flat warts also present as skin color papules, but characteristically are flat, not round and shiny as our patient’s lesions were. Angiofibromas, as seen in individuals with tuberous sclerosis, also can start at an early age in the same location as trichoepitheliomas in BSS, but clinically the lesions are pinker and redder rather than the skin-color, round shape papules characteristic of trichoepitheliomas. Patients may have other findings suggestive of tuberous sclerosis including confetti hypopigmentation, ash leaf spots, shagreen patch, and a history of seizures or developmental delay – none of which were present in our patient. Children with basal cell nevus syndrome can present with skin color to shiny telangiectatic papules (basal cell carcinomas) that can be single or multiple on the face, chest, and back. The lesions usually are not seen in clusters around the nose and central face as seen in patients with BSS. Patients with basal cell nevus syndrome can develop jaw bone cysts, brain tumors (medulloblastoma), and fibromas on the heart or ovaries, palmar pits and be macrocephalic.4
Trichoepitheliomas usually are treated surgically but other nonsurgical removing techniques include laser resurfacing, curettage, and electrocautery.5 Malignant transformation can occur in 5%-10% of the individuals and should be managed by a multidisciplinary team. Topical treatment with sirolimus previously has been reported to be effective in young patients.6
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email Dr. Matiz at pdnews@mdedge.com.
References
1. Acta Dermatovenerol Croat. 2018 Jun;26(2):162-5.
2. Eur J Med Genet. 2015;58(5):271-8.
3. Am J Dermatopathol. 2014;36(11):868-74.
4. Int J Dermatol. 2016 Apr;55(4):367-75.
5. Int J Dermatol. 2007;46(6):583-6.
6. Dermatol Ther. 2017 Mar. doi: 10.1111/dth.12458.
A shave biopsy of one of the lesions was performed that showed a proliferation of nests of basaloid cells on the dermis with palisading and rare vacuolated clear cell change. A rare ductal structure with luminal proteinaceous contents was noted. The findings were consistent with a trichoepithelioma.
Trichoepitheliomas are rare, benign, adnexal skin tumors that can start in early childhood or during puberty. The lesions are most commonly seen in girls as skin color papules on the face, and sometimes on the trunk and the neck. Trichoepitheliomas can appear as a benign single lesion nonfamilial form or as a familial form with multiple lesions.1 Brooke-Spiegler syndrome (BSS) is a rare autosomal dominant condition where affected individuals have multiple trichoepitheliomas, cylindromas, and spiradenomas. Depending on the predominant type of lesion, phenotypic variants include multiple familial trichoepithelioma type 1 and familial cylindromatosis.2 BSS is caused by mutations within CYLD, a tumor-suppressor gene located on chromosome 16q12-q13.3 Our patient presented only with trichoepitheliomas with no other lesions on the scalp, neck, or torso.
Multiple trichoepitheliomas also can be seen in other syndromes including Rombo syndrome, which is characterized by basal cell carcinomas, milia, hypotrichosis, distal vasodilation, and atrophoderma vermiculata; none seen in our patient. Bazex-Dupré-Christol syndrome is an X-linked dominant condition in which affected individuals can present with multiple trichoepitheliomas, as well as milia, hypotrichosis, follicular atrophoderma, and basal cell carcinomas.
The differential diagnosis of skin color papules on the central face on a child should include acne, flat warts, and angiofibromas seen in tuberous sclerosis. Our patient’s lesions were monomorphous, and there were no comedones, pustules, or inflammatory papules characteristic of acne.
He had warts on his hands which could make it suspicious for the face lesions to be verrucous in nature. Flat warts also present as skin color papules, but characteristically are flat, not round and shiny as our patient’s lesions were. Angiofibromas, as seen in individuals with tuberous sclerosis, also can start at an early age in the same location as trichoepitheliomas in BSS, but clinically the lesions are pinker and redder rather than the skin-color, round shape papules characteristic of trichoepitheliomas. Patients may have other findings suggestive of tuberous sclerosis including confetti hypopigmentation, ash leaf spots, shagreen patch, and a history of seizures or developmental delay – none of which were present in our patient. Children with basal cell nevus syndrome can present with skin color to shiny telangiectatic papules (basal cell carcinomas) that can be single or multiple on the face, chest, and back. The lesions usually are not seen in clusters around the nose and central face as seen in patients with BSS. Patients with basal cell nevus syndrome can develop jaw bone cysts, brain tumors (medulloblastoma), and fibromas on the heart or ovaries, palmar pits and be macrocephalic.4
Trichoepitheliomas usually are treated surgically but other nonsurgical removing techniques include laser resurfacing, curettage, and electrocautery.5 Malignant transformation can occur in 5%-10% of the individuals and should be managed by a multidisciplinary team. Topical treatment with sirolimus previously has been reported to be effective in young patients.6
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email Dr. Matiz at pdnews@mdedge.com.
References
1. Acta Dermatovenerol Croat. 2018 Jun;26(2):162-5.
2. Eur J Med Genet. 2015;58(5):271-8.
3. Am J Dermatopathol. 2014;36(11):868-74.
4. Int J Dermatol. 2016 Apr;55(4):367-75.
5. Int J Dermatol. 2007;46(6):583-6.
6. Dermatol Ther. 2017 Mar. doi: 10.1111/dth.12458.
A shave biopsy of one of the lesions was performed that showed a proliferation of nests of basaloid cells on the dermis with palisading and rare vacuolated clear cell change. A rare ductal structure with luminal proteinaceous contents was noted. The findings were consistent with a trichoepithelioma.
Trichoepitheliomas are rare, benign, adnexal skin tumors that can start in early childhood or during puberty. The lesions are most commonly seen in girls as skin color papules on the face, and sometimes on the trunk and the neck. Trichoepitheliomas can appear as a benign single lesion nonfamilial form or as a familial form with multiple lesions.1 Brooke-Spiegler syndrome (BSS) is a rare autosomal dominant condition where affected individuals have multiple trichoepitheliomas, cylindromas, and spiradenomas. Depending on the predominant type of lesion, phenotypic variants include multiple familial trichoepithelioma type 1 and familial cylindromatosis.2 BSS is caused by mutations within CYLD, a tumor-suppressor gene located on chromosome 16q12-q13.3 Our patient presented only with trichoepitheliomas with no other lesions on the scalp, neck, or torso.
Multiple trichoepitheliomas also can be seen in other syndromes including Rombo syndrome, which is characterized by basal cell carcinomas, milia, hypotrichosis, distal vasodilation, and atrophoderma vermiculata; none seen in our patient. Bazex-Dupré-Christol syndrome is an X-linked dominant condition in which affected individuals can present with multiple trichoepitheliomas, as well as milia, hypotrichosis, follicular atrophoderma, and basal cell carcinomas.
The differential diagnosis of skin color papules on the central face on a child should include acne, flat warts, and angiofibromas seen in tuberous sclerosis. Our patient’s lesions were monomorphous, and there were no comedones, pustules, or inflammatory papules characteristic of acne.
He had warts on his hands which could make it suspicious for the face lesions to be verrucous in nature. Flat warts also present as skin color papules, but characteristically are flat, not round and shiny as our patient’s lesions were. Angiofibromas, as seen in individuals with tuberous sclerosis, also can start at an early age in the same location as trichoepitheliomas in BSS, but clinically the lesions are pinker and redder rather than the skin-color, round shape papules characteristic of trichoepitheliomas. Patients may have other findings suggestive of tuberous sclerosis including confetti hypopigmentation, ash leaf spots, shagreen patch, and a history of seizures or developmental delay – none of which were present in our patient. Children with basal cell nevus syndrome can present with skin color to shiny telangiectatic papules (basal cell carcinomas) that can be single or multiple on the face, chest, and back. The lesions usually are not seen in clusters around the nose and central face as seen in patients with BSS. Patients with basal cell nevus syndrome can develop jaw bone cysts, brain tumors (medulloblastoma), and fibromas on the heart or ovaries, palmar pits and be macrocephalic.4
Trichoepitheliomas usually are treated surgically but other nonsurgical removing techniques include laser resurfacing, curettage, and electrocautery.5 Malignant transformation can occur in 5%-10% of the individuals and should be managed by a multidisciplinary team. Topical treatment with sirolimus previously has been reported to be effective in young patients.6
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email Dr. Matiz at pdnews@mdedge.com.
