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‘Deeper dive’ into opioid overdose deaths during COVID pandemic
Opioid overdose deaths were significantly higher during 2020, but occurrences were not homogeneous across nine states. Male deaths were higher than in the 2 previous years in two states, according to a new, granular examination of data collected by researchers at the Massachusetts General Hospital (Mass General), Boston.
The analysis also showed that synthetic opioids such as fentanyl played an outsized role in most of the states that were reviewed. Additional drugs of abuse found in decedents, such as cocaine and psychostimulants, were more prevalent in some states than in others.
The Centers for Disease Control and Prevention used provisional death data in its recent report. It found that opioid-related deaths substantially rose in 2020 and that synthetic opioids were a primary driver.
The current Mass General analysis provides a more timely and detailed dive, senior author Mohammad Jalali, PhD, who is a senior scientist at Mass General’s Institute for Technology Assessment, told this news organization.
The findings, which have not yet been peer reviewed, were published in MedRxiv.
Shifting sands of opioid use disorder
to analyze and project trends and also to be better prepared to address the shifting sands of opioid use disorder in the United States.
They attempted to collect data on confirmed opioid overdose deaths from all 50 states and Washington, D.C. to assess what might have changed during the COVID-19 pandemic. Only nine states provided enough data for the analysis, which has been submitted to a peer reviewed publication.
These states were Alaska, Connecticut, Indiana, Massachusetts, North Carolina, Rhode Island, Colorado, Utah, and Wyoming.
“Drug overdose data are collected and reported more slowly than COVID-19 data,” Dr. Jalali said in a press release. The data reflected a lag time of about 4 to 8 months in Massachusetts and North Carolina to more than a year in Maryland and Ohio, he noted.
The reporting lag “has clouded the understanding of the effects of the COVID-19 pandemic on opioid-related overdose deaths,” said Dr. Jalali.
Commenting on the findings, Brandon Marshall, PhD, associate professor of epidemiology at Brown University, Providence, R.I, said that “the overall pattern of what’s being reported here is not surprising,” given the national trends seen in the CDC data.
“This paper adds a deeper dive into some of the sociodemographic trends that we’re starting to observe in specific states,” Dr. Marshall said.
Also commenting for this news organization, Brian Fuehrlein, MD, PhD, director of the psychiatric emergency department at the VA Connecticut Healthcare System in West Haven, Connecticut, noted that the current study “highlights things that we are currently seeing at VA Connecticut.”
Decrease in heroin, rise in fentanyl
The investigators found a significant reduction in overdose deaths that involved heroin in Alaska, Connecticut, Indiana, Massachusetts, North Carolina, and Rhode Island. That was a new trend for Alaska, Indiana, and Rhode Island, although with only 3 years of data, it’s hard to say whether it will continue, Dr. Jalali noted.
The decrease in heroin involvement seemed to continue a trend previously observed in Colorado, Connecticut, Massachusetts, and North Carolina.
In Connecticut, heroin was involved in 36% of deaths in 2018, 30% in 2019, and 16% in 2020, according to the study.
“We have begun seeing more and more heroin-negative, fentanyl-positive drug screens,” said Dr. Fuehrlein, who is also associate professor of psychiatry at Yale University, New Haven, Conn.
“There is a shift from fentanyl being an adulterant to fentanyl being what is sold and used exclusively,” he added.
In 2020, 92% (n = 887) of deaths in Connecticut involved synthetic opioids, continuing a trend. In Alaska, however, synthetic opioids were involved in 60% (44) of deaths, which is a big jump from 23% (9) in 2018.
Synthetic opioids were involved in the largest percentage of overdoses in all of the states studied. The fewest deaths, 17 (49%), occurred in Wyoming.
Cocaine is also increasingly found in addition to other substances in decedents. In Alaska, about 14% of individuals who overdosed in 2020 also had cocaine in their system, which was a jump from 2% in the prior year.
In Colorado, 19% (94) of those who died also had taken cocaine, up from 13% in 2019. Cocaine was also frequently found in those who died in the northeast: 39% (467) of those who died in Massachusetts, 29% (280) in Connecticut, and 47% (109) in Rhode Island.
There was also an increase in psychostimulants found in those who had died in Massachusetts in 2020.
More male overdoses in 2020
Results also showed that, compared to 2019, significantly more men died from overdoses in 2020 in Colorado (61% vs. 70%, P = .017) and Indiana (62% vs. 70%, P = .026).
This finding was unexpected, said Dr. Marshall, who has observed the same phenomenon in Rhode Island. He is the scientific director of PreventOverdoseRI, Rhode Island’s drug overdose surveillance and information dashboard.
Dr. Marshall and his colleagues conducted a study that also found disproportionate increases in overdoses among men. The findings of that study will be published in September.
“We’re still trying to wrap our head around why that is,” he said. He added that a deeper dive into the Rhode Island data showed that the deaths were increased especially among middle-aged men who had been diagnosed with depression and anxiety.
The same patterns were not seen among women in either Dr. Jalali’s study or his own analysis of the Rhode Island data, said Dr. Marshall.
“That suggests the COVID-19 pandemic impacted men who are at risk for overdose in some particularly severe way,” he noted.
Dr. Fuehrlein said he believes a variety of factors have led to an increase in overdose deaths during the pandemic, including the fact that many patients who would normally seek help avoided care or dropped out of treatment because of COVID fears. In addition, other support systems, such as group therapy and Narcotics Anonymous, were unavailable.
The pandemic increased stress, which can lead to worsening substance use, said Dr. Fuehrlein. He also noted that regular opioid suppliers were often not available, which led some to buy from different dealers, “which can lead to overdose if the fentanyl content is different.”
Identifying at-risk individuals
Dr. Jalali and colleagues note that clinicians and policymakers could use the new study to help identify and treat at-risk individuals.
“Practitioners and policy makers can use our findings to help them anticipate which groups of people might be most affected by opioid overdose and which types of policy interventions might be most effective given each state’s unique situation,” said lead study author Gian-Gabriel P. Garcia, PhD, in a press release. At the time of the study, Dr. Garcia was a postdoctoral fellow at Mass General and Harvard Medical School. He is currently an assistant professor at Georgia Tech, Atlanta.
Dr. Marshall pointed out that Dr. Jalali’s study is also relevant for emergency departments.
ED clinicians “are and will be seeing patients coming in who have no idea they were exposed to an opioid, nevermind fentanyl,” he said. ED clinicians can discuss with patients various harm reduction techniques, including the use of naloxone as well as test strips that can detect fentanyl in the drug supply, he added.
“Given the increasing use of fentanyl, which is very dangerous in overdose, clinicians need to be well versed in a harm reduction/overdose prevention approach to patient care,” Dr. Fuehrlein agreed.
A version of this article first appeared on Medscape.com.
Opioid overdose deaths were significantly higher during 2020, but occurrences were not homogeneous across nine states. Male deaths were higher than in the 2 previous years in two states, according to a new, granular examination of data collected by researchers at the Massachusetts General Hospital (Mass General), Boston.
The analysis also showed that synthetic opioids such as fentanyl played an outsized role in most of the states that were reviewed. Additional drugs of abuse found in decedents, such as cocaine and psychostimulants, were more prevalent in some states than in others.
The Centers for Disease Control and Prevention used provisional death data in its recent report. It found that opioid-related deaths substantially rose in 2020 and that synthetic opioids were a primary driver.
The current Mass General analysis provides a more timely and detailed dive, senior author Mohammad Jalali, PhD, who is a senior scientist at Mass General’s Institute for Technology Assessment, told this news organization.
The findings, which have not yet been peer reviewed, were published in MedRxiv.
Shifting sands of opioid use disorder
to analyze and project trends and also to be better prepared to address the shifting sands of opioid use disorder in the United States.
They attempted to collect data on confirmed opioid overdose deaths from all 50 states and Washington, D.C. to assess what might have changed during the COVID-19 pandemic. Only nine states provided enough data for the analysis, which has been submitted to a peer reviewed publication.
These states were Alaska, Connecticut, Indiana, Massachusetts, North Carolina, Rhode Island, Colorado, Utah, and Wyoming.
“Drug overdose data are collected and reported more slowly than COVID-19 data,” Dr. Jalali said in a press release. The data reflected a lag time of about 4 to 8 months in Massachusetts and North Carolina to more than a year in Maryland and Ohio, he noted.
The reporting lag “has clouded the understanding of the effects of the COVID-19 pandemic on opioid-related overdose deaths,” said Dr. Jalali.
Commenting on the findings, Brandon Marshall, PhD, associate professor of epidemiology at Brown University, Providence, R.I, said that “the overall pattern of what’s being reported here is not surprising,” given the national trends seen in the CDC data.
“This paper adds a deeper dive into some of the sociodemographic trends that we’re starting to observe in specific states,” Dr. Marshall said.
Also commenting for this news organization, Brian Fuehrlein, MD, PhD, director of the psychiatric emergency department at the VA Connecticut Healthcare System in West Haven, Connecticut, noted that the current study “highlights things that we are currently seeing at VA Connecticut.”
Decrease in heroin, rise in fentanyl
The investigators found a significant reduction in overdose deaths that involved heroin in Alaska, Connecticut, Indiana, Massachusetts, North Carolina, and Rhode Island. That was a new trend for Alaska, Indiana, and Rhode Island, although with only 3 years of data, it’s hard to say whether it will continue, Dr. Jalali noted.
The decrease in heroin involvement seemed to continue a trend previously observed in Colorado, Connecticut, Massachusetts, and North Carolina.
In Connecticut, heroin was involved in 36% of deaths in 2018, 30% in 2019, and 16% in 2020, according to the study.
“We have begun seeing more and more heroin-negative, fentanyl-positive drug screens,” said Dr. Fuehrlein, who is also associate professor of psychiatry at Yale University, New Haven, Conn.
“There is a shift from fentanyl being an adulterant to fentanyl being what is sold and used exclusively,” he added.
In 2020, 92% (n = 887) of deaths in Connecticut involved synthetic opioids, continuing a trend. In Alaska, however, synthetic opioids were involved in 60% (44) of deaths, which is a big jump from 23% (9) in 2018.
