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Don't just blame Facebook for fake news: It's us, too
Critics such as Zeynep Tufekci are quite right to take Facebook and Twitter to task for allowing nefarious and hostile actors, likely including the Russian state, to hold sway on social media (“Facebook’s Ad Scandal Isn’t a ‘Fail,’ It’s a Feature,” New York Times, Sept. 23, 2017).
These actors must be reined in online, for the very simple reason that so many of us are immersed in our news feeds and Twitter streams, and thus susceptible to whatever toxins are allowed to proliferate there.
Some have called apps, including social media, “the race to the bottom of the brainstem.” The most primitive parts of our brain, responsible for fight-flight and survival, are always on the lookout for perceived threats. In our restless, clicking and scrolling state, we are often naturally attracted to and activated by tantalizing, titillating, and emotionally charged posts that are lacking in reason, but are inflammatory and viscerally captivating. Viral news, click bait, gossip, rumors, and scandals get a disproportionate share of our attention. And since we become what we do, our reason is overwhelmed by reaction. In fact, a recent 60 Minutes segment demonstrated how President Trump’s political operatives optimized Facebook ads for reaction, not thought. As we engage in social media, we may become less reasonable, and prone to reacting out of our most base and primal fears.
The late neurologist and psychiatrist Viktor E. Frankl pointed out our freedom lies in our ability to put space between stimulus and response. In this space lies our freedom to choose, he wrote. Online, this inner life can shrink. Our wandering minds look for cheap thrills and anything that confirms our biases of threat. We reduce the world to simplistic one-size-fits-all narratives, and heap blame on our usual suspects. I call the Internet the angernet. Anger is the most viral and contagious emotion on social networks, and as we use social media, we deepen the groove of anger – making our anger more likely and the most readily shared.
But we’ve been racing to the bottom of the brainstem, where fear, anger, hatred, and reactivity reside, for decades in this country. Again, we can’t simply blame social media. Trust has been eroding for decades, for many reasons. No matter the generation, only a minority of us trust each other, according to the Pew Research Center’s surveys. Millennials are the least trusting of all: Only 19% of them agree that “generally speaking, people are to be trusted.” Any scroll of the news feed quickly confirms this dangerous bias to mistrust, as we are besieged by a near cataclysmic barrage of traumatic events. We are also more polarized than ever, with a great percentage of partisans believing that the other side aims at the destruction of all they hold dear in America. As we feel more vulnerable, we are more likely to mistrust and become further polarized, and the cycle continues.
More importantly, as we flee real-world relationships and interaction for the ease and seeming reach of the online world, we lose subtle cues and important connections that would normally soothe our reactivity. Humanity has evolved and progressed precisely because of our social connections. We are who happens to us, and what we make of the happening. When we connect in more superficial ways, we endanger our very identities. As a nation, we are having an identity crisis: We have not worked out who we are in relation to one another, and to ourselves. This is expressed politically, and in our confused and fearful opinions and appraisals of each other and government. Without the good graces that come out of shared presence in real-world relationships, we are more likely to think badly of each other. We are more likely to retreat into narrow and tribal identities where we think safety resides, and deemphasize communal identity. In this space of narrow identity, ideological self-righteousness and dogma prevail, and we are less likely to listen and cultivate curiosity, understanding, and empathy for others. One example lies in how representatives and senators spend less time socializing with each other than in years past, and are thus less likely to forge compromise. Online, we are all refugees from the real world, and we fall to building our own personal walls and exiling those with whom we disagree – who then become those we hate, fear, blame, and fight.
We have met the enemy, and it is us.
The antidote to mistrust is in cultivating the top of our nervous systems, where long-term planning and positive emotions reside. We can only do this through real-world relationships. Social media will not ultimately take us to a feeling of society. It might provide a glimmer of connection, but its inherent vectors of disconnection and division are proving deadly, from Internet radicalization, to the increased levels of depression, anxiety, loneliness, and suicidality noted with increasing Internet and social media use.
We each have incredible human possibilities, but to reach them, we have to transcend the biases and reactivity of our habitually and usually unconsciously self-centered egos. We can start with awareness of what the Internet siren is doing to us and steer our ships in a more fruitful direction. Toward home, toward our hearts, and toward each other.
Dr. Chandra is a psychiatrist and writer in San Francisco. He is the author of Facebuddha: Transcendence in the Age of Social Networks (Pacific Heart Books, 2017).
Critics such as Zeynep Tufekci are quite right to take Facebook and Twitter to task for allowing nefarious and hostile actors, likely including the Russian state, to hold sway on social media (“Facebook’s Ad Scandal Isn’t a ‘Fail,’ It’s a Feature,” New York Times, Sept. 23, 2017).
These actors must be reined in online, for the very simple reason that so many of us are immersed in our news feeds and Twitter streams, and thus susceptible to whatever toxins are allowed to proliferate there.
Some have called apps, including social media, “the race to the bottom of the brainstem.” The most primitive parts of our brain, responsible for fight-flight and survival, are always on the lookout for perceived threats. In our restless, clicking and scrolling state, we are often naturally attracted to and activated by tantalizing, titillating, and emotionally charged posts that are lacking in reason, but are inflammatory and viscerally captivating. Viral news, click bait, gossip, rumors, and scandals get a disproportionate share of our attention. And since we become what we do, our reason is overwhelmed by reaction. In fact, a recent 60 Minutes segment demonstrated how President Trump’s political operatives optimized Facebook ads for reaction, not thought. As we engage in social media, we may become less reasonable, and prone to reacting out of our most base and primal fears.
The late neurologist and psychiatrist Viktor E. Frankl pointed out our freedom lies in our ability to put space between stimulus and response. In this space lies our freedom to choose, he wrote. Online, this inner life can shrink. Our wandering minds look for cheap thrills and anything that confirms our biases of threat. We reduce the world to simplistic one-size-fits-all narratives, and heap blame on our usual suspects. I call the Internet the angernet. Anger is the most viral and contagious emotion on social networks, and as we use social media, we deepen the groove of anger – making our anger more likely and the most readily shared.
But we’ve been racing to the bottom of the brainstem, where fear, anger, hatred, and reactivity reside, for decades in this country. Again, we can’t simply blame social media. Trust has been eroding for decades, for many reasons. No matter the generation, only a minority of us trust each other, according to the Pew Research Center’s surveys. Millennials are the least trusting of all: Only 19% of them agree that “generally speaking, people are to be trusted.” Any scroll of the news feed quickly confirms this dangerous bias to mistrust, as we are besieged by a near cataclysmic barrage of traumatic events. We are also more polarized than ever, with a great percentage of partisans believing that the other side aims at the destruction of all they hold dear in America. As we feel more vulnerable, we are more likely to mistrust and become further polarized, and the cycle continues.
More importantly, as we flee real-world relationships and interaction for the ease and seeming reach of the online world, we lose subtle cues and important connections that would normally soothe our reactivity. Humanity has evolved and progressed precisely because of our social connections. We are who happens to us, and what we make of the happening. When we connect in more superficial ways, we endanger our very identities. As a nation, we are having an identity crisis: We have not worked out who we are in relation to one another, and to ourselves. This is expressed politically, and in our confused and fearful opinions and appraisals of each other and government. Without the good graces that come out of shared presence in real-world relationships, we are more likely to think badly of each other. We are more likely to retreat into narrow and tribal identities where we think safety resides, and deemphasize communal identity. In this space of narrow identity, ideological self-righteousness and dogma prevail, and we are less likely to listen and cultivate curiosity, understanding, and empathy for others. One example lies in how representatives and senators spend less time socializing with each other than in years past, and are thus less likely to forge compromise. Online, we are all refugees from the real world, and we fall to building our own personal walls and exiling those with whom we disagree – who then become those we hate, fear, blame, and fight.
We have met the enemy, and it is us.
The antidote to mistrust is in cultivating the top of our nervous systems, where long-term planning and positive emotions reside. We can only do this through real-world relationships. Social media will not ultimately take us to a feeling of society. It might provide a glimmer of connection, but its inherent vectors of disconnection and division are proving deadly, from Internet radicalization, to the increased levels of depression, anxiety, loneliness, and suicidality noted with increasing Internet and social media use.
We each have incredible human possibilities, but to reach them, we have to transcend the biases and reactivity of our habitually and usually unconsciously self-centered egos. We can start with awareness of what the Internet siren is doing to us and steer our ships in a more fruitful direction. Toward home, toward our hearts, and toward each other.
Dr. Chandra is a psychiatrist and writer in San Francisco. He is the author of Facebuddha: Transcendence in the Age of Social Networks (Pacific Heart Books, 2017).
Critics such as Zeynep Tufekci are quite right to take Facebook and Twitter to task for allowing nefarious and hostile actors, likely including the Russian state, to hold sway on social media (“Facebook’s Ad Scandal Isn’t a ‘Fail,’ It’s a Feature,” New York Times, Sept. 23, 2017).
These actors must be reined in online, for the very simple reason that so many of us are immersed in our news feeds and Twitter streams, and thus susceptible to whatever toxins are allowed to proliferate there.
Some have called apps, including social media, “the race to the bottom of the brainstem.” The most primitive parts of our brain, responsible for fight-flight and survival, are always on the lookout for perceived threats. In our restless, clicking and scrolling state, we are often naturally attracted to and activated by tantalizing, titillating, and emotionally charged posts that are lacking in reason, but are inflammatory and viscerally captivating. Viral news, click bait, gossip, rumors, and scandals get a disproportionate share of our attention. And since we become what we do, our reason is overwhelmed by reaction. In fact, a recent 60 Minutes segment demonstrated how President Trump’s political operatives optimized Facebook ads for reaction, not thought. As we engage in social media, we may become less reasonable, and prone to reacting out of our most base and primal fears.
The late neurologist and psychiatrist Viktor E. Frankl pointed out our freedom lies in our ability to put space between stimulus and response. In this space lies our freedom to choose, he wrote. Online, this inner life can shrink. Our wandering minds look for cheap thrills and anything that confirms our biases of threat. We reduce the world to simplistic one-size-fits-all narratives, and heap blame on our usual suspects. I call the Internet the angernet. Anger is the most viral and contagious emotion on social networks, and as we use social media, we deepen the groove of anger – making our anger more likely and the most readily shared.
But we’ve been racing to the bottom of the brainstem, where fear, anger, hatred, and reactivity reside, for decades in this country. Again, we can’t simply blame social media. Trust has been eroding for decades, for many reasons. No matter the generation, only a minority of us trust each other, according to the Pew Research Center’s surveys. Millennials are the least trusting of all: Only 19% of them agree that “generally speaking, people are to be trusted.” Any scroll of the news feed quickly confirms this dangerous bias to mistrust, as we are besieged by a near cataclysmic barrage of traumatic events. We are also more polarized than ever, with a great percentage of partisans believing that the other side aims at the destruction of all they hold dear in America. As we feel more vulnerable, we are more likely to mistrust and become further polarized, and the cycle continues.
