Study highlights role of structural racism in delayed autism diagnoses

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An analysis of a large cohort of African American children with autism spectrum disorder (ASD) reveals a more than 3-year time lag between parental recognition of a development delay and an ASD diagnosis, reported John N. Constantino, MD, of the department of psychiatry at Washington University, St. Louis, and coauthors.

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The analysis also highlights the need to further understand – and act on – the disproportionate burden of intellectual disability comorbidity among these children, the investigators say.

Their analysis, published in Pediatrics, builds on national community surveillance data from the Centers for Disease Control and Prevention published in 2018 showing near-equal rates of identification of ASD among African American (and other minorities) and non-Hispanic white children, but greater delays in diagnosis for African American children as well as twice the rate of comorbid intellectual disability, compared with non-Hispanic white children (44% vs. 22%).

To explore potential drivers of both diagnostic delays and the intellectual disability disparity, the investigators tapped into a repository of data on 584 African American children with ASD and their first-degree relatives who were consecutively enrolled in the National Institutes of Health–funded Autism Genetic Resource Exchange across four academic sites. The program aims to improve the representation of families of self-reported African ancestry in ASD genetics research.

The mean age of diagnosis was 65 months, which came at an average of more than 3 years after parents reported having concerns about their child’s language, behavior or development – and “the period when early developmental therapies (typically delivered through part C interventions in the United States) are initiated to ameliorate the disability associated with ASD,” Dr. Constantino and associates said.

Approximately 42% reported seeing multiple professionals before receiving an ASD diagnosis (14% saw six or more), and 31% said that a lack of available professionals had contributed to the delay. Almost all families – 98% – reported having some type of health insurance at the time of their first concerns (49% private, 46% public, and 5% others).

The data also show that excess intellectual disability comorbidity seen in African American children cannot be explained by familial or sociodemographic factors that have traditionally been associated with variation in IQ in the general population. Nor can it be explained by overclassification of intellectual disability, the authors said.

“The persistence of an unexplained excess of [intellectual disability] comorbidity of this magnitude in the [African American] population constitutes an urgent public health concern,” they wrote.

The NIH-funded program involved parental completion of “Diagnostic Odyssey” interviews (characterizing service-seeking experiences and obstacles to diagnosis, treatment, and care) and several in-person cognitive assessments and measurements of adaptive functioning. “These were in-depth [highly validated] intellectual assessments based on IQ measures that were tailored to the level of functioning of the children and backed by extensive assessments of adaptive functioning,” Dr. Constantino said in an interview.

Historically, autism has been underdiagnosed among minority children. Now that this is no longer the case, as demonstrated in the CDC’s 2018 report from its Autism and Developmental Disabilities Monitoring Network, the thought that higher rates of intellectual disability comorbidity among minority children are due to ascertainment bias – to “our only diagnosing the most serious cases” – “is no longer true,” he said.

And now, with use of data from the largest-available repository of diagnostic and phenotypic information on African American children with ASD, “we’ve dispelled other misperceptions, other factors that might be used to dismiss or explain away why Black children might have a high rate of intellectual disability,” Dr. Constantino said in the interview, referring to the absence of association between the IQ scores of children with ASD and those of their first-degree relatives as well as the lack of significant associations between the IQ of children with ASD and factors such as family income (above versus below the median income of the cohort), the mother having or not having a college degree, and the estimated gestational age at birth (before versus after 37 weeks).

“This kind of complication of autism lasts for the life of a child and profoundly impairs their functioning,” he said. “If anyone thinks there isn’t an opportunity to improve the timing of diagnosis and to improve access to services and appropriate developmental therapies, that’s wrong. There is opportunity – parents are raising the alarm, and we are not coming to these children’s rescue.”

In an accompanying editorial, Sarabeth Broder-Fingert, MD, MPH, of Boston University and Boston Medical Center, and associates wrote that the “confluence of findings [in this study] are suggestive of structural racism leading to inequity.”

For example, they said, “although the causes of delays from first parental concern to ASD diagnosis are complex, they can result from a number of issues, including racial bias and discrimination experienced by families, a lack of diversity in health professionals (impacting patient-provider relationships), and/or concentration of specialists in geographic areas with fewer minority residents.” Each of these issues, they wrote, can be linked to racism, both structural and individual.

Combined with previous research on inequity in ASD, the new data “necessitate an immediate evaluation of how issues of structural racism have impacted ASD diagnosis and, more importantly, an action plan to address inequity,” they said.

Issues of workforce capacity for ASD diagnosis need to be addressed by evaluating Medicaid reimbursement rates for ASD diagnosis, for instance, and removing restrictions on who is qualified to make a diagnosis, increasing adherence to evidence-based practices, “increasing workforce cultural humility, and recruiting a workforce that reflects the diverse communities they serve,” Dr. Broder-Fingert and associates said.

Jeremiah Dickerson, MD, a child and adolescent psychiatrist at the University of Vermont, Burlington, said he is hopeful that the inequities and structural obstacles that he sees in his patients are “being informed more and more by science” and that “we’re taking steps in exploring our own cultural humility and focusing on problems ... that have been under the surface for decades.”

Years of diagnostic delay and missed intervention for ASD can lead to increasing lifelong functional difficulties, which in turn can be compounded by enduring inequities and stigma, he said when asked to comment on the study.

“Diagnosing and teasing apart ID [intellectual disability] versus ASD, and ID co-occurring with ASD, can be very complicated, particularly in young children with significant language impairments,” he added. “If indeed there is a higher proportion of African American children with co-occurring ASD and ID ... we have to do a much better job with identifying those children earlier and providing longitudinal follow-up/assessment that can help provide diagnostic clarity and inform recommendations.”

Understanding better why this occurs “without repeating the history of assigning cause based upon racist thinking” is also important, said Dr. Dickerson, who directs the autism assessment clinic at the university’s Vermont Center for Children, Youth & Families.

Dr. Constantino, who has been involved in the CDC’s 11-site ASD surveillance network, said it is unclear to what extent broad implementation of early and high-quality interventions can reduce the proportion of African American children with autism and comorbid intellectual disability. “We may be only half-successful in closing the gap, or there may be other factors involved that we don’t understand yet,” he said. “But we haven’t even attempted to close the gap [through] reasonable application of an intervention strategy that is available and that we know can improve cognitive outcomes.”

“Some primary care doctors are reluctant to make the diagnosis in the first place because they have nothing to offer the families,” Dr. Constantino noted.

Continued research on the interactions between genetic background and specific biological susceptibilities to autism is an ongoing objective of the Autism Genetic Resource Exchange.

The CDC recently published its latest report on the prevalence of ASD in children aged 8 years, concluding again that continued efforts are needed for “early and equitable identification of ASD and timely enrollment in services.

The study was supported by grants from the National Institutes of Health and from the Intellectual and Developmental Disabilities Research Center at Washington University. Dr. Constantino is author of the Social Responsiveness Scale-2, from which he receives royalties. A coauthor helped author the Vineland-3 and receives royalties, and this coauthor and another associate also have ties to pharmaceutical companies or other organizations; the remaining authors of the study said they had no relevant financial disclosures. Dr. Broder-Fingert and associates said they have no relevant financial relationships; the editorial was funded by the National Institutes of Health. Dr. Dickerson said he had no relevant financial disclosures.

SOURCE: Constantino JN et al. Pediatrics. 2020. doi: 10.1542/peds.2019-3629.

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An analysis of a large cohort of African American children with autism spectrum disorder (ASD) reveals a more than 3-year time lag between parental recognition of a development delay and an ASD diagnosis, reported John N. Constantino, MD, of the department of psychiatry at Washington University, St. Louis, and coauthors.

FreshSplash/E+

The analysis also highlights the need to further understand – and act on – the disproportionate burden of intellectual disability comorbidity among these children, the investigators say.

Their analysis, published in Pediatrics, builds on national community surveillance data from the Centers for Disease Control and Prevention published in 2018 showing near-equal rates of identification of ASD among African American (and other minorities) and non-Hispanic white children, but greater delays in diagnosis for African American children as well as twice the rate of comorbid intellectual disability, compared with non-Hispanic white children (44% vs. 22%).

To explore potential drivers of both diagnostic delays and the intellectual disability disparity, the investigators tapped into a repository of data on 584 African American children with ASD and their first-degree relatives who were consecutively enrolled in the National Institutes of Health–funded Autism Genetic Resource Exchange across four academic sites. The program aims to improve the representation of families of self-reported African ancestry in ASD genetics research.

The mean age of diagnosis was 65 months, which came at an average of more than 3 years after parents reported having concerns about their child’s language, behavior or development – and “the period when early developmental therapies (typically delivered through part C interventions in the United States) are initiated to ameliorate the disability associated with ASD,” Dr. Constantino and associates said.

Approximately 42% reported seeing multiple professionals before receiving an ASD diagnosis (14% saw six or more), and 31% said that a lack of available professionals had contributed to the delay. Almost all families – 98% – reported having some type of health insurance at the time of their first concerns (49% private, 46% public, and 5% others).

The data also show that excess intellectual disability comorbidity seen in African American children cannot be explained by familial or sociodemographic factors that have traditionally been associated with variation in IQ in the general population. Nor can it be explained by overclassification of intellectual disability, the authors said.

“The persistence of an unexplained excess of [intellectual disability] comorbidity of this magnitude in the [African American] population constitutes an urgent public health concern,” they wrote.

The NIH-funded program involved parental completion of “Diagnostic Odyssey” interviews (characterizing service-seeking experiences and obstacles to diagnosis, treatment, and care) and several in-person cognitive assessments and measurements of adaptive functioning. “These were in-depth [highly validated] intellectual assessments based on IQ measures that were tailored to the level of functioning of the children and backed by extensive assessments of adaptive functioning,” Dr. Constantino said in an interview.

Historically, autism has been underdiagnosed among minority children. Now that this is no longer the case, as demonstrated in the CDC’s 2018 report from its Autism and Developmental Disabilities Monitoring Network, the thought that higher rates of intellectual disability comorbidity among minority children are due to ascertainment bias – to “our only diagnosing the most serious cases” – “is no longer true,” he said.

And now, with use of data from the largest-available repository of diagnostic and phenotypic information on African American children with ASD, “we’ve dispelled other misperceptions, other factors that might be used to dismiss or explain away why Black children might have a high rate of intellectual disability,” Dr. Constantino said in the interview, referring to the absence of association between the IQ scores of children with ASD and those of their first-degree relatives as well as the lack of significant associations between the IQ of children with ASD and factors such as family income (above versus below the median income of the cohort), the mother having or not having a college degree, and the estimated gestational age at birth (before versus after 37 weeks).

“This kind of complication of autism lasts for the life of a child and profoundly impairs their functioning,” he said. “If anyone thinks there isn’t an opportunity to improve the timing of diagnosis and to improve access to services and appropriate developmental therapies, that’s wrong. There is opportunity – parents are raising the alarm, and we are not coming to these children’s rescue.”

In an accompanying editorial, Sarabeth Broder-Fingert, MD, MPH, of Boston University and Boston Medical Center, and associates wrote that the “confluence of findings [in this study] are suggestive of structural racism leading to inequity.”

For example, they said, “although the causes of delays from first parental concern to ASD diagnosis are complex, they can result from a number of issues, including racial bias and discrimination experienced by families, a lack of diversity in health professionals (impacting patient-provider relationships), and/or concentration of specialists in geographic areas with fewer minority residents.” Each of these issues, they wrote, can be linked to racism, both structural and individual.