References
1. Acta Dermatovenerol Croat. 2018 Jun;26(2):162-5.
2. Eur J Med Genet. 2015;58(5):271-8.
3. Am J Dermatopathol. 2014;36(11):868-74.
4. Int J Dermatol. 2016 Apr;55(4):367-75.
5. Int J Dermatol. 2007;46(6):583-6.
6. Dermatol Ther. 2017 Mar. doi: 10.1111/dth.12458.
A white 8-year-old boy comes to our pediatric dermatology clinic with his mother for evaluation of acne. The lesions started about a year ago on his nose and now have spread to his cheeks. The bumps are not symptomatic. He has been applying over the counter salicylic acid and benzoyl peroxide gels with no help. The mother reports he has been growing well, denies any growth spurt, no axillary or genital hair or body odor noted.
None of the family members have a history of acne. The mother cannot recall any family members with similar lesions on the face. He has had some warts on his fingers for years and has been treated with over the counter salicylic acid. There is no family history of skin cancer.
On physical exam, he is a healthy young boy with several skin color, round papules 1-3 mm on the nose, forehead, and cheeks. There are no lesions on the scalp. He has abundant brown hair. He has few verrucous papules on the fingers. Axillary and genital hair is not noted. There is no body odor and he is Tanner stage I.
No cardiovascular benefit from vitamin D supplementation
There are no benefits from vitamin D supplementation in reducing the risk of major adverse cardiovascular events or all-cause mortality, according to a meta-analysis published in JAMA Cardiology.
Researchers analyzed data from 83,291 patients enrolled in 21 randomized, placebo-controlled clinical trials of at least 1 year of vitamin D supplementation.
They found the incidence of major adverse cardiovascular events was the same among patients taking vitamin D supplements and those taking placebo (risk ratio, 1; P = .85). Even stratifying by age, sex, postmenopausal status, pretreatment vitamin D levels, vitamin D dosage and formulation, chronic kidney disease, or excluding studies that used vitamin D analogues made no significant difference.
However, there was the suggestion of reduced incidence of major adverse cardiovascular events with vitamin D supplementation in individuals of advanced age, but the authors wrote that the finding should be interpreted with caution.
The analysis found no benefit from vitamin D supplementation on the secondary endpoints of MI, stroke, cardiovascular mortality, or all-cause mortality risk.
Mahmoud Barbarawi, MD, from the Hurley Medical Center at Michigan State University, East Lansing, and coauthors commented that previous observational studies have found significant associations between low vitamin D levels and cardiovascular events and all-cause mortality.
“However, observational studies are susceptible to uncontrolled confounding by outdoor physical activity, nutritional status, and prevalent chronic disease, which may influence serum 25-hydroxyvitamin D levels,” they wrote.
This updated analysis extended earlier clinical trial findings and added in some more-recent randomized trial outcomes, including the massive VITAL trial, which showed that neither daily vitamin D nor omega-3 fatty acids reduce cancer or cardiovascular event risk (N Engl J Med. 2019;380[1]:33-44).
Still, the authors noted that most of the trials included in the analysis had not prespecified cardiovascular disease as the primary endpoint and were underpowered to detect an effect on cardiovascular events. They also pointed out that few trials included data on heart failure, and a previous meta-analysis had suggested a potential benefit of supplementation in reducing the risk of this condition.
“Additional trials of higher-dose vitamin D supplementation, perhaps targeting members of older age groups and with attention to other [cardiovascular disease] endpoints such as heart failure, are of interest,” they wrote.
One author reported receiving funding from the National Institutes of Health and in-kind support from the pharmaceutical sector for a vitamin D study. No other disclosures were reported.
SOURCE: Barbarawi M et al. JAMA Cardiol. 2019 Jun 19. doi: 10.1001/jamacardio.2019.1870.
The past decade has seen a nearly 100-fold increase in vitamin D testing and supplementation, driven by a widespread fascination with the notion of vitamin D as a panacea. Vitamin D assessments alone are costing the United States an estimated $350 million annually.
Population and cohort studies have shown a clear link between vitamin D status and cardiovascular disease, but this link is complicated by the possibility that low serum 25-hydroxyvitamin D levels may be a result of, rather than the cause of, cardiovascular disease.
The findings of this meta-analysis, that vitamin D supplementation does not reduce the risk of major cardiovascular events and all-cause mortality, should support efforts to reduce unnecessary vitamin D testing and treatment in populations not at risk for deficiency or to prevent cardiovascular disease morbidity and mortality.
Arshed A. Quyyumi, MD, and Ibhar Al Mheid, MD, are from the division of cardiology at Emory University, Atlanta. The comments are adapted from an accompanying editorial (JAMA Cardiol. 2019 Jun 19. doi:10.1001/jamacardio.2019.1906). No conflicts of interest were reported.
The past decade has seen a nearly 100-fold increase in vitamin D testing and supplementation, driven by a widespread fascination with the notion of vitamin D as a panacea. Vitamin D assessments alone are costing the United States an estimated $350 million annually.
Population and cohort studies have shown a clear link between vitamin D status and cardiovascular disease, but this link is complicated by the possibility that low serum 25-hydroxyvitamin D levels may be a result of, rather than the cause of, cardiovascular disease.
The findings of this meta-analysis, that vitamin D supplementation does not reduce the risk of major cardiovascular events and all-cause mortality, should support efforts to reduce unnecessary vitamin D testing and treatment in populations not at risk for deficiency or to prevent cardiovascular disease morbidity and mortality.
Arshed A. Quyyumi, MD, and Ibhar Al Mheid, MD, are from the division of cardiology at Emory University, Atlanta. The comments are adapted from an accompanying editorial (JAMA Cardiol. 2019 Jun 19. doi:10.1001/jamacardio.2019.1906). No conflicts of interest were reported.
The past decade has seen a nearly 100-fold increase in vitamin D testing and supplementation, driven by a widespread fascination with the notion of vitamin D as a panacea. Vitamin D assessments alone are costing the United States an estimated $350 million annually.
Population and cohort studies have shown a clear link between vitamin D status and cardiovascular disease, but this link is complicated by the possibility that low serum 25-hydroxyvitamin D levels may be a result of, rather than the cause of, cardiovascular disease.
The findings of this meta-analysis, that vitamin D supplementation does not reduce the risk of major cardiovascular events and all-cause mortality, should support efforts to reduce unnecessary vitamin D testing and treatment in populations not at risk for deficiency or to prevent cardiovascular disease morbidity and mortality.
Arshed A. Quyyumi, MD, and Ibhar Al Mheid, MD, are from the division of cardiology at Emory University, Atlanta. The comments are adapted from an accompanying editorial (JAMA Cardiol. 2019 Jun 19. doi:10.1001/jamacardio.2019.1906). No conflicts of interest were reported.
There are no benefits from vitamin D supplementation in reducing the risk of major adverse cardiovascular events or all-cause mortality, according to a meta-analysis published in JAMA Cardiology.
Researchers analyzed data from 83,291 patients enrolled in 21 randomized, placebo-controlled clinical trials of at least 1 year of vitamin D supplementation.
They found the incidence of major adverse cardiovascular events was the same among patients taking vitamin D supplements and those taking placebo (risk ratio, 1; P = .85). Even stratifying by age, sex, postmenopausal status, pretreatment vitamin D levels, vitamin D dosage and formulation, chronic kidney disease, or excluding studies that used vitamin D analogues made no significant difference.
However, there was the suggestion of reduced incidence of major adverse cardiovascular events with vitamin D supplementation in individuals of advanced age, but the authors wrote that the finding should be interpreted with caution.