More importantly, as we flee real-world relationships and interaction for the ease and seeming reach of the online world, we lose subtle cues and important connections that would normally soothe our reactivity. Humanity has evolved and progressed precisely because of our social connections. We are who happens to us, and what we make of the happening. When we connect in more superficial ways, we endanger our very identities. As a nation, we are having an identity crisis: We have not worked out who we are in relation to one another, and to ourselves. This is expressed politically, and in our confused and fearful opinions and appraisals of each other and government. Without the good graces that come out of shared presence in real-world relationships, we are more likely to think badly of each other. We are more likely to retreat into narrow and tribal identities where we think safety resides, and deemphasize communal identity. In this space of narrow identity, ideological self-righteousness and dogma prevail, and we are less likely to listen and cultivate curiosity, understanding, and empathy for others. One example lies in how representatives and senators spend less time socializing with each other than in years past, and are thus less likely to forge compromise. Online, we are all refugees from the real world, and we fall to building our own personal walls and exiling those with whom we disagree – who then become those we hate, fear, blame, and fight.
We have met the enemy, and it is us.
The antidote to mistrust is in cultivating the top of our nervous systems, where long-term planning and positive emotions reside. We can only do this through real-world relationships. Social media will not ultimately take us to a feeling of society. It might provide a glimmer of connection, but its inherent vectors of disconnection and division are proving deadly, from Internet radicalization, to the increased levels of depression, anxiety, loneliness, and suicidality noted with increasing Internet and social media use.
We each have incredible human possibilities, but to reach them, we have to transcend the biases and reactivity of our habitually and usually unconsciously self-centered egos. We can start with awareness of what the Internet siren is doing to us and steer our ships in a more fruitful direction. Toward home, toward our hearts, and toward each other.
Dr. Chandra is a psychiatrist and writer in San Francisco. He is the author of Facebuddha: Transcendence in the Age of Social Networks (Pacific Heart Books, 2017).
This Month in CHEST Editor’s Picks
A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.
By Dr. M. W. Semler, et al.
Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.
By Dr. I. Cano-Pumarega, et al.
A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.
By Dr. M. W. Semler, et al.
Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.
By Dr. I. Cano-Pumarega, et al.
A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.
By Dr. M. W. Semler, et al.
Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.
By Dr. I. Cano-Pumarega, et al.
Changes to CPT® codes coming January 2018
There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.
There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.
CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO2 production, O2 uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.
There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.
There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.
CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO2 production, O2 uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.
There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.
There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.
CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO2 production, O2 uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.
Evidence is mixed on probiotics in pediatric patients
CHICAGO – Outside of that, things are less clear.
“In terms of diarrhea, the evidence is positive, but probiotics only provide about 25 hours of benefit. And treatment of antibiotic-associated diarrhea is really dependent on patient adherence,” said Michael D. Cabana, MD. When it comes to treating colic, there is a particular probiotic that looks promising, he added, but the research so far demonstrating effectiveness is limited to breastfed babies. Also, the probiotic therapy appears to work best when started relatively early.
You are very likely to be asked your take on probiotics for a wide range of conditions, Dr. Cabana said, Overall, however, skepticism is warranted. Advise patients and families to be aware of advertising that promotes many different products as “probiotic,” especially around claims of improved “gut health” or “balanced microbiota.” He emphasized: “Make sure what your patients are using has some evidence behind it.”
Knowing the particular probiotic strain is essential to researching the evidence around its use, said Dr. Cabana, professor of pediatrics at the University of California, San Francisco. “I used the Canis familiaris example. All dogs are C. familiaris. But there are different breeds. You want to make sure you match the right breed to the task. If you were in an avalanche in the Swiss Alps, you would want a St. Bernard to rescue you, not a Chihuahua,” he said. “Similarly, when you are using probiotics you want to make sure you have the right strain, not just the genus and species.” For example, if a product label states it contains Bifidobacterium breve C50, the “C50” is the strain.
Another tip is to look for labeling that lists probiotic concentrations in colony-forming units or CFUs, Dr. Cabana said. He’s seen concentrations listed in mg, a red flag that a product is not legitimate.
Families also might ask if it’s better to take a probiotic supplement or choose food that contains probiotics. “Food products offer additional nutritional benefits, but you can give a relatively higher dose with supplements with a much lower volume ingested,” Dr. Cabana said. “And supplements theoretically provide a more consistent dose.” Speaking of dose, it’s difficult to counsel patients on dosing and frequency in general because probiotics really vary by the indication and formulation.
“As a pediatrician, I also get this question: Should kids get a lower dose of probiotic?” Dr. Cabana said. There are no known reports of toxicity associated with probiotic use in either adults or children, he said. “Unless a dose modification has been documented in a clinical trial, it is not clear that this is necessary. You’re just giving less of the probiotic.”
Treating diarrhea and antibiotic-associated diarrhea
When it comes to probiotics for treating acute diarrhea in children, “the literature is actually fairly good here,” Dr. Cabana said. More than 60 studies with an excess of 8,000 participants, the majority with rotavirus infection, suggests probiotics are not associated with any adverse effects and generally shorten duration of diarrhea.
In fact, Dr. Cabana added, multiple meta-analyses support a shorter course of diarrhea. He added, “Look at the units here – it’s hours, not days. You can treat, but on average it’s only 25 hours.” He added that a day less of diarrhea can be significant for patients and parents, however.
In another meta-analysis probiotics, particularly Lactobacillus strains, were analyzed for prevention of antibiotic-associated diarrhea (JAMA. 2012 May 9;307[18]:1959-69). Researchers assessed 63 randomized controlled trials with nearly 12,000 participants. The pooled results showed a statistically significant positive reduction in antibiotic-associated diarrhea (relative risk, 0.58; P less than .001). “Note the number needed to treat to see the effect is 13, so it won’t work in every patient,” Dr. Cabana said.
“So prevention of antibiotic-associated diarrhea is well documented. However, it’s also highly dependent on patent adherence,” he emphasized.
The clinical evidence on colic
For treating babies with colic, the best evidence is behind use of Lactobacilus reuteri DSM 17938, Dr. Cabana said. It tends to work best in breastfed infants, babies not on any gastrointestinal meds, and babies that start therapy early in the course of symptoms. “Use in formula-fed infants is unknown, because there are not enough data so far,” he said.
In some cases, during a prenatal visit, soon-to-be-parents will ask if they should start a probiotic to prevent colic. Dr. Cabana has seen only one prophylaxis study for this indication (JAMA Pediatr. 2014 Mar;168[3]:228-33). In the study, 589 infants were randomly allocated to take L. reuteri DSM 17938 or placebo daily for 90 days. At 3 months of age, the researchers discovered a significantly shorter mean duration of daily crying in the probiotic group (38 vs. 71 minutes; P less than .01).
What’s known about efficacy for eczema
The evidence for treating a child who presents with eczema with probiotics does not support efficacy in general, Dr. Cabana said. And the evidence on prevention of atopic eczema is mixed.
For example, in a randomized, controlled study from Finland, investigators randomized mothers to receive Lactobacillus GG or placebo during the prenatal period (Lancet. 2001;357:1076-9). Of 132 of the children, 35% were later diagnosed with atopic eczema, and the rate in the probiotic group, 23%, was half the 46% rate in the placebo group.
In contrast, researchers found no benefit regarding prevention of atopic dermatitis when 105 pregnant women were randomized to Lactobacillus GG or placebo. At the age of 2 years, atopic dermatitis was diagnosed in 28% of the 50 children in the probiotic group and 27.3% of the 44 in the placebo group (Pediatrics. 2008;121:e850-6).
The region of Germany where the study was conducted was rural/agricultural, so the diet could be different, Dr. Cabana said. Also, the median duration of breastfeeding differed between the Finnish and German study population, 6.8 months versus 9.2 months, respectively. “So that could potentially explain it, or there are just differences that cannot be explained.”
For more information, Dr. Cabana recommended information provided by the International Scientific Association of Prebiotics & Probiotics (https://isappscience.org/infographics/). The association’s website has easy to understand infographics including: What are probiotics and what can they do for you?; What’s so special about fermented foods?; and How do you read a probiotic label?
Dr. Cabana reported he receives research support from the National Institutes of Health, Wyeth Nutrition, and Nestle; is on the speakers bureau for Merck; owns stocks or bonds in Abbot and AbbVie; and is a consultant for Mead Johnson, Abbott, Genentech, Biogaia, General Mills, and Nestle.
CHICAGO – Outside of that, things are less clear.
“In terms of diarrhea, the evidence is positive, but probiotics only provide about 25 hours of benefit. And treatment of antibiotic-associated diarrhea is really dependent on patient adherence,” said Michael D. Cabana, MD. When it comes to treating colic, there is a particular probiotic that looks promising, he added, but the research so far demonstrating effectiveness is limited to breastfed babies. Also, the probiotic therapy appears to work best when started relatively early.
You are very likely to be asked your take on probiotics for a wide range of conditions, Dr. Cabana said, Overall, however, skepticism is warranted. Advise patients and families to be aware of advertising that promotes many different products as “probiotic,” especially around claims of improved “gut health” or “balanced microbiota.” He emphasized: “Make sure what your patients are using has some evidence behind it.”
Knowing the particular probiotic strain is essential to researching the evidence around its use, said Dr. Cabana, professor of pediatrics at the University of California, San Francisco. “I used the Canis familiaris example. All dogs are C. familiaris. But there are different breeds. You want to make sure you match the right breed to the task. If you were in an avalanche in the Swiss Alps, you would want a St. Bernard to rescue you, not a Chihuahua,” he said. “Similarly, when you are using probiotics you want to make sure you have the right strain, not just the genus and species.” For example, if a product label states it contains Bifidobacterium breve C50, the “C50” is the strain.
Another tip is to look for labeling that lists probiotic concentrations in colony-forming units or CFUs, Dr. Cabana said. He’s seen concentrations listed in mg, a red flag that a product is not legitimate.
Families also might ask if it’s better to take a probiotic supplement or choose food that contains probiotics. “Food products offer additional nutritional benefits, but you can give a relatively higher dose with supplements with a much lower volume ingested,” Dr. Cabana said. “And supplements theoretically provide a more consistent dose.” Speaking of dose, it’s difficult to counsel patients on dosing and frequency in general because probiotics really vary by the indication and formulation.
“As a pediatrician, I also get this question: Should kids get a lower dose of probiotic?” Dr. Cabana said. There are no known reports of toxicity associated with probiotic use in either adults or children, he said. “Unless a dose modification has been documented in a clinical trial, it is not clear that this is necessary. You’re just giving less of the probiotic.”
Treating diarrhea and antibiotic-associated diarrhea
When it comes to probiotics for treating acute diarrhea in children, “the literature is actually fairly good here,” Dr. Cabana said. More than 60 studies with an excess of 8,000 participants, the majority with rotavirus infection, suggests probiotics are not associated with any adverse effects and generally shorten duration of diarrhea.