Combined with previous research on inequity in ASD, the new data “necessitate an immediate evaluation of how issues of structural racism have impacted ASD diagnosis and, more importantly, an action plan to address inequity,” they said.

Issues of workforce capacity for ASD diagnosis need to be addressed by evaluating Medicaid reimbursement rates for ASD diagnosis, for instance, and removing restrictions on who is qualified to make a diagnosis, increasing adherence to evidence-based practices, “increasing workforce cultural humility, and recruiting a workforce that reflects the diverse communities they serve,” Dr. Broder-Fingert and associates said.

Jeremiah Dickerson, MD, a child and adolescent psychiatrist at the University of Vermont, Burlington, said he is hopeful that the inequities and structural obstacles that he sees in his patients are “being informed more and more by science” and that “we’re taking steps in exploring our own cultural humility and focusing on problems ... that have been under the surface for decades.”

Years of diagnostic delay and missed intervention for ASD can lead to increasing lifelong functional difficulties, which in turn can be compounded by enduring inequities and stigma, he said when asked to comment on the study.

“Diagnosing and teasing apart ID [intellectual disability] versus ASD, and ID co-occurring with ASD, can be very complicated, particularly in young children with significant language impairments,” he added. “If indeed there is a higher proportion of African American children with co-occurring ASD and ID ... we have to do a much better job with identifying those children earlier and providing longitudinal follow-up/assessment that can help provide diagnostic clarity and inform recommendations.”

Understanding better why this occurs “without repeating the history of assigning cause based upon racist thinking” is also important, said Dr. Dickerson, who directs the autism assessment clinic at the university’s Vermont Center for Children, Youth & Families.

Dr. Constantino, who has been involved in the CDC’s 11-site ASD surveillance network, said it is unclear to what extent broad implementation of early and high-quality interventions can reduce the proportion of African American children with autism and comorbid intellectual disability. “We may be only half-successful in closing the gap, or there may be other factors involved that we don’t understand yet,” he said. “But we haven’t even attempted to close the gap [through] reasonable application of an intervention strategy that is available and that we know can improve cognitive outcomes.”

“Some primary care doctors are reluctant to make the diagnosis in the first place because they have nothing to offer the families,” Dr. Constantino noted.

Continued research on the interactions between genetic background and specific biological susceptibilities to autism is an ongoing objective of the Autism Genetic Resource Exchange.

The CDC recently published its latest report on the prevalence of ASD in children aged 8 years, concluding again that continued efforts are needed for “early and equitable identification of ASD and timely enrollment in services.

The study was supported by grants from the National Institutes of Health and from the Intellectual and Developmental Disabilities Research Center at Washington University. Dr. Constantino is author of the Social Responsiveness Scale-2, from which he receives royalties. A coauthor helped author the Vineland-3 and receives royalties, and this coauthor and another associate also have ties to pharmaceutical companies or other organizations; the remaining authors of the study said they had no relevant financial disclosures. Dr. Broder-Fingert and associates said they have no relevant financial relationships; the editorial was funded by the National Institutes of Health. Dr. Dickerson said he had no relevant financial disclosures.

SOURCE: Constantino JN et al. Pediatrics. 2020. doi: 10.1542/peds.2019-3629.

An analysis of a large cohort of African American children with autism spectrum disorder (ASD) reveals a more than 3-year time lag between parental recognition of a development delay and an ASD diagnosis, reported John N. Constantino, MD, of the department of psychiatry at Washington University, St. Louis, and coauthors.

FreshSplash/E+

The analysis also highlights the need to further understand – and act on – the disproportionate burden of intellectual disability comorbidity among these children, the investigators say.

Their analysis, published in Pediatrics, builds on national community surveillance data from the Centers for Disease Control and Prevention published in 2018 showing near-equal rates of identification of ASD among African American (and other minorities) and non-Hispanic white children, but greater delays in diagnosis for African American children as well as twice the rate of comorbid intellectual disability, compared with non-Hispanic white children (44% vs. 22%).

To explore potential drivers of both diagnostic delays and the intellectual disability disparity, the investigators tapped into a repository of data on 584 African American children with ASD and their first-degree relatives who were consecutively enrolled in the National Institutes of Health–funded Autism Genetic Resource Exchange across four academic sites. The program aims to improve the representation of families of self-reported African ancestry in ASD genetics research.

The mean age of diagnosis was 65 months, which came at an average of more than 3 years after parents reported having concerns about their child’s language, behavior or development – and “the period when early developmental therapies (typically delivered through part C interventions in the United States) are initiated to ameliorate the disability associated with ASD,” Dr. Constantino and associates said.

Approximately 42% reported seeing multiple professionals before receiving an ASD diagnosis (14% saw six or more), and 31% said that a lack of available professionals had contributed to the delay. Almost all families – 98% – reported having some type of health insurance at the time of their first concerns (49% private, 46% public, and 5% others).

The data also show that excess intellectual disability comorbidity seen in African American children cannot be explained by familial or sociodemographic factors that have traditionally been associated with variation in IQ in the general population. Nor can it be explained by overclassification of intellectual disability, the authors said.

“The persistence of an unexplained excess of [intellectual disability] comorbidity of this magnitude in the [African American] population constitutes an urgent public health concern,” they wrote.

The NIH-funded program involved parental completion of “Diagnostic Odyssey” interviews (characterizing service-seeking experiences and obstacles to diagnosis, treatment, and care) and several in-person cognitive assessments and measurements of adaptive functioning. “These were in-depth [highly validated] intellectual assessments based on IQ measures that were tailored to the level of functioning of the children and backed by extensive assessments of adaptive functioning,” Dr. Constantino said in an interview.

Historically, autism has been underdiagnosed among minority children. Now that this is no longer the case, as demonstrated in the CDC’s 2018 report from its Autism and Developmental Disabilities Monitoring Network, the thought that higher rates of intellectual disability comorbidity among minority children are due to ascertainment bias – to “our only diagnosing the most serious cases” – “is no longer true,” he said.

And now, with use of data from the largest-available repository of diagnostic and phenotypic information on African American children with ASD, “we’ve dispelled other misperceptions, other factors that might be used to dismiss or explain away why Black children might have a high rate of intellectual disability,” Dr. Constantino said in the interview, referring to the absence of association between the IQ scores of children with ASD and those of their first-degree relatives as well as the lack of significant associations between the IQ of children with ASD and factors such as family income (above versus below the median income of the cohort), the mother having or not having a college degree, and the estimated gestational age at birth (before versus after 37 weeks).

“This kind of complication of autism lasts for the life of a child and profoundly impairs their functioning,” he said. “If anyone thinks there isn’t an opportunity to improve the timing of diagnosis and to improve access to services and appropriate developmental therapies, that’s wrong. There is opportunity – parents are raising the alarm, and we are not coming to these children’s rescue.”

In an accompanying editorial, Sarabeth Broder-Fingert, MD, MPH, of Boston University and Boston Medical Center, and associates wrote that the “confluence of findings [in this study] are suggestive of structural racism leading to inequity.”

For example, they said, “although the causes of delays from first parental concern to ASD diagnosis are complex, they can result from a number of issues, including racial bias and discrimination experienced by families, a lack of diversity in health professionals (impacting patient-provider relationships), and/or concentration of specialists in geographic areas with fewer minority residents.” Each of these issues, they wrote, can be linked to racism, both structural and individual.

Combined with previous research on inequity in ASD, the new data “necessitate an immediate evaluation of how issues of structural racism have impacted ASD diagnosis and, more importantly, an action plan to address inequity,” they said.

Issues of workforce capacity for ASD diagnosis need to be addressed by evaluating Medicaid reimbursement rates for ASD diagnosis, for instance, and removing restrictions on who is qualified to make a diagnosis, increasing adherence to evidence-based practices, “increasing workforce cultural humility, and recruiting a workforce that reflects the diverse communities they serve,” Dr. Broder-Fingert and associates said.

Jeremiah Dickerson, MD, a child and adolescent psychiatrist at the University of Vermont, Burlington, said he is hopeful that the inequities and structural obstacles that he sees in his patients are “being informed more and more by science” and that “we’re taking steps in exploring our own cultural humility and focusing on problems ... that have been under the surface for decades.”

Years of diagnostic delay and missed intervention for ASD can lead to increasing lifelong functional difficulties, which in turn can be compounded by enduring inequities and stigma, he said when asked to comment on the study.

“Diagnosing and teasing apart ID [intellectual disability] versus ASD, and ID co-occurring with ASD, can be very complicated, particularly in young children with significant language impairments,” he added. “If indeed there is a higher proportion of African American children with co-occurring ASD and ID ... we have to do a much better job with identifying those children earlier and providing longitudinal follow-up/assessment that can help provide diagnostic clarity and inform recommendations.”

Understanding better why this occurs “without repeating the history of assigning cause based upon racist thinking” is also important, said Dr. Dickerson, who directs the autism assessment clinic at the university’s Vermont Center for Children, Youth & Families.

Dr. Constantino, who has been involved in the CDC’s 11-site ASD surveillance network, said it is unclear to what extent broad implementation of early and high-quality interventions can reduce the proportion of African American children with autism and comorbid intellectual disability. “We may be only half-successful in closing the gap, or there may be other factors involved that we don’t understand yet,” he said. “But we haven’t even attempted to close the gap [through] reasonable application of an intervention strategy that is available and that we know can improve cognitive outcomes.”

“Some primary care doctors are reluctant to make the diagnosis in the first place because they have nothing to offer the families,” Dr. Constantino noted.

Continued research on the interactions between genetic background and specific biological susceptibilities to autism is an ongoing objective of the Autism Genetic Resource Exchange.

The CDC recently published its latest report on the prevalence of ASD in children aged 8 years, concluding again that continued efforts are needed for “early and equitable identification of ASD and timely enrollment in services.

The study was supported by grants from the National Institutes of Health and from the Intellectual and Developmental Disabilities Research Center at Washington University. Dr. Constantino is author of the Social Responsiveness Scale-2, from which he receives royalties. A coauthor helped author the Vineland-3 and receives royalties, and this coauthor and another associate also have ties to pharmaceutical companies or other organizations; the remaining authors of the study said they had no relevant financial disclosures. Dr. Broder-Fingert and associates said they have no relevant financial relationships; the editorial was funded by the National Institutes of Health. Dr. Dickerson said he had no relevant financial disclosures.

SOURCE: Constantino JN et al. Pediatrics. 2020. doi: 10.1542/peds.2019-3629.

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FDA OKs new ‘artificial pancreas’ Medtronic 770G

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The Food and Drug Administration has approved the MiniMed 770G (Medtronic) automated insulin delivery system for children aged 2-6 years.

The 770G system adds Bluetooth smartphone connectivity to the SmartGuard technology that is present in the hybrid closed-loop MiniMed 670G system, which has been available in the United States since 2016 for individuals aged 14 years and older who have type 1 diabetes. It has been available since 2018 for children aged 7 years.

The 770G will also be available to older children and adults once it has been launched.

As with other so-called artificial pancreas systems, the 770G is made up of an insulin pump and continuous glucose monitor that are connected via software that allows the pump to deliver or withhold insulin on the basis of glucose readings.

It is a “hybrid closed-loop” system in that users or caregivers must still manually signal carbohydrate consumption.

The 770G includes a “share” feature that allows health care providers, users, and caregivers to follow the user’s glucose levels remotely via smartphones. In-app notices indicate when glucose levels are out of range. The data can be uploaded prior to telehealth visits.