The analysis found no benefit from vitamin D supplementation on the secondary endpoints of MI, stroke, cardiovascular mortality, or all-cause mortality risk.
Mahmoud Barbarawi, MD, from the Hurley Medical Center at Michigan State University, East Lansing, and coauthors commented that previous observational studies have found significant associations between low vitamin D levels and cardiovascular events and all-cause mortality.
“However, observational studies are susceptible to uncontrolled confounding by outdoor physical activity, nutritional status, and prevalent chronic disease, which may influence serum 25-hydroxyvitamin D levels,” they wrote.
This updated analysis extended earlier clinical trial findings and added in some more-recent randomized trial outcomes, including the massive VITAL trial, which showed that neither daily vitamin D nor omega-3 fatty acids reduce cancer or cardiovascular event risk (N Engl J Med. 2019;380[1]:33-44).
Still, the authors noted that most of the trials included in the analysis had not prespecified cardiovascular disease as the primary endpoint and were underpowered to detect an effect on cardiovascular events. They also pointed out that few trials included data on heart failure, and a previous meta-analysis had suggested a potential benefit of supplementation in reducing the risk of this condition.
“Additional trials of higher-dose vitamin D supplementation, perhaps targeting members of older age groups and with attention to other [cardiovascular disease] endpoints such as heart failure, are of interest,” they wrote.
One author reported receiving funding from the National Institutes of Health and in-kind support from the pharmaceutical sector for a vitamin D study. No other disclosures were reported.
SOURCE: Barbarawi M et al. JAMA Cardiol. 2019 Jun 19. doi: 10.1001/jamacardio.2019.1870.
There are no benefits from vitamin D supplementation in reducing the risk of major adverse cardiovascular events or all-cause mortality, according to a meta-analysis published in JAMA Cardiology.
Researchers analyzed data from 83,291 patients enrolled in 21 randomized, placebo-controlled clinical trials of at least 1 year of vitamin D supplementation.
They found the incidence of major adverse cardiovascular events was the same among patients taking vitamin D supplements and those taking placebo (risk ratio, 1; P = .85). Even stratifying by age, sex, postmenopausal status, pretreatment vitamin D levels, vitamin D dosage and formulation, chronic kidney disease, or excluding studies that used vitamin D analogues made no significant difference.
However, there was the suggestion of reduced incidence of major adverse cardiovascular events with vitamin D supplementation in individuals of advanced age, but the authors wrote that the finding should be interpreted with caution.
The analysis found no benefit from vitamin D supplementation on the secondary endpoints of MI, stroke, cardiovascular mortality, or all-cause mortality risk.
Mahmoud Barbarawi, MD, from the Hurley Medical Center at Michigan State University, East Lansing, and coauthors commented that previous observational studies have found significant associations between low vitamin D levels and cardiovascular events and all-cause mortality.
“However, observational studies are susceptible to uncontrolled confounding by outdoor physical activity, nutritional status, and prevalent chronic disease, which may influence serum 25-hydroxyvitamin D levels,” they wrote.
This updated analysis extended earlier clinical trial findings and added in some more-recent randomized trial outcomes, including the massive VITAL trial, which showed that neither daily vitamin D nor omega-3 fatty acids reduce cancer or cardiovascular event risk (N Engl J Med. 2019;380[1]:33-44).
Still, the authors noted that most of the trials included in the analysis had not prespecified cardiovascular disease as the primary endpoint and were underpowered to detect an effect on cardiovascular events. They also pointed out that few trials included data on heart failure, and a previous meta-analysis had suggested a potential benefit of supplementation in reducing the risk of this condition.
“Additional trials of higher-dose vitamin D supplementation, perhaps targeting members of older age groups and with attention to other [cardiovascular disease] endpoints such as heart failure, are of interest,” they wrote.
One author reported receiving funding from the National Institutes of Health and in-kind support from the pharmaceutical sector for a vitamin D study. No other disclosures were reported.
SOURCE: Barbarawi M et al. JAMA Cardiol. 2019 Jun 19. doi: 10.1001/jamacardio.2019.1870.
FROM JAMA CARDIOLOGY
HM19: Sepsis care update
Presenter
Patricia Kritek MD, EdM
Session Title
Sepsis update: From screening to refractory shock
Background
Each year 1.7 million adults in America develop sepsis, and 270,000 Americans die from sepsis annually. Sepsis costs U.S. health care over $27 billion dollars each year. Because of the wide range of etiologies and variation in presentation and intensity, it is a challenge to establish homogeneous evidence based guidelines.1
The definition of sepsis based on the “SIRS” criterion was developed initially in 1992, later revised as Sepsis-2 in 2001. The latest Sepsis-3 definition – “life-threatening organ dysfunction due to a dysregulated host response to infection” – was developed in 2016 by the Third International Consensus Definitions for Sepsis and Septic Shock. This newest definition has renounced the SIRS criterion and adopted the Sequential Organ Failure Assessment (SOFA) score. Treatment guidelines in sepsis were developed by the Surviving Sepsis Campaign starting with the Barcelona Declaration in 2002 and revised multiple times, with the development of 3-hour and 6-hour care bundles in 2012. The latest revision, in 2018, consolidated to a 1-hour bundle.2
Sepsis is a continuum of every severe infection, and with the combined efforts of the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, evidence-based guidelines have been developed over the past 2 decades, with the latest iteration in 2018. The Centers for Medicare & Medicaid Services still uses Sepsis-2 for diagnosis, and the 3-hr/6-hr bundle compliance (2016) for expected care.3
Session summary
Dr. Kritek, of the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle, presented to a room of over 1,000 enthusiastic hospitalists. She was able to capture everyone’s attention with a great presentation. As sepsis is one of the most common and serious conditions we encounter, most hospitalists are fairly well versed in evidence-based practices, and Dr. Kritek was able to keep us engaged, describing in detail the evolving definition, pathophysiology, and screening procedures for sepsis. She also spoke about important studies and the latest evidence that will positively impact each hospitalist’s practice in treating sepsis.
Dr. Kritek explained clearly how the Surviving Sepsis Campaign developed a vital and nontraditional guideline that “recommends health systems have a performance improvement program for sepsis including screening for high-risk patients.” In a 1-hour session, Dr. Kritek did a commendable job untangling this bewildering health care challenge, and aligned each component to explain how to best use available resources and address sepsis in individual hospitals.
She talked about the statistics and historical aspects involved in the definition of sepsis, and the Surviving Sepsis Campaign. With three good case scenarios, Dr. Kritek explained how it was difficult to accurately diagnose sepsis using the Sepsis-2/SIRS criterion, and how the SIRS criterion led to several false positives. This created a need for the new Sepsis-3 definition, which used delta SOFA score of 2 indicating “organ failure.”
Key takeaways: Screening
- Sepsis-3 with delta SOFA score of at least 2 and Quick SOFA (qSOFA) of at least 2 was best at predicting in-hospital death, ICU admission, and long ICU stay in ED.
- qSOFA was not helpful in the admitted ICU population. An increase of at least 2 points in SOFA score within 24 hours of admission to the ICU was the best predictor of in-hospital mortality and long ICU stays.
- SIRS has high sensitivity and low specificity. The Early Warning Score has accuracy similar to qSOFA.
- Understanding that there is no perfect answer regarding screening, but having a process is vital for each organization. This approach led to the Surviving Sepsis Campaign guideline: “Recommend health systems have a performance improvement program for sepsis including screening for high-risk patients.”
Key takeaways: Treatment
- Meta-analysis showed that specifically targeted, early goal–directed treatment (specifically, central venous pressure 8-12 mm Hg, central venous oxygen saturation greater than 70%, packed red blood cell inotropes used) did not show any improvement in 90-day mortality, and actually generated worse outcomes, including cirrhosis, as well as higher costs of care.