In fact, Dr. Cabana added, multiple meta-analyses support a shorter course of diarrhea. He added, “Look at the units here – it’s hours, not days. You can treat, but on average it’s only 25 hours.” He added that a day less of diarrhea can be significant for patients and parents, however.
In another meta-analysis probiotics, particularly Lactobacillus strains, were analyzed for prevention of antibiotic-associated diarrhea (JAMA. 2012 May 9;307[18]:1959-69). Researchers assessed 63 randomized controlled trials with nearly 12,000 participants. The pooled results showed a statistically significant positive reduction in antibiotic-associated diarrhea (relative risk, 0.58; P less than .001). “Note the number needed to treat to see the effect is 13, so it won’t work in every patient,” Dr. Cabana said.
“So prevention of antibiotic-associated diarrhea is well documented. However, it’s also highly dependent on patent adherence,” he emphasized.
The clinical evidence on colic
For treating babies with colic, the best evidence is behind use of Lactobacilus reuteri DSM 17938, Dr. Cabana said. It tends to work best in breastfed infants, babies not on any gastrointestinal meds, and babies that start therapy early in the course of symptoms. “Use in formula-fed infants is unknown, because there are not enough data so far,” he said.
In some cases, during a prenatal visit, soon-to-be-parents will ask if they should start a probiotic to prevent colic. Dr. Cabana has seen only one prophylaxis study for this indication (JAMA Pediatr. 2014 Mar;168[3]:228-33). In the study, 589 infants were randomly allocated to take L. reuteri DSM 17938 or placebo daily for 90 days. At 3 months of age, the researchers discovered a significantly shorter mean duration of daily crying in the probiotic group (38 vs. 71 minutes; P less than .01).
What’s known about efficacy for eczema
The evidence for treating a child who presents with eczema with probiotics does not support efficacy in general, Dr. Cabana said. And the evidence on prevention of atopic eczema is mixed.
For example, in a randomized, controlled study from Finland, investigators randomized mothers to receive Lactobacillus GG or placebo during the prenatal period (Lancet. 2001;357:1076-9). Of 132 of the children, 35% were later diagnosed with atopic eczema, and the rate in the probiotic group, 23%, was half the 46% rate in the placebo group.
In contrast, researchers found no benefit regarding prevention of atopic dermatitis when 105 pregnant women were randomized to Lactobacillus GG or placebo. At the age of 2 years, atopic dermatitis was diagnosed in 28% of the 50 children in the probiotic group and 27.3% of the 44 in the placebo group (Pediatrics. 2008;121:e850-6).
The region of Germany where the study was conducted was rural/agricultural, so the diet could be different, Dr. Cabana said. Also, the median duration of breastfeeding differed between the Finnish and German study population, 6.8 months versus 9.2 months, respectively. “So that could potentially explain it, or there are just differences that cannot be explained.”
For more information, Dr. Cabana recommended information provided by the International Scientific Association of Prebiotics & Probiotics (https://isappscience.org/infographics/). The association’s website has easy to understand infographics including: What are probiotics and what can they do for you?; What’s so special about fermented foods?; and How do you read a probiotic label?
Dr. Cabana reported he receives research support from the National Institutes of Health, Wyeth Nutrition, and Nestle; is on the speakers bureau for Merck; owns stocks or bonds in Abbot and AbbVie; and is a consultant for Mead Johnson, Abbott, Genentech, Biogaia, General Mills, and Nestle.
CHICAGO – Outside of that, things are less clear.
“In terms of diarrhea, the evidence is positive, but probiotics only provide about 25 hours of benefit. And treatment of antibiotic-associated diarrhea is really dependent on patient adherence,” said Michael D. Cabana, MD. When it comes to treating colic, there is a particular probiotic that looks promising, he added, but the research so far demonstrating effectiveness is limited to breastfed babies. Also, the probiotic therapy appears to work best when started relatively early.
You are very likely to be asked your take on probiotics for a wide range of conditions, Dr. Cabana said, Overall, however, skepticism is warranted. Advise patients and families to be aware of advertising that promotes many different products as “probiotic,” especially around claims of improved “gut health” or “balanced microbiota.” He emphasized: “Make sure what your patients are using has some evidence behind it.”
Knowing the particular probiotic strain is essential to researching the evidence around its use, said Dr. Cabana, professor of pediatrics at the University of California, San Francisco. “I used the Canis familiaris example. All dogs are C. familiaris. But there are different breeds. You want to make sure you match the right breed to the task. If you were in an avalanche in the Swiss Alps, you would want a St. Bernard to rescue you, not a Chihuahua,” he said. “Similarly, when you are using probiotics you want to make sure you have the right strain, not just the genus and species.” For example, if a product label states it contains Bifidobacterium breve C50, the “C50” is the strain.
Another tip is to look for labeling that lists probiotic concentrations in colony-forming units or CFUs, Dr. Cabana said. He’s seen concentrations listed in mg, a red flag that a product is not legitimate.
Families also might ask if it’s better to take a probiotic supplement or choose food that contains probiotics. “Food products offer additional nutritional benefits, but you can give a relatively higher dose with supplements with a much lower volume ingested,” Dr. Cabana said. “And supplements theoretically provide a more consistent dose.” Speaking of dose, it’s difficult to counsel patients on dosing and frequency in general because probiotics really vary by the indication and formulation.
“As a pediatrician, I also get this question: Should kids get a lower dose of probiotic?” Dr. Cabana said. There are no known reports of toxicity associated with probiotic use in either adults or children, he said. “Unless a dose modification has been documented in a clinical trial, it is not clear that this is necessary. You’re just giving less of the probiotic.”
Treating diarrhea and antibiotic-associated diarrhea
When it comes to probiotics for treating acute diarrhea in children, “the literature is actually fairly good here,” Dr. Cabana said. More than 60 studies with an excess of 8,000 participants, the majority with rotavirus infection, suggests probiotics are not associated with any adverse effects and generally shorten duration of diarrhea.
In fact, Dr. Cabana added, multiple meta-analyses support a shorter course of diarrhea. He added, “Look at the units here – it’s hours, not days. You can treat, but on average it’s only 25 hours.” He added that a day less of diarrhea can be significant for patients and parents, however.
In another meta-analysis probiotics, particularly Lactobacillus strains, were analyzed for prevention of antibiotic-associated diarrhea (JAMA. 2012 May 9;307[18]:1959-69). Researchers assessed 63 randomized controlled trials with nearly 12,000 participants. The pooled results showed a statistically significant positive reduction in antibiotic-associated diarrhea (relative risk, 0.58; P less than .001). “Note the number needed to treat to see the effect is 13, so it won’t work in every patient,” Dr. Cabana said.
“So prevention of antibiotic-associated diarrhea is well documented. However, it’s also highly dependent on patent adherence,” he emphasized.
The clinical evidence on colic
For treating babies with colic, the best evidence is behind use of Lactobacilus reuteri DSM 17938, Dr. Cabana said. It tends to work best in breastfed infants, babies not on any gastrointestinal meds, and babies that start therapy early in the course of symptoms. “Use in formula-fed infants is unknown, because there are not enough data so far,” he said.
In some cases, during a prenatal visit, soon-to-be-parents will ask if they should start a probiotic to prevent colic. Dr. Cabana has seen only one prophylaxis study for this indication (JAMA Pediatr. 2014 Mar;168[3]:228-33). In the study, 589 infants were randomly allocated to take L. reuteri DSM 17938 or placebo daily for 90 days. At 3 months of age, the researchers discovered a significantly shorter mean duration of daily crying in the probiotic group (38 vs. 71 minutes; P less than .01).
What’s known about efficacy for eczema
The evidence for treating a child who presents with eczema with probiotics does not support efficacy in general, Dr. Cabana said. And the evidence on prevention of atopic eczema is mixed.
For example, in a randomized, controlled study from Finland, investigators randomized mothers to receive Lactobacillus GG or placebo during the prenatal period (Lancet. 2001;357:1076-9). Of 132 of the children, 35% were later diagnosed with atopic eczema, and the rate in the probiotic group, 23%, was half the 46% rate in the placebo group.
In contrast, researchers found no benefit regarding prevention of atopic dermatitis when 105 pregnant women were randomized to Lactobacillus GG or placebo. At the age of 2 years, atopic dermatitis was diagnosed in 28% of the 50 children in the probiotic group and 27.3% of the 44 in the placebo group (Pediatrics. 2008;121:e850-6).
The region of Germany where the study was conducted was rural/agricultural, so the diet could be different, Dr. Cabana said. Also, the median duration of breastfeeding differed between the Finnish and German study population, 6.8 months versus 9.2 months, respectively. “So that could potentially explain it, or there are just differences that cannot be explained.”
For more information, Dr. Cabana recommended information provided by the International Scientific Association of Prebiotics & Probiotics (https://isappscience.org/infographics/). The association’s website has easy to understand infographics including: What are probiotics and what can they do for you?; What’s so special about fermented foods?; and How do you read a probiotic label?
Dr. Cabana reported he receives research support from the National Institutes of Health, Wyeth Nutrition, and Nestle; is on the speakers bureau for Merck; owns stocks or bonds in Abbot and AbbVie; and is a consultant for Mead Johnson, Abbott, Genentech, Biogaia, General Mills, and Nestle.
EXPERT ANALYSIS FROM AAP 2017
Bedside imaging finds best PEEP settings
A noninvasive bedside imaging technique can individually calibrate positive end-expiratory pressure settings in patients on extracorporeal membrane oxygenation (ECMO) for severe acute respiratory distress syndrome (ARDS), a study showed.
The step-down PEEP (positive end-expiratory pressure) trial could not identify a single PEEP setting that optimally balanced lung overdistension and lung collapse for all 15 patients. But, electrical impedance tomography (EIT) allowed investigators to individually titrate PEEP settings for each patient, Guillaume Franchineau, MD, wrote (Am J Respir Crit Care Med. 2017;196[4]:447-57. doi: 10.1164/rccm.201605-1055OC).
The 4-month study involved 15 patients (aged, 18-79 years) who were in acute respiratory distress syndrome for a variety of reasons, including influenza (7 patients), pneumonia (3), leukemia (2), and 1 case each of Pneumocystis, antisynthetase syndrome, and trauma. All patients were receiving ECMO with a constant driving pressure of 14 cm H2O. After verifying that the inspiratory flow was 0 at the end of inspiration, PEEP was increased to 20 cm H2O (PEEP 20) with a peak inspiratory pressure of 34 cm H2O. PEEP 20 was held for 20 minutes and then lowered by 5-cm H2O decrements with the potential of reaching PEEP 0.
The EIT device, consisting of a silicone belt with 16 surface electrodes, was placed around the thorax aligning with the sixth intercostal parasternal space and connected to a monitor. By measuring conductivity and impeditivity in the underlying tissues, the device generates a low-resolution, two-dimensional image. The image was sufficient to show lung distension and collapse as the PEEP settings changed. Investigators looked for the best compromise between overdistension and collapsed zones, which they defined as the lowest pressure able to limit EIT-assessed collapse to no more than 15% with the least overdistension.