The approval was based on a 3-month study of 151 children aged 2-6 years who showed improvement in outcomes comparable with those seen in 124 older adolescents and adults with the 770G system as compared to patients who used manual (nonlooped) mode over a 2-week period. There were no episodes of severe hypoglycemia or diabetic ketoacidosis and no serious device-related adverse events while in hybrid closed-loop mode.

The FDA will require Medtronic to conduct a postmarketing study to evaluate the 770G in real-world settings. It is not approved for use in children younger than 2 years nor in any patient who requires less than 8 units of insulin per day.

The next-generation Medtronic closed-loop system, the 780G, has already been approved in Europe. It improves on the technology by delivering automated bolus correction doses in addition to basal insulin every 5 minutes. The company is preparing to submit the 780G for approval in the United States.

A version of this article originally appeared on Medscape.com.

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The Food and Drug Administration has approved the MiniMed 770G (Medtronic) automated insulin delivery system for children aged 2-6 years.

The 770G system adds Bluetooth smartphone connectivity to the SmartGuard technology that is present in the hybrid closed-loop MiniMed 670G system, which has been available in the United States since 2016 for individuals aged 14 years and older who have type 1 diabetes. It has been available since 2018 for children aged 7 years.

The 770G will also be available to older children and adults once it has been launched.

As with other so-called artificial pancreas systems, the 770G is made up of an insulin pump and continuous glucose monitor that are connected via software that allows the pump to deliver or withhold insulin on the basis of glucose readings.

It is a “hybrid closed-loop” system in that users or caregivers must still manually signal carbohydrate consumption.

The 770G includes a “share” feature that allows health care providers, users, and caregivers to follow the user’s glucose levels remotely via smartphones. In-app notices indicate when glucose levels are out of range. The data can be uploaded prior to telehealth visits.

The approval was based on a 3-month study of 151 children aged 2-6 years who showed improvement in outcomes comparable with those seen in 124 older adolescents and adults with the 770G system as compared to patients who used manual (nonlooped) mode over a 2-week period. There were no episodes of severe hypoglycemia or diabetic ketoacidosis and no serious device-related adverse events while in hybrid closed-loop mode.

The FDA will require Medtronic to conduct a postmarketing study to evaluate the 770G in real-world settings. It is not approved for use in children younger than 2 years nor in any patient who requires less than 8 units of insulin per day.

The next-generation Medtronic closed-loop system, the 780G, has already been approved in Europe. It improves on the technology by delivering automated bolus correction doses in addition to basal insulin every 5 minutes. The company is preparing to submit the 780G for approval in the United States.

A version of this article originally appeared on Medscape.com.

 

The Food and Drug Administration has approved the MiniMed 770G (Medtronic) automated insulin delivery system for children aged 2-6 years.

The 770G system adds Bluetooth smartphone connectivity to the SmartGuard technology that is present in the hybrid closed-loop MiniMed 670G system, which has been available in the United States since 2016 for individuals aged 14 years and older who have type 1 diabetes. It has been available since 2018 for children aged 7 years.

The 770G will also be available to older children and adults once it has been launched.

As with other so-called artificial pancreas systems, the 770G is made up of an insulin pump and continuous glucose monitor that are connected via software that allows the pump to deliver or withhold insulin on the basis of glucose readings.

It is a “hybrid closed-loop” system in that users or caregivers must still manually signal carbohydrate consumption.

The 770G includes a “share” feature that allows health care providers, users, and caregivers to follow the user’s glucose levels remotely via smartphones. In-app notices indicate when glucose levels are out of range. The data can be uploaded prior to telehealth visits.

The approval was based on a 3-month study of 151 children aged 2-6 years who showed improvement in outcomes comparable with those seen in 124 older adolescents and adults with the 770G system as compared to patients who used manual (nonlooped) mode over a 2-week period. There were no episodes of severe hypoglycemia or diabetic ketoacidosis and no serious device-related adverse events while in hybrid closed-loop mode.

The FDA will require Medtronic to conduct a postmarketing study to evaluate the 770G in real-world settings. It is not approved for use in children younger than 2 years nor in any patient who requires less than 8 units of insulin per day.

The next-generation Medtronic closed-loop system, the 780G, has already been approved in Europe. It improves on the technology by delivering automated bolus correction doses in addition to basal insulin every 5 minutes. The company is preparing to submit the 780G for approval in the United States.

A version of this article originally appeared on Medscape.com.

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CagA-positive H. pylori patients at higher risk of osteoporosis, fracture

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CagA-positive H. pylori patients at higher risk of osteoporosis, fracture

A new study has found that older patients who test positive for the cytotoxin associated gene-A (CagA) strain of Helicobacter pylori may be more at risk of both osteoporosis and fractures.

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“Further studies will be required to replicate these findings in other cohorts and to better clarify the underlying pathogenetic mechanisms leading to increased bone fragility in subjects infected by CagA-positive H. pylori strains,” wrote Luigi Gennari, MD, PhD, of the University of Siena (Italy), and coauthors. The study was published in the Journal of Bone and Mineral Research.

To determine the effects of H. pylori on bone health and potential fracture risk, the researchers launched a population-based cohort study of 1,149 adults between the ages of 50 and 80 in Siena. The cohort comprised 174 males with an average (SD) age of 65.9 (plus or minus 6 years) and 975 females with an average age of 62.5 (plus or minus 6 years). All subjects were examined for H. pylori antibodies, and those who were infected were also examined for anti-CagA serum antibodies. As blood was sampled, bone mineral density (BMD) of the lumbar spine, femoral neck, total hip, and total body was measured via dual-energy x-ray absorptiometry.

In total, 53% of male participants and 49% of female participants tested positive for H. pylori, with CagA-positive strains found in 27% of males and 26% of females. No differences in infection rates were discovered in regard to socioeconomic status, age, weight, or height. Patients with normal BMD (45%), osteoporosis (51%), or osteopenia (49%) had similar prevalence of H. pylori infection, but CagA-positive strains were more frequently found in osteoporotic (30%) and osteopenic (26%) patients, compared to patients with normal BMD (21%, P < .01). CagA-positive female patients also had lower lumbar (0.950 g/cm2) and femoral (0.795 g/cm2) BMD, compared to CagA-negative (0.987 and 0.813 g/cm2) or H. pylori-negative women (0.997 and 0.821 g/cm2), respectively.

After an average follow-up period of 11.8 years, 199 nontraumatic fractures (72 vertebral and 127 nonvertebral) had occurred in 158 participants. Patients with CagA-positive strains of H. pylori had significantly increased risk of a clinical vertebral fracture (hazard ratio [HR], 5.27; 95% confidence interval, 2.23-12.63; P < .0001) or a nonvertebral incident fracture (HR, 2.09; 95% CI, 1.27-2.46; P < .01), compared to patients without H. pylori. After adjustment for age, sex, and body mass index, the risk among CagA-positive patients remained similarly significantly elevated for both vertebral (aHR, 4.78; 95% CI, 1.99-11.47; P < .0001) and nonvertebral fractures (aHR, 2.04; 95% CI, 1.22-3.41; P < .01).

The authors acknowledged their study’s limitations, including a cohort that was notably low in male participants, an inability to assess the effects of eradicating H. pylori on bone, and uncertainty as to which specific effects of H. pylori infection increase the risk of osteoporosis or fracture. Along those lines, they noted that an association between serum CagA antibody titer and gastric mucosal inflammation could lead to malabsorption of calcium, hypothesizing that antibody titer rather than antibody positivity “might be a more relevant marker for assessing the risk of bone fragility in patients affected by H. pylori infection.”

The study was supported in part by a grant from the Italian Association for Osteoporosis. The authors reported no potential conflicts of interest.

SOURCE: Gennari L et al. J Bone Miner Res. 2020 Aug 13. doi: 10.1002/jbmr.4162.

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A new study has found that older patients who test positive for the cytotoxin associated gene-A (CagA) strain of Helicobacter pylori may be more at risk of both osteoporosis and fractures.

Patho/Wikimedia Commons/CC BY-SA 3.0

“Further studies will be required to replicate these findings in other cohorts and to better clarify the underlying pathogenetic mechanisms leading to increased bone fragility in subjects infected by CagA-positive H. pylori strains,” wrote Luigi Gennari, MD, PhD, of the University of Siena (Italy), and coauthors. The study was published in the Journal of Bone and Mineral Research.

To determine the effects of H. pylori on bone health and potential fracture risk, the researchers launched a population-based cohort study of 1,149 adults between the ages of 50 and 80 in Siena. The cohort comprised 174 males with an average (SD) age of 65.9 (plus or minus 6 years) and 975 females with an average age of 62.5 (plus or minus 6 years). All subjects were examined for H. pylori antibodies, and those who were infected were also examined for anti-CagA serum antibodies. As blood was sampled, bone mineral density (BMD) of the lumbar spine, femoral neck, total hip, and total body was measured via dual-energy x-ray absorptiometry.

In total, 53% of male participants and 49% of female participants tested positive for H. pylori, with CagA-positive strains found in 27% of males and 26% of females. No differences in infection rates were discovered in regard to socioeconomic status, age, weight, or height. Patients with normal BMD (45%), osteoporosis (51%), or osteopenia (49%) had similar prevalence of H. pylori infection, but CagA-positive strains were more frequently found in osteoporotic (30%) and osteopenic (26%) patients, compared to patients with normal BMD (21%, P < .01). CagA-positive female patients also had lower lumbar (0.950 g/cm2) and femoral (0.795 g/cm2) BMD, compared to CagA-negative (0.987 and 0.813 g/cm2) or H. pylori-negative women (0.997 and 0.821 g/cm2), respectively.

After an average follow-up period of 11.8 years, 199 nontraumatic fractures (72 vertebral and 127 nonvertebral) had occurred in 158 participants. Patients with CagA-positive strains of H. pylori had significantly increased risk of a clinical vertebral fracture (hazard ratio [HR], 5.27; 95% confidence interval, 2.23-12.63; P < .0001) or a nonvertebral incident fracture (HR, 2.09; 95% CI, 1.27-2.46; P < .01), compared to patients without H. pylori. After adjustment for age, sex, and body mass index, the risk among CagA-positive patients remained similarly significantly elevated for both vertebral (aHR, 4.78; 95% CI, 1.99-11.47; P < .0001) and nonvertebral fractures (aHR, 2.04; 95% CI, 1.22-3.41; P < .01).

The authors acknowledged their study’s limitations, including a cohort that was notably low in male participants, an inability to assess the effects of eradicating H. pylori on bone, and uncertainty as to which specific effects of H. pylori infection increase the risk of osteoporosis or fracture. Along those lines, they noted that an association between serum CagA antibody titer and gastric mucosal inflammation could lead to malabsorption of calcium, hypothesizing that antibody titer rather than antibody positivity “might be a more relevant marker for assessing the risk of bone fragility in patients affected by H. pylori infection.”

The study was supported in part by a grant from the Italian Association for Osteoporosis. The authors reported no potential conflicts of interest.

SOURCE: Gennari L et al. J Bone Miner Res. 2020 Aug 13. doi: 10.1002/jbmr.4162.

A new study has found that older patients who test positive for the cytotoxin associated gene-A (CagA) strain of Helicobacter pylori may be more at risk of both osteoporosis and fractures.

Patho/Wikimedia Commons/CC BY-SA 3.0

“Further studies will be required to replicate these findings in other cohorts and to better clarify the underlying pathogenetic mechanisms leading to increased bone fragility in subjects infected by CagA-positive H. pylori strains,” wrote Luigi Gennari, MD, PhD, of the University of Siena (Italy), and coauthors. The study was published in the Journal of Bone and Mineral Research.