Synthetic opioids were involved in the largest percentage of overdoses in all of the states studied. The fewest deaths, 17 (49%), occurred in Wyoming.
Cocaine is also increasingly found in addition to other substances in decedents. In Alaska, about 14% of individuals who overdosed in 2020 also had cocaine in their system, which was a jump from 2% in the prior year.
In Colorado, 19% (94) of those who died also had taken cocaine, up from 13% in 2019. Cocaine was also frequently found in those who died in the northeast: 39% (467) of those who died in Massachusetts, 29% (280) in Connecticut, and 47% (109) in Rhode Island.
There was also an increase in psychostimulants found in those who had died in Massachusetts in 2020.
More male overdoses in 2020
Results also showed that, compared to 2019, significantly more men died from overdoses in 2020 in Colorado (61% vs. 70%, P = .017) and Indiana (62% vs. 70%, P = .026).
This finding was unexpected, said Dr. Marshall, who has observed the same phenomenon in Rhode Island. He is the scientific director of PreventOverdoseRI, Rhode Island’s drug overdose surveillance and information dashboard.
Dr. Marshall and his colleagues conducted a study that also found disproportionate increases in overdoses among men. The findings of that study will be published in September.
“We’re still trying to wrap our head around why that is,” he said. He added that a deeper dive into the Rhode Island data showed that the deaths were increased especially among middle-aged men who had been diagnosed with depression and anxiety.
The same patterns were not seen among women in either Dr. Jalali’s study or his own analysis of the Rhode Island data, said Dr. Marshall.
“That suggests the COVID-19 pandemic impacted men who are at risk for overdose in some particularly severe way,” he noted.
Dr. Fuehrlein said he believes a variety of factors have led to an increase in overdose deaths during the pandemic, including the fact that many patients who would normally seek help avoided care or dropped out of treatment because of COVID fears. In addition, other support systems, such as group therapy and Narcotics Anonymous, were unavailable.
The pandemic increased stress, which can lead to worsening substance use, said Dr. Fuehrlein. He also noted that regular opioid suppliers were often not available, which led some to buy from different dealers, “which can lead to overdose if the fentanyl content is different.”
Identifying at-risk individuals
Dr. Jalali and colleagues note that clinicians and policymakers could use the new study to help identify and treat at-risk individuals.
“Practitioners and policy makers can use our findings to help them anticipate which groups of people might be most affected by opioid overdose and which types of policy interventions might be most effective given each state’s unique situation,” said lead study author Gian-Gabriel P. Garcia, PhD, in a press release. At the time of the study, Dr. Garcia was a postdoctoral fellow at Mass General and Harvard Medical School. He is currently an assistant professor at Georgia Tech, Atlanta.
Dr. Marshall pointed out that Dr. Jalali’s study is also relevant for emergency departments.
ED clinicians “are and will be seeing patients coming in who have no idea they were exposed to an opioid, nevermind fentanyl,” he said. ED clinicians can discuss with patients various harm reduction techniques, including the use of naloxone as well as test strips that can detect fentanyl in the drug supply, he added.
“Given the increasing use of fentanyl, which is very dangerous in overdose, clinicians need to be well versed in a harm reduction/overdose prevention approach to patient care,” Dr. Fuehrlein agreed.
A version of this article first appeared on Medscape.com.
Opioid overdose deaths were significantly higher during 2020, but occurrences were not homogeneous across nine states. Male deaths were higher than in the 2 previous years in two states, according to a new, granular examination of data collected by researchers at the Massachusetts General Hospital (Mass General), Boston.
The analysis also showed that synthetic opioids such as fentanyl played an outsized role in most of the states that were reviewed. Additional drugs of abuse found in decedents, such as cocaine and psychostimulants, were more prevalent in some states than in others.
The Centers for Disease Control and Prevention used provisional death data in its recent report. It found that opioid-related deaths substantially rose in 2020 and that synthetic opioids were a primary driver.
The current Mass General analysis provides a more timely and detailed dive, senior author Mohammad Jalali, PhD, who is a senior scientist at Mass General’s Institute for Technology Assessment, told this news organization.
The findings, which have not yet been peer reviewed, were published in MedRxiv.
Shifting sands of opioid use disorder
to analyze and project trends and also to be better prepared to address the shifting sands of opioid use disorder in the United States.
They attempted to collect data on confirmed opioid overdose deaths from all 50 states and Washington, D.C. to assess what might have changed during the COVID-19 pandemic. Only nine states provided enough data for the analysis, which has been submitted to a peer reviewed publication.
These states were Alaska, Connecticut, Indiana, Massachusetts, North Carolina, Rhode Island, Colorado, Utah, and Wyoming.
“Drug overdose data are collected and reported more slowly than COVID-19 data,” Dr. Jalali said in a press release. The data reflected a lag time of about 4 to 8 months in Massachusetts and North Carolina to more than a year in Maryland and Ohio, he noted.
The reporting lag “has clouded the understanding of the effects of the COVID-19 pandemic on opioid-related overdose deaths,” said Dr. Jalali.
Commenting on the findings, Brandon Marshall, PhD, associate professor of epidemiology at Brown University, Providence, R.I, said that “the overall pattern of what’s being reported here is not surprising,” given the national trends seen in the CDC data.
“This paper adds a deeper dive into some of the sociodemographic trends that we’re starting to observe in specific states,” Dr. Marshall said.
Also commenting for this news organization, Brian Fuehrlein, MD, PhD, director of the psychiatric emergency department at the VA Connecticut Healthcare System in West Haven, Connecticut, noted that the current study “highlights things that we are currently seeing at VA Connecticut.”
Decrease in heroin, rise in fentanyl
The investigators found a significant reduction in overdose deaths that involved heroin in Alaska, Connecticut, Indiana, Massachusetts, North Carolina, and Rhode Island. That was a new trend for Alaska, Indiana, and Rhode Island, although with only 3 years of data, it’s hard to say whether it will continue, Dr. Jalali noted.
The decrease in heroin involvement seemed to continue a trend previously observed in Colorado, Connecticut, Massachusetts, and North Carolina.
In Connecticut, heroin was involved in 36% of deaths in 2018, 30% in 2019, and 16% in 2020, according to the study.
“We have begun seeing more and more heroin-negative, fentanyl-positive drug screens,” said Dr. Fuehrlein, who is also associate professor of psychiatry at Yale University, New Haven, Conn.
“There is a shift from fentanyl being an adulterant to fentanyl being what is sold and used exclusively,” he added.
In 2020, 92% (n = 887) of deaths in Connecticut involved synthetic opioids, continuing a trend. In Alaska, however, synthetic opioids were involved in 60% (44) of deaths, which is a big jump from 23% (9) in 2018.
Synthetic opioids were involved in the largest percentage of overdoses in all of the states studied. The fewest deaths, 17 (49%), occurred in Wyoming.
Cocaine is also increasingly found in addition to other substances in decedents. In Alaska, about 14% of individuals who overdosed in 2020 also had cocaine in their system, which was a jump from 2% in the prior year.
In Colorado, 19% (94) of those who died also had taken cocaine, up from 13% in 2019. Cocaine was also frequently found in those who died in the northeast: 39% (467) of those who died in Massachusetts, 29% (280) in Connecticut, and 47% (109) in Rhode Island.
There was also an increase in psychostimulants found in those who had died in Massachusetts in 2020.
More male overdoses in 2020
Results also showed that, compared to 2019, significantly more men died from overdoses in 2020 in Colorado (61% vs. 70%, P = .017) and Indiana (62% vs. 70%, P = .026).
This finding was unexpected, said Dr. Marshall, who has observed the same phenomenon in Rhode Island. He is the scientific director of PreventOverdoseRI, Rhode Island’s drug overdose surveillance and information dashboard.
Dr. Marshall and his colleagues conducted a study that also found disproportionate increases in overdoses among men. The findings of that study will be published in September.
“We’re still trying to wrap our head around why that is,” he said. He added that a deeper dive into the Rhode Island data showed that the deaths were increased especially among middle-aged men who had been diagnosed with depression and anxiety.
The same patterns were not seen among women in either Dr. Jalali’s study or his own analysis of the Rhode Island data, said Dr. Marshall.
“That suggests the COVID-19 pandemic impacted men who are at risk for overdose in some particularly severe way,” he noted.
Dr. Fuehrlein said he believes a variety of factors have led to an increase in overdose deaths during the pandemic, including the fact that many patients who would normally seek help avoided care or dropped out of treatment because of COVID fears. In addition, other support systems, such as group therapy and Narcotics Anonymous, were unavailable.
The pandemic increased stress, which can lead to worsening substance use, said Dr. Fuehrlein. He also noted that regular opioid suppliers were often not available, which led some to buy from different dealers, “which can lead to overdose if the fentanyl content is different.”
Identifying at-risk individuals
Dr. Jalali and colleagues note that clinicians and policymakers could use the new study to help identify and treat at-risk individuals.
“Practitioners and policy makers can use our findings to help them anticipate which groups of people might be most affected by opioid overdose and which types of policy interventions might be most effective given each state’s unique situation,” said lead study author Gian-Gabriel P. Garcia, PhD, in a press release. At the time of the study, Dr. Garcia was a postdoctoral fellow at Mass General and Harvard Medical School. He is currently an assistant professor at Georgia Tech, Atlanta.
Dr. Marshall pointed out that Dr. Jalali’s study is also relevant for emergency departments.
ED clinicians “are and will be seeing patients coming in who have no idea they were exposed to an opioid, nevermind fentanyl,” he said. ED clinicians can discuss with patients various harm reduction techniques, including the use of naloxone as well as test strips that can detect fentanyl in the drug supply, he added.
“Given the increasing use of fentanyl, which is very dangerous in overdose, clinicians need to be well versed in a harm reduction/overdose prevention approach to patient care,” Dr. Fuehrlein agreed.
A version of this article first appeared on Medscape.com.
Early end for trial of experimental oxygenation strategies in ARDS
Background: Both observational studies and clinical trials have found that a liberal oxygenation strategy in multiple inpatient settings may be harmful. Furthermore, a conservative strategy is what has been recommended in guidelines. Conversely, the relevance of this recent concept has been challenged in a large trial of a critically ill population (ICU-ROX).