There was no one-size-fits-all PEEP setting, the authors found. The setting that minimized both overdistension and collapse was PEEP 15 in seven patients, PEEP 10 in six patients, and PEEP 5 in two patients.
At each patient’s optimal PEEP setting, the median tidal volume was similar: 3.8 mL/kg ideal body weight for PEEP 15, 3.9 mL/kg ideal body weight for PEEP 10, and 4.3 mL/kg ideal body weight for PEEP 5.
Respiratory system compliance was also similar among the groups, at 20 mL/cm H2O, 18 mL/cm H2O, and 21 mL/cm H2O, respectively. However, arterial partial pressure of oxygen decreased as the PEEP setting decreased, dropping from 148 mm Hg to 128 mm Hg to 100 mm Hg, respectively. Conversely, arterial partial pressure of CO2 increased (32-41 mm Hg).
EIT also allowed clinicians to pinpoint areas of distension or collapse. As PEEP decreased, there was steady ventilation loss in the medial-dorsal and dorsal regions, which shifted to the medial-ventral and ventral regions.
“Most end-expiratory lung impedances were located in medial-dorsal and medial-ventral regions, whereas the dorsal region constantly contributed less than 10% of total end-expiratory lung impedance,” the authors noted.
“The broad variability of EIT-based best compromise PEEPs in these patients with severe ARDS reinforces the need to provide ventilation settings individually tailored to the regional ARDS-lesion distribution,” they concluded. “To achieve that goal, EIT seems to be an interesting bedside noninvasive tool to provide real-time monitoring of the PEEP effect and ventilation distribution on ECMO.”
Positive PEEP trial, but questions remain
This first study to examine EIT in patients under extracorporeal membrane oxygenation shows important clinical potential, but also raises important questions, Claude Guerin, MD, wrote in an accompanying editorial. (Am J Respir Crit Care Med. doi: 10.1164/rccm.201701-0167ed).
The ability to titrate PEEP settings to a patient’s individual needs could substantially reduce the risk of lung derecruitment or damage by overdistension.
The current study, however, has limitations that must be addressed in the next phase of research, before this technique can be adopted into clinical practice, noted Dr. Guerin, a pulmonologist at the Hospital de la Croix Rousse, Lyon, France. The 5-cm H20 PEEP steps may be too large to detect relevant changes, he said.
In several other studies, PEEP was reduced more gradually in 2- to 3-cm H2O increments. “Surprisingly, PEEP was reduced to 0 cm H2O in this study, with this step maintained for 20 minutes, raising the risk of derecruitment and further stretching once higher PEEP levels were resumed.”
The investigators did not perform any recruitment maneuvers before proceeding with PEEP adjustment. This is contrary to what has been done in prior animal and human studies.
The computation of driving pressure was done without taking total PEEP into account. “As total PEEP is frequently greater than PEEP in patients with [acute respiratory distress syndrome], driving pressure can be overestimated with the common computation.”
The optimal PEEP that the investigators aimed for was determined retrospectively from an offline analysis of the data; this technique would not be suitable for bedside management. “When ‘optimal’ PEEP was defined from [EIT criteria], from a higher PaO2 [arterial partial pressure of oxygen] or from a higher compliance of the respiratory system during the decremental PEEP trial, these three criteria were observed together in only four patients with [acute respiratory distress syndrome].”
The study was done only once and cannot comply with the need for regular PEEP-level assessments over time, as could be done with some other strategies.
“Further studies should also consider taking into account the role of chest wall mechanics,” Dr. Guerin said.
Nevertheless, he concluded, EIT-based PEEP titration for each individual patient represents a prospective tool for assisting with the treatment of acute respiratory distress syndrome, and should be fully investigated in a large, prospective trial.
Dr. Franchineau reported receiving speakers fees from Mapquet. Dr. Guerin had no relevant financial disclosures.
[email protected]
On Twitter @alz_gal
A noninvasive bedside imaging technique can individually calibrate positive end-expiratory pressure settings in patients on extracorporeal membrane oxygenation (ECMO) for severe acute respiratory distress syndrome (ARDS), a study showed.
The step-down PEEP (positive end-expiratory pressure) trial could not identify a single PEEP setting that optimally balanced lung overdistension and lung collapse for all 15 patients. But, electrical impedance tomography (EIT) allowed investigators to individually titrate PEEP settings for each patient, Guillaume Franchineau, MD, wrote (Am J Respir Crit Care Med. 2017;196[4]:447-57. doi: 10.1164/rccm.201605-1055OC).
The 4-month study involved 15 patients (aged, 18-79 years) who were in acute respiratory distress syndrome for a variety of reasons, including influenza (7 patients), pneumonia (3), leukemia (2), and 1 case each of Pneumocystis, antisynthetase syndrome, and trauma. All patients were receiving ECMO with a constant driving pressure of 14 cm H2O. After verifying that the inspiratory flow was 0 at the end of inspiration, PEEP was increased to 20 cm H2O (PEEP 20) with a peak inspiratory pressure of 34 cm H2O. PEEP 20 was held for 20 minutes and then lowered by 5-cm H2O decrements with the potential of reaching PEEP 0.
The EIT device, consisting of a silicone belt with 16 surface electrodes, was placed around the thorax aligning with the sixth intercostal parasternal space and connected to a monitor. By measuring conductivity and impeditivity in the underlying tissues, the device generates a low-resolution, two-dimensional image. The image was sufficient to show lung distension and collapse as the PEEP settings changed. Investigators looked for the best compromise between overdistension and collapsed zones, which they defined as the lowest pressure able to limit EIT-assessed collapse to no more than 15% with the least overdistension.
There was no one-size-fits-all PEEP setting, the authors found. The setting that minimized both overdistension and collapse was PEEP 15 in seven patients, PEEP 10 in six patients, and PEEP 5 in two patients.
At each patient’s optimal PEEP setting, the median tidal volume was similar: 3.8 mL/kg ideal body weight for PEEP 15, 3.9 mL/kg ideal body weight for PEEP 10, and 4.3 mL/kg ideal body weight for PEEP 5.
Respiratory system compliance was also similar among the groups, at 20 mL/cm H2O, 18 mL/cm H2O, and 21 mL/cm H2O, respectively. However, arterial partial pressure of oxygen decreased as the PEEP setting decreased, dropping from 148 mm Hg to 128 mm Hg to 100 mm Hg, respectively. Conversely, arterial partial pressure of CO2 increased (32-41 mm Hg).
EIT also allowed clinicians to pinpoint areas of distension or collapse. As PEEP decreased, there was steady ventilation loss in the medial-dorsal and dorsal regions, which shifted to the medial-ventral and ventral regions.
“Most end-expiratory lung impedances were located in medial-dorsal and medial-ventral regions, whereas the dorsal region constantly contributed less than 10% of total end-expiratory lung impedance,” the authors noted.
“The broad variability of EIT-based best compromise PEEPs in these patients with severe ARDS reinforces the need to provide ventilation settings individually tailored to the regional ARDS-lesion distribution,” they concluded. “To achieve that goal, EIT seems to be an interesting bedside noninvasive tool to provide real-time monitoring of the PEEP effect and ventilation distribution on ECMO.”
Positive PEEP trial, but questions remain
This first study to examine EIT in patients under extracorporeal membrane oxygenation shows important clinical potential, but also raises important questions, Claude Guerin, MD, wrote in an accompanying editorial. (Am J Respir Crit Care Med. doi: 10.1164/rccm.201701-0167ed).
The ability to titrate PEEP settings to a patient’s individual needs could substantially reduce the risk of lung derecruitment or damage by overdistension.
The current study, however, has limitations that must be addressed in the next phase of research, before this technique can be adopted into clinical practice, noted Dr. Guerin, a pulmonologist at the Hospital de la Croix Rousse, Lyon, France. The 5-cm H20 PEEP steps may be too large to detect relevant changes, he said.
In several other studies, PEEP was reduced more gradually in 2- to 3-cm H2O increments. “Surprisingly, PEEP was reduced to 0 cm H2O in this study, with this step maintained for 20 minutes, raising the risk of derecruitment and further stretching once higher PEEP levels were resumed.”
The investigators did not perform any recruitment maneuvers before proceeding with PEEP adjustment. This is contrary to what has been done in prior animal and human studies.
The computation of driving pressure was done without taking total PEEP into account. “As total PEEP is frequently greater than PEEP in patients with [acute respiratory distress syndrome], driving pressure can be overestimated with the common computation.”
The optimal PEEP that the investigators aimed for was determined retrospectively from an offline analysis of the data; this technique would not be suitable for bedside management. “When ‘optimal’ PEEP was defined from [EIT criteria], from a higher PaO2 [arterial partial pressure of oxygen] or from a higher compliance of the respiratory system during the decremental PEEP trial, these three criteria were observed together in only four patients with [acute respiratory distress syndrome].”
The study was done only once and cannot comply with the need for regular PEEP-level assessments over time, as could be done with some other strategies.
“Further studies should also consider taking into account the role of chest wall mechanics,” Dr. Guerin said.
Nevertheless, he concluded, EIT-based PEEP titration for each individual patient represents a prospective tool for assisting with the treatment of acute respiratory distress syndrome, and should be fully investigated in a large, prospective trial.
Dr. Franchineau reported receiving speakers fees from Mapquet. Dr. Guerin had no relevant financial disclosures.
[email protected]
On Twitter @alz_gal
A noninvasive bedside imaging technique can individually calibrate positive end-expiratory pressure settings in patients on extracorporeal membrane oxygenation (ECMO) for severe acute respiratory distress syndrome (ARDS), a study showed.
The step-down PEEP (positive end-expiratory pressure) trial could not identify a single PEEP setting that optimally balanced lung overdistension and lung collapse for all 15 patients. But, electrical impedance tomography (EIT) allowed investigators to individually titrate PEEP settings for each patient, Guillaume Franchineau, MD, wrote (Am J Respir Crit Care Med. 2017;196[4]:447-57. doi: 10.1164/rccm.201605-1055OC).
The 4-month study involved 15 patients (aged, 18-79 years) who were in acute respiratory distress syndrome for a variety of reasons, including influenza (7 patients), pneumonia (3), leukemia (2), and 1 case each of Pneumocystis, antisynthetase syndrome, and trauma. All patients were receiving ECMO with a constant driving pressure of 14 cm H2O. After verifying that the inspiratory flow was 0 at the end of inspiration, PEEP was increased to 20 cm H2O (PEEP 20) with a peak inspiratory pressure of 34 cm H2O. PEEP 20 was held for 20 minutes and then lowered by 5-cm H2O decrements with the potential of reaching PEEP 0.