To determine the effects of H. pylori on bone health and potential fracture risk, the researchers launched a population-based cohort study of 1,149 adults between the ages of 50 and 80 in Siena. The cohort comprised 174 males with an average (SD) age of 65.9 (plus or minus 6 years) and 975 females with an average age of 62.5 (plus or minus 6 years). All subjects were examined for H. pylori antibodies, and those who were infected were also examined for anti-CagA serum antibodies. As blood was sampled, bone mineral density (BMD) of the lumbar spine, femoral neck, total hip, and total body was measured via dual-energy x-ray absorptiometry.

In total, 53% of male participants and 49% of female participants tested positive for H. pylori, with CagA-positive strains found in 27% of males and 26% of females. No differences in infection rates were discovered in regard to socioeconomic status, age, weight, or height. Patients with normal BMD (45%), osteoporosis (51%), or osteopenia (49%) had similar prevalence of H. pylori infection, but CagA-positive strains were more frequently found in osteoporotic (30%) and osteopenic (26%) patients, compared to patients with normal BMD (21%, P < .01). CagA-positive female patients also had lower lumbar (0.950 g/cm2) and femoral (0.795 g/cm2) BMD, compared to CagA-negative (0.987 and 0.813 g/cm2) or H. pylori-negative women (0.997 and 0.821 g/cm2), respectively.

After an average follow-up period of 11.8 years, 199 nontraumatic fractures (72 vertebral and 127 nonvertebral) had occurred in 158 participants. Patients with CagA-positive strains of H. pylori had significantly increased risk of a clinical vertebral fracture (hazard ratio [HR], 5.27; 95% confidence interval, 2.23-12.63; P < .0001) or a nonvertebral incident fracture (HR, 2.09; 95% CI, 1.27-2.46; P < .01), compared to patients without H. pylori. After adjustment for age, sex, and body mass index, the risk among CagA-positive patients remained similarly significantly elevated for both vertebral (aHR, 4.78; 95% CI, 1.99-11.47; P < .0001) and nonvertebral fractures (aHR, 2.04; 95% CI, 1.22-3.41; P < .01).

The authors acknowledged their study’s limitations, including a cohort that was notably low in male participants, an inability to assess the effects of eradicating H. pylori on bone, and uncertainty as to which specific effects of H. pylori infection increase the risk of osteoporosis or fracture. Along those lines, they noted that an association between serum CagA antibody titer and gastric mucosal inflammation could lead to malabsorption of calcium, hypothesizing that antibody titer rather than antibody positivity “might be a more relevant marker for assessing the risk of bone fragility in patients affected by H. pylori infection.”

The study was supported in part by a grant from the Italian Association for Osteoporosis. The authors reported no potential conflicts of interest.

SOURCE: Gennari L et al. J Bone Miner Res. 2020 Aug 13. doi: 10.1002/jbmr.4162.

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FROM THE JOURNAL OF BONE AND MINERAL RESEARCH

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The joys of telemedicine

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Tue, 07/06/2021 - 13:26

Another great morning, seeing patients in the comfort of quarantine!

Here goes. I’ll invite Gretchen by text: 617-555-5555. “TOO LONG.” How can 10 digits be too long? Trying again: 617-555-5555. “TOO LONG!” What the heck, let me leave off the last digit: 617-555-555. “TOO SHORT.”

Never mind, I’ll invite her by email.

Five minutes have gone by. Better call to see if she got the invite.

“Hello, is this Gretchen? Don’t hang up, I’m not a telemarketer! This is Dr. Rockoff. I sent you an invitation for our computer visit.

“You got it, great. Yes, you have to click on it to sign in. I know, your appointment’s at 8:30. It’s now 8:28. Let’s start early, why not?

“Hi, there! I can see you. Can you hear me? You’re nodding and your lips are moving. I can’t hear you. Did you enable your microphone?

“Nope, still can’t hear. I’ll call your cell, and we’ll talk that way.

“Yes, it’s me, Dr. Rockoff. What’s that? You enabled the microphone along with your video when you logged on? Well, there we go. How can I help today?

“You want a refill on your tretinoin gel for age management? Not a problem. Let’s see, you’ve been using it since 1996. No, you look great! Not a day over 76, really! I’ll have the staff escribe it right over.

“Okay, take care. Three years should be about right. Happy 80th!”

Wonder what happened there. Maybe things will go better for the next patient. Okay, I’m emailing an invite to Rob.

There he is! “Hi. Can you see me? Hear me? Nope, can’t hear you. Let me just call your cell.”

Okay, 972-555-5555. Ringing ... oh no, right to voicemail. “You have reached 972-555-5555. The mailbox is full and cannot accept messages. Please try some other time.”

“Okay, I’m back with you on the screen, Rob. Nope, still can’t hear you. I tried your cell but it went to voicemail. Yes, I see you’re holding the phone in your hand. Let me try you again.

Dr. Alan Rockoff

“972-555-5555. Right to voicemail. Doesn’t your phone ring? You never make voice calls, only send texts? Look, please call me: 781-555-5555, write it down.

“Excellent, we’re in business. You’re worried about a mole that’s changing. You sent a photo to the office. Great, I’ll look right now on your record ... nope, not uploaded. Can you email me the photo? Please write down my email address: alanrockoffmdskincarespecialistist@myfabuloustelemedicineportal.now. Got that? Okay, please send the picture ...

“Returned as undeliverable? Show me what you typed ... Oh, wait. It’s ‘telemedicine,’ not ‘TellaMedicine.’ ” Yeah, that should do it.

“Okay, got the picture. You do fabulous super-closeups! Is that your navel next to it? Your left nostril? Okay. You tried to razor off the hair growing out it? Yes, that could account for the bleeding. Tell you what, go easy on it for the next 2 weeks, and send me another picture. Same email address.



“You have another question? Sure. You want a refill of your clindamycin gel because the tube from 2013 ran out? Guess you haven’t grown out of your acne yet. Sure, happy to send it in for you. Same pharmacy we have on file? You’re bunking with your parents in Wichita? No problem. Just need the pharmacy name and street. Boston, Wichita, whatever.

“Sure, happy to help. Enjoy your stay with your parents. You’ve been there 4 months? Are you cleaning your room? Mostly? Good. Take care. I’ll respond to your email in 2 weeks. Meantime, you might empty out your full voicemail box ... Oh, right, your generation only texts ...”

Okay, one more. Here’s Henrietta. I emailed her an invitation ... Holy Cow, she’s checked in! Let’s see, click “Join.” I can see her!

“Henrietta, is that you? Can you hear me? You can? You can hear me! Henrietta can hear me! And I can hear her!

“Yes, Henrietta, I’m all right. Just doing cartwheels around my study. Between COVID and the 95-degree heat and 100% humidity, it’s all the exercise I get.

“How can I help you today?

“Henrietta? HENRIETTA! Where have you gone, Henrietta?”

THERE IS A PROBLEM WITH YOUR CALL. DISCONNECT YOUR ROUTER, WAIT 65 SECONDS, RECONNECT, THEN RESTART YOUR WIFI, AND LOG IN AGAIN.

Maybe it’s time to go back to the office. A face shield and HAZMAT suit are sounding better all the time.

Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available online. Write to him at [email protected].

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Another great morning, seeing patients in the comfort of quarantine!

Here goes. I’ll invite Gretchen by text: 617-555-5555. “TOO LONG.” How can 10 digits be too long? Trying again: 617-555-5555. “TOO LONG!” What the heck, let me leave off the last digit: 617-555-555. “TOO SHORT.”

Never mind, I’ll invite her by email.

Five minutes have gone by. Better call to see if she got the invite.

“Hello, is this Gretchen? Don’t hang up, I’m not a telemarketer! This is Dr. Rockoff. I sent you an invitation for our computer visit.

“You got it, great. Yes, you have to click on it to sign in. I know, your appointment’s at 8:30. It’s now 8:28. Let’s start early, why not?

“Hi, there! I can see you. Can you hear me? You’re nodding and your lips are moving. I can’t hear you. Did you enable your microphone?

“Nope, still can’t hear. I’ll call your cell, and we’ll talk that way.

“Yes, it’s me, Dr. Rockoff. What’s that? You enabled the microphone along with your video when you logged on? Well, there we go. How can I help today?

“You want a refill on your tretinoin gel for age management? Not a problem. Let’s see, you’ve been using it since 1996. No, you look great! Not a day over 76, really! I’ll have the staff escribe it right over.

“Okay, take care. Three years should be about right. Happy 80th!”

Wonder what happened there. Maybe things will go better for the next patient. Okay, I’m emailing an invite to Rob.

There he is! “Hi. Can you see me? Hear me? Nope, can’t hear you. Let me just call your cell.”

Okay, 972-555-5555. Ringing ... oh no, right to voicemail. “You have reached 972-555-5555. The mailbox is full and cannot accept messages. Please try some other time.”

“Okay, I’m back with you on the screen, Rob. Nope, still can’t hear you. I tried your cell but it went to voicemail. Yes, I see you’re holding the phone in your hand. Let me try you again.

Dr. Alan Rockoff

“972-555-5555. Right to voicemail. Doesn’t your phone ring? You never make voice calls, only send texts? Look, please call me: 781-555-5555, write it down.

“Excellent, we’re in business. You’re worried about a mole that’s changing. You sent a photo to the office. Great, I’ll look right now on your record ... nope, not uploaded. Can you email me the photo? Please write down my email address: alanrockoffmdskincarespecialistist@myfabuloustelemedicineportal.now. Got that? Okay, please send the picture ...

“Returned as undeliverable? Show me what you typed ... Oh, wait. It’s ‘telemedicine,’ not ‘TellaMedicine.’ ” Yeah, that should do it.

“Okay, got the picture. You do fabulous super-closeups! Is that your navel next to it? Your left nostril? Okay. You tried to razor off the hair growing out it? Yes, that could account for the bleeding. Tell you what, go easy on it for the next 2 weeks, and send me another picture. Same email address.



“You have another question? Sure. You want a refill of your clindamycin gel because the tube from 2013 ran out? Guess you haven’t grown out of your acne yet. Sure, happy to send it in for you. Same pharmacy we have on file? You’re bunking with your parents in Wichita? No problem. Just need the pharmacy name and street. Boston, Wichita, whatever.

“Sure, happy to help. Enjoy your stay with your parents. You’ve been there 4 months? Are you cleaning your room? Mostly? Good. Take care. I’ll respond to your email in 2 weeks. Meantime, you might empty out your full voicemail box ... Oh, right, your generation only texts ...”

Okay, one more. Here’s Henrietta. I emailed her an invitation ... Holy Cow, she’s checked in! Let’s see, click “Join.” I can see her!

“Henrietta, is that you? Can you hear me? You can? You can hear me! Henrietta can hear me! And I can hear her!

“Yes, Henrietta, I’m all right. Just doing cartwheels around my study. Between COVID and the 95-degree heat and 100% humidity, it’s all the exercise I get.

“How can I help you today?

“Henrietta? HENRIETTA! Where have you gone, Henrietta?”

THERE IS A PROBLEM WITH YOUR CALL. DISCONNECT YOUR ROUTER, WAIT 65 SECONDS, RECONNECT, THEN RESTART YOUR WIFI, AND LOG IN AGAIN.

Maybe it’s time to go back to the office. A face shield and HAZMAT suit are sounding better all the time.

Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available online. Write to him at [email protected].

Another great morning, seeing patients in the comfort of quarantine!