Study design: Randomized clinical trial, unblinded.
Setting: Thirteen sites in France.
Synopsis: In a multicenter randomized clinical trial, investigators enrolled patients with ARDS to either a liberal oxygenation group (PaO2 target 90-105 mm Hg or SpO2 of 96% or greater) or a conservative oxygenation group (PaO2 target 55-70 mm Hg or SpO2 88%-92%). The trial was planned for inclusion of 850 patients, but the data and safety monitoring board decided to stop the trial after inclusion of 205 patients. Although the primary outcome (28-day all-cause mortality) was not significantly different between groups (34.3% vs 26.5%; absolute difference, 7.8%; 95% confidence interval, –4.8 to 20.6), the direction was signaling possible harm and there were five episodes of mesenteric ischemia in the conservative oxygenation group (none in the liberal oxygenation group).
Bottom line: A conservative oxygenation strategy cannot be currently recommended to patients with ARDS in the ICU. A minimum SpO2 of 90% was suggested in an accompanying editorial.
Editorial commentary: Interestingly, the supplemental results of the article show that prone positioning was used much less frequently in the conservative oxygenation group (34.3 vs 51.0%). If the impressive results of Guerin (2013) would be repeated in this population, this difference could help explain the higher observed mortality in the conservative oxygenation group. It is possible that, by aiming to be less aggressive in improving the PaO2, clinicians inadvertently withheld effective treatments for ARDS. The results of this trial bring up several interesting questions, but provide the bedside clinician with few answers. The complex interplay of treatment factors needs to be dissected in future trials.
Citation: Barrot L et al. Liberal or conservative oxygen therapy for acute respiratory distress syndrome. N Eng J Med. 2020;382:999-1008.
Dr. Saraiva is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Background: Both observational studies and clinical trials have found that a liberal oxygenation strategy in multiple inpatient settings may be harmful. Furthermore, a conservative strategy is what has been recommended in guidelines. Conversely, the relevance of this recent concept has been challenged in a large trial of a critically ill population (ICU-ROX).
Study design: Randomized clinical trial, unblinded.
Setting: Thirteen sites in France.
Synopsis: In a multicenter randomized clinical trial, investigators enrolled patients with ARDS to either a liberal oxygenation group (PaO2 target 90-105 mm Hg or SpO2 of 96% or greater) or a conservative oxygenation group (PaO2 target 55-70 mm Hg or SpO2 88%-92%). The trial was planned for inclusion of 850 patients, but the data and safety monitoring board decided to stop the trial after inclusion of 205 patients. Although the primary outcome (28-day all-cause mortality) was not significantly different between groups (34.3% vs 26.5%; absolute difference, 7.8%; 95% confidence interval, –4.8 to 20.6), the direction was signaling possible harm and there were five episodes of mesenteric ischemia in the conservative oxygenation group (none in the liberal oxygenation group).
Bottom line: A conservative oxygenation strategy cannot be currently recommended to patients with ARDS in the ICU. A minimum SpO2 of 90% was suggested in an accompanying editorial.
Editorial commentary: Interestingly, the supplemental results of the article show that prone positioning was used much less frequently in the conservative oxygenation group (34.3 vs 51.0%). If the impressive results of Guerin (2013) would be repeated in this population, this difference could help explain the higher observed mortality in the conservative oxygenation group. It is possible that, by aiming to be less aggressive in improving the PaO2, clinicians inadvertently withheld effective treatments for ARDS. The results of this trial bring up several interesting questions, but provide the bedside clinician with few answers. The complex interplay of treatment factors needs to be dissected in future trials.
Citation: Barrot L et al. Liberal or conservative oxygen therapy for acute respiratory distress syndrome. N Eng J Med. 2020;382:999-1008.
Dr. Saraiva is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Background: Both observational studies and clinical trials have found that a liberal oxygenation strategy in multiple inpatient settings may be harmful. Furthermore, a conservative strategy is what has been recommended in guidelines. Conversely, the relevance of this recent concept has been challenged in a large trial of a critically ill population (ICU-ROX).
Study design: Randomized clinical trial, unblinded.
Setting: Thirteen sites in France.
Synopsis: In a multicenter randomized clinical trial, investigators enrolled patients with ARDS to either a liberal oxygenation group (PaO2 target 90-105 mm Hg or SpO2 of 96% or greater) or a conservative oxygenation group (PaO2 target 55-70 mm Hg or SpO2 88%-92%). The trial was planned for inclusion of 850 patients, but the data and safety monitoring board decided to stop the trial after inclusion of 205 patients. Although the primary outcome (28-day all-cause mortality) was not significantly different between groups (34.3% vs 26.5%; absolute difference, 7.8%; 95% confidence interval, –4.8 to 20.6), the direction was signaling possible harm and there were five episodes of mesenteric ischemia in the conservative oxygenation group (none in the liberal oxygenation group).
Bottom line: A conservative oxygenation strategy cannot be currently recommended to patients with ARDS in the ICU. A minimum SpO2 of 90% was suggested in an accompanying editorial.
Editorial commentary: Interestingly, the supplemental results of the article show that prone positioning was used much less frequently in the conservative oxygenation group (34.3 vs 51.0%). If the impressive results of Guerin (2013) would be repeated in this population, this difference could help explain the higher observed mortality in the conservative oxygenation group. It is possible that, by aiming to be less aggressive in improving the PaO2, clinicians inadvertently withheld effective treatments for ARDS. The results of this trial bring up several interesting questions, but provide the bedside clinician with few answers. The complex interplay of treatment factors needs to be dissected in future trials.
Citation: Barrot L et al. Liberal or conservative oxygen therapy for acute respiratory distress syndrome. N Eng J Med. 2020;382:999-1008.
Dr. Saraiva is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Advocates seek to reframe masks as a disability accommodation
As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.
For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.
argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.
This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
How did you come to think about mask requirements as a form of disability accommodation?
I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?
I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.
For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?
The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.
The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.
In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
In your view, can this argument be used in the mask debates happening right now across the country?
This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.
I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?
I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.
We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.
A version of this article first appeared on Medscape.com.
As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.
For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.
argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.
This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
How did you come to think about mask requirements as a form of disability accommodation?
I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?
I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.
For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?
The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.
The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.
In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
In your view, can this argument be used in the mask debates happening right now across the country?
This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.
I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?
I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.
We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.
A version of this article first appeared on Medscape.com.
As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.
For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.
argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.
This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
How did you come to think about mask requirements as a form of disability accommodation?
I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?
I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.
For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?
The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.
The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.
In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
In your view, can this argument be used in the mask debates happening right now across the country?
This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.
I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?
I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.
We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.
A version of this article first appeared on Medscape.com.
EAACI review urges reduction in antibiotic overuse with allergy
Urgent recommendations from a European Academy of Allergy and Clinical Immunology (EAACI) task force are aimed at reducing antibiotic overuse with allergic disease.
Top recommendations include limiting antibiotic therapy in pregnancy and early childhood to help reduce the allergy epidemic in children, and restricting antibiotic therapy in exacerbations and chronic treatment of allergic diseases, especially asthma and atopic dermatitis.
The review, by lead author Gerdien Tramper-Stranders, MD, PhD, department of pediatrics, Franciscus Gasthuis & Vlietland Hospital, Rotterdam, the Netherlands, and colleagues, was published online Aug. 13 in the journal Allergy.
Several studies have shown that use of antibiotics in childhood and during pregnancy is associated with disturbing the intestinal and respiratory microbiome, which in turn leads to dysbiosis and an increased risk of acquiring allergic diseases, the authors noted.
In addition, patients with allergic diseases such as asthma have a higher risk of being prescribed antibiotics for infections compared with the general population, despite lack of clear clinical benefit.
“In fact, there are no clear data supporting antibiotic prescriptions for acute exacerbations; and clinical and/or laboratory criteria are lacking,” the authors wrote.
Despite that lack of data, antibiotics are often prescribed for exacerbations along with oral corticosteroids, Dr. Tramper-Stranders said in an interview. Some patients may benefit from antibiotics in a flare-up, she said, but more research is needed to determine which ones.
Dr. Tramper-Stranders said Franciscus has begun a large study that includes patients with asthma exacerbations to find biomarkers that might predict the type or origin of exacerbation to personalize treatment.
Recommendations have global relevance
She said although the recommendations are coming from the EAACI group, they apply worldwide.
“Especially in countries outside Northern Europe, antibiotic use is tremendous, leading to high rates of antibiotic resistance; but also increasing the risk for developing allergic diseases when prescribed in infancy,” she said.
She pointed out that in the United States, as many as one in six children receive unnecessary antibiotics for an asthma exacerbation. Overtreatment in adults with flare-ups is also prevalent, at rates from 40%-50%.
Millie Kwan, MD, PhD, an allergy specialist at University of North Carolina in Chapel Hill, said in an interview that in the U.S. there’s been a culture change in the direction of antibiotic restraint – but there are still problems.
“It’s a lot easier for us to whip out our prescription pads and prescribe antibiotics for an asthma patient who’s having a flare-up or a patient who has atopic dermatitis before addressing the underlying mechanism directly,” Dr. Kwan said. She agreed that antibiotic overuse is prevalent in pregnancies in the U.S., and she said that starts with the high prevalence of cesarean births. Nearly one-third of all births in the U.S. are by C-section, twice the rate recommended by the World Health Organization.
“Just bypassing the birth canal actually changes what kind of microflora the infant is being exposed to,” Dr. Kwan said. “That’s the first huge problem.”
The second problem, she said, is the potential for overuse of antibiotics with the surgical procedure.
The researchers wrote that pre-, pro- or postbiotics might alter the course of allergic disease, but clear evidence is lacking.
Until now, Dr. Tramper-Stranders said, pre- or probiotic treatment in infancy, irrespective of previous antibiotic use, has not proved effective in preventing allergies.
Data describing the effect of pre- or probiotics after an antibiotic course are scarce, are limited to older children and adults, and are focused on short-term effects, such as diarrhea prevention, she explained.