- Antibiotics: Though part of the 3-hour bundle, antibiotics are recommended to be administered within 1 hour.
- Intravenous fluids: Patients with sepsis-induced hypoperfusion need 30 mL/kg crystalloids. Normal saline and lactated ringer are preferred. Lactated ringer has the advantage over normal saline, with a reduced incidence of major adverse kidney events.
- Importance of bundle compliance: N.Y. study showed use of protocols cut mortality from 30.2% to 25.4%.
Refractory septic shock
- Adding hydrocortisone and fludrocortisone improved mortality at 28 days, helped patients get off vasopressors sooner, and ultimately resulted in less organ failure. But no difference in 90-day mortality.
- A study of vitamin C use in septic patients needs further studies to validate, as it only included 47 patients.
- Early renal replacement therapy showed no difference in mortality or length of stay.
Dr. Kritek’s presentation made a positive impact by helping to explain the reasoning behind the established and evolving best practices and guidelines for care of patients with sepsis and septic shock. Her approach will help hospitalists provide cost-effective care, by understanding which expensive interventions and practices do not make a difference in patient care.
Dr. Odeti is hospitalist medical director at Johnston Memorial Hospital in Abingdon, Va. JMH is part of Ballad Health, a health system operating 21 hospitals in northeast Tennessee and southwest Virginia.
References
1. https://www.sepsis.org/wp-content/uploads/2017/05/Sepsis-Fact-Sheet-2018.pdf.
2. http://www.survivingsepsis.org/News/Pages/SCCM-and-ACEP-Release-Joint-Statement-About-the-Surviving-Sepsis-Campaign-Hour-1-Bundle.aspx
3. Specifications Manual for National Hospital Inpatient Quality Measures Discharges 01-01-17 (1Q17) through 12-31-17 (4Q17).
Presenter
Patricia Kritek MD, EdM
Session Title
Sepsis update: From screening to refractory shock
Background
Each year 1.7 million adults in America develop sepsis, and 270,000 Americans die from sepsis annually. Sepsis costs U.S. health care over $27 billion dollars each year. Because of the wide range of etiologies and variation in presentation and intensity, it is a challenge to establish homogeneous evidence based guidelines.1
The definition of sepsis based on the “SIRS” criterion was developed initially in 1992, later revised as Sepsis-2 in 2001. The latest Sepsis-3 definition – “life-threatening organ dysfunction due to a dysregulated host response to infection” – was developed in 2016 by the Third International Consensus Definitions for Sepsis and Septic Shock. This newest definition has renounced the SIRS criterion and adopted the Sequential Organ Failure Assessment (SOFA) score. Treatment guidelines in sepsis were developed by the Surviving Sepsis Campaign starting with the Barcelona Declaration in 2002 and revised multiple times, with the development of 3-hour and 6-hour care bundles in 2012. The latest revision, in 2018, consolidated to a 1-hour bundle.2
Sepsis is a continuum of every severe infection, and with the combined efforts of the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, evidence-based guidelines have been developed over the past 2 decades, with the latest iteration in 2018. The Centers for Medicare & Medicaid Services still uses Sepsis-2 for diagnosis, and the 3-hr/6-hr bundle compliance (2016) for expected care.3
Session summary
Dr. Kritek, of the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle, presented to a room of over 1,000 enthusiastic hospitalists. She was able to capture everyone’s attention with a great presentation. As sepsis is one of the most common and serious conditions we encounter, most hospitalists are fairly well versed in evidence-based practices, and Dr. Kritek was able to keep us engaged, describing in detail the evolving definition, pathophysiology, and screening procedures for sepsis. She also spoke about important studies and the latest evidence that will positively impact each hospitalist’s practice in treating sepsis.
Dr. Kritek explained clearly how the Surviving Sepsis Campaign developed a vital and nontraditional guideline that “recommends health systems have a performance improvement program for sepsis including screening for high-risk patients.” In a 1-hour session, Dr. Kritek did a commendable job untangling this bewildering health care challenge, and aligned each component to explain how to best use available resources and address sepsis in individual hospitals.
She talked about the statistics and historical aspects involved in the definition of sepsis, and the Surviving Sepsis Campaign. With three good case scenarios, Dr. Kritek explained how it was difficult to accurately diagnose sepsis using the Sepsis-2/SIRS criterion, and how the SIRS criterion led to several false positives. This created a need for the new Sepsis-3 definition, which used delta SOFA score of 2 indicating “organ failure.”
Key takeaways: Screening
- Sepsis-3 with delta SOFA score of at least 2 and Quick SOFA (qSOFA) of at least 2 was best at predicting in-hospital death, ICU admission, and long ICU stay in ED.
- qSOFA was not helpful in the admitted ICU population. An increase of at least 2 points in SOFA score within 24 hours of admission to the ICU was the best predictor of in-hospital mortality and long ICU stays.
- SIRS has high sensitivity and low specificity. The Early Warning Score has accuracy similar to qSOFA.
- Understanding that there is no perfect answer regarding screening, but having a process is vital for each organization. This approach led to the Surviving Sepsis Campaign guideline: “Recommend health systems have a performance improvement program for sepsis including screening for high-risk patients.”
Key takeaways: Treatment
- Meta-analysis showed that specifically targeted, early goal–directed treatment (specifically, central venous pressure 8-12 mm Hg, central venous oxygen saturation greater than 70%, packed red blood cell inotropes used) did not show any improvement in 90-day mortality, and actually generated worse outcomes, including cirrhosis, as well as higher costs of care.
- Antibiotics: Though part of the 3-hour bundle, antibiotics are recommended to be administered within 1 hour.
- Intravenous fluids: Patients with sepsis-induced hypoperfusion need 30 mL/kg crystalloids. Normal saline and lactated ringer are preferred. Lactated ringer has the advantage over normal saline, with a reduced incidence of major adverse kidney events.
- Importance of bundle compliance: N.Y. study showed use of protocols cut mortality from 30.2% to 25.4%.
Refractory septic shock
- Adding hydrocortisone and fludrocortisone improved mortality at 28 days, helped patients get off vasopressors sooner, and ultimately resulted in less organ failure. But no difference in 90-day mortality.
- A study of vitamin C use in septic patients needs further studies to validate, as it only included 47 patients.
- Early renal replacement therapy showed no difference in mortality or length of stay.
Dr. Kritek’s presentation made a positive impact by helping to explain the reasoning behind the established and evolving best practices and guidelines for care of patients with sepsis and septic shock. Her approach will help hospitalists provide cost-effective care, by understanding which expensive interventions and practices do not make a difference in patient care.
Dr. Odeti is hospitalist medical director at Johnston Memorial Hospital in Abingdon, Va. JMH is part of Ballad Health, a health system operating 21 hospitals in northeast Tennessee and southwest Virginia.
References
1. https://www.sepsis.org/wp-content/uploads/2017/05/Sepsis-Fact-Sheet-2018.pdf.
2. http://www.survivingsepsis.org/News/Pages/SCCM-and-ACEP-Release-Joint-Statement-About-the-Surviving-Sepsis-Campaign-Hour-1-Bundle.aspx
3. Specifications Manual for National Hospital Inpatient Quality Measures Discharges 01-01-17 (1Q17) through 12-31-17 (4Q17).