Here goes. I’ll invite Gretchen by text: 617-555-5555. “TOO LONG.” How can 10 digits be too long? Trying again: 617-555-5555. “TOO LONG!” What the heck, let me leave off the last digit: 617-555-555. “TOO SHORT.”

Never mind, I’ll invite her by email.

Five minutes have gone by. Better call to see if she got the invite.

“Hello, is this Gretchen? Don’t hang up, I’m not a telemarketer! This is Dr. Rockoff. I sent you an invitation for our computer visit.

“You got it, great. Yes, you have to click on it to sign in. I know, your appointment’s at 8:30. It’s now 8:28. Let’s start early, why not?

“Hi, there! I can see you. Can you hear me? You’re nodding and your lips are moving. I can’t hear you. Did you enable your microphone?

“Nope, still can’t hear. I’ll call your cell, and we’ll talk that way.

“Yes, it’s me, Dr. Rockoff. What’s that? You enabled the microphone along with your video when you logged on? Well, there we go. How can I help today?

“You want a refill on your tretinoin gel for age management? Not a problem. Let’s see, you’ve been using it since 1996. No, you look great! Not a day over 76, really! I’ll have the staff escribe it right over.

“Okay, take care. Three years should be about right. Happy 80th!”

Wonder what happened there. Maybe things will go better for the next patient. Okay, I’m emailing an invite to Rob.

There he is! “Hi. Can you see me? Hear me? Nope, can’t hear you. Let me just call your cell.”

Okay, 972-555-5555. Ringing ... oh no, right to voicemail. “You have reached 972-555-5555. The mailbox is full and cannot accept messages. Please try some other time.”

“Okay, I’m back with you on the screen, Rob. Nope, still can’t hear you. I tried your cell but it went to voicemail. Yes, I see you’re holding the phone in your hand. Let me try you again.

Dr. Alan Rockoff

“972-555-5555. Right to voicemail. Doesn’t your phone ring? You never make voice calls, only send texts? Look, please call me: 781-555-5555, write it down.

“Excellent, we’re in business. You’re worried about a mole that’s changing. You sent a photo to the office. Great, I’ll look right now on your record ... nope, not uploaded. Can you email me the photo? Please write down my email address: alanrockoffmdskincarespecialistist@myfabuloustelemedicineportal.now. Got that? Okay, please send the picture ...

“Returned as undeliverable? Show me what you typed ... Oh, wait. It’s ‘telemedicine,’ not ‘TellaMedicine.’ ” Yeah, that should do it.

“Okay, got the picture. You do fabulous super-closeups! Is that your navel next to it? Your left nostril? Okay. You tried to razor off the hair growing out it? Yes, that could account for the bleeding. Tell you what, go easy on it for the next 2 weeks, and send me another picture. Same email address.



“You have another question? Sure. You want a refill of your clindamycin gel because the tube from 2013 ran out? Guess you haven’t grown out of your acne yet. Sure, happy to send it in for you. Same pharmacy we have on file? You’re bunking with your parents in Wichita? No problem. Just need the pharmacy name and street. Boston, Wichita, whatever.

“Sure, happy to help. Enjoy your stay with your parents. You’ve been there 4 months? Are you cleaning your room? Mostly? Good. Take care. I’ll respond to your email in 2 weeks. Meantime, you might empty out your full voicemail box ... Oh, right, your generation only texts ...”

Okay, one more. Here’s Henrietta. I emailed her an invitation ... Holy Cow, she’s checked in! Let’s see, click “Join.” I can see her!

“Henrietta, is that you? Can you hear me? You can? You can hear me! Henrietta can hear me! And I can hear her!

“Yes, Henrietta, I’m all right. Just doing cartwheels around my study. Between COVID and the 95-degree heat and 100% humidity, it’s all the exercise I get.

“How can I help you today?

“Henrietta? HENRIETTA! Where have you gone, Henrietta?”

THERE IS A PROBLEM WITH YOUR CALL. DISCONNECT YOUR ROUTER, WAIT 65 SECONDS, RECONNECT, THEN RESTART YOUR WIFI, AND LOG IN AGAIN.

Maybe it’s time to go back to the office. A face shield and HAZMAT suit are sounding better all the time.

Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available online. Write to him at [email protected].

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Obesity boosts risks in COVID-19 from diagnosis to death

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Thu, 08/26/2021 - 16:00

A new analysis of existing research confirms a stark link between excess weight and COVID-19: People with obesity are much more likely to be diagnosed with the novel coronavirus, undergo hospitalization and ICU admission, and die.

Obese patients faced the greatest bump in risk on the hospitalization front, with their odds of being admitted listed as 113% higher. The odds of diagnosis, ICU admission, and death were 46% higher (odds ratio [OR], 1.46; 95% confidence interval [CI], 1.30-1.65; P < .0001); 74% higher (OR, 1.74, CI, 1.46-2.08, P < .0001); 48% (OR, 1.48, CI, 1.22–1.80, P < .001, all pooled analyses and 95% CI), respectively. All differences were highly significantly different, investigators reported in a systematic review and meta-analysis published online Aug. 26 in Obesity Reviews.

“Essentially, these are pretty scary statistics,” nutrition researcher and study lead author Barry M. Popkin, PhD, of the University of North Carolina at Chapel Hill School of Public Health, said in an interview. “Other studies have talked about an increase in mortality, and we were thinking there’d be a little increase like 10% – nothing like 48%.”

According to the Johns Hopkins University of Medicine tracker, nearly 6 million people in the United States had been diagnosed with COVID-19 as of Aug. 30. The number of deaths had surpassed 183,000.

The authors of the new review launched their project to better understand the link between obesity and COVID-19 “all the way from being diagnosed to death,” Dr. Popkin said, adding that the meta-analysis is the largest of its kind to examine the link.

Dr. Popkin and colleagues analyzed 75 studies during January to June 2020 that tracked 399,461 patients (55% of whom were male) diagnosed with COVID-19. They found that 18 of 20 studies linked obesity with a 46% higher risk of diagnosis, but Dr. Popkin cautioned that this may be misleading. “I suspect it’s because they’re sicker and getting tested more for COVID,” he said. “I don’t think obesity enhances your likelihood of getting COVID. We don’t have a biological rationale for that.”

The researchers examined 19 studies that explored a link between obesity and hospitalization; all 19 found a higher risk of hospitalization in patients with obesity (pooled OR, 2.13). Twenty-one of 22 studies that looked at ICU admissions discovered a higher risk for patients with obesity (pooled OR, 1.74). And 27 of 35 studies that examined COVID-19 mortality found a higher death rate in patients with obesity (pooled OR, 1.48).

The review also looked at 14 studies that examined links between obesity and administration of invasive mechanical ventilation. All the studies found a higher risk for patients with obesity (pooled OR, 1.66; 95% CI, 1.38-1.99; P < .0001).



Could socioeconomic factors explain the difference in risk for people with obesity? It’s not clear. According to Dr. Popkin, most of the studies don’t examine factors such as income. While he believes physical factors are the key to the higher risk, he said “there’s clearly a social side to this.”

On the biological front, it appears that “the immune system is much weaker if you’re obese,” he said, and excess weight may worsen the course of a respiratory disease such as COVID-19 because of lung disorders such as sleep apnea.

In addition to highlighting inflammation and a weakened immune system, the review offers multiple explanations for why patients with obesity face worse outcomes in COVID-19. It may be more difficult for medical professionals to care for them in the hospital because of their weight, the authors wrote, and “obesity may also impair therapeutic treatments during COVID-19 infections.” The authors noted that ACE inhibitors may worsen COVID-19 in patients with type 2 diabetes.

The researchers noted that “potentially the vaccines developed to address COVID-19 will be less effective for individuals with obesity due to a weakened immune response.” They pointed to research that suggests T-cell responses are weaker and antibody titers wane at a faster rate in people with obesity who are vaccinated against influenza.

Dr. Joshua L. Denson


Pulmonologist Joshua L. Denson, MD, MS, of Tulane University, New Orleans, praised the review in an interview, but noted that some of the included studies have wide confidence intervals. One study that links COVID-19 to a sixfold higher mortality rate (OR, 6.29) has a confidence interval of 1.76-22.45.

Dr. Denson said he’s seen about 100 patients with COVID-19, and many are obese and have metabolic syndrome.

Like the authors of the study, he believes higher levels of inflammation play a crucial role in making these patients more vulnerable. “For whatever reason, the virus tends to really like that state. That’s driving these people to get sick,” he said.

Moving forward, Dr. Popkin urged physicians to redouble their efforts to warn patients about the risks of obesity and the importance of healthy eating. He also said COVID-19 vaccine researchers must stratify obese vs. nonobese subjects in clinical trials.

The review was funded by Bloomberg Philanthropies, the Carolina Population Center, World Bank, and Saudi Health Council. The review authors report no relevant disclosures. Dr. Denson reports no relevant disclosures.

SOURCE: Popkin BM et al. Obes Rev. 2020 Aug 26. doi: 10.1111/obr.13128.

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A new analysis of existing research confirms a stark link between excess weight and COVID-19: People with obesity are much more likely to be diagnosed with the novel coronavirus, undergo hospitalization and ICU admission, and die.

Obese patients faced the greatest bump in risk on the hospitalization front, with their odds of being admitted listed as 113% higher. The odds of diagnosis, ICU admission, and death were 46% higher (odds ratio [OR], 1.46; 95% confidence interval [CI], 1.30-1.65; P < .0001); 74% higher (OR, 1.74, CI, 1.46-2.08, P < .0001); 48% (OR, 1.48, CI, 1.22–1.80, P < .001, all pooled analyses and 95% CI), respectively. All differences were highly significantly different, investigators reported in a systematic review and meta-analysis published online Aug. 26 in Obesity Reviews.

“Essentially, these are pretty scary statistics,” nutrition researcher and study lead author Barry M. Popkin, PhD, of the University of North Carolina at Chapel Hill School of Public Health, said in an interview. “Other studies have talked about an increase in mortality, and we were thinking there’d be a little increase like 10% – nothing like 48%.”

According to the Johns Hopkins University of Medicine tracker, nearly 6 million people in the United States had been diagnosed with COVID-19 as of Aug. 30. The number of deaths had surpassed 183,000.

The authors of the new review launched their project to better understand the link between obesity and COVID-19 “all the way from being diagnosed to death,” Dr. Popkin said, adding that the meta-analysis is the largest of its kind to examine the link.

Dr. Popkin and colleagues analyzed 75 studies during January to June 2020 that tracked 399,461 patients (55% of whom were male) diagnosed with COVID-19. They found that 18 of 20 studies linked obesity with a 46% higher risk of diagnosis, but Dr. Popkin cautioned that this may be misleading. “I suspect it’s because they’re sicker and getting tested more for COVID,” he said. “I don’t think obesity enhances your likelihood of getting COVID. We don’t have a biological rationale for that.”

The researchers examined 19 studies that explored a link between obesity and hospitalization; all 19 found a higher risk of hospitalization in patients with obesity (pooled OR, 2.13). Twenty-one of 22 studies that looked at ICU admissions discovered a higher risk for patients with obesity (pooled OR, 1.74). And 27 of 35 studies that examined COVID-19 mortality found a higher death rate in patients with obesity (pooled OR, 1.48).

The review also looked at 14 studies that examined links between obesity and administration of invasive mechanical ventilation. All the studies found a higher risk for patients with obesity (pooled OR, 1.66; 95% CI, 1.38-1.99; P < .0001).



Could socioeconomic factors explain the difference in risk for people with obesity? It’s not clear. According to Dr. Popkin, most of the studies don’t examine factors such as income. While he believes physical factors are the key to the higher risk, he said “there’s clearly a social side to this.”