Dr. Kwan says she agrees that current data are not strong enough to recommend one over another.
“We don’t even know what the normal amount of bacteria should be to constitute an environment where the immune system develops ‘normally,’ “ she said.
Antibiotics should be prescribed cautiously and by following current recommendations to use the narrowest spectrum available, the authors wrote. Future research in antibiotic stewardship should incorporate biomarker-guided therapy to determine which patients might benefit most from antibiotic therapy.
“Practicing antibiotic stewardship needs recurrent attention and we hope that with this initiative, we specifically reach allergy doctors who will rethink their next [antibiotic] prescription. Within our EAACI task force, we will next work on a guideline for rational antibiotic use in asthma,” Dr. Tramper-Stranders said.
The review’s authors and Dr. Kwan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Urgent recommendations from a European Academy of Allergy and Clinical Immunology (EAACI) task force are aimed at reducing antibiotic overuse with allergic disease.
Top recommendations include limiting antibiotic therapy in pregnancy and early childhood to help reduce the allergy epidemic in children, and restricting antibiotic therapy in exacerbations and chronic treatment of allergic diseases, especially asthma and atopic dermatitis.
The review, by lead author Gerdien Tramper-Stranders, MD, PhD, department of pediatrics, Franciscus Gasthuis & Vlietland Hospital, Rotterdam, the Netherlands, and colleagues, was published online Aug. 13 in the journal Allergy.
Several studies have shown that use of antibiotics in childhood and during pregnancy is associated with disturbing the intestinal and respiratory microbiome, which in turn leads to dysbiosis and an increased risk of acquiring allergic diseases, the authors noted.
In addition, patients with allergic diseases such as asthma have a higher risk of being prescribed antibiotics for infections compared with the general population, despite lack of clear clinical benefit.
“In fact, there are no clear data supporting antibiotic prescriptions for acute exacerbations; and clinical and/or laboratory criteria are lacking,” the authors wrote.
Despite that lack of data, antibiotics are often prescribed for exacerbations along with oral corticosteroids, Dr. Tramper-Stranders said in an interview. Some patients may benefit from antibiotics in a flare-up, she said, but more research is needed to determine which ones.
Dr. Tramper-Stranders said Franciscus has begun a large study that includes patients with asthma exacerbations to find biomarkers that might predict the type or origin of exacerbation to personalize treatment.
Recommendations have global relevance
She said although the recommendations are coming from the EAACI group, they apply worldwide.
“Especially in countries outside Northern Europe, antibiotic use is tremendous, leading to high rates of antibiotic resistance; but also increasing the risk for developing allergic diseases when prescribed in infancy,” she said.
She pointed out that in the United States, as many as one in six children receive unnecessary antibiotics for an asthma exacerbation. Overtreatment in adults with flare-ups is also prevalent, at rates from 40%-50%.
Millie Kwan, MD, PhD, an allergy specialist at University of North Carolina in Chapel Hill, said in an interview that in the U.S. there’s been a culture change in the direction of antibiotic restraint – but there are still problems.
“It’s a lot easier for us to whip out our prescription pads and prescribe antibiotics for an asthma patient who’s having a flare-up or a patient who has atopic dermatitis before addressing the underlying mechanism directly,” Dr. Kwan said. She agreed that antibiotic overuse is prevalent in pregnancies in the U.S., and she said that starts with the high prevalence of cesarean births. Nearly one-third of all births in the U.S. are by C-section, twice the rate recommended by the World Health Organization.
“Just bypassing the birth canal actually changes what kind of microflora the infant is being exposed to,” Dr. Kwan said. “That’s the first huge problem.”
The second problem, she said, is the potential for overuse of antibiotics with the surgical procedure.
The researchers wrote that pre-, pro- or postbiotics might alter the course of allergic disease, but clear evidence is lacking.
Until now, Dr. Tramper-Stranders said, pre- or probiotic treatment in infancy, irrespective of previous antibiotic use, has not proved effective in preventing allergies.
Data describing the effect of pre- or probiotics after an antibiotic course are scarce, are limited to older children and adults, and are focused on short-term effects, such as diarrhea prevention, she explained.
Dr. Kwan says she agrees that current data are not strong enough to recommend one over another.
“We don’t even know what the normal amount of bacteria should be to constitute an environment where the immune system develops ‘normally,’ “ she said.
Antibiotics should be prescribed cautiously and by following current recommendations to use the narrowest spectrum available, the authors wrote. Future research in antibiotic stewardship should incorporate biomarker-guided therapy to determine which patients might benefit most from antibiotic therapy.
“Practicing antibiotic stewardship needs recurrent attention and we hope that with this initiative, we specifically reach allergy doctors who will rethink their next [antibiotic] prescription. Within our EAACI task force, we will next work on a guideline for rational antibiotic use in asthma,” Dr. Tramper-Stranders said.
The review’s authors and Dr. Kwan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Urgent recommendations from a European Academy of Allergy and Clinical Immunology (EAACI) task force are aimed at reducing antibiotic overuse with allergic disease.
Top recommendations include limiting antibiotic therapy in pregnancy and early childhood to help reduce the allergy epidemic in children, and restricting antibiotic therapy in exacerbations and chronic treatment of allergic diseases, especially asthma and atopic dermatitis.
The review, by lead author Gerdien Tramper-Stranders, MD, PhD, department of pediatrics, Franciscus Gasthuis & Vlietland Hospital, Rotterdam, the Netherlands, and colleagues, was published online Aug. 13 in the journal Allergy.
Several studies have shown that use of antibiotics in childhood and during pregnancy is associated with disturbing the intestinal and respiratory microbiome, which in turn leads to dysbiosis and an increased risk of acquiring allergic diseases, the authors noted.
In addition, patients with allergic diseases such as asthma have a higher risk of being prescribed antibiotics for infections compared with the general population, despite lack of clear clinical benefit.
“In fact, there are no clear data supporting antibiotic prescriptions for acute exacerbations; and clinical and/or laboratory criteria are lacking,” the authors wrote.
Despite that lack of data, antibiotics are often prescribed for exacerbations along with oral corticosteroids, Dr. Tramper-Stranders said in an interview. Some patients may benefit from antibiotics in a flare-up, she said, but more research is needed to determine which ones.
Dr. Tramper-Stranders said Franciscus has begun a large study that includes patients with asthma exacerbations to find biomarkers that might predict the type or origin of exacerbation to personalize treatment.
Recommendations have global relevance
She said although the recommendations are coming from the EAACI group, they apply worldwide.
“Especially in countries outside Northern Europe, antibiotic use is tremendous, leading to high rates of antibiotic resistance; but also increasing the risk for developing allergic diseases when prescribed in infancy,” she said.
She pointed out that in the United States, as many as one in six children receive unnecessary antibiotics for an asthma exacerbation. Overtreatment in adults with flare-ups is also prevalent, at rates from 40%-50%.
Millie Kwan, MD, PhD, an allergy specialist at University of North Carolina in Chapel Hill, said in an interview that in the U.S. there’s been a culture change in the direction of antibiotic restraint – but there are still problems.
“It’s a lot easier for us to whip out our prescription pads and prescribe antibiotics for an asthma patient who’s having a flare-up or a patient who has atopic dermatitis before addressing the underlying mechanism directly,” Dr. Kwan said. She agreed that antibiotic overuse is prevalent in pregnancies in the U.S., and she said that starts with the high prevalence of cesarean births. Nearly one-third of all births in the U.S. are by C-section, twice the rate recommended by the World Health Organization.
“Just bypassing the birth canal actually changes what kind of microflora the infant is being exposed to,” Dr. Kwan said. “That’s the first huge problem.”
The second problem, she said, is the potential for overuse of antibiotics with the surgical procedure.
The researchers wrote that pre-, pro- or postbiotics might alter the course of allergic disease, but clear evidence is lacking.
Until now, Dr. Tramper-Stranders said, pre- or probiotic treatment in infancy, irrespective of previous antibiotic use, has not proved effective in preventing allergies.
Data describing the effect of pre- or probiotics after an antibiotic course are scarce, are limited to older children and adults, and are focused on short-term effects, such as diarrhea prevention, she explained.
Dr. Kwan says she agrees that current data are not strong enough to recommend one over another.
“We don’t even know what the normal amount of bacteria should be to constitute an environment where the immune system develops ‘normally,’ “ she said.
Antibiotics should be prescribed cautiously and by following current recommendations to use the narrowest spectrum available, the authors wrote. Future research in antibiotic stewardship should incorporate biomarker-guided therapy to determine which patients might benefit most from antibiotic therapy.
“Practicing antibiotic stewardship needs recurrent attention and we hope that with this initiative, we specifically reach allergy doctors who will rethink their next [antibiotic] prescription. Within our EAACI task force, we will next work on a guideline for rational antibiotic use in asthma,” Dr. Tramper-Stranders said.
The review’s authors and Dr. Kwan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Genetic link may tie cannabis use disorder to severe COVID-19
The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”
“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”
The study was published in the journal Biological Psychiatry Global Open Science.
Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.
As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.
The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.
He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”
According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.
Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.
“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”
The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.
In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”
As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”
However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”
Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.
The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”
“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”
The study was published in the journal Biological Psychiatry Global Open Science.
Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.
As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.
The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.
He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”
According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.
Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.
“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”
The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.
In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”
As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”
However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”
Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.
The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”
“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”
The study was published in the journal Biological Psychiatry Global Open Science.
Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.
As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.
The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.
He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”
According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.
Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.
“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”
The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.
In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”
As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”
However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”
Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.
FROM BIOLOGICAL PSYCHIATRY GLOBAL OPEN SCIENCE
AHA targets rising prevalence of obstructive sleep apnea in children
Obstructive sleep apnea is becoming more common in children and adolescents as the prevalence of obesity increases, but it may also be a preventable risk factor for cardiovascular disease, according to a new scientific statement from the American Heart Association.
The statement focuses on the links between OSA and CVD risk factors in children and adolescents, and reviews diagnostic strategies and treatments. The writing committee reported that 1%-6% of children and adolescents have OSA, as do up to 60% of adolescents considered obese.