The EIT device, consisting of a silicone belt with 16 surface electrodes, was placed around the thorax aligning with the sixth intercostal parasternal space and connected to a monitor. By measuring conductivity and impeditivity in the underlying tissues, the device generates a low-resolution, two-dimensional image. The image was sufficient to show lung distension and collapse as the PEEP settings changed. Investigators looked for the best compromise between overdistension and collapsed zones, which they defined as the lowest pressure able to limit EIT-assessed collapse to no more than 15% with the least overdistension.
There was no one-size-fits-all PEEP setting, the authors found. The setting that minimized both overdistension and collapse was PEEP 15 in seven patients, PEEP 10 in six patients, and PEEP 5 in two patients.
At each patient’s optimal PEEP setting, the median tidal volume was similar: 3.8 mL/kg ideal body weight for PEEP 15, 3.9 mL/kg ideal body weight for PEEP 10, and 4.3 mL/kg ideal body weight for PEEP 5.
Respiratory system compliance was also similar among the groups, at 20 mL/cm H2O, 18 mL/cm H2O, and 21 mL/cm H2O, respectively. However, arterial partial pressure of oxygen decreased as the PEEP setting decreased, dropping from 148 mm Hg to 128 mm Hg to 100 mm Hg, respectively. Conversely, arterial partial pressure of CO2 increased (32-41 mm Hg).
EIT also allowed clinicians to pinpoint areas of distension or collapse. As PEEP decreased, there was steady ventilation loss in the medial-dorsal and dorsal regions, which shifted to the medial-ventral and ventral regions.
“Most end-expiratory lung impedances were located in medial-dorsal and medial-ventral regions, whereas the dorsal region constantly contributed less than 10% of total end-expiratory lung impedance,” the authors noted.
“The broad variability of EIT-based best compromise PEEPs in these patients with severe ARDS reinforces the need to provide ventilation settings individually tailored to the regional ARDS-lesion distribution,” they concluded. “To achieve that goal, EIT seems to be an interesting bedside noninvasive tool to provide real-time monitoring of the PEEP effect and ventilation distribution on ECMO.”
Positive PEEP trial, but questions remain
This first study to examine EIT in patients under extracorporeal membrane oxygenation shows important clinical potential, but also raises important questions, Claude Guerin, MD, wrote in an accompanying editorial. (Am J Respir Crit Care Med. doi: 10.1164/rccm.201701-0167ed).
The ability to titrate PEEP settings to a patient’s individual needs could substantially reduce the risk of lung derecruitment or damage by overdistension.
The current study, however, has limitations that must be addressed in the next phase of research, before this technique can be adopted into clinical practice, noted Dr. Guerin, a pulmonologist at the Hospital de la Croix Rousse, Lyon, France. The 5-cm H20 PEEP steps may be too large to detect relevant changes, he said.
In several other studies, PEEP was reduced more gradually in 2- to 3-cm H2O increments. “Surprisingly, PEEP was reduced to 0 cm H2O in this study, with this step maintained for 20 minutes, raising the risk of derecruitment and further stretching once higher PEEP levels were resumed.”
The investigators did not perform any recruitment maneuvers before proceeding with PEEP adjustment. This is contrary to what has been done in prior animal and human studies.
The computation of driving pressure was done without taking total PEEP into account. “As total PEEP is frequently greater than PEEP in patients with [acute respiratory distress syndrome], driving pressure can be overestimated with the common computation.”
The optimal PEEP that the investigators aimed for was determined retrospectively from an offline analysis of the data; this technique would not be suitable for bedside management. “When ‘optimal’ PEEP was defined from [EIT criteria], from a higher PaO2 [arterial partial pressure of oxygen] or from a higher compliance of the respiratory system during the decremental PEEP trial, these three criteria were observed together in only four patients with [acute respiratory distress syndrome].”
The study was done only once and cannot comply with the need for regular PEEP-level assessments over time, as could be done with some other strategies.
“Further studies should also consider taking into account the role of chest wall mechanics,” Dr. Guerin said.
Nevertheless, he concluded, EIT-based PEEP titration for each individual patient represents a prospective tool for assisting with the treatment of acute respiratory distress syndrome, and should be fully investigated in a large, prospective trial.
Dr. Franchineau reported receiving speakers fees from Mapquet. Dr. Guerin had no relevant financial disclosures.
[email protected]
On Twitter @alz_gal
Tezepelumab reduces exacerbations in asthma
Patients whose asthma remains uncontrolled despite treatment may benefit from a new monoclonal antibody that targets an inflammatory cytokine known to be promoted in asthmatic airways, according to data presented at the annual congress of the European Respiratory Society.
Writing in the Sept. 7 issue of the New England Journal of Medicine, researchers reported on a phase 2, randomized placebo-controlled trial of three dosing regimens of subcutaneous tezepelumab, which targets the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP). The trial involved 584 patients with uncontrolled asthma, despite treatment with long-acting beta-agonists and medium to high doses of inhaled glucocorticoids.
At 70 mg every 4 weeks, exacerbation rates were 61% lower than in the placebo group; at 210 mg every 4 weeks, they were 71% lower; and at 280 mg every 2 weeks, they were 66% lower (P was less than .001 in comparisons between each group and the placebo).The overall annualized exacerbation rates by week 52 were 0.26 for the 70-mg group, 0.19 for the 210-mg group, and 0.22 for the 280-mg group, compared with 0.67 in the placebo group, regardless of a patient’s baseline eosinophil count. Patients treated with tezepelumab had a longer time to first asthma exacerbation. They also experienced a significantly higher change from baseline in their prebronchodilator forced expiratory volume in 1 second at week 52, when compared with patients on the placebo. “The observed improvements in disease control in patients who received tezepelumab highlight the potential pathogenic role of TSLP across different asthma phenotypes,” reported Jonathan Corren, MD, of the University of California, Los Angeles, and his coauthors. “... Although TSLP is central to the regulation of type 2 immunity, many cell types that are activated by or respond to TSLP, such as mast cells, basophils, natural killer T cells, innate lymphoid cells, and neutrophils, may play a role in inflammation in asthma beyond type 2 inflammation.”The incidences of adverse events and serious adverse events were similar across all groups in the study. Three serious adverse events – pneumonia and stroke in the same patient and one case of Guillain-Barré syndrome – in patients taking tezepelumab, were deemed to be related to the treatment.
Tezepelumab ‘most promising’ asthma biologic to date
Tezepelumab is the first biologic that has a substantial positive effect on two important markers of the inflammation of asthma – namely, blood eosinophil counts and the fraction of exhaled nitric oxide, noted Elisabeth H. Bel, MD, PhD, in an editorial accompanying the New England Journal of Medicine’s publication of this study (2017;377:989-91). It appears to be the broadest and most promising biologic for the treatment of persistent uncontrolled asthma to date, said Dr. Bel, of the department of respiratory medicine, Academic Medical Center, the University of Amsterdam.
The observation that tezepelumab reduces the level of both inflammatory markers shows that it hits a more upstream target and that it blocks at least two relevant inflammatory pathways in asthma, she noted. This is likely to be clinically relevant, since simultaneously increased exhaled nitric oxide levels and blood eosinophil counts are related to increased morbidity due to asthma.
The study was supported by tezepelumab manufacturers MedImmune (a member of the AstraZeneca group) and Amgen. Six of the seven authors are employees of MedImmune or Amgen. One author declared support and honoraria from several pharmaceutical companies, one declared a related patent, and five also had stock options in either MedImmune or Amgen.
Dr. Bel declared consultancies and grants from pharmaceutical companies including AstraZeneca.
Patients whose asthma remains uncontrolled despite treatment may benefit from a new monoclonal antibody that targets an inflammatory cytokine known to be promoted in asthmatic airways, according to data presented at the annual congress of the European Respiratory Society.
Writing in the Sept. 7 issue of the New England Journal of Medicine, researchers reported on a phase 2, randomized placebo-controlled trial of three dosing regimens of subcutaneous tezepelumab, which targets the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP). The trial involved 584 patients with uncontrolled asthma, despite treatment with long-acting beta-agonists and medium to high doses of inhaled glucocorticoids.
At 70 mg every 4 weeks, exacerbation rates were 61% lower than in the placebo group; at 210 mg every 4 weeks, they were 71% lower; and at 280 mg every 2 weeks, they were 66% lower (P was less than .001 in comparisons between each group and the placebo).The overall annualized exacerbation rates by week 52 were 0.26 for the 70-mg group, 0.19 for the 210-mg group, and 0.22 for the 280-mg group, compared with 0.67 in the placebo group, regardless of a patient’s baseline eosinophil count. Patients treated with tezepelumab had a longer time to first asthma exacerbation. They also experienced a significantly higher change from baseline in their prebronchodilator forced expiratory volume in 1 second at week 52, when compared with patients on the placebo. “The observed improvements in disease control in patients who received tezepelumab highlight the potential pathogenic role of TSLP across different asthma phenotypes,” reported Jonathan Corren, MD, of the University of California, Los Angeles, and his coauthors. “... Although TSLP is central to the regulation of type 2 immunity, many cell types that are activated by or respond to TSLP, such as mast cells, basophils, natural killer T cells, innate lymphoid cells, and neutrophils, may play a role in inflammation in asthma beyond type 2 inflammation.”The incidences of adverse events and serious adverse events were similar across all groups in the study. Three serious adverse events – pneumonia and stroke in the same patient and one case of Guillain-Barré syndrome – in patients taking tezepelumab, were deemed to be related to the treatment.
Tezepelumab ‘most promising’ asthma biologic to date
Tezepelumab is the first biologic that has a substantial positive effect on two important markers of the inflammation of asthma – namely, blood eosinophil counts and the fraction of exhaled nitric oxide, noted Elisabeth H. Bel, MD, PhD, in an editorial accompanying the New England Journal of Medicine’s publication of this study (2017;377:989-91). It appears to be the broadest and most promising biologic for the treatment of persistent uncontrolled asthma to date, said Dr. Bel, of the department of respiratory medicine, Academic Medical Center, the University of Amsterdam.
The observation that tezepelumab reduces the level of both inflammatory markers shows that it hits a more upstream target and that it blocks at least two relevant inflammatory pathways in asthma, she noted. This is likely to be clinically relevant, since simultaneously increased exhaled nitric oxide levels and blood eosinophil counts are related to increased morbidity due to asthma.
The study was supported by tezepelumab manufacturers MedImmune (a member of the AstraZeneca group) and Amgen. Six of the seven authors are employees of MedImmune or Amgen. One author declared support and honoraria from several pharmaceutical companies, one declared a related patent, and five also had stock options in either MedImmune or Amgen.
Dr. Bel declared consultancies and grants from pharmaceutical companies including AstraZeneca.
Patients whose asthma remains uncontrolled despite treatment may benefit from a new monoclonal antibody that targets an inflammatory cytokine known to be promoted in asthmatic airways, according to data presented at the annual congress of the European Respiratory Society.
Writing in the Sept. 7 issue of the New England Journal of Medicine, researchers reported on a phase 2, randomized placebo-controlled trial of three dosing regimens of subcutaneous tezepelumab, which targets the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP). The trial involved 584 patients with uncontrolled asthma, despite treatment with long-acting beta-agonists and medium to high doses of inhaled glucocorticoids.