On the biological front, it appears that “the immune system is much weaker if you’re obese,” he said, and excess weight may worsen the course of a respiratory disease such as COVID-19 because of lung disorders such as sleep apnea.

In addition to highlighting inflammation and a weakened immune system, the review offers multiple explanations for why patients with obesity face worse outcomes in COVID-19. It may be more difficult for medical professionals to care for them in the hospital because of their weight, the authors wrote, and “obesity may also impair therapeutic treatments during COVID-19 infections.” The authors noted that ACE inhibitors may worsen COVID-19 in patients with type 2 diabetes.

The researchers noted that “potentially the vaccines developed to address COVID-19 will be less effective for individuals with obesity due to a weakened immune response.” They pointed to research that suggests T-cell responses are weaker and antibody titers wane at a faster rate in people with obesity who are vaccinated against influenza.

Dr. Joshua L. Denson


Pulmonologist Joshua L. Denson, MD, MS, of Tulane University, New Orleans, praised the review in an interview, but noted that some of the included studies have wide confidence intervals. One study that links COVID-19 to a sixfold higher mortality rate (OR, 6.29) has a confidence interval of 1.76-22.45.

Dr. Denson said he’s seen about 100 patients with COVID-19, and many are obese and have metabolic syndrome.

Like the authors of the study, he believes higher levels of inflammation play a crucial role in making these patients more vulnerable. “For whatever reason, the virus tends to really like that state. That’s driving these people to get sick,” he said.

Moving forward, Dr. Popkin urged physicians to redouble their efforts to warn patients about the risks of obesity and the importance of healthy eating. He also said COVID-19 vaccine researchers must stratify obese vs. nonobese subjects in clinical trials.

The review was funded by Bloomberg Philanthropies, the Carolina Population Center, World Bank, and Saudi Health Council. The review authors report no relevant disclosures. Dr. Denson reports no relevant disclosures.

SOURCE: Popkin BM et al. Obes Rev. 2020 Aug 26. doi: 10.1111/obr.13128.

A new analysis of existing research confirms a stark link between excess weight and COVID-19: People with obesity are much more likely to be diagnosed with the novel coronavirus, undergo hospitalization and ICU admission, and die.

Obese patients faced the greatest bump in risk on the hospitalization front, with their odds of being admitted listed as 113% higher. The odds of diagnosis, ICU admission, and death were 46% higher (odds ratio [OR], 1.46; 95% confidence interval [CI], 1.30-1.65; P < .0001); 74% higher (OR, 1.74, CI, 1.46-2.08, P < .0001); 48% (OR, 1.48, CI, 1.22–1.80, P < .001, all pooled analyses and 95% CI), respectively. All differences were highly significantly different, investigators reported in a systematic review and meta-analysis published online Aug. 26 in Obesity Reviews.

“Essentially, these are pretty scary statistics,” nutrition researcher and study lead author Barry M. Popkin, PhD, of the University of North Carolina at Chapel Hill School of Public Health, said in an interview. “Other studies have talked about an increase in mortality, and we were thinking there’d be a little increase like 10% – nothing like 48%.”

According to the Johns Hopkins University of Medicine tracker, nearly 6 million people in the United States had been diagnosed with COVID-19 as of Aug. 30. The number of deaths had surpassed 183,000.

The authors of the new review launched their project to better understand the link between obesity and COVID-19 “all the way from being diagnosed to death,” Dr. Popkin said, adding that the meta-analysis is the largest of its kind to examine the link.

Dr. Popkin and colleagues analyzed 75 studies during January to June 2020 that tracked 399,461 patients (55% of whom were male) diagnosed with COVID-19. They found that 18 of 20 studies linked obesity with a 46% higher risk of diagnosis, but Dr. Popkin cautioned that this may be misleading. “I suspect it’s because they’re sicker and getting tested more for COVID,” he said. “I don’t think obesity enhances your likelihood of getting COVID. We don’t have a biological rationale for that.”

The researchers examined 19 studies that explored a link between obesity and hospitalization; all 19 found a higher risk of hospitalization in patients with obesity (pooled OR, 2.13). Twenty-one of 22 studies that looked at ICU admissions discovered a higher risk for patients with obesity (pooled OR, 1.74). And 27 of 35 studies that examined COVID-19 mortality found a higher death rate in patients with obesity (pooled OR, 1.48).

The review also looked at 14 studies that examined links between obesity and administration of invasive mechanical ventilation. All the studies found a higher risk for patients with obesity (pooled OR, 1.66; 95% CI, 1.38-1.99; P < .0001).



Could socioeconomic factors explain the difference in risk for people with obesity? It’s not clear. According to Dr. Popkin, most of the studies don’t examine factors such as income. While he believes physical factors are the key to the higher risk, he said “there’s clearly a social side to this.”

On the biological front, it appears that “the immune system is much weaker if you’re obese,” he said, and excess weight may worsen the course of a respiratory disease such as COVID-19 because of lung disorders such as sleep apnea.

In addition to highlighting inflammation and a weakened immune system, the review offers multiple explanations for why patients with obesity face worse outcomes in COVID-19. It may be more difficult for medical professionals to care for them in the hospital because of their weight, the authors wrote, and “obesity may also impair therapeutic treatments during COVID-19 infections.” The authors noted that ACE inhibitors may worsen COVID-19 in patients with type 2 diabetes.

The researchers noted that “potentially the vaccines developed to address COVID-19 will be less effective for individuals with obesity due to a weakened immune response.” They pointed to research that suggests T-cell responses are weaker and antibody titers wane at a faster rate in people with obesity who are vaccinated against influenza.

Dr. Joshua L. Denson


Pulmonologist Joshua L. Denson, MD, MS, of Tulane University, New Orleans, praised the review in an interview, but noted that some of the included studies have wide confidence intervals. One study that links COVID-19 to a sixfold higher mortality rate (OR, 6.29) has a confidence interval of 1.76-22.45.

Dr. Denson said he’s seen about 100 patients with COVID-19, and many are obese and have metabolic syndrome.

Like the authors of the study, he believes higher levels of inflammation play a crucial role in making these patients more vulnerable. “For whatever reason, the virus tends to really like that state. That’s driving these people to get sick,” he said.

Moving forward, Dr. Popkin urged physicians to redouble their efforts to warn patients about the risks of obesity and the importance of healthy eating. He also said COVID-19 vaccine researchers must stratify obese vs. nonobese subjects in clinical trials.

The review was funded by Bloomberg Philanthropies, the Carolina Population Center, World Bank, and Saudi Health Council. The review authors report no relevant disclosures. Dr. Denson reports no relevant disclosures.

SOURCE: Popkin BM et al. Obes Rev. 2020 Aug 26. doi: 10.1111/obr.13128.

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More research needed on how fetal exposure affects later development

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Tue, 09/01/2020 - 09:13

The number of genes in humans seems inadequate to account for the diversity seen in people. While maternal and paternal factors do play a role in the development of offspring, increased attention is being paid to the forces that express these genes and the impact they have on the health of a person, including development of psychiatric conditions, according to Dolores Malaspina, MD.

Epigenetics, or changes that occur in a fetal phenotype that do not involve changes to the genotype, involve factors such as DNA methylation to control gene expression, histone modification or the wrapping of genes, or the silencing and activation of certain genes with noncoding RNA-associated factors, said Dr. Malaspina of the Icahn School of Medicine at Mount Sinai, New York.

When this occurs during pregnancy, “the fetus does not simply develop from a genetic blueprint of the genes from its father and mother. Instead, signals are received throughout the pregnancy as to the health of the mother and signals about the environment,” she said in a virtual meeting presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

There is an evolutionary advantage to this so-called survival phenotype. “If, during the pregnancy, there’s a deficit of available nutrition, that may be a signal to the fetus that food will be scarce. In the setting of food scarcity, certain physiological adaptations during development can make the fetus more likely to survive to adulthood,” Dr. Malaspina said at the meeting, presented by Global Academy for Medical Education. But a fetus programmed to adapt to scarcity of food may also develop cardiovascular disease, metabolic disease, or mortality later in life if the prediction of scarce nutrition proved incorrect.

This approach to thinking about the developmental origins of health and disease, which examines how prenatal and perinatal exposure to environmental factors affect disease in adulthood, has also found a link between some exposures and psychiatric disorders. The most famous example, the Dutch Hunger Winter Families Study, found an increased risk of schizophrenia among children born during the height of the famine (Int J Epidemiol. 2007 Dec;36[6]:1196-204). During the Arab-Israeli war of 1967 (the Six-Day War), which took place in June, the fetuses of mothers who were pregnant during that month had a higher risk of schizophrenia if the fetus was in the second month (relative risk, 2.3; 95% confidence interval, 1.1-4.7) or third month (RR, 2.5; 95% CI, 1.2-5.2) of fetal life during June 1967, Dr. Malaspina and associates wrote (BMC Psychiatry. 2008 Aug 21;8:71).



“The key aspect is the ascertainment of individuals during a circumscribed period, the assessment and then the longitudinal follow-up,” she said. “Obviously, these are not easy studies to do, but enough of them have been done such that for the last decade at least, the general population should be aware of the developmental origins of health and disease.”

Maternal depression is another psychiatric condition that can serve as a prenatal exposure to adversity. A recent review found that children of women with untreated depression were 56% more likely to be born preterm and 96% more likely to have a low birth weight (Pediatr Res. 2019 Jan;85[2]:134-45). “Preterm birth and early birth along with low birth weight, these have ramifying effects throughout life, not only on neonatal and infant mortality, but on developmental disorders and lifetime morbidity,” she said. “These effects of maternal depression withstand all sorts of accounting for other correlated exposures, including maternal age and her medical complications or substance use.”

Maternal stress and depression can also harm neurocognitive development and effective functioning of the children, Dr. Malaspina noted. “The modulation of mood and affect can affect temperament and affect mental health. Studies exist linking maternal depression to autism, attention-deficit disorder, developmental delay, behavioral problems, sleep problems, externalizing behavior and depression, showing a very large effect of maternal depression on offspring well-being.”

To complicate matters, at least 15% of women will experience major depression during pregnancy, but of these, major depression is not being addressed in about half. Nonpharmacologic interventions can include cognitive-behavioral therapy and relaxation practices, but medication should be considered as well. “There’s an ongoing debate about whether antidepressant medications are harmful for the offspring,” she said. However, reviews conducted by Dr. Malaspina’s group have found low evidence of serious harm.

“My summary would be the depression itself holds much more evidence for disrupting offspring health and development than medications,” Dr. Malaspina said. “Most studies find no adverse birth effects when they properly controlled accounting for maternal age and the other conditions and other medications.”

Global Academy and this news organization are owned by the same parent company. Dr. Malaspina reported no relevant conflicts of interest.

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The number of genes in humans seems inadequate to account for the diversity seen in people. While maternal and paternal factors do play a role in the development of offspring, increased attention is being paid to the forces that express these genes and the impact they have on the health of a person, including development of psychiatric conditions, according to Dolores Malaspina, MD.

Epigenetics, or changes that occur in a fetal phenotype that do not involve changes to the genotype, involve factors such as DNA methylation to control gene expression, histone modification or the wrapping of genes, or the silencing and activation of certain genes with noncoding RNA-associated factors, said Dr. Malaspina of the Icahn School of Medicine at Mount Sinai, New York.