Presenter
Patricia Kritek MD, EdM
Session Title
Sepsis update: From screening to refractory shock
Background
Each year 1.7 million adults in America develop sepsis, and 270,000 Americans die from sepsis annually. Sepsis costs U.S. health care over $27 billion dollars each year. Because of the wide range of etiologies and variation in presentation and intensity, it is a challenge to establish homogeneous evidence based guidelines.1
The definition of sepsis based on the “SIRS” criterion was developed initially in 1992, later revised as Sepsis-2 in 2001. The latest Sepsis-3 definition – “life-threatening organ dysfunction due to a dysregulated host response to infection” – was developed in 2016 by the Third International Consensus Definitions for Sepsis and Septic Shock. This newest definition has renounced the SIRS criterion and adopted the Sequential Organ Failure Assessment (SOFA) score. Treatment guidelines in sepsis were developed by the Surviving Sepsis Campaign starting with the Barcelona Declaration in 2002 and revised multiple times, with the development of 3-hour and 6-hour care bundles in 2012. The latest revision, in 2018, consolidated to a 1-hour bundle.2
Sepsis is a continuum of every severe infection, and with the combined efforts of the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, evidence-based guidelines have been developed over the past 2 decades, with the latest iteration in 2018. The Centers for Medicare & Medicaid Services still uses Sepsis-2 for diagnosis, and the 3-hr/6-hr bundle compliance (2016) for expected care.3
Session summary
Dr. Kritek, of the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle, presented to a room of over 1,000 enthusiastic hospitalists. She was able to capture everyone’s attention with a great presentation. As sepsis is one of the most common and serious conditions we encounter, most hospitalists are fairly well versed in evidence-based practices, and Dr. Kritek was able to keep us engaged, describing in detail the evolving definition, pathophysiology, and screening procedures for sepsis. She also spoke about important studies and the latest evidence that will positively impact each hospitalist’s practice in treating sepsis.
Dr. Kritek explained clearly how the Surviving Sepsis Campaign developed a vital and nontraditional guideline that “recommends health systems have a performance improvement program for sepsis including screening for high-risk patients.” In a 1-hour session, Dr. Kritek did a commendable job untangling this bewildering health care challenge, and aligned each component to explain how to best use available resources and address sepsis in individual hospitals.
She talked about the statistics and historical aspects involved in the definition of sepsis, and the Surviving Sepsis Campaign. With three good case scenarios, Dr. Kritek explained how it was difficult to accurately diagnose sepsis using the Sepsis-2/SIRS criterion, and how the SIRS criterion led to several false positives. This created a need for the new Sepsis-3 definition, which used delta SOFA score of 2 indicating “organ failure.”
Key takeaways: Screening
- Sepsis-3 with delta SOFA score of at least 2 and Quick SOFA (qSOFA) of at least 2 was best at predicting in-hospital death, ICU admission, and long ICU stay in ED.
- qSOFA was not helpful in the admitted ICU population. An increase of at least 2 points in SOFA score within 24 hours of admission to the ICU was the best predictor of in-hospital mortality and long ICU stays.
- SIRS has high sensitivity and low specificity. The Early Warning Score has accuracy similar to qSOFA.
- Understanding that there is no perfect answer regarding screening, but having a process is vital for each organization. This approach led to the Surviving Sepsis Campaign guideline: “Recommend health systems have a performance improvement program for sepsis including screening for high-risk patients.”
Key takeaways: Treatment
- Meta-analysis showed that specifically targeted, early goal–directed treatment (specifically, central venous pressure 8-12 mm Hg, central venous oxygen saturation greater than 70%, packed red blood cell inotropes used) did not show any improvement in 90-day mortality, and actually generated worse outcomes, including cirrhosis, as well as higher costs of care.
- Antibiotics: Though part of the 3-hour bundle, antibiotics are recommended to be administered within 1 hour.
- Intravenous fluids: Patients with sepsis-induced hypoperfusion need 30 mL/kg crystalloids. Normal saline and lactated ringer are preferred. Lactated ringer has the advantage over normal saline, with a reduced incidence of major adverse kidney events.
- Importance of bundle compliance: N.Y. study showed use of protocols cut mortality from 30.2% to 25.4%.
Refractory septic shock
- Adding hydrocortisone and fludrocortisone improved mortality at 28 days, helped patients get off vasopressors sooner, and ultimately resulted in less organ failure. But no difference in 90-day mortality.
- A study of vitamin C use in septic patients needs further studies to validate, as it only included 47 patients.
- Early renal replacement therapy showed no difference in mortality or length of stay.
Dr. Kritek’s presentation made a positive impact by helping to explain the reasoning behind the established and evolving best practices and guidelines for care of patients with sepsis and septic shock. Her approach will help hospitalists provide cost-effective care, by understanding which expensive interventions and practices do not make a difference in patient care.
Dr. Odeti is hospitalist medical director at Johnston Memorial Hospital in Abingdon, Va. JMH is part of Ballad Health, a health system operating 21 hospitals in northeast Tennessee and southwest Virginia.
References
1. https://www.sepsis.org/wp-content/uploads/2017/05/Sepsis-Fact-Sheet-2018.pdf.
2. http://www.survivingsepsis.org/News/Pages/SCCM-and-ACEP-Release-Joint-Statement-About-the-Surviving-Sepsis-Campaign-Hour-1-Bundle.aspx
3. Specifications Manual for National Hospital Inpatient Quality Measures Discharges 01-01-17 (1Q17) through 12-31-17 (4Q17).
Quick Byte: Conversations about cost
Patients want to talk
Seventy percent of Americans would like to have conversations about the costs of care with their health care providers, but only 28% do so, according to polling conducted for the Robert Wood Johnson Foundation (RWJF) by Avalere Health.
With those polling results in hand, 2 years ago RWJF and Avalere Health launched the Cost Conversation projects to help. Practice briefs for these kinds of conversations are now available on America’s Essential Hospitals’ website (https://essentialhospitals.org/cost-care/practice-briefs/).
Reference
1. Ganos E, Steinberg K, Seidman J, Masi D, Gomez-Rexode A, Fraser A. Talking About Costs: Innovation In Clinician-Patient Conversations. Health Affairs. Published online Nov. 27, 2018. doi: 10.1377/hblog20181126.366161. Accessed Dec. 11, 2018.
Patients want to talk
Patients want to talk
Seventy percent of Americans would like to have conversations about the costs of care with their health care providers, but only 28% do so, according to polling conducted for the Robert Wood Johnson Foundation (RWJF) by Avalere Health.
With those polling results in hand, 2 years ago RWJF and Avalere Health launched the Cost Conversation projects to help. Practice briefs for these kinds of conversations are now available on America’s Essential Hospitals’ website (https://essentialhospitals.org/cost-care/practice-briefs/).
Reference
1. Ganos E, Steinberg K, Seidman J, Masi D, Gomez-Rexode A, Fraser A. Talking About Costs: Innovation In Clinician-Patient Conversations. Health Affairs. Published online Nov. 27, 2018. doi: 10.1377/hblog20181126.366161. Accessed Dec. 11, 2018.
Seventy percent of Americans would like to have conversations about the costs of care with their health care providers, but only 28% do so, according to polling conducted for the Robert Wood Johnson Foundation (RWJF) by Avalere Health.
With those polling results in hand, 2 years ago RWJF and Avalere Health launched the Cost Conversation projects to help. Practice briefs for these kinds of conversations are now available on America’s Essential Hospitals’ website (https://essentialhospitals.org/cost-care/practice-briefs/).
Reference
1. Ganos E, Steinberg K, Seidman J, Masi D, Gomez-Rexode A, Fraser A. Talking About Costs: Innovation In Clinician-Patient Conversations. Health Affairs. Published online Nov. 27, 2018. doi: 10.1377/hblog20181126.366161. Accessed Dec. 11, 2018.
Hippocampal cerebral blood flow upped with antihypertensive use in Alzheimer’s
according to a new study.
Cerebral blood flow in other regions of the brain did not significantly change in patients who took the antihypertensive drug nilvadipine, according to a report on the trial published in Hypertension. Reduced cerebral blood flow is an early marker of Alzheimer’s disease, and the SPRINT MIND study suggests that intensive blood pressure control may reduce the risk of cognitive impairment.
“These findings [of the new study] not only indicate preserved cerebral autoregulation in Alzheimer’s disease but also point toward beneficial cerebrovascular effects of antihypertensive treatment,” said Jurgen A.H.R. Claassen, MD, PhD of Radboud University Medical Center in Nijmegen, the Netherlands, and coauthors. “An important question is whether this observed increase in [cerebral blood flow] translates to clinical benefits. Unfortunately, sample sizes were too small and follow-up time too short to reliably study the effects ... on structural brain measures and cognitive measures.”