The statement was created by the AHA’s Atherosclerosis, Hypertension, and Obesity in the Young subcommittee of the Council on Cardiovascular Disease in the Young and was published online in the Journal of the American Heart Association.
Carissa M. Baker-Smith, MD, chair of the writing group chair and director of pediatric preventive cardiology at Nemours Cardiac Center, Alfred I. duPont Hospital for Children, Wilmington, Del., explained the rationale for issuing the statement at this time, noting that the relationship between OSA and CVD in adults is well documented.
“There has been less focus on the importance of recognizing and treating sleep apnea in youth,” she said in an interview. “Thus, we felt that it was vitally important to get the word out to parents and to providers that paying attention to the quality and duration of your child’s sleep is vitally important to a child’s long-term heart health. Risk factors for heart disease, when present in childhood, can persist into adulthood.”
Clarity on polysomnography
For making the diagnosis of OSA in children, the statement provides clarity on the use of polysomnography and the role of the apnea-hypopnea index, which is lower in children with OSA than in adults. “One controversy, or at least as I saw it, was whether or not polysomnography testing is always required to make the diagnosis of OSA and before proceeding with tonsil and adenoid removal among children for whom enlarged tonsils and adenoids are present,” Dr. Baker-Smith said. “Polysomnography testing is not always needed before an ear, nose, and throat surgeon may recommend surgery.”
The statement also noted that history and physical examination may not yield enough reliable information to distinguish OSA from snoring.
In areas where sleep laboratories that work with children aren’t available, alternative tests such as daytime nap polysomnography, nocturnal oximetry, and nocturnal video recording may be used – with a caveat. “These alternative tests have weaker positive and negative predictive values when compared with polysomnography,” the writing committee noted. Home sleep apnea tests aren’t recommended in children. Questionnaires “are useful as screening, but not as diagnostic tools.”
Pediatric patients being evaluated for OSA should also be screened for hypertension and metabolic syndrome, as well as central nervous system and behavioral disorders. Diagnosing OSA in children and adolescents requires “a high index of suspicion,” the committee wrote.
Pediatricians and pediatric cardiologists should exercise that high index of suspicion when receiving referrals for cardiac evaluations for attention deficit hyperactivity disorder medication, Dr. Baker-Smith said. “Take the time to ask about a child’s sleep – snoring, apnea, etc. – especially if the child has obesity, difficulty focusing during the day, and if there is evidence of systemic hypertension or other signs of metabolic syndrome,” she said.
Risk factors for OSA in children
The statement also reviewed risk factors for OSA, among them obesity, particularly among children younger than 6 years. Other risk factors include upper and lower airway disease, hypotonia, parental history of hyperplasia of the adenoids and tonsils, craniofacial malformations, and neuromuscular disorders. However, the committee cited “limited data” to support that children with congenital heart disease may be at greater risk for OSA and sleep-disordered breathing (SDB).
Black children are at significantly greater risk, and socioeconomic factors “may be potential confounders,” the committee stated. Other risk factors include allergic rhinitis and sickle cell disease.
But the statement underscores that “obesity is the main risk factor” for OSA in children and adolescents, and that the presence of increased inflammation may explain this relationship. Steroids may alleviate these symptoms, even in nonobese children, and removal of the adenoids or tonsils is an option to reduce inflammation in children with OSA.
“Obesity is a significant risk factor for sleep disturbances and obstructive sleep apnea, and the severity of sleep apnea may be improved by weight-loss interventions, which then improves metabolic syndrome factors such as insulin sensitivity,” Dr. Baker-Smith said. “We need to increase awareness about how the rising prevalence of obesity may be impacting sleep quality in kids and recognize sleep-disordered breathing as something that could contribute to risks for hypertension and later cardiovascular disease.”
Children in whom OSA is suspected should also undergo screening for metabolic syndrome, and central nervous system and behavioral disorders.
Cardiovascular risks
The statement explores the connection between cardiovascular complications and SDB and OSA in depth.
“Inadequate sleep duration of < 5 hours per night in children and adolescents has been linked to an increased risk of hypertension and is also associated with an increased prevalence of obesity,” the committee wrote.
However, the statement left one question hanging: whether OSA alone or obesity cause higher BP in younger patients with OSA. But the committee concluded that BP levels increase with the severity of OSA, although the effects can vary with age. OSA in children peaks between ages 2 and 8, corresponding to the peak prevalence of hypertrophy of the tonsils and adenoids. Children aged 10-11 with more severe OSA may have BP dysregulation, while older adolescents develop higher sustained BP. Obesity may be a confounder for daytime BP elevations, while nighttime hypertension depends less on obesity and more on OSA severity.
“OSA is associated with abnormal BP in youth and, in particular, higher nighttime blood pressures and loss of the normal decline in BP that should occur during sleep,” Dr. Baker-Smith said. “Children with OSA appear to have higher BP than controls during both sleep and wake times, and BP levels increase with increasing severity of OSA.”
Nonetheless, children with OSA are at greater risk for other cardiovascular problems. Left ventricular hypertrophy may be a secondary outcome. “The presence of obstructive sleep apnea in children is associated with an 11-fold increased risk for LVH in children, a relationship not seen in the presence of primary snoring alone,” Dr. Baker-Smith said.
Dr. Baker-Smith had no relevant disclosures. Coauthor Amal Isaiah, MD, is coinventor of an imaging system for sleep apnea and receives royalties from the University of Maryland. The other coauthors have no relevant financial relationships to disclose.
Obstructive sleep apnea is becoming more common in children and adolescents as the prevalence of obesity increases, but it may also be a preventable risk factor for cardiovascular disease, according to a new scientific statement from the American Heart Association.
The statement focuses on the links between OSA and CVD risk factors in children and adolescents, and reviews diagnostic strategies and treatments. The writing committee reported that 1%-6% of children and adolescents have OSA, as do up to 60% of adolescents considered obese.
The statement was created by the AHA’s Atherosclerosis, Hypertension, and Obesity in the Young subcommittee of the Council on Cardiovascular Disease in the Young and was published online in the Journal of the American Heart Association.
Carissa M. Baker-Smith, MD, chair of the writing group chair and director of pediatric preventive cardiology at Nemours Cardiac Center, Alfred I. duPont Hospital for Children, Wilmington, Del., explained the rationale for issuing the statement at this time, noting that the relationship between OSA and CVD in adults is well documented.
“There has been less focus on the importance of recognizing and treating sleep apnea in youth,” she said in an interview. “Thus, we felt that it was vitally important to get the word out to parents and to providers that paying attention to the quality and duration of your child’s sleep is vitally important to a child’s long-term heart health. Risk factors for heart disease, when present in childhood, can persist into adulthood.”
Clarity on polysomnography
For making the diagnosis of OSA in children, the statement provides clarity on the use of polysomnography and the role of the apnea-hypopnea index, which is lower in children with OSA than in adults. “One controversy, or at least as I saw it, was whether or not polysomnography testing is always required to make the diagnosis of OSA and before proceeding with tonsil and adenoid removal among children for whom enlarged tonsils and adenoids are present,” Dr. Baker-Smith said. “Polysomnography testing is not always needed before an ear, nose, and throat surgeon may recommend surgery.”
The statement also noted that history and physical examination may not yield enough reliable information to distinguish OSA from snoring.
In areas where sleep laboratories that work with children aren’t available, alternative tests such as daytime nap polysomnography, nocturnal oximetry, and nocturnal video recording may be used – with a caveat. “These alternative tests have weaker positive and negative predictive values when compared with polysomnography,” the writing committee noted. Home sleep apnea tests aren’t recommended in children. Questionnaires “are useful as screening, but not as diagnostic tools.”
Pediatric patients being evaluated for OSA should also be screened for hypertension and metabolic syndrome, as well as central nervous system and behavioral disorders. Diagnosing OSA in children and adolescents requires “a high index of suspicion,” the committee wrote.
Pediatricians and pediatric cardiologists should exercise that high index of suspicion when receiving referrals for cardiac evaluations for attention deficit hyperactivity disorder medication, Dr. Baker-Smith said. “Take the time to ask about a child’s sleep – snoring, apnea, etc. – especially if the child has obesity, difficulty focusing during the day, and if there is evidence of systemic hypertension or other signs of metabolic syndrome,” she said.
Risk factors for OSA in children
The statement also reviewed risk factors for OSA, among them obesity, particularly among children younger than 6 years. Other risk factors include upper and lower airway disease, hypotonia, parental history of hyperplasia of the adenoids and tonsils, craniofacial malformations, and neuromuscular disorders. However, the committee cited “limited data” to support that children with congenital heart disease may be at greater risk for OSA and sleep-disordered breathing (SDB).
Black children are at significantly greater risk, and socioeconomic factors “may be potential confounders,” the committee stated. Other risk factors include allergic rhinitis and sickle cell disease.
But the statement underscores that “obesity is the main risk factor” for OSA in children and adolescents, and that the presence of increased inflammation may explain this relationship. Steroids may alleviate these symptoms, even in nonobese children, and removal of the adenoids or tonsils is an option to reduce inflammation in children with OSA.
“Obesity is a significant risk factor for sleep disturbances and obstructive sleep apnea, and the severity of sleep apnea may be improved by weight-loss interventions, which then improves metabolic syndrome factors such as insulin sensitivity,” Dr. Baker-Smith said. “We need to increase awareness about how the rising prevalence of obesity may be impacting sleep quality in kids and recognize sleep-disordered breathing as something that could contribute to risks for hypertension and later cardiovascular disease.”
Children in whom OSA is suspected should also undergo screening for metabolic syndrome, and central nervous system and behavioral disorders.
Cardiovascular risks
The statement explores the connection between cardiovascular complications and SDB and OSA in depth.
“Inadequate sleep duration of < 5 hours per night in children and adolescents has been linked to an increased risk of hypertension and is also associated with an increased prevalence of obesity,” the committee wrote.
However, the statement left one question hanging: whether OSA alone or obesity cause higher BP in younger patients with OSA. But the committee concluded that BP levels increase with the severity of OSA, although the effects can vary with age. OSA in children peaks between ages 2 and 8, corresponding to the peak prevalence of hypertrophy of the tonsils and adenoids. Children aged 10-11 with more severe OSA may have BP dysregulation, while older adolescents develop higher sustained BP. Obesity may be a confounder for daytime BP elevations, while nighttime hypertension depends less on obesity and more on OSA severity.