When this occurs during pregnancy, “the fetus does not simply develop from a genetic blueprint of the genes from its father and mother. Instead, signals are received throughout the pregnancy as to the health of the mother and signals about the environment,” she said in a virtual meeting presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

There is an evolutionary advantage to this so-called survival phenotype. “If, during the pregnancy, there’s a deficit of available nutrition, that may be a signal to the fetus that food will be scarce. In the setting of food scarcity, certain physiological adaptations during development can make the fetus more likely to survive to adulthood,” Dr. Malaspina said at the meeting, presented by Global Academy for Medical Education. But a fetus programmed to adapt to scarcity of food may also develop cardiovascular disease, metabolic disease, or mortality later in life if the prediction of scarce nutrition proved incorrect.

This approach to thinking about the developmental origins of health and disease, which examines how prenatal and perinatal exposure to environmental factors affect disease in adulthood, has also found a link between some exposures and psychiatric disorders. The most famous example, the Dutch Hunger Winter Families Study, found an increased risk of schizophrenia among children born during the height of the famine (Int J Epidemiol. 2007 Dec;36[6]:1196-204). During the Arab-Israeli war of 1967 (the Six-Day War), which took place in June, the fetuses of mothers who were pregnant during that month had a higher risk of schizophrenia if the fetus was in the second month (relative risk, 2.3; 95% confidence interval, 1.1-4.7) or third month (RR, 2.5; 95% CI, 1.2-5.2) of fetal life during June 1967, Dr. Malaspina and associates wrote (BMC Psychiatry. 2008 Aug 21;8:71).



“The key aspect is the ascertainment of individuals during a circumscribed period, the assessment and then the longitudinal follow-up,” she said. “Obviously, these are not easy studies to do, but enough of them have been done such that for the last decade at least, the general population should be aware of the developmental origins of health and disease.”

Maternal depression is another psychiatric condition that can serve as a prenatal exposure to adversity. A recent review found that children of women with untreated depression were 56% more likely to be born preterm and 96% more likely to have a low birth weight (Pediatr Res. 2019 Jan;85[2]:134-45). “Preterm birth and early birth along with low birth weight, these have ramifying effects throughout life, not only on neonatal and infant mortality, but on developmental disorders and lifetime morbidity,” she said. “These effects of maternal depression withstand all sorts of accounting for other correlated exposures, including maternal age and her medical complications or substance use.”

Maternal stress and depression can also harm neurocognitive development and effective functioning of the children, Dr. Malaspina noted. “The modulation of mood and affect can affect temperament and affect mental health. Studies exist linking maternal depression to autism, attention-deficit disorder, developmental delay, behavioral problems, sleep problems, externalizing behavior and depression, showing a very large effect of maternal depression on offspring well-being.”

To complicate matters, at least 15% of women will experience major depression during pregnancy, but of these, major depression is not being addressed in about half. Nonpharmacologic interventions can include cognitive-behavioral therapy and relaxation practices, but medication should be considered as well. “There’s an ongoing debate about whether antidepressant medications are harmful for the offspring,” she said. However, reviews conducted by Dr. Malaspina’s group have found low evidence of serious harm.

“My summary would be the depression itself holds much more evidence for disrupting offspring health and development than medications,” Dr. Malaspina said. “Most studies find no adverse birth effects when they properly controlled accounting for maternal age and the other conditions and other medications.”

Global Academy and this news organization are owned by the same parent company. Dr. Malaspina reported no relevant conflicts of interest.

The number of genes in humans seems inadequate to account for the diversity seen in people. While maternal and paternal factors do play a role in the development of offspring, increased attention is being paid to the forces that express these genes and the impact they have on the health of a person, including development of psychiatric conditions, according to Dolores Malaspina, MD.

Epigenetics, or changes that occur in a fetal phenotype that do not involve changes to the genotype, involve factors such as DNA methylation to control gene expression, histone modification or the wrapping of genes, or the silencing and activation of certain genes with noncoding RNA-associated factors, said Dr. Malaspina of the Icahn School of Medicine at Mount Sinai, New York.

When this occurs during pregnancy, “the fetus does not simply develop from a genetic blueprint of the genes from its father and mother. Instead, signals are received throughout the pregnancy as to the health of the mother and signals about the environment,” she said in a virtual meeting presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

There is an evolutionary advantage to this so-called survival phenotype. “If, during the pregnancy, there’s a deficit of available nutrition, that may be a signal to the fetus that food will be scarce. In the setting of food scarcity, certain physiological adaptations during development can make the fetus more likely to survive to adulthood,” Dr. Malaspina said at the meeting, presented by Global Academy for Medical Education. But a fetus programmed to adapt to scarcity of food may also develop cardiovascular disease, metabolic disease, or mortality later in life if the prediction of scarce nutrition proved incorrect.

This approach to thinking about the developmental origins of health and disease, which examines how prenatal and perinatal exposure to environmental factors affect disease in adulthood, has also found a link between some exposures and psychiatric disorders. The most famous example, the Dutch Hunger Winter Families Study, found an increased risk of schizophrenia among children born during the height of the famine (Int J Epidemiol. 2007 Dec;36[6]:1196-204). During the Arab-Israeli war of 1967 (the Six-Day War), which took place in June, the fetuses of mothers who were pregnant during that month had a higher risk of schizophrenia if the fetus was in the second month (relative risk, 2.3; 95% confidence interval, 1.1-4.7) or third month (RR, 2.5; 95% CI, 1.2-5.2) of fetal life during June 1967, Dr. Malaspina and associates wrote (BMC Psychiatry. 2008 Aug 21;8:71).



“The key aspect is the ascertainment of individuals during a circumscribed period, the assessment and then the longitudinal follow-up,” she said. “Obviously, these are not easy studies to do, but enough of them have been done such that for the last decade at least, the general population should be aware of the developmental origins of health and disease.”

Maternal depression is another psychiatric condition that can serve as a prenatal exposure to adversity. A recent review found that children of women with untreated depression were 56% more likely to be born preterm and 96% more likely to have a low birth weight (Pediatr Res. 2019 Jan;85[2]:134-45). “Preterm birth and early birth along with low birth weight, these have ramifying effects throughout life, not only on neonatal and infant mortality, but on developmental disorders and lifetime morbidity,” she said. “These effects of maternal depression withstand all sorts of accounting for other correlated exposures, including maternal age and her medical complications or substance use.”

Maternal stress and depression can also harm neurocognitive development and effective functioning of the children, Dr. Malaspina noted. “The modulation of mood and affect can affect temperament and affect mental health. Studies exist linking maternal depression to autism, attention-deficit disorder, developmental delay, behavioral problems, sleep problems, externalizing behavior and depression, showing a very large effect of maternal depression on offspring well-being.”

To complicate matters, at least 15% of women will experience major depression during pregnancy, but of these, major depression is not being addressed in about half. Nonpharmacologic interventions can include cognitive-behavioral therapy and relaxation practices, but medication should be considered as well. “There’s an ongoing debate about whether antidepressant medications are harmful for the offspring,” she said. However, reviews conducted by Dr. Malaspina’s group have found low evidence of serious harm.

“My summary would be the depression itself holds much more evidence for disrupting offspring health and development than medications,” Dr. Malaspina said. “Most studies find no adverse birth effects when they properly controlled accounting for maternal age and the other conditions and other medications.”

Global Academy and this news organization are owned by the same parent company. Dr. Malaspina reported no relevant conflicts of interest.

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HOME-PE trial clarifies which pulmonary embolism patients to treat at home

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Wed, 09/02/2020 - 09:58

The pragmatic Hestia criteria proved as safe as the more structured, points-based simplified Pulmonary Embolism Severity Index (sPESI) score for selection of patients with acute pulmonary embolism for outpatient care in the large, randomized HOME-PE trial presented at the virtual annual congress of the European Society of Cardiology.

Courtesy Wikimedia Commons/Walter Serra, Giuseppe De Iaco, Claudio Reverberi, and Tiziano Gherli/Creative Commons License

“These results support outpatient management of acute pulmonary embolism patients using either the Hestia method or the sPESI score with the option for the physician-in-charge to override the decision. In hospitals organized for outpatient management, both triaging strategies enable more than a third of pulmonary embolism patients to be managed at home with a low rate of complications,” Pierre-Marie Roy, MD, said in presenting the HOME-PE findings.

The study clarifies a transatlantic controversy regarding how best to triage patients with acute pulmonary embolism (PE) for outpatient care. The answer? It’s basically a tie between the points-based sPESI score recommended in the current ESC guidelines (Eur Respir J. 2019 Oct 9;54[3]:1901647) and the Hestia method endorsed in the American College of Chest Physician guidelines (Chest. 2016 Feb;149[2]:315-52).

The sPESI is a validated tool that grants 1 point each for age over 80 years, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%. A patient needs a score of zero to be eligible for outpatient management. In contrast, the Hestia method relies upon 11 simple bedside criteria rather than a points system, explained Dr. Roy of University Hospital of Angers, France (J Thromb Haemost. 2011 Aug;9[8]:1500-7).

HOME-PE was a randomized, open-label, noninferiority trial conducted at 26 hospitals in France, Belgium, Switzerland, and the Netherlands. The study included 1,974 patients presenting to the emergency department with non–high-risk acute PE as defined by hemodynamic stability. About 39% of patients in the Hestia group were eligible for outpatient care on the basis of ‘no’ answers regarding all 11 criteria, while 48% of patients had an sPESI score of 0 and were thus initially considered appropriate for outpatient management.

However, the investigators recognized that no scoring system for acute PE is perfect, and that the judgment of a physician with extensive experience in managing this life-threatening condition counts for a lot. So they stipulated that a patient’s physician-in-charge could overrule a decision for early discharge. This happened 29% of the time in patients with a sPESI score of 0, as compared with a 3% overrule rate with the Hestia rule. The physician-in-charge also moved small numbers of patients who were Hestia or sPESI positive into the outpatient care group. As a result, a similar proportion of patients in both groups were discharged home within 24 hours for outpatient treatment: 38% of the total Hestia group and 37% in the sPESI arm.

Major adverse event rates were reassuringly low in both groups managed on an outpatient basis. The composite of recurrent venous thromboembolism, bleeding, or death within 30 days occurred in 1.3% of Hestia outpatients and 1.1% of sPESI outpatients. Among patients managed in the hospital, these rates were 5.6% in the Hestia group and 4.7% in the sPESI group.

Discussant Stavros V. Konstantinides, MD, who chaired the ESC guideline committee, asked rhetorically, “who’s happy with the HOME-PE trial? I think everybody.”

“The Hestia criteria integrate the feasibility of family support of the individual patient. This is a good thing. And eligibility based on the Hestia criteria, unlike sPESI, does not require age younger than 80 years or no cancer, and it appears from the HOME-PE study that this is okay,” observed Dr. Konstantinides of the Center for Thrombosis and Hemostasis at the University of Mainz (Germany).

In an interview, Hadley Wilson, MD, called the HOME-PE trial “transformative” and predicted it will change clinical practice. He was particularly impressed with the high quality of the trial, noting that 87% of participants managed as outpatients received a direct oral anticoagulant.

The Hestia rule is simpler and more user-friendly. And greater use of this triaging strategy might have advantages in terms of economics and health care utilization by potentially encouraging movement of decision-making regarding outpatient management of acute PE out of the hospital wards and into emergency departments, said Dr. Wilson, executive vice chair of the Sanger Heart and Vascular Institute and a cardiologist at the University of North Carolina at Chapel Hill.

Dr. Roy reported receiving research grants to conduct HOME-PE from the French Ministry of Health, the study sponsor. In addition, he is on scientific advisory boards and/or speakers’ panels for Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, Aspen, Daiichi Sankyo, and Sanofi Aventis.
 