At 70 mg every 4 weeks, exacerbation rates were 61% lower than in the placebo group; at 210 mg every 4 weeks, they were 71% lower; and at 280 mg every 2 weeks, they were 66% lower (P was less than .001 in comparisons between each group and the placebo).The overall annualized exacerbation rates by week 52 were 0.26 for the 70-mg group, 0.19 for the 210-mg group, and 0.22 for the 280-mg group, compared with 0.67 in the placebo group, regardless of a patient’s baseline eosinophil count. Patients treated with tezepelumab had a longer time to first asthma exacerbation. They also experienced a significantly higher change from baseline in their prebronchodilator forced expiratory volume in 1 second at week 52, when compared with patients on the placebo. “The observed improvements in disease control in patients who received tezepelumab highlight the potential pathogenic role of TSLP across different asthma phenotypes,” reported Jonathan Corren, MD, of the University of California, Los Angeles, and his coauthors. “... Although TSLP is central to the regulation of type 2 immunity, many cell types that are activated by or respond to TSLP, such as mast cells, basophils, natural killer T cells, innate lymphoid cells, and neutrophils, may play a role in inflammation in asthma beyond type 2 inflammation.”The incidences of adverse events and serious adverse events were similar across all groups in the study. Three serious adverse events – pneumonia and stroke in the same patient and one case of Guillain-Barré syndrome – in patients taking tezepelumab, were deemed to be related to the treatment.
Tezepelumab ‘most promising’ asthma biologic to date
Tezepelumab is the first biologic that has a substantial positive effect on two important markers of the inflammation of asthma – namely, blood eosinophil counts and the fraction of exhaled nitric oxide, noted Elisabeth H. Bel, MD, PhD, in an editorial accompanying the New England Journal of Medicine’s publication of this study (2017;377:989-91). It appears to be the broadest and most promising biologic for the treatment of persistent uncontrolled asthma to date, said Dr. Bel, of the department of respiratory medicine, Academic Medical Center, the University of Amsterdam.
The observation that tezepelumab reduces the level of both inflammatory markers shows that it hits a more upstream target and that it blocks at least two relevant inflammatory pathways in asthma, she noted. This is likely to be clinically relevant, since simultaneously increased exhaled nitric oxide levels and blood eosinophil counts are related to increased morbidity due to asthma.
The study was supported by tezepelumab manufacturers MedImmune (a member of the AstraZeneca group) and Amgen. Six of the seven authors are employees of MedImmune or Amgen. One author declared support and honoraria from several pharmaceutical companies, one declared a related patent, and five also had stock options in either MedImmune or Amgen.
Dr. Bel declared consultancies and grants from pharmaceutical companies including AstraZeneca.
Statins linked to lower death rates in COPD
Receiving a statin prescription within a year after diagnosis of chronic obstructive pulmonary disease was associated with a 21% decrease in the subsequent risk of all-cause mortality and a 45% drop in risk of pulmonary mortality, according to the results of a large retrospective administrative database study.
The findings belie those of the recent Simvastatin in the Prevention of COPD Exacerbation (STATCOPE) trial, in which daily simvastatin (40 mg) did not affect exacerbation rates or time to first exacerbation in high-risk COPD patients, wrote Larry D. Lynd, PhD, a professor at the at the University of British Columbia, Vancouver, and his associates. Their study was observational, but the association between statin use and decreased mortality “persisted across several measures of statin exposure,” they wrote. “Our findings, in conjunction with previously reported evidence, suggest that there may be a specific subtype of COPD patients that may benefit from statin use.” The study appears in the September issue of CHEST (2017;152;486-93).
To further explore the question, the researchers analyzed linked health databases from nearly 40,000 patients aged 50 years and older who had received at least three prescriptions for an anticholinergic or a short-acting beta agonist in 12 months some time between 1998 and 2007. The first prescription was considered the date of COPD “diagnosis.” The average age of the patients was 71 years; 55% were female.
A total of 7,775 patients (19.6%) who met this definition of incident COPD were prescribed a statin at least once during the subsequent year. These patients had a significantly reduced risk of subsequent all-cause mortality in univariate and multivariate analyses, with hazard ratios of 0.79 (95% confidence intervals, 0.68-0.91; P less than .002). Statins also showed a protective effect against pulmonary mortality, with univariate and multivariate hazard ratios of 0.52 (P = .01) and 0.55 (P = .03), respectively.
The protective effect of statins held up when the investigators narrowed the exposure period to 6 months after COPD diagnosis and when they expanded it to 18 months. Exposure to statins for 80% of the 1-year window after COPD diagnosis – a proxy for statin adherence – also led to a reduced risk of all-cause mortality, but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.71- 1.01; P = .06).
The most common prescription was for atorvastatin (49%), usually for 90 days (23%), 100 days (20%), or 30 days (15%), the researchers said. While the “possibility of the ‘healthy user’ or the ‘healthy adherer’ cannot be ignored,” they adjusted for other prescriptions, comorbidities, and income level, which should have helped eliminate this effect, they added. However, they lacked data on smoking and lung function assessments, both of which are “important confounders and contributors to mortality,” they acknowledged.
Despite [its] limitations, the study results are intriguing and in line with findings from other retrospective cohorts, noted Or Kalchiem-Dekel, MD, and Robert M. Reed, MD, in an editorial published in CHEST (2017;152:456-7. doi: 10.1016/j.chest.2017.04.156).
How then can we reconcile the apparent benefits observed in retrospective studies with the lack of clinical effect seen in prospective trials, particularly the in the STATCOPE study? Could it be that both negative and positive studies are “correct”? Prospective studies have thus far not been adequately powered for mortality as an endpoint, said the editorialists, who are both at the pulmonary and critical care medicine division, University of Maryland, Baltimore.This most recent study reinforces the idea that statins may play a beneficial role in COPD, but it isn’t clear which patients to target for therapy. It is unlikely that the findings will reverse recent recommendations by the American College of Chest Physicians and Canadian Thoracic Society against the use of statins for the purpose of prevention of COPD exacerbations, but the suggestion of survival advantage related to statins certainly may breathe new life into an enthusiasm greatly tempered by STATCOPE, they said.
Canadian Institutes of Health Research supported the study. One coinvestigator disclosed consulting relationships with Teva, Pfizer, and Novartis; the others had no conflicts of interest. Neither editorialist had conflicts of interest.
Receiving a statin prescription within a year after diagnosis of chronic obstructive pulmonary disease was associated with a 21% decrease in the subsequent risk of all-cause mortality and a 45% drop in risk of pulmonary mortality, according to the results of a large retrospective administrative database study.
The findings belie those of the recent Simvastatin in the Prevention of COPD Exacerbation (STATCOPE) trial, in which daily simvastatin (40 mg) did not affect exacerbation rates or time to first exacerbation in high-risk COPD patients, wrote Larry D. Lynd, PhD, a professor at the at the University of British Columbia, Vancouver, and his associates. Their study was observational, but the association between statin use and decreased mortality “persisted across several measures of statin exposure,” they wrote. “Our findings, in conjunction with previously reported evidence, suggest that there may be a specific subtype of COPD patients that may benefit from statin use.” The study appears in the September issue of CHEST (2017;152;486-93).
To further explore the question, the researchers analyzed linked health databases from nearly 40,000 patients aged 50 years and older who had received at least three prescriptions for an anticholinergic or a short-acting beta agonist in 12 months some time between 1998 and 2007. The first prescription was considered the date of COPD “diagnosis.” The average age of the patients was 71 years; 55% were female.
A total of 7,775 patients (19.6%) who met this definition of incident COPD were prescribed a statin at least once during the subsequent year. These patients had a significantly reduced risk of subsequent all-cause mortality in univariate and multivariate analyses, with hazard ratios of 0.79 (95% confidence intervals, 0.68-0.91; P less than .002). Statins also showed a protective effect against pulmonary mortality, with univariate and multivariate hazard ratios of 0.52 (P = .01) and 0.55 (P = .03), respectively.
The protective effect of statins held up when the investigators narrowed the exposure period to 6 months after COPD diagnosis and when they expanded it to 18 months. Exposure to statins for 80% of the 1-year window after COPD diagnosis – a proxy for statin adherence – also led to a reduced risk of all-cause mortality, but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.71- 1.01; P = .06).
The most common prescription was for atorvastatin (49%), usually for 90 days (23%), 100 days (20%), or 30 days (15%), the researchers said. While the “possibility of the ‘healthy user’ or the ‘healthy adherer’ cannot be ignored,” they adjusted for other prescriptions, comorbidities, and income level, which should have helped eliminate this effect, they added. However, they lacked data on smoking and lung function assessments, both of which are “important confounders and contributors to mortality,” they acknowledged.
Despite [its] limitations, the study results are intriguing and in line with findings from other retrospective cohorts, noted Or Kalchiem-Dekel, MD, and Robert M. Reed, MD, in an editorial published in CHEST (2017;152:456-7. doi: 10.1016/j.chest.2017.04.156).
How then can we reconcile the apparent benefits observed in retrospective studies with the lack of clinical effect seen in prospective trials, particularly the in the STATCOPE study? Could it be that both negative and positive studies are “correct”? Prospective studies have thus far not been adequately powered for mortality as an endpoint, said the editorialists, who are both at the pulmonary and critical care medicine division, University of Maryland, Baltimore.This most recent study reinforces the idea that statins may play a beneficial role in COPD, but it isn’t clear which patients to target for therapy. It is unlikely that the findings will reverse recent recommendations by the American College of Chest Physicians and Canadian Thoracic Society against the use of statins for the purpose of prevention of COPD exacerbations, but the suggestion of survival advantage related to statins certainly may breathe new life into an enthusiasm greatly tempered by STATCOPE, they said.
Canadian Institutes of Health Research supported the study. One coinvestigator disclosed consulting relationships with Teva, Pfizer, and Novartis; the others had no conflicts of interest. Neither editorialist had conflicts of interest.
Receiving a statin prescription within a year after diagnosis of chronic obstructive pulmonary disease was associated with a 21% decrease in the subsequent risk of all-cause mortality and a 45% drop in risk of pulmonary mortality, according to the results of a large retrospective administrative database study.
The findings belie those of the recent Simvastatin in the Prevention of COPD Exacerbation (STATCOPE) trial, in which daily simvastatin (40 mg) did not affect exacerbation rates or time to first exacerbation in high-risk COPD patients, wrote Larry D. Lynd, PhD, a professor at the at the University of British Columbia, Vancouver, and his associates. Their study was observational, but the association between statin use and decreased mortality “persisted across several measures of statin exposure,” they wrote. “Our findings, in conjunction with previously reported evidence, suggest that there may be a specific subtype of COPD patients that may benefit from statin use.” The study appears in the September issue of CHEST (2017;152;486-93).