Nilvadipine is a dihydropyridine calcium antagonist used to treat hypertension. In the NILVAD trial, investigators assessed the effects of nilvadipine versus placebo in approximately 500 patients with Alzheimer’s disease. The 18-month trial found no beneficial effects of nilvadipine on cognitive function, but subgroup analyses suggested a potential benefit among patients in the early stages of the disease (PLoS Med. 2018 Sep 24;15[9]:e1002660.).
The cerebral blood flow analysis was a preplanned substudy of NILVAD designed to assess how 6 months of treatment with the drug affects cerebral blood flow as measured using MRI arterial spin labeling. The researchers looked at cerebral blood flow in whole-brain gray matter and in specific regions such as the hippocampus.
The substudy analysis included 22 patients who received nilvadipine and 22 who received placebo during the randomized, double-blind study. Participants had a mean age of 72.8 years and a mean Mini-Mental State Examination score of 20.4.
At 6 months, nilvadipine lowered systolic BP by 11.5 mm Hg, and whole-brain gray matter cerebral blood flow remained stable. Blood flow to the hippocampus increased by approximately 20% among patients treated with nilvadipine – by 24.4 mL/100 g per minute to the left hippocampus and by 20.1 mL/100 g per minute to the right hippocampus.
The increased hippocampal cerebral blood flow could be related to nilvadipine’s antihypertensive effects or its effects on amyloid-beta, the authors noted.
“These findings indicate that the known decrease in [cerebral blood flow] in patients with [Alzheimer’s disease] can in some regions be reversed,” they wrote.
“Even though no medical treatment is without risk, getting treatment for high blood pressure could be important to maintain brain health in patients with Alzheimer’s disease,” Dr. Claassen said in a statement. “In the future, we need to find out whether the improvement in blood flow, especially in the hippocampus, can be used as a supportive treatment to slow down progression of Alzheimer’s disease, especially in earlier states of disease.”
The researchers wrote they lacked biomarkers to confirm Alzheimer’s disease pathology. Most of the study participants were white Europeans, which “limits extrapolation [of the findings] to other populations,” they added.
The Alzheimer’s Drug Discovery Foundation and the Dutch Alzheimer Society funded the NILVAD cerebral blood flow substudy. NILVAD was funded by the European Commission Framework 7 Program Health Theme. Dr. Claassen had no disclosures; one coauthor disclosed a pending patent for nilvadipine.
SOURCE: Claassen JAHR et al. Hypertension. 2019 Jun 17. doi: 10.1161/HYPERTENSIONAHA.119.12892.
according to a new study.
Cerebral blood flow in other regions of the brain did not significantly change in patients who took the antihypertensive drug nilvadipine, according to a report on the trial published in Hypertension. Reduced cerebral blood flow is an early marker of Alzheimer’s disease, and the SPRINT MIND study suggests that intensive blood pressure control may reduce the risk of cognitive impairment.
“These findings [of the new study] not only indicate preserved cerebral autoregulation in Alzheimer’s disease but also point toward beneficial cerebrovascular effects of antihypertensive treatment,” said Jurgen A.H.R. Claassen, MD, PhD of Radboud University Medical Center in Nijmegen, the Netherlands, and coauthors. “An important question is whether this observed increase in [cerebral blood flow] translates to clinical benefits. Unfortunately, sample sizes were too small and follow-up time too short to reliably study the effects ... on structural brain measures and cognitive measures.”
Nilvadipine is a dihydropyridine calcium antagonist used to treat hypertension. In the NILVAD trial, investigators assessed the effects of nilvadipine versus placebo in approximately 500 patients with Alzheimer’s disease. The 18-month trial found no beneficial effects of nilvadipine on cognitive function, but subgroup analyses suggested a potential benefit among patients in the early stages of the disease (PLoS Med. 2018 Sep 24;15[9]:e1002660.).
The cerebral blood flow analysis was a preplanned substudy of NILVAD designed to assess how 6 months of treatment with the drug affects cerebral blood flow as measured using MRI arterial spin labeling. The researchers looked at cerebral blood flow in whole-brain gray matter and in specific regions such as the hippocampus.
The substudy analysis included 22 patients who received nilvadipine and 22 who received placebo during the randomized, double-blind study. Participants had a mean age of 72.8 years and a mean Mini-Mental State Examination score of 20.4.
At 6 months, nilvadipine lowered systolic BP by 11.5 mm Hg, and whole-brain gray matter cerebral blood flow remained stable. Blood flow to the hippocampus increased by approximately 20% among patients treated with nilvadipine – by 24.4 mL/100 g per minute to the left hippocampus and by 20.1 mL/100 g per minute to the right hippocampus.
The increased hippocampal cerebral blood flow could be related to nilvadipine’s antihypertensive effects or its effects on amyloid-beta, the authors noted.
“These findings indicate that the known decrease in [cerebral blood flow] in patients with [Alzheimer’s disease] can in some regions be reversed,” they wrote.
“Even though no medical treatment is without risk, getting treatment for high blood pressure could be important to maintain brain health in patients with Alzheimer’s disease,” Dr. Claassen said in a statement. “In the future, we need to find out whether the improvement in blood flow, especially in the hippocampus, can be used as a supportive treatment to slow down progression of Alzheimer’s disease, especially in earlier states of disease.”
The researchers wrote they lacked biomarkers to confirm Alzheimer’s disease pathology. Most of the study participants were white Europeans, which “limits extrapolation [of the findings] to other populations,” they added.
The Alzheimer’s Drug Discovery Foundation and the Dutch Alzheimer Society funded the NILVAD cerebral blood flow substudy. NILVAD was funded by the European Commission Framework 7 Program Health Theme. Dr. Claassen had no disclosures; one coauthor disclosed a pending patent for nilvadipine.
SOURCE: Claassen JAHR et al. Hypertension. 2019 Jun 17. doi: 10.1161/HYPERTENSIONAHA.119.12892.
according to a new study.
Cerebral blood flow in other regions of the brain did not significantly change in patients who took the antihypertensive drug nilvadipine, according to a report on the trial published in Hypertension. Reduced cerebral blood flow is an early marker of Alzheimer’s disease, and the SPRINT MIND study suggests that intensive blood pressure control may reduce the risk of cognitive impairment.
“These findings [of the new study] not only indicate preserved cerebral autoregulation in Alzheimer’s disease but also point toward beneficial cerebrovascular effects of antihypertensive treatment,” said Jurgen A.H.R. Claassen, MD, PhD of Radboud University Medical Center in Nijmegen, the Netherlands, and coauthors. “An important question is whether this observed increase in [cerebral blood flow] translates to clinical benefits. Unfortunately, sample sizes were too small and follow-up time too short to reliably study the effects ... on structural brain measures and cognitive measures.”
Nilvadipine is a dihydropyridine calcium antagonist used to treat hypertension. In the NILVAD trial, investigators assessed the effects of nilvadipine versus placebo in approximately 500 patients with Alzheimer’s disease. The 18-month trial found no beneficial effects of nilvadipine on cognitive function, but subgroup analyses suggested a potential benefit among patients in the early stages of the disease (PLoS Med. 2018 Sep 24;15[9]:e1002660.).
The cerebral blood flow analysis was a preplanned substudy of NILVAD designed to assess how 6 months of treatment with the drug affects cerebral blood flow as measured using MRI arterial spin labeling. The researchers looked at cerebral blood flow in whole-brain gray matter and in specific regions such as the hippocampus.
The substudy analysis included 22 patients who received nilvadipine and 22 who received placebo during the randomized, double-blind study. Participants had a mean age of 72.8 years and a mean Mini-Mental State Examination score of 20.4.