“OSA is associated with abnormal BP in youth and, in particular, higher nighttime blood pressures and loss of the normal decline in BP that should occur during sleep,” Dr. Baker-Smith said. “Children with OSA appear to have higher BP than controls during both sleep and wake times, and BP levels increase with increasing severity of OSA.”
Nonetheless, children with OSA are at greater risk for other cardiovascular problems. Left ventricular hypertrophy may be a secondary outcome. “The presence of obstructive sleep apnea in children is associated with an 11-fold increased risk for LVH in children, a relationship not seen in the presence of primary snoring alone,” Dr. Baker-Smith said.
Dr. Baker-Smith had no relevant disclosures. Coauthor Amal Isaiah, MD, is coinventor of an imaging system for sleep apnea and receives royalties from the University of Maryland. The other coauthors have no relevant financial relationships to disclose.
Obstructive sleep apnea is becoming more common in children and adolescents as the prevalence of obesity increases, but it may also be a preventable risk factor for cardiovascular disease, according to a new scientific statement from the American Heart Association.
The statement focuses on the links between OSA and CVD risk factors in children and adolescents, and reviews diagnostic strategies and treatments. The writing committee reported that 1%-6% of children and adolescents have OSA, as do up to 60% of adolescents considered obese.
The statement was created by the AHA’s Atherosclerosis, Hypertension, and Obesity in the Young subcommittee of the Council on Cardiovascular Disease in the Young and was published online in the Journal of the American Heart Association.
Carissa M. Baker-Smith, MD, chair of the writing group chair and director of pediatric preventive cardiology at Nemours Cardiac Center, Alfred I. duPont Hospital for Children, Wilmington, Del., explained the rationale for issuing the statement at this time, noting that the relationship between OSA and CVD in adults is well documented.
“There has been less focus on the importance of recognizing and treating sleep apnea in youth,” she said in an interview. “Thus, we felt that it was vitally important to get the word out to parents and to providers that paying attention to the quality and duration of your child’s sleep is vitally important to a child’s long-term heart health. Risk factors for heart disease, when present in childhood, can persist into adulthood.”
Clarity on polysomnography
For making the diagnosis of OSA in children, the statement provides clarity on the use of polysomnography and the role of the apnea-hypopnea index, which is lower in children with OSA than in adults. “One controversy, or at least as I saw it, was whether or not polysomnography testing is always required to make the diagnosis of OSA and before proceeding with tonsil and adenoid removal among children for whom enlarged tonsils and adenoids are present,” Dr. Baker-Smith said. “Polysomnography testing is not always needed before an ear, nose, and throat surgeon may recommend surgery.”
The statement also noted that history and physical examination may not yield enough reliable information to distinguish OSA from snoring.
In areas where sleep laboratories that work with children aren’t available, alternative tests such as daytime nap polysomnography, nocturnal oximetry, and nocturnal video recording may be used – with a caveat. “These alternative tests have weaker positive and negative predictive values when compared with polysomnography,” the writing committee noted. Home sleep apnea tests aren’t recommended in children. Questionnaires “are useful as screening, but not as diagnostic tools.”
Pediatric patients being evaluated for OSA should also be screened for hypertension and metabolic syndrome, as well as central nervous system and behavioral disorders. Diagnosing OSA in children and adolescents requires “a high index of suspicion,” the committee wrote.
Pediatricians and pediatric cardiologists should exercise that high index of suspicion when receiving referrals for cardiac evaluations for attention deficit hyperactivity disorder medication, Dr. Baker-Smith said. “Take the time to ask about a child’s sleep – snoring, apnea, etc. – especially if the child has obesity, difficulty focusing during the day, and if there is evidence of systemic hypertension or other signs of metabolic syndrome,” she said.
Risk factors for OSA in children
The statement also reviewed risk factors for OSA, among them obesity, particularly among children younger than 6 years. Other risk factors include upper and lower airway disease, hypotonia, parental history of hyperplasia of the adenoids and tonsils, craniofacial malformations, and neuromuscular disorders. However, the committee cited “limited data” to support that children with congenital heart disease may be at greater risk for OSA and sleep-disordered breathing (SDB).
Black children are at significantly greater risk, and socioeconomic factors “may be potential confounders,” the committee stated. Other risk factors include allergic rhinitis and sickle cell disease.
But the statement underscores that “obesity is the main risk factor” for OSA in children and adolescents, and that the presence of increased inflammation may explain this relationship. Steroids may alleviate these symptoms, even in nonobese children, and removal of the adenoids or tonsils is an option to reduce inflammation in children with OSA.
“Obesity is a significant risk factor for sleep disturbances and obstructive sleep apnea, and the severity of sleep apnea may be improved by weight-loss interventions, which then improves metabolic syndrome factors such as insulin sensitivity,” Dr. Baker-Smith said. “We need to increase awareness about how the rising prevalence of obesity may be impacting sleep quality in kids and recognize sleep-disordered breathing as something that could contribute to risks for hypertension and later cardiovascular disease.”
Children in whom OSA is suspected should also undergo screening for metabolic syndrome, and central nervous system and behavioral disorders.
Cardiovascular risks
The statement explores the connection between cardiovascular complications and SDB and OSA in depth.
“Inadequate sleep duration of < 5 hours per night in children and adolescents has been linked to an increased risk of hypertension and is also associated with an increased prevalence of obesity,” the committee wrote.
However, the statement left one question hanging: whether OSA alone or obesity cause higher BP in younger patients with OSA. But the committee concluded that BP levels increase with the severity of OSA, although the effects can vary with age. OSA in children peaks between ages 2 and 8, corresponding to the peak prevalence of hypertrophy of the tonsils and adenoids. Children aged 10-11 with more severe OSA may have BP dysregulation, while older adolescents develop higher sustained BP. Obesity may be a confounder for daytime BP elevations, while nighttime hypertension depends less on obesity and more on OSA severity.
“OSA is associated with abnormal BP in youth and, in particular, higher nighttime blood pressures and loss of the normal decline in BP that should occur during sleep,” Dr. Baker-Smith said. “Children with OSA appear to have higher BP than controls during both sleep and wake times, and BP levels increase with increasing severity of OSA.”
Nonetheless, children with OSA are at greater risk for other cardiovascular problems. Left ventricular hypertrophy may be a secondary outcome. “The presence of obstructive sleep apnea in children is associated with an 11-fold increased risk for LVH in children, a relationship not seen in the presence of primary snoring alone,” Dr. Baker-Smith said.
Dr. Baker-Smith had no relevant disclosures. Coauthor Amal Isaiah, MD, is coinventor of an imaging system for sleep apnea and receives royalties from the University of Maryland. The other coauthors have no relevant financial relationships to disclose.
FROM JOURNAL OF THE AMERICAN HEART ASSOCIATION
CRP as a biomarker for community-acquired pneumonia
Background: In the United States, CAP was responsible for nearly 50,000 deaths in 2017. Prompt and accurate diagnosis promotes early treatment and avoids unnecessary antibiotic treatment for nonpneumonia lower respiratory tract infection patients. Diagnosis is based on signs and symptoms, as well as available imaging. Inflammatory markers such as CRP, white blood cell count, and procalcitonin are readily available in the ED and outpatient settings.
Study design: Bivariate meta-analysis.
Setting: A systematic review of literature was done via PubMed search to identify prospective studies evaluating the accuracy of biomarkers in patients with cough or suspected CAP.
Synopsis: Fourteen studies met the criteria to be included in the meta-analysis. Summary receiver operating characteristic (ROC) curves generated reported area under the curve of 0.802 for CRP (95% confidence interval, 0.78-0.85), 0.777 for leukocytosis (95% CI, 0.74-0.81), and 0.771 for procalcitonin (95% CI, 0.74-0.81). The combination of CRP greater than 49.5 mg/L and procalcitonin greater than 0.1 mcg/L had a positive likelihood ratio of 2.24 and a negative likelihood ratio of 0.44.
The study had a some of limitations. The blinding of the person performing the index test to the reference standard and vice versa was not clear. Further, it was unclear if the person interpreting the reference standard was blinded to the index test in five studies and absent in one. Other limitations were inconsistent reporting of abnormal post hoc cutoffs and only two biomarkers being reported in a single study.
Combining a biomarker with signs and symptoms has the potential to improve diagnostic accuracy in the outpatient setting further. CRP was found to be most accurate regardless of the cutoff used; however, further studies without threshold effect will prove beneficial.
Bottom line: CRP is a more accurate and useful biomarker for outpatient CAP diagnosis than procalcitonin or leukocytosis.
Citation: Ebell MH et al. Accuracy of biomarkers for the diagnosis of adult community-acquired pneumonia: A meta-analysis. Acad Emerg Med. 2020;27(3):195-206.
Dr. Castellanos is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Background: In the United States, CAP was responsible for nearly 50,000 deaths in 2017. Prompt and accurate diagnosis promotes early treatment and avoids unnecessary antibiotic treatment for nonpneumonia lower respiratory tract infection patients. Diagnosis is based on signs and symptoms, as well as available imaging. Inflammatory markers such as CRP, white blood cell count, and procalcitonin are readily available in the ED and outpatient settings.
Study design: Bivariate meta-analysis.
Setting: A systematic review of literature was done via PubMed search to identify prospective studies evaluating the accuracy of biomarkers in patients with cough or suspected CAP.
Synopsis: Fourteen studies met the criteria to be included in the meta-analysis. Summary receiver operating characteristic (ROC) curves generated reported area under the curve of 0.802 for CRP (95% confidence interval, 0.78-0.85), 0.777 for leukocytosis (95% CI, 0.74-0.81), and 0.771 for procalcitonin (95% CI, 0.74-0.81). The combination of CRP greater than 49.5 mg/L and procalcitonin greater than 0.1 mcg/L had a positive likelihood ratio of 2.24 and a negative likelihood ratio of 0.44.