To further explore the question, the researchers analyzed linked health databases from nearly 40,000 patients aged 50 years and older who had received at least three prescriptions for an anticholinergic or a short-acting beta agonist in 12 months some time between 1998 and 2007. The first prescription was considered the date of COPD “diagnosis.” The average age of the patients was 71 years; 55% were female.
A total of 7,775 patients (19.6%) who met this definition of incident COPD were prescribed a statin at least once during the subsequent year. These patients had a significantly reduced risk of subsequent all-cause mortality in univariate and multivariate analyses, with hazard ratios of 0.79 (95% confidence intervals, 0.68-0.91; P less than .002). Statins also showed a protective effect against pulmonary mortality, with univariate and multivariate hazard ratios of 0.52 (P = .01) and 0.55 (P = .03), respectively.
The protective effect of statins held up when the investigators narrowed the exposure period to 6 months after COPD diagnosis and when they expanded it to 18 months. Exposure to statins for 80% of the 1-year window after COPD diagnosis – a proxy for statin adherence – also led to a reduced risk of all-cause mortality, but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.71- 1.01; P = .06).
The most common prescription was for atorvastatin (49%), usually for 90 days (23%), 100 days (20%), or 30 days (15%), the researchers said. While the “possibility of the ‘healthy user’ or the ‘healthy adherer’ cannot be ignored,” they adjusted for other prescriptions, comorbidities, and income level, which should have helped eliminate this effect, they added. However, they lacked data on smoking and lung function assessments, both of which are “important confounders and contributors to mortality,” they acknowledged.
Despite [its] limitations, the study results are intriguing and in line with findings from other retrospective cohorts, noted Or Kalchiem-Dekel, MD, and Robert M. Reed, MD, in an editorial published in CHEST (2017;152:456-7. doi: 10.1016/j.chest.2017.04.156).
How then can we reconcile the apparent benefits observed in retrospective studies with the lack of clinical effect seen in prospective trials, particularly the in the STATCOPE study? Could it be that both negative and positive studies are “correct”? Prospective studies have thus far not been adequately powered for mortality as an endpoint, said the editorialists, who are both at the pulmonary and critical care medicine division, University of Maryland, Baltimore.This most recent study reinforces the idea that statins may play a beneficial role in COPD, but it isn’t clear which patients to target for therapy. It is unlikely that the findings will reverse recent recommendations by the American College of Chest Physicians and Canadian Thoracic Society against the use of statins for the purpose of prevention of COPD exacerbations, but the suggestion of survival advantage related to statins certainly may breathe new life into an enthusiasm greatly tempered by STATCOPE, they said.
Canadian Institutes of Health Research supported the study. One coinvestigator disclosed consulting relationships with Teva, Pfizer, and Novartis; the others had no conflicts of interest. Neither editorialist had conflicts of interest.
FROM CHEST
Payment gaps seen for child visits
, according to the Agency for Healthcare Research and Quality.
Child visits covered by private insurance brought in a mean $214 for office-based physicians of all specialties in 2015, which was $88 more than the $126 they received for Medicaid-covered visits, the AHRQ said.
That gap has been consistent since 2010, even as payments rose from 2010 to 2013 and fell in 2014 and 2015. The payment gap was even larger in 2015 when looking at the most expensive 10% of child visits: $406 for those that were privately insured and $215 for those covered by Medicaid, the AHRQ reported in a recent Statistical Brief.
Variations in payments also were seen between geographic regions and among the different physician specialties. Mean payments to physicians in the Midwest were highest for both private insurance ($249) and Medicaid ($152), while the lowest payments – $192 from private insurance and $120 from Medicaid – went to physicians in the South. The South also had the smallest gap between private and Medicaid coverage at $72, and the West had the largest gap at an even $100, but none of the variation across regions was significant, the AHRQ said.
There were statistically significant gaps between private and Medicaid payments by specialty, although only for visits to orthopedists ($423 private – $162 Medicaid = $261) and primary care physicians such as family physicians and internists ($174 private – $122 Medicaid = $52). Payments to pediatricians were $190 private/$115 Medicaid, and the psychiatrists’ $111 mean payment from Medicaid represented the lowest for any specialty, data from Medical Expenditure Panel Survey’s household component show.
, according to the Agency for Healthcare Research and Quality.
Child visits covered by private insurance brought in a mean $214 for office-based physicians of all specialties in 2015, which was $88 more than the $126 they received for Medicaid-covered visits, the AHRQ said.
That gap has been consistent since 2010, even as payments rose from 2010 to 2013 and fell in 2014 and 2015. The payment gap was even larger in 2015 when looking at the most expensive 10% of child visits: $406 for those that were privately insured and $215 for those covered by Medicaid, the AHRQ reported in a recent Statistical Brief.
Variations in payments also were seen between geographic regions and among the different physician specialties. Mean payments to physicians in the Midwest were highest for both private insurance ($249) and Medicaid ($152), while the lowest payments – $192 from private insurance and $120 from Medicaid – went to physicians in the South. The South also had the smallest gap between private and Medicaid coverage at $72, and the West had the largest gap at an even $100, but none of the variation across regions was significant, the AHRQ said.
There were statistically significant gaps between private and Medicaid payments by specialty, although only for visits to orthopedists ($423 private – $162 Medicaid = $261) and primary care physicians such as family physicians and internists ($174 private – $122 Medicaid = $52). Payments to pediatricians were $190 private/$115 Medicaid, and the psychiatrists’ $111 mean payment from Medicaid represented the lowest for any specialty, data from Medical Expenditure Panel Survey’s household component show.
, according to the Agency for Healthcare Research and Quality.
Child visits covered by private insurance brought in a mean $214 for office-based physicians of all specialties in 2015, which was $88 more than the $126 they received for Medicaid-covered visits, the AHRQ said.
That gap has been consistent since 2010, even as payments rose from 2010 to 2013 and fell in 2014 and 2015. The payment gap was even larger in 2015 when looking at the most expensive 10% of child visits: $406 for those that were privately insured and $215 for those covered by Medicaid, the AHRQ reported in a recent Statistical Brief.
Variations in payments also were seen between geographic regions and among the different physician specialties. Mean payments to physicians in the Midwest were highest for both private insurance ($249) and Medicaid ($152), while the lowest payments – $192 from private insurance and $120 from Medicaid – went to physicians in the South. The South also had the smallest gap between private and Medicaid coverage at $72, and the West had the largest gap at an even $100, but none of the variation across regions was significant, the AHRQ said.
There were statistically significant gaps between private and Medicaid payments by specialty, although only for visits to orthopedists ($423 private – $162 Medicaid = $261) and primary care physicians such as family physicians and internists ($174 private – $122 Medicaid = $52). Payments to pediatricians were $190 private/$115 Medicaid, and the psychiatrists’ $111 mean payment from Medicaid represented the lowest for any specialty, data from Medical Expenditure Panel Survey’s household component show.
Tdap during pregnancy, or before, offers infants pertussis protection
during the early months of life, according to Tami H. Skoff of the Centers for Disease Control and Prevention, Atlanta, and her associates.
In an analysis of 240 infants younger than 2 months with pertussis cough onset between 2011 and 2015 and 535 control infants, 57% of case mothers and 67% of control mothers had at least one valid Tdap dose; 13% of vaccinated case mothers and 14% of vaccinated control mothers had more than one valid dose of Tdap reported. 
Of Tdap doses received during pregnancy in 22 cases and 117 controls, 77% were received during the third trimester, most during the Advisory Committee on Immunization Practices’ recommended 27-36 weeks of gestation. Of the Tdap doses received before pregnancy in mothers of 24 cases and 67 controls, 25% of the case mothers and 67% of the control mothers received Tdap 2 or fewer years before pregnancy.
The effectiveness of Tdap vaccination during the third trimester of pregnancy was 78%, and effectiveness during the first or second trimester was 64%. Effectiveness of Tdap given 2 or fewer years before pregnancy was 83%. This study was not powered to determine a difference if the vaccine was administered in the ACIP-recommended time period during the third trimester.
A reported 49% of U.S. pregnant women received Tdap during the 2015-2016 flu season, an increase of 22% from the 2013-2014 season, according to a CDC Internet panel survey.
“While maternal immunization during pregnancy will help bridge the gap until next-generation pertussis vaccines are licensed and available for use, this highly effective strategy will likely remain an integral component of pertussis prevention and control, even in the setting of new vaccines,” the investigators said.
Read more in Clinical Infectious Diseases (2017 Sep 28. doi: 10.1093/cid/cix724).
during the early months of life, according to Tami H. Skoff of the Centers for Disease Control and Prevention, Atlanta, and her associates.
In an analysis of 240 infants younger than 2 months with pertussis cough onset between 2011 and 2015 and 535 control infants, 57% of case mothers and 67% of control mothers had at least one valid Tdap dose; 13% of vaccinated case mothers and 14% of vaccinated control mothers had more than one valid dose of Tdap reported.
Of Tdap doses received during pregnancy in 22 cases and 117 controls, 77% were received during the third trimester, most during the Advisory Committee on Immunization Practices’ recommended 27-36 weeks of gestation. Of the Tdap doses received before pregnancy in mothers of 24 cases and 67 controls, 25% of the case mothers and 67% of the control mothers received Tdap 2 or fewer years before pregnancy.
The effectiveness of Tdap vaccination during the third trimester of pregnancy was 78%, and effectiveness during the first or second trimester was 64%. Effectiveness of Tdap given 2 or fewer years before pregnancy was 83%. This study was not powered to determine a difference if the vaccine was administered in the ACIP-recommended time period during the third trimester.
A reported 49% of U.S. pregnant women received Tdap during the 2015-2016 flu season, an increase of 22% from the 2013-2014 season, according to a CDC Internet panel survey.
“While maternal immunization during pregnancy will help bridge the gap until next-generation pertussis vaccines are licensed and available for use, this highly effective strategy will likely remain an integral component of pertussis prevention and control, even in the setting of new vaccines,” the investigators said.
Read more in Clinical Infectious Diseases (2017 Sep 28. doi: 10.1093/cid/cix724).
during the early months of life, according to Tami H. Skoff of the Centers for Disease Control and Prevention, Atlanta, and her associates.
In an analysis of 240 infants younger than 2 months with pertussis cough onset between 2011 and 2015 and 535 control infants, 57% of case mothers and 67% of control mothers had at least one valid Tdap dose; 13% of vaccinated case mothers and 14% of vaccinated control mothers had more than one valid dose of Tdap reported.
Of Tdap doses received during pregnancy in 22 cases and 117 controls, 77% were received during the third trimester, most during the Advisory Committee on Immunization Practices’ recommended 27-36 weeks of gestation. Of the Tdap doses received before pregnancy in mothers of 24 cases and 67 controls, 25% of the case mothers and 67% of the control mothers received Tdap 2 or fewer years before pregnancy.