At 6 months, nilvadipine lowered systolic BP by 11.5 mm Hg, and whole-brain gray matter cerebral blood flow remained stable. Blood flow to the hippocampus increased by approximately 20% among patients treated with nilvadipine – by 24.4 mL/100 g per minute to the left hippocampus and by 20.1 mL/100 g per minute to the right hippocampus.
The increased hippocampal cerebral blood flow could be related to nilvadipine’s antihypertensive effects or its effects on amyloid-beta, the authors noted.
“These findings indicate that the known decrease in [cerebral blood flow] in patients with [Alzheimer’s disease] can in some regions be reversed,” they wrote.
“Even though no medical treatment is without risk, getting treatment for high blood pressure could be important to maintain brain health in patients with Alzheimer’s disease,” Dr. Claassen said in a statement. “In the future, we need to find out whether the improvement in blood flow, especially in the hippocampus, can be used as a supportive treatment to slow down progression of Alzheimer’s disease, especially in earlier states of disease.”
The researchers wrote they lacked biomarkers to confirm Alzheimer’s disease pathology. Most of the study participants were white Europeans, which “limits extrapolation [of the findings] to other populations,” they added.
The Alzheimer’s Drug Discovery Foundation and the Dutch Alzheimer Society funded the NILVAD cerebral blood flow substudy. NILVAD was funded by the European Commission Framework 7 Program Health Theme. Dr. Claassen had no disclosures; one coauthor disclosed a pending patent for nilvadipine.
SOURCE: Claassen JAHR et al. Hypertension. 2019 Jun 17. doi: 10.1161/HYPERTENSIONAHA.119.12892.
FROM HYPERTENSION
Frailty Tools are Not Yet Ready for Prime Time in High-Risk Identification
In this issue of the Journal of Hospital Medicine, McAlister et al.1 compared the ability of the Clinical Frailty Scale (CFS) and the Hospital Frailty Risk Score (HFRS) to predict 30-day readmission or death. The authors prospectively assessed adult patients aged ≥18 years without cognitive impairment being discharged back to the community after medical admissions. They demonstrated only modest overlap in frailty designation between HFRS and CFS and concluded that CFS is better than HFRS for predicting the outcomes of interest.
Before a prediction rule is widely adopted for use in routine practice, robust external validation is needed.2 Factors such as the prevalence of disease in a population, the clinical competencies of a health system, the socioeconomic status, and the ethnicity of the population can all affect how well a clinical rule performs, but may not become apparent until a prospective validation in a different population is attempted.
In developing the HFRS, Gilbert et al. aimed to create a low-cost, highly generalizable method of identifying frailty using International Classification of Diseases (ICD) 10 billing codes.3 The derivation and validation cohorts for HFRS included older adults aged >75 years in the United Kingdom, many of whom had cognitive impairment. Therefore, it is not surprising that the tool behaved very differently in the younger Canadian cohort described by McAlister et al. where persons with cognitive impairment were excluded. That the HFRS had less predictability in the Canadian cohort may simply indicate that it performs better in an older population with cognitive vulnerabilities; given the frailty constructs of the CFS, it may provide less insights in older populations.
We applaud the efforts to find a way to better identify high-risk groups of adults. We also appreciate the increasing attention to function and other frailty-related domains in risk prediction models. Nevertheless, we recommend caution in using any of the many existing frailty indices4 in risk prediction tools unless it is clear what domains of frailty are most relevant for the predicted outcome and what population is the subject of interest.
One of the challenges of choosing an appropriate frailty tool is that different tools are measuring different domains or constructs of frailty. Most consider frailty either as a physical phenotype5 or as a more multifaceted construct with impairments in physical and mental health, function, and social interaction.6 There is often poor overlap between those individuals identified as frail by different measures, highlighting that they are in fact identifying different people within the population studied and have different predictive abilities.
An ideal frailty tool for clinical use would allow clinicians to identify high-risk patients relative to specific outcome(s) in real time prior to discharge from hospital or prior to a sentinel event in the community. CFS can be calculated at the bedside, but HFRS calculation can only be done retrospectively when medical records are coded for claims after discharge. This makes HFRS more suited to research or post hoc quality measure work and CFS more suited to clinical use as the authors describe.
Although using a frailty indicator to help determine those at high risk of early readmission is an important objective, the presence of frailty accounts for only part of a person’s risk for readmission or other untoward events. Reasons for readmissions are complex and often heavily weighted on a lack of social and community supports. A deeper understanding of the reasons for readmission is needed to establish whether readmission of these complex patients has more to do with frailty or other drivers such as poor transitions of care.
The prevalence of frailty will continue to increase as our population ages. Definitions of frailty vary, but there is a broad agreement that frailty, regardless of how it is constructed, increases with age, results in multisystem changes, and leads to increased healthcare utilization and costs. Preventing the development of frailty, identifying frailty, and developing interventions to address frailty in and out of the hospital setting are all vital. We welcome further research regarding the biopsychosocial constructs of frailty, how they overlap with the frailty phenotype, and how these constructs inform both our understanding of frailty and the use of frailty tools.
Disclosures
The authors have no conflicts of interest to report.
1. McAlister FA, Lin M, Bakal JA. Prevalence and Postdischarge Outcomes Associated with Frailty in Medical Inpatients: Impact of Different Frailty Definitions. J Hosp Med. 2019;14(7):407-410. doi: 10.12788/jhm.3174 PubMed
2. Wasson JH, Sox HC, Neff RK, Goldman L. Clinical prediction rules. Applications and methodological standards. N Engl J Med. 1985;313(13):793-799. doi: 10.1056/NEJM198509263131306. PubMed
3. Gilbert T, Neuburger J, Kraindler J, et al. Development and validation of a Hospital Frailty Risk Score focusing on older people in acute care settings using electronic hospital records: an observational study. Lancet. 2018;391(10132):1775-1782. doi: 10.1016/S0140-6736(18)30668-8. PubMed
4. de Vries NM, Staal JB, van Ravensberg CD, et al. Outcome instruments to measure frailty: a systematic review. Ageing Res Rev. 2011;10(1):104-114. doi: 0.1016/j.arr.2010.09.001. PubMed
5. Fried LP, Tangen CM, Walston J, et al. Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001;56(3);M146-M156. PubMed
6. Cesari M, Gambassi G, van Kan GA, Vellas B. The frailty phenotype and the frailty index: different instruments for different purposes. Age Ageing. 2014;43(1):10-12. doi: 10.1093/ageing/aft160. PubMed
In this issue of the Journal of Hospital Medicine, McAlister et al.1 compared the ability of the Clinical Frailty Scale (CFS) and the Hospital Frailty Risk Score (HFRS) to predict 30-day readmission or death. The authors prospectively assessed adult patients aged ≥18 years without cognitive impairment being discharged back to the community after medical admissions. They demonstrated only modest overlap in frailty designation between HFRS and CFS and concluded that CFS is better than HFRS for predicting the outcomes of interest.
Before a prediction rule is widely adopted for use in routine practice, robust external validation is needed.2 Factors such as the prevalence of disease in a population, the clinical competencies of a health system, the socioeconomic status, and the ethnicity of the population can all affect how well a clinical rule performs, but may not become apparent until a prospective validation in a different population is attempted.
In developing the HFRS, Gilbert et al. aimed to create a low-cost, highly generalizable method of identifying frailty using International Classification of Diseases (ICD) 10 billing codes.3 The derivation and validation cohorts for HFRS included older adults aged >75 years in the United Kingdom, many of whom had cognitive impairment. Therefore, it is not surprising that the tool behaved very differently in the younger Canadian cohort described by McAlister et al. where persons with cognitive impairment were excluded. That the HFRS had less predictability in the Canadian cohort may simply indicate that it performs better in an older population with cognitive vulnerabilities; given the frailty constructs of the CFS, it may provide less insights in older populations.
We applaud the efforts to find a way to better identify high-risk groups of adults. We also appreciate the increasing attention to function and other frailty-related domains in risk prediction models. Nevertheless, we recommend caution in using any of the many existing frailty indices4 in risk prediction tools unless it is clear what domains of frailty are most relevant for the predicted outcome and what population is the subject of interest.