The study had a some of limitations. The blinding of the person performing the index test to the reference standard and vice versa was not clear. Further, it was unclear if the person interpreting the reference standard was blinded to the index test in five studies and absent in one. Other limitations were inconsistent reporting of abnormal post hoc cutoffs and only two biomarkers being reported in a single study.
Combining a biomarker with signs and symptoms has the potential to improve diagnostic accuracy in the outpatient setting further. CRP was found to be most accurate regardless of the cutoff used; however, further studies without threshold effect will prove beneficial.
Bottom line: CRP is a more accurate and useful biomarker for outpatient CAP diagnosis than procalcitonin or leukocytosis.
Citation: Ebell MH et al. Accuracy of biomarkers for the diagnosis of adult community-acquired pneumonia: A meta-analysis. Acad Emerg Med. 2020;27(3):195-206.
Dr. Castellanos is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Background: In the United States, CAP was responsible for nearly 50,000 deaths in 2017. Prompt and accurate diagnosis promotes early treatment and avoids unnecessary antibiotic treatment for nonpneumonia lower respiratory tract infection patients. Diagnosis is based on signs and symptoms, as well as available imaging. Inflammatory markers such as CRP, white blood cell count, and procalcitonin are readily available in the ED and outpatient settings.
Study design: Bivariate meta-analysis.
Setting: A systematic review of literature was done via PubMed search to identify prospective studies evaluating the accuracy of biomarkers in patients with cough or suspected CAP.
Synopsis: Fourteen studies met the criteria to be included in the meta-analysis. Summary receiver operating characteristic (ROC) curves generated reported area under the curve of 0.802 for CRP (95% confidence interval, 0.78-0.85), 0.777 for leukocytosis (95% CI, 0.74-0.81), and 0.771 for procalcitonin (95% CI, 0.74-0.81). The combination of CRP greater than 49.5 mg/L and procalcitonin greater than 0.1 mcg/L had a positive likelihood ratio of 2.24 and a negative likelihood ratio of 0.44.
The study had a some of limitations. The blinding of the person performing the index test to the reference standard and vice versa was not clear. Further, it was unclear if the person interpreting the reference standard was blinded to the index test in five studies and absent in one. Other limitations were inconsistent reporting of abnormal post hoc cutoffs and only two biomarkers being reported in a single study.
Combining a biomarker with signs and symptoms has the potential to improve diagnostic accuracy in the outpatient setting further. CRP was found to be most accurate regardless of the cutoff used; however, further studies without threshold effect will prove beneficial.
Bottom line: CRP is a more accurate and useful biomarker for outpatient CAP diagnosis than procalcitonin or leukocytosis.
Citation: Ebell MH et al. Accuracy of biomarkers for the diagnosis of adult community-acquired pneumonia: A meta-analysis. Acad Emerg Med. 2020;27(3):195-206.
Dr. Castellanos is a hospitalist and assistant professor of medicine at UK HealthCare, Lexington, Ky.
Not all interstitial lung abnormalities represent disease
CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.
Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).
What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!
Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?
A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.
The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.
Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).
What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!
Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?
A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.
The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.
Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).
What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!
Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?
A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.
The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
What is the most likely cause of this patient’s fever?
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
A 63-year-old man undergoes cardiac bypass surgery. He is able to be extubated at 8 hours. The next morning he has a fever to 38.5° C His exam shows no redness at the surgical site, or at his IV sites. His lung exam is unremarkable. His urinalysis is without white blood cells. His white blood cell count is 8,500, and his chest x-ray shows atelectasis without other abnormalities.
One of the earliest things I was taught in my clinical years were the causes of postoperative fever, or the 5Ws, which are wind, water, wound, walk, and wonder drug.
Atelectasis was touted as the cause of early postoperative fever. This became clear fact in my medical student mind, not something that I had ever questioned. But investigation into whether there is evidence of this shows it is only a myth. In actuality, there is scant evidence, if any, for atelectasis causing fever. Frequently, no cause of postoperative fever has been found, despite aggressive attempts to look for one.
What the research says
Fanning and colleagues prospectively looked at 537 women who were undergoing major gynecologic surgery.1 Postoperative fever occurred in 211 of them. In 92% of these patients, no cause for fever was found.
Atelectasis is frequently seen postoperatively. Schlenker and colleagues reported that, in patients with postoperative atelectasis, temperature elevation on the first postoperative day was directly related to the degree of atelectasis, but the white blood cell count elevation was inversely related.2
In this study, atelectasis was diagnosed by auscultation, with chest x-rays ordered at the discretion of the physician. There was little correlation with the auscultatory findings and presence or absence of atelectasis in the patients who did receive chest x-rays.
Engoren did a study to prospectively evaluate 100 postoperative patients with daily chest x-rays and continuous temperature monitoring.3 Results from the day of surgery (day 0) to the second postoperative day showed an increase in presence of atelectasis from 43% on the day of surgery to 79% by day 2.
Fever, defined as temperature greater than 38° C, fell from 37% on the day of surgery to 17% by day 2. Engoren found no association between fever and degree of atelectasis.
Mavros and colleagues did a comprehensive review to determine whether there was evidence to support atelectasis causing fever.4 They concluded that there was no clinical evidence supporting the concept that atelectasis is associated with early postoperative fever.
A possible cause of fever
Mavros and colleagues’ paper suggested that early postoperative fever was caused by stress derived by surgery, which can increase the patient’s interleukin-6 levels and thermostatic set point. This was demonstrated in a small study by Wortel and colleagues, who measured IL-6 levels in the portal and peripheral blood of patients following pancreaticoduodenectomy.5 They found IL-6 levels correlated strongly with peak body temperature.
In conclusion, atelectasis is not a well-established cause of postoperative fever.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].
References
1. Fanning J et al. Infect Dis Obstet Gynecol. 1998; 6(6):252-5 .
2. Schlenker JD and Hubay CA. Arch Surg 1973;107:846-50
3. Engoren M. Chest. 1995;107(1):81-4 .
4. Michael N et al. Chest. 2011;140(2):418-24
5. Wortel CH et al. Surgery. 1993;114(3):564-70 .
Parental smoking linked to more adult RA in women
Childhood exposure to parental smoking appears to greatly boost the risk of confirmed cases of rheumatoid arthritis in adult women, although the overall rate is small, a new study reports. The findings, published Aug. 18, 2021, in Arthritis & Rheumatology, follows other evidence that early second-hand smoke exposure can trigger lifelong damage to the immune system.
“We estimated that there is 75% increased risk of adult seropositive RA due to the direct impact of childhood parental smoking,” said study lead author and Brigham & Women’s Hospital epidemiologist Kazuki Yoshida, MD, ScD, referring to an adjusted analysis conducted in the study. “Passive smoking is likely harmful throughout an individual’s life course regarding rheumatoid arthritis but potentially more harmful during the childhood period.”
The researchers launched the study to fill an evidence gap, Dr. Yoshida said in an interview. “Active smoking is a well-established risk factor for RA. However, studies on passive smoking’s impact on RA are sparse, and few studies had a well-characterized cohort of participants with comprehensive data of passive smoking during life course – in utero exposure, childhood exposure, adult exposure – and chart review–adjudicated RA outcomes.”
The study authors retrospectively tracked 90,923 subjects who joined the Nurses’ Health Study II in 1989 when they were aged 25-42. At the study’s start, the average age of subjects was 34.5, 93% were White, and 98% were premenopausal. Almost two-thirds had never smoked themselves, and 65% said their parents had smoked during their childhoods.
Of the subjects, the researchers found that 532 were identified as having RA over a median follow-up period of 27.7 years. Two-thirds of those cases (n = 352) were confirmed as seropositive by clinical testing.
The study linked maternal smoking during pregnancy to confirmed RA in adulthood via a confounder-adjusted analysis (hazard ratio, 1.25; 95% confidence interval, 1.03-1.52), but the connection vanished after researchers adjusted their statistics to reflect possible influences by later exposures to smoke.
After adjustment for confounders, the study linked childhood exposure to parental smoking to a 41% in increase in risk of confirmed adulthood RA (HR, 1.41; 95% CI, 1.08-1.83). A controlled direct effect analysis boosted the excess risk to 75% (HR, 1.75; 95% CI, 1.03-2.98).
This analysis reveals that “childhood parental smoking seems to be associated with adult rheumatoid arthritis beyond what is explained by the fact that childhood passive smoking can promote personal smoking uptake, a known risk factor for rheumatoid arthritis,” Dr. Yoshida said.
The overall rate of RA in the study population – roughly 0.6% – aligns with risk levels in the general population, he said. As a result, “the absolute risk increase may not be extremely high. But the concept that early life exposure may affect immunological health later in life is important.”
Potential pathophysiological mechanisms
Why might parental smoking boost the risk of RA? Exposure to secondhand smoke may irritate the lungs and cause abnormal proteins to form, Dr. Yoshida said. “The immune system produces antibodies in an attempt to attack such abnormal proteins. This immune reaction can spread to other body sites and attack normal tissues, including the joints.”
In addition, “smoking increases the risk of infections, which could in turn increase the risk of RA. Smoking is also known to result in epigenetic changes which could trigger RA in susceptible people,” University of California, San Francisco, autoimmune disease epidemiologist Milena A. Gianfrancesco, PhD, MPH, said in an interview. She cowrote a commentary accompanying the new study.
Other studies have linked smoking exposure to autoimmune disorders. Earlier this year, researchers who tracked 79,806 French women reported at the EULAR 2021 annual meeting that they found a link between exposure to second-hand smoking during childhood or adulthood and higher rates of RA.
Dr. Yoshida and colleagues noted their study’s limitations, including the inability to track cases of RA in subjects up to the age when they entered the nurses research project. Also, only one questionnaire over the entire period of the Nurses’ Health Study II asks subjects about whether they were exposed to secondhand smoke as adults.
The study also says nothing about whether a similar risk exists for males, and the nurse subjects are overwhelmingly White.
Still, Dr. Gianfrancesco praised the study and said it relies on extensive data and strong statistical methods. “The findings are important because they drive home the importance of reducing cigarette smoke exposure to reduce risk of disease,” she said. “They highlight the need to not only focus on one’s personal smoking habits, but also other sources of secondhand smoke exposure.”