The effectiveness of Tdap vaccination during the third trimester of pregnancy was 78%, and effectiveness during the first or second trimester was 64%. Effectiveness of Tdap given 2 or fewer years before pregnancy was 83%. This study was not powered to determine a difference if the vaccine was administered in the ACIP-recommended time period during the third trimester.
A reported 49% of U.S. pregnant women received Tdap during the 2015-2016 flu season, an increase of 22% from the 2013-2014 season, according to a CDC Internet panel survey.
“While maternal immunization during pregnancy will help bridge the gap until next-generation pertussis vaccines are licensed and available for use, this highly effective strategy will likely remain an integral component of pertussis prevention and control, even in the setting of new vaccines,” the investigators said.
Read more in Clinical Infectious Diseases (2017 Sep 28. doi: 10.1093/cid/cix724).
FROM CLINICAL INFECTIOUS DISEASES
Avoid sildenafil for pulmonary hypertension after corrected valvular disease
BARCELONA – Off-label use of the phosphodiesterase-5 inhibitor sildenafil to treat residual pulmonary hypertension after successful correction of valvular heart disease is not merely ineffective, it’s counterproductive, according to the results of the randomized, placebo-controlled SIOVAC study.
“We believe based upon our results that off-label use of sildenafil in patients with left heart disease-pulmonary hypertension due to valvular disease should be discouraged,” Javier Bermejo, MD, declared at the annual congress of the European Society of Cardiology. 
Sildenafil is approved with a solid, evidence-based indication for treating some other types of pulmonary hypertension. Many cardiologists also prescribe the drug off label for residual pulmonary hypertension in patients with corrected valve disease, hoping that it will be of benefit, since there is currently no approved treatment for this common and serious condition associated with increased mortality. But because the anecdotal literature on sildenafil for this specific type of pulmonary hypertension is mixed, Dr. Bermejo and his coinvestigators in the Spanish Network Center for Cardiovascular Research decided to conduct a multicenter randomized trial.
SIOVAC (Sildenafil for Improving Clinical Outcomes After Valvular Correction) comprised 200 patients with residual pulmonary hypertension after corrected valvular heart disease at 17 Spanish general hospitals. The patients were randomized to receive sildenafil at 40 mg t.i.d. or placebo for 6 months in this double-blind trial.
The primary endpoint was a standardized composite clinical score widely used in heart failure trials. It consists of all-cause mortality, hospital admission for heart failure, worsening exercise tolerance, and deterioration in a global self-assessment rating.
The shocker for the investigators – who had expected a positive study – was that 33% of patients in the sildenafil group worsened significantly on the composite clinical score at 6 months, compared with 14% of placebo-treated controls, said Dr. Bermejo, a cardiologist at Gregorio Marañón University Hospital in Madrid.
Moreover, only 27% of the sildenafil group improved, compared with 44% of controls. About one-third of patients in both groups remained unchanged over the course of the 6-month trial.
Dr. Bermejo noted that valvular disease is considered the next cardiac epidemic because of its strong association with advancing age and the rapid aging of the population worldwide. Pulmonary hypertension occurs is virtually all patients with severe mitral disease and in up to two-thirds of those with asymptomatic aortic stenosis. Regression of the pulmonary hypertension is often incomplete after successful surgical or transcatheter correction of the valvular lesion.
Discussant Irene M. Lang, MD, called SIOVAC “a very clear study.” It convincingly establishes that sildenafil – a vasodilator – is ineffective for the treatment of what the current ESC/European Respiratory Society guidelines on pulmonary hypertension call isolated post-capillary pulmonary hypertension, a condition defined hemodynamically by a diastolic pulmonary vascular pressure gradient of less than 7 mm Hg and/or a pulmonary vascular resistance below 3 Wood units (Eur Heart J. 2016 Jan 1;37[1]:67-119.)
The SIOVAC findings underscore the strong IIIC recommendation in the European guidelines that the use of approved therapies for pulmonary arterial hypertension is not recommended in patients with left heart disease-pulmonary hypertension, added Dr. Lang, a coauthor of the guidelines and professor of vascular biology at the Medical University of Vienna.
The Spanish government funded SIOVAC. Dr. Bermejo reported having no financial conflicts of interest.
BARCELONA – Off-label use of the phosphodiesterase-5 inhibitor sildenafil to treat residual pulmonary hypertension after successful correction of valvular heart disease is not merely ineffective, it’s counterproductive, according to the results of the randomized, placebo-controlled SIOVAC study.
“We believe based upon our results that off-label use of sildenafil in patients with left heart disease-pulmonary hypertension due to valvular disease should be discouraged,” Javier Bermejo, MD, declared at the annual congress of the European Society of Cardiology.
Sildenafil is approved with a solid, evidence-based indication for treating some other types of pulmonary hypertension. Many cardiologists also prescribe the drug off label for residual pulmonary hypertension in patients with corrected valve disease, hoping that it will be of benefit, since there is currently no approved treatment for this common and serious condition associated with increased mortality. But because the anecdotal literature on sildenafil for this specific type of pulmonary hypertension is mixed, Dr. Bermejo and his coinvestigators in the Spanish Network Center for Cardiovascular Research decided to conduct a multicenter randomized trial.
SIOVAC (Sildenafil for Improving Clinical Outcomes After Valvular Correction) comprised 200 patients with residual pulmonary hypertension after corrected valvular heart disease at 17 Spanish general hospitals. The patients were randomized to receive sildenafil at 40 mg t.i.d. or placebo for 6 months in this double-blind trial.
The primary endpoint was a standardized composite clinical score widely used in heart failure trials. It consists of all-cause mortality, hospital admission for heart failure, worsening exercise tolerance, and deterioration in a global self-assessment rating.
The shocker for the investigators – who had expected a positive study – was that 33% of patients in the sildenafil group worsened significantly on the composite clinical score at 6 months, compared with 14% of placebo-treated controls, said Dr. Bermejo, a cardiologist at Gregorio Marañón University Hospital in Madrid.
Moreover, only 27% of the sildenafil group improved, compared with 44% of controls. About one-third of patients in both groups remained unchanged over the course of the 6-month trial.
Dr. Bermejo noted that valvular disease is considered the next cardiac epidemic because of its strong association with advancing age and the rapid aging of the population worldwide. Pulmonary hypertension occurs is virtually all patients with severe mitral disease and in up to two-thirds of those with asymptomatic aortic stenosis. Regression of the pulmonary hypertension is often incomplete after successful surgical or transcatheter correction of the valvular lesion.
Discussant Irene M. Lang, MD, called SIOVAC “a very clear study.” It convincingly establishes that sildenafil – a vasodilator – is ineffective for the treatment of what the current ESC/European Respiratory Society guidelines on pulmonary hypertension call isolated post-capillary pulmonary hypertension, a condition defined hemodynamically by a diastolic pulmonary vascular pressure gradient of less than 7 mm Hg and/or a pulmonary vascular resistance below 3 Wood units (Eur Heart J. 2016 Jan 1;37[1]:67-119.)
The SIOVAC findings underscore the strong IIIC recommendation in the European guidelines that the use of approved therapies for pulmonary arterial hypertension is not recommended in patients with left heart disease-pulmonary hypertension, added Dr. Lang, a coauthor of the guidelines and professor of vascular biology at the Medical University of Vienna.
The Spanish government funded SIOVAC. Dr. Bermejo reported having no financial conflicts of interest.
BARCELONA – Off-label use of the phosphodiesterase-5 inhibitor sildenafil to treat residual pulmonary hypertension after successful correction of valvular heart disease is not merely ineffective, it’s counterproductive, according to the results of the randomized, placebo-controlled SIOVAC study.
“We believe based upon our results that off-label use of sildenafil in patients with left heart disease-pulmonary hypertension due to valvular disease should be discouraged,” Javier Bermejo, MD, declared at the annual congress of the European Society of Cardiology.
Sildenafil is approved with a solid, evidence-based indication for treating some other types of pulmonary hypertension. Many cardiologists also prescribe the drug off label for residual pulmonary hypertension in patients with corrected valve disease, hoping that it will be of benefit, since there is currently no approved treatment for this common and serious condition associated with increased mortality. But because the anecdotal literature on sildenafil for this specific type of pulmonary hypertension is mixed, Dr. Bermejo and his coinvestigators in the Spanish Network Center for Cardiovascular Research decided to conduct a multicenter randomized trial.
SIOVAC (Sildenafil for Improving Clinical Outcomes After Valvular Correction) comprised 200 patients with residual pulmonary hypertension after corrected valvular heart disease at 17 Spanish general hospitals. The patients were randomized to receive sildenafil at 40 mg t.i.d. or placebo for 6 months in this double-blind trial.
The primary endpoint was a standardized composite clinical score widely used in heart failure trials. It consists of all-cause mortality, hospital admission for heart failure, worsening exercise tolerance, and deterioration in a global self-assessment rating.
The shocker for the investigators – who had expected a positive study – was that 33% of patients in the sildenafil group worsened significantly on the composite clinical score at 6 months, compared with 14% of placebo-treated controls, said Dr. Bermejo, a cardiologist at Gregorio Marañón University Hospital in Madrid.
Moreover, only 27% of the sildenafil group improved, compared with 44% of controls. About one-third of patients in both groups remained unchanged over the course of the 6-month trial.
Dr. Bermejo noted that valvular disease is considered the next cardiac epidemic because of its strong association with advancing age and the rapid aging of the population worldwide. Pulmonary hypertension occurs is virtually all patients with severe mitral disease and in up to two-thirds of those with asymptomatic aortic stenosis. Regression of the pulmonary hypertension is often incomplete after successful surgical or transcatheter correction of the valvular lesion.
Discussant Irene M. Lang, MD, called SIOVAC “a very clear study.” It convincingly establishes that sildenafil – a vasodilator – is ineffective for the treatment of what the current ESC/European Respiratory Society guidelines on pulmonary hypertension call isolated post-capillary pulmonary hypertension, a condition defined hemodynamically by a diastolic pulmonary vascular pressure gradient of less than 7 mm Hg and/or a pulmonary vascular resistance below 3 Wood units (Eur Heart J. 2016 Jan 1;37[1]:67-119.)
The SIOVAC findings underscore the strong IIIC recommendation in the European guidelines that the use of approved therapies for pulmonary arterial hypertension is not recommended in patients with left heart disease-pulmonary hypertension, added Dr. Lang, a coauthor of the guidelines and professor of vascular biology at the Medical University of Vienna.
The Spanish government funded SIOVAC. Dr. Bermejo reported having no financial conflicts of interest.
AT THE ESC CONGRESS 2017
Key clinical point:
Major finding: One-third of patients with residual pulmonary hypertension after successful correction of valvular heart disease experienced significant clinical worsening during 6 months of sildenafil therapy, compared with 14% on placebo.
Data source: SIOVAC, a 6-month, double-blind, placebo-controlled study of 200 patients with residual pulmonary hypertension after correction for valvular heart disease.
Disclosures: The Spanish government funded SIOVAC. The presenter reported having no financial conflicts of interest.