One of the challenges of choosing an appropriate frailty tool is that different tools are measuring different domains or constructs of frailty. Most consider frailty either as a physical phenotype5 or as a more multifaceted construct with impairments in physical and mental health, function, and social interaction.6 There is often poor overlap between those individuals identified as frail by different measures, highlighting that they are in fact identifying different people within the population studied and have different predictive abilities.
An ideal frailty tool for clinical use would allow clinicians to identify high-risk patients relative to specific outcome(s) in real time prior to discharge from hospital or prior to a sentinel event in the community. CFS can be calculated at the bedside, but HFRS calculation can only be done retrospectively when medical records are coded for claims after discharge. This makes HFRS more suited to research or post hoc quality measure work and CFS more suited to clinical use as the authors describe.
Although using a frailty indicator to help determine those at high risk of early readmission is an important objective, the presence of frailty accounts for only part of a person’s risk for readmission or other untoward events. Reasons for readmissions are complex and often heavily weighted on a lack of social and community supports. A deeper understanding of the reasons for readmission is needed to establish whether readmission of these complex patients has more to do with frailty or other drivers such as poor transitions of care.
The prevalence of frailty will continue to increase as our population ages. Definitions of frailty vary, but there is a broad agreement that frailty, regardless of how it is constructed, increases with age, results in multisystem changes, and leads to increased healthcare utilization and costs. Preventing the development of frailty, identifying frailty, and developing interventions to address frailty in and out of the hospital setting are all vital. We welcome further research regarding the biopsychosocial constructs of frailty, how they overlap with the frailty phenotype, and how these constructs inform both our understanding of frailty and the use of frailty tools.
Disclosures
The authors have no conflicts of interest to report.
In this issue of the Journal of Hospital Medicine, McAlister et al.1 compared the ability of the Clinical Frailty Scale (CFS) and the Hospital Frailty Risk Score (HFRS) to predict 30-day readmission or death. The authors prospectively assessed adult patients aged ≥18 years without cognitive impairment being discharged back to the community after medical admissions. They demonstrated only modest overlap in frailty designation between HFRS and CFS and concluded that CFS is better than HFRS for predicting the outcomes of interest.
Before a prediction rule is widely adopted for use in routine practice, robust external validation is needed.2 Factors such as the prevalence of disease in a population, the clinical competencies of a health system, the socioeconomic status, and the ethnicity of the population can all affect how well a clinical rule performs, but may not become apparent until a prospective validation in a different population is attempted.
In developing the HFRS, Gilbert et al. aimed to create a low-cost, highly generalizable method of identifying frailty using International Classification of Diseases (ICD) 10 billing codes.3 The derivation and validation cohorts for HFRS included older adults aged >75 years in the United Kingdom, many of whom had cognitive impairment. Therefore, it is not surprising that the tool behaved very differently in the younger Canadian cohort described by McAlister et al. where persons with cognitive impairment were excluded. That the HFRS had less predictability in the Canadian cohort may simply indicate that it performs better in an older population with cognitive vulnerabilities; given the frailty constructs of the CFS, it may provide less insights in older populations.
We applaud the efforts to find a way to better identify high-risk groups of adults. We also appreciate the increasing attention to function and other frailty-related domains in risk prediction models. Nevertheless, we recommend caution in using any of the many existing frailty indices4 in risk prediction tools unless it is clear what domains of frailty are most relevant for the predicted outcome and what population is the subject of interest.
One of the challenges of choosing an appropriate frailty tool is that different tools are measuring different domains or constructs of frailty. Most consider frailty either as a physical phenotype5 or as a more multifaceted construct with impairments in physical and mental health, function, and social interaction.6 There is often poor overlap between those individuals identified as frail by different measures, highlighting that they are in fact identifying different people within the population studied and have different predictive abilities.
An ideal frailty tool for clinical use would allow clinicians to identify high-risk patients relative to specific outcome(s) in real time prior to discharge from hospital or prior to a sentinel event in the community. CFS can be calculated at the bedside, but HFRS calculation can only be done retrospectively when medical records are coded for claims after discharge. This makes HFRS more suited to research or post hoc quality measure work and CFS more suited to clinical use as the authors describe.
Although using a frailty indicator to help determine those at high risk of early readmission is an important objective, the presence of frailty accounts for only part of a person’s risk for readmission or other untoward events. Reasons for readmissions are complex and often heavily weighted on a lack of social and community supports. A deeper understanding of the reasons for readmission is needed to establish whether readmission of these complex patients has more to do with frailty or other drivers such as poor transitions of care.
The prevalence of frailty will continue to increase as our population ages. Definitions of frailty vary, but there is a broad agreement that frailty, regardless of how it is constructed, increases with age, results in multisystem changes, and leads to increased healthcare utilization and costs. Preventing the development of frailty, identifying frailty, and developing interventions to address frailty in and out of the hospital setting are all vital. We welcome further research regarding the biopsychosocial constructs of frailty, how they overlap with the frailty phenotype, and how these constructs inform both our understanding of frailty and the use of frailty tools.
Disclosures
The authors have no conflicts of interest to report.
1. McAlister FA, Lin M, Bakal JA. Prevalence and Postdischarge Outcomes Associated with Frailty in Medical Inpatients: Impact of Different Frailty Definitions. J Hosp Med. 2019;14(7):407-410. doi: 10.12788/jhm.3174 PubMed
2. Wasson JH, Sox HC, Neff RK, Goldman L. Clinical prediction rules. Applications and methodological standards. N Engl J Med. 1985;313(13):793-799. doi: 10.1056/NEJM198509263131306. PubMed
3. Gilbert T, Neuburger J, Kraindler J, et al. Development and validation of a Hospital Frailty Risk Score focusing on older people in acute care settings using electronic hospital records: an observational study. Lancet. 2018;391(10132):1775-1782. doi: 10.1016/S0140-6736(18)30668-8. PubMed
4. de Vries NM, Staal JB, van Ravensberg CD, et al. Outcome instruments to measure frailty: a systematic review. Ageing Res Rev. 2011;10(1):104-114. doi: 0.1016/j.arr.2010.09.001. PubMed
5. Fried LP, Tangen CM, Walston J, et al. Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001;56(3);M146-M156. PubMed
6. Cesari M, Gambassi G, van Kan GA, Vellas B. The frailty phenotype and the frailty index: different instruments for different purposes. Age Ageing. 2014;43(1):10-12. doi: 10.1093/ageing/aft160. PubMed
1. McAlister FA, Lin M, Bakal JA. Prevalence and Postdischarge Outcomes Associated with Frailty in Medical Inpatients: Impact of Different Frailty Definitions. J Hosp Med. 2019;14(7):407-410. doi: 10.12788/jhm.3174 PubMed
2. Wasson JH, Sox HC, Neff RK, Goldman L. Clinical prediction rules. Applications and methodological standards. N Engl J Med. 1985;313(13):793-799. doi: 10.1056/NEJM198509263131306. PubMed
3. Gilbert T, Neuburger J, Kraindler J, et al. Development and validation of a Hospital Frailty Risk Score focusing on older people in acute care settings using electronic hospital records: an observational study. Lancet. 2018;391(10132):1775-1782. doi: 10.1016/S0140-6736(18)30668-8. PubMed
4. de Vries NM, Staal JB, van Ravensberg CD, et al. Outcome instruments to measure frailty: a systematic review. Ageing Res Rev. 2011;10(1):104-114. doi: 0.1016/j.arr.2010.09.001. PubMed
5. Fried LP, Tangen CM, Walston J, et al. Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001;56(3);M146-M156. PubMed
6. Cesari M, Gambassi G, van Kan GA, Vellas B. The frailty phenotype and the frailty index: different instruments for different purposes. Age Ageing. 2014;43(1):10-12. doi: 10.1093/ageing/aft160. PubMed
© 2019 Society of Hospital Medicine