She added that children with a family history of RA or other autoimmune diseases are especially vulnerable to the effects of secondhand smoke because they may be more susceptible to developing the diseases themselves. “Rheumatologists and other health care providers should be sure to discuss the risks of smoking with their patients, as well as the risk of secondhand smoke,” she said. “And parents should keep their children away from secondhand smoke in the home or other environments in which smoke is prevalent, such as the home of another caregiver or a workplace if the child accompanies their parent to work.”
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Institutes of Health. The study and commentary authors, including Dr. Yoshida and Dr. Gianfrancesco, reported having no relevant disclosures.
Childhood exposure to parental smoking appears to greatly boost the risk of confirmed cases of rheumatoid arthritis in adult women, although the overall rate is small, a new study reports. The findings, published Aug. 18, 2021, in Arthritis & Rheumatology, follows other evidence that early second-hand smoke exposure can trigger lifelong damage to the immune system.
“We estimated that there is 75% increased risk of adult seropositive RA due to the direct impact of childhood parental smoking,” said study lead author and Brigham & Women’s Hospital epidemiologist Kazuki Yoshida, MD, ScD, referring to an adjusted analysis conducted in the study. “Passive smoking is likely harmful throughout an individual’s life course regarding rheumatoid arthritis but potentially more harmful during the childhood period.”
The researchers launched the study to fill an evidence gap, Dr. Yoshida said in an interview. “Active smoking is a well-established risk factor for RA. However, studies on passive smoking’s impact on RA are sparse, and few studies had a well-characterized cohort of participants with comprehensive data of passive smoking during life course – in utero exposure, childhood exposure, adult exposure – and chart review–adjudicated RA outcomes.”
The study authors retrospectively tracked 90,923 subjects who joined the Nurses’ Health Study II in 1989 when they were aged 25-42. At the study’s start, the average age of subjects was 34.5, 93% were White, and 98% were premenopausal. Almost two-thirds had never smoked themselves, and 65% said their parents had smoked during their childhoods.
Of the subjects, the researchers found that 532 were identified as having RA over a median follow-up period of 27.7 years. Two-thirds of those cases (n = 352) were confirmed as seropositive by clinical testing.
The study linked maternal smoking during pregnancy to confirmed RA in adulthood via a confounder-adjusted analysis (hazard ratio, 1.25; 95% confidence interval, 1.03-1.52), but the connection vanished after researchers adjusted their statistics to reflect possible influences by later exposures to smoke.
After adjustment for confounders, the study linked childhood exposure to parental smoking to a 41% in increase in risk of confirmed adulthood RA (HR, 1.41; 95% CI, 1.08-1.83). A controlled direct effect analysis boosted the excess risk to 75% (HR, 1.75; 95% CI, 1.03-2.98).
This analysis reveals that “childhood parental smoking seems to be associated with adult rheumatoid arthritis beyond what is explained by the fact that childhood passive smoking can promote personal smoking uptake, a known risk factor for rheumatoid arthritis,” Dr. Yoshida said.
The overall rate of RA in the study population – roughly 0.6% – aligns with risk levels in the general population, he said. As a result, “the absolute risk increase may not be extremely high. But the concept that early life exposure may affect immunological health later in life is important.”
Potential pathophysiological mechanisms
Why might parental smoking boost the risk of RA? Exposure to secondhand smoke may irritate the lungs and cause abnormal proteins to form, Dr. Yoshida said. “The immune system produces antibodies in an attempt to attack such abnormal proteins. This immune reaction can spread to other body sites and attack normal tissues, including the joints.”
In addition, “smoking increases the risk of infections, which could in turn increase the risk of RA. Smoking is also known to result in epigenetic changes which could trigger RA in susceptible people,” University of California, San Francisco, autoimmune disease epidemiologist Milena A. Gianfrancesco, PhD, MPH, said in an interview. She cowrote a commentary accompanying the new study.
Other studies have linked smoking exposure to autoimmune disorders. Earlier this year, researchers who tracked 79,806 French women reported at the EULAR 2021 annual meeting that they found a link between exposure to second-hand smoking during childhood or adulthood and higher rates of RA.
Dr. Yoshida and colleagues noted their study’s limitations, including the inability to track cases of RA in subjects up to the age when they entered the nurses research project. Also, only one questionnaire over the entire period of the Nurses’ Health Study II asks subjects about whether they were exposed to secondhand smoke as adults.
The study also says nothing about whether a similar risk exists for males, and the nurse subjects are overwhelmingly White.
Still, Dr. Gianfrancesco praised the study and said it relies on extensive data and strong statistical methods. “The findings are important because they drive home the importance of reducing cigarette smoke exposure to reduce risk of disease,” she said. “They highlight the need to not only focus on one’s personal smoking habits, but also other sources of secondhand smoke exposure.”
She added that children with a family history of RA or other autoimmune diseases are especially vulnerable to the effects of secondhand smoke because they may be more susceptible to developing the diseases themselves. “Rheumatologists and other health care providers should be sure to discuss the risks of smoking with their patients, as well as the risk of secondhand smoke,” she said. “And parents should keep their children away from secondhand smoke in the home or other environments in which smoke is prevalent, such as the home of another caregiver or a workplace if the child accompanies their parent to work.”
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Institutes of Health. The study and commentary authors, including Dr. Yoshida and Dr. Gianfrancesco, reported having no relevant disclosures.
Childhood exposure to parental smoking appears to greatly boost the risk of confirmed cases of rheumatoid arthritis in adult women, although the overall rate is small, a new study reports. The findings, published Aug. 18, 2021, in Arthritis & Rheumatology, follows other evidence that early second-hand smoke exposure can trigger lifelong damage to the immune system.
“We estimated that there is 75% increased risk of adult seropositive RA due to the direct impact of childhood parental smoking,” said study lead author and Brigham & Women’s Hospital epidemiologist Kazuki Yoshida, MD, ScD, referring to an adjusted analysis conducted in the study. “Passive smoking is likely harmful throughout an individual’s life course regarding rheumatoid arthritis but potentially more harmful during the childhood period.”
The researchers launched the study to fill an evidence gap, Dr. Yoshida said in an interview. “Active smoking is a well-established risk factor for RA. However, studies on passive smoking’s impact on RA are sparse, and few studies had a well-characterized cohort of participants with comprehensive data of passive smoking during life course – in utero exposure, childhood exposure, adult exposure – and chart review–adjudicated RA outcomes.”
The study authors retrospectively tracked 90,923 subjects who joined the Nurses’ Health Study II in 1989 when they were aged 25-42. At the study’s start, the average age of subjects was 34.5, 93% were White, and 98% were premenopausal. Almost two-thirds had never smoked themselves, and 65% said their parents had smoked during their childhoods.
Of the subjects, the researchers found that 532 were identified as having RA over a median follow-up period of 27.7 years. Two-thirds of those cases (n = 352) were confirmed as seropositive by clinical testing.
The study linked maternal smoking during pregnancy to confirmed RA in adulthood via a confounder-adjusted analysis (hazard ratio, 1.25; 95% confidence interval, 1.03-1.52), but the connection vanished after researchers adjusted their statistics to reflect possible influences by later exposures to smoke.
After adjustment for confounders, the study linked childhood exposure to parental smoking to a 41% in increase in risk of confirmed adulthood RA (HR, 1.41; 95% CI, 1.08-1.83). A controlled direct effect analysis boosted the excess risk to 75% (HR, 1.75; 95% CI, 1.03-2.98).
This analysis reveals that “childhood parental smoking seems to be associated with adult rheumatoid arthritis beyond what is explained by the fact that childhood passive smoking can promote personal smoking uptake, a known risk factor for rheumatoid arthritis,” Dr. Yoshida said.
The overall rate of RA in the study population – roughly 0.6% – aligns with risk levels in the general population, he said. As a result, “the absolute risk increase may not be extremely high. But the concept that early life exposure may affect immunological health later in life is important.”
Potential pathophysiological mechanisms
Why might parental smoking boost the risk of RA? Exposure to secondhand smoke may irritate the lungs and cause abnormal proteins to form, Dr. Yoshida said. “The immune system produces antibodies in an attempt to attack such abnormal proteins. This immune reaction can spread to other body sites and attack normal tissues, including the joints.”
In addition, “smoking increases the risk of infections, which could in turn increase the risk of RA. Smoking is also known to result in epigenetic changes which could trigger RA in susceptible people,” University of California, San Francisco, autoimmune disease epidemiologist Milena A. Gianfrancesco, PhD, MPH, said in an interview. She cowrote a commentary accompanying the new study.
Other studies have linked smoking exposure to autoimmune disorders. Earlier this year, researchers who tracked 79,806 French women reported at the EULAR 2021 annual meeting that they found a link between exposure to second-hand smoking during childhood or adulthood and higher rates of RA.
Dr. Yoshida and colleagues noted their study’s limitations, including the inability to track cases of RA in subjects up to the age when they entered the nurses research project. Also, only one questionnaire over the entire period of the Nurses’ Health Study II asks subjects about whether they were exposed to secondhand smoke as adults.
The study also says nothing about whether a similar risk exists for males, and the nurse subjects are overwhelmingly White.
Still, Dr. Gianfrancesco praised the study and said it relies on extensive data and strong statistical methods. “The findings are important because they drive home the importance of reducing cigarette smoke exposure to reduce risk of disease,” she said. “They highlight the need to not only focus on one’s personal smoking habits, but also other sources of secondhand smoke exposure.”
She added that children with a family history of RA or other autoimmune diseases are especially vulnerable to the effects of secondhand smoke because they may be more susceptible to developing the diseases themselves. “Rheumatologists and other health care providers should be sure to discuss the risks of smoking with their patients, as well as the risk of secondhand smoke,” she said. “And parents should keep their children away from secondhand smoke in the home or other environments in which smoke is prevalent, such as the home of another caregiver or a workplace if the child accompanies their parent to work.”
The study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Institutes of Health. The study and commentary authors, including Dr. Yoshida and Dr. Gianfrancesco, reported having no relevant disclosures.
FROM ARTHRITIS & RHEUMATOLOGY