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The pragmatic Hestia criteria proved as safe as the more structured, points-based simplified Pulmonary Embolism Severity Index (sPESI) score for selection of patients with acute pulmonary embolism for outpatient care in the large, randomized HOME-PE trial presented at the virtual annual congress of the European Society of Cardiology.

Courtesy Wikimedia Commons/Walter Serra, Giuseppe De Iaco, Claudio Reverberi, and Tiziano Gherli/Creative Commons License

“These results support outpatient management of acute pulmonary embolism patients using either the Hestia method or the sPESI score with the option for the physician-in-charge to override the decision. In hospitals organized for outpatient management, both triaging strategies enable more than a third of pulmonary embolism patients to be managed at home with a low rate of complications,” Pierre-Marie Roy, MD, said in presenting the HOME-PE findings.

The study clarifies a transatlantic controversy regarding how best to triage patients with acute pulmonary embolism (PE) for outpatient care. The answer? It’s basically a tie between the points-based sPESI score recommended in the current ESC guidelines (Eur Respir J. 2019 Oct 9;54[3]:1901647) and the Hestia method endorsed in the American College of Chest Physician guidelines (Chest. 2016 Feb;149[2]:315-52).

The sPESI is a validated tool that grants 1 point each for age over 80 years, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%. A patient needs a score of zero to be eligible for outpatient management. In contrast, the Hestia method relies upon 11 simple bedside criteria rather than a points system, explained Dr. Roy of University Hospital of Angers, France (J Thromb Haemost. 2011 Aug;9[8]:1500-7).

HOME-PE was a randomized, open-label, noninferiority trial conducted at 26 hospitals in France, Belgium, Switzerland, and the Netherlands. The study included 1,974 patients presenting to the emergency department with non–high-risk acute PE as defined by hemodynamic stability. About 39% of patients in the Hestia group were eligible for outpatient care on the basis of ‘no’ answers regarding all 11 criteria, while 48% of patients had an sPESI score of 0 and were thus initially considered appropriate for outpatient management.

However, the investigators recognized that no scoring system for acute PE is perfect, and that the judgment of a physician with extensive experience in managing this life-threatening condition counts for a lot. So they stipulated that a patient’s physician-in-charge could overrule a decision for early discharge. This happened 29% of the time in patients with a sPESI score of 0, as compared with a 3% overrule rate with the Hestia rule. The physician-in-charge also moved small numbers of patients who were Hestia or sPESI positive into the outpatient care group. As a result, a similar proportion of patients in both groups were discharged home within 24 hours for outpatient treatment: 38% of the total Hestia group and 37% in the sPESI arm.

Major adverse event rates were reassuringly low in both groups managed on an outpatient basis. The composite of recurrent venous thromboembolism, bleeding, or death within 30 days occurred in 1.3% of Hestia outpatients and 1.1% of sPESI outpatients. Among patients managed in the hospital, these rates were 5.6% in the Hestia group and 4.7% in the sPESI group.

Discussant Stavros V. Konstantinides, MD, who chaired the ESC guideline committee, asked rhetorically, “who’s happy with the HOME-PE trial? I think everybody.”

“The Hestia criteria integrate the feasibility of family support of the individual patient. This is a good thing. And eligibility based on the Hestia criteria, unlike sPESI, does not require age younger than 80 years or no cancer, and it appears from the HOME-PE study that this is okay,” observed Dr. Konstantinides of the Center for Thrombosis and Hemostasis at the University of Mainz (Germany).

In an interview, Hadley Wilson, MD, called the HOME-PE trial “transformative” and predicted it will change clinical practice. He was particularly impressed with the high quality of the trial, noting that 87% of participants managed as outpatients received a direct oral anticoagulant.

The Hestia rule is simpler and more user-friendly. And greater use of this triaging strategy might have advantages in terms of economics and health care utilization by potentially encouraging movement of decision-making regarding outpatient management of acute PE out of the hospital wards and into emergency departments, said Dr. Wilson, executive vice chair of the Sanger Heart and Vascular Institute and a cardiologist at the University of North Carolina at Chapel Hill.

Dr. Roy reported receiving research grants to conduct HOME-PE from the French Ministry of Health, the study sponsor. In addition, he is on scientific advisory boards and/or speakers’ panels for Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, Aspen, Daiichi Sankyo, and Sanofi Aventis.
 

The pragmatic Hestia criteria proved as safe as the more structured, points-based simplified Pulmonary Embolism Severity Index (sPESI) score for selection of patients with acute pulmonary embolism for outpatient care in the large, randomized HOME-PE trial presented at the virtual annual congress of the European Society of Cardiology.

Courtesy Wikimedia Commons/Walter Serra, Giuseppe De Iaco, Claudio Reverberi, and Tiziano Gherli/Creative Commons License

“These results support outpatient management of acute pulmonary embolism patients using either the Hestia method or the sPESI score with the option for the physician-in-charge to override the decision. In hospitals organized for outpatient management, both triaging strategies enable more than a third of pulmonary embolism patients to be managed at home with a low rate of complications,” Pierre-Marie Roy, MD, said in presenting the HOME-PE findings.

The study clarifies a transatlantic controversy regarding how best to triage patients with acute pulmonary embolism (PE) for outpatient care. The answer? It’s basically a tie between the points-based sPESI score recommended in the current ESC guidelines (Eur Respir J. 2019 Oct 9;54[3]:1901647) and the Hestia method endorsed in the American College of Chest Physician guidelines (Chest. 2016 Feb;149[2]:315-52).

The sPESI is a validated tool that grants 1 point each for age over 80 years, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%. A patient needs a score of zero to be eligible for outpatient management. In contrast, the Hestia method relies upon 11 simple bedside criteria rather than a points system, explained Dr. Roy of University Hospital of Angers, France (J Thromb Haemost. 2011 Aug;9[8]:1500-7).

HOME-PE was a randomized, open-label, noninferiority trial conducted at 26 hospitals in France, Belgium, Switzerland, and the Netherlands. The study included 1,974 patients presenting to the emergency department with non–high-risk acute PE as defined by hemodynamic stability. About 39% of patients in the Hestia group were eligible for outpatient care on the basis of ‘no’ answers regarding all 11 criteria, while 48% of patients had an sPESI score of 0 and were thus initially considered appropriate for outpatient management.

However, the investigators recognized that no scoring system for acute PE is perfect, and that the judgment of a physician with extensive experience in managing this life-threatening condition counts for a lot. So they stipulated that a patient’s physician-in-charge could overrule a decision for early discharge. This happened 29% of the time in patients with a sPESI score of 0, as compared with a 3% overrule rate with the Hestia rule. The physician-in-charge also moved small numbers of patients who were Hestia or sPESI positive into the outpatient care group. As a result, a similar proportion of patients in both groups were discharged home within 24 hours for outpatient treatment: 38% of the total Hestia group and 37% in the sPESI arm.

Major adverse event rates were reassuringly low in both groups managed on an outpatient basis. The composite of recurrent venous thromboembolism, bleeding, or death within 30 days occurred in 1.3% of Hestia outpatients and 1.1% of sPESI outpatients. Among patients managed in the hospital, these rates were 5.6% in the Hestia group and 4.7% in the sPESI group.

Discussant Stavros V. Konstantinides, MD, who chaired the ESC guideline committee, asked rhetorically, “who’s happy with the HOME-PE trial? I think everybody.”

“The Hestia criteria integrate the feasibility of family support of the individual patient. This is a good thing. And eligibility based on the Hestia criteria, unlike sPESI, does not require age younger than 80 years or no cancer, and it appears from the HOME-PE study that this is okay,” observed Dr. Konstantinides of the Center for Thrombosis and Hemostasis at the University of Mainz (Germany).

In an interview, Hadley Wilson, MD, called the HOME-PE trial “transformative” and predicted it will change clinical practice. He was particularly impressed with the high quality of the trial, noting that 87% of participants managed as outpatients received a direct oral anticoagulant.

The Hestia rule is simpler and more user-friendly. And greater use of this triaging strategy might have advantages in terms of economics and health care utilization by potentially encouraging movement of decision-making regarding outpatient management of acute PE out of the hospital wards and into emergency departments, said Dr. Wilson, executive vice chair of the Sanger Heart and Vascular Institute and a cardiologist at the University of North Carolina at Chapel Hill.

Dr. Roy reported receiving research grants to conduct HOME-PE from the French Ministry of Health, the study sponsor. In addition, he is on scientific advisory boards and/or speakers’ panels for Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, Aspen, Daiichi Sankyo, and Sanofi Aventis.
 

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AGA updates endoscopic management of nonvariceal upper GI bleeding

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The American Gastroenterological Association (AGA) has published a clinical practice update for endoscopic management of nonvariceal upper GI bleeding (NVUGIB).

The update includes 10 best practice recommendations based on clinical experience and a comprehensive literature review, reported lead author Daniel K. Mullady, MD, of Washington University in St. Louis.

“Numerous endoscopic devices have been developed over the past 30 years with demonstrated effectiveness in treating NVUGIB,” Dr. Mullady and colleagues wrote in Gastroenterology. “The purpose of this clinical practice update is to review the key concepts, new devices, and therapeutic strategies in endoscopically combating this age-old clinical dilemma.”

According to the investigators, endoscopy is central to management of NVUGIB, but only after patients are appropriately triaged and stabilized.

“[E]ndoscopy should be performed to determine the source of bleeding, to assess rebleeding risk, and to treat lesions at high risk for rebleeding,” they wrote. “Exactly when the endoscopy should be performed is a clinical judgment made by the gastroenterologist in consultation with the primary service.”

The investigators recommended that endoscopy be performed within 12 hours for emergent cases and within 24 hours for urgent cases, whereas elective cases could wait longer.

They noted that NVUGIB can range from mild and self-limiting, allowing for outpatient management, to severe and life-threatening, necessitating intensive care. Because of this broad range, the investigators recommended familiarity with triage scoring systems, including the Glasgow-Blatchford Score, the Rockall Score, and AIMS-65.

“A common decision is deciding whether or not to wait until the next morning to perform endoscopy on a patient presenting after hours with suspected NVUGIB,” the investigators wrote.

The investigators cautioned that emergent endoscopy may actually be associated with poorer outcomes because of “inadequate resuscitation,” and suggested that “[p]atients who are hemodynamically stable, do not have ongoing hematemesis, and have melena only can generally be deferred to the following morning.”

Concerning hemostatic technique, Dr. Mullady and colleagues recommended familiarity with conventional thermal therapy and placement of hemoclips. If these approaches are unsuccessful, or deemed unlikely to succeed, they recommended an over-the-scope clip.

For ulcers “with a rigid and fibrotic base,” or those that are hard to reach, the investigators recommended monopolar hemostatic forceps with low-voltage coagulation.

According to the update, hemostatic powder should be reserved for scenarios in which bleeding is diffuse and difficult to locate.

“In most instances, hemostatic powder should be preferentially used as a rescue therapy and not for primary hemostasis, except in cases of malignant bleeding or massive bleeding with inability to perform thermal therapy or hemoclip placement,” the investigators wrote.

They noted that hemostatic powder generally dissolves in less than 24 hours, so additional treatment approaches should be considered, particular when there is a high risk of rebleeding.

When deciding between transcatheter arterial embolization (TAE) and surgery after endoscopic failure, the update calls for a comprehensive clinical assessment that incorporates patient factors, such as coagulopathy, hemodynamic instability, and multiorgan failure; bleeding etiology; potential adverse effects; and rebleeding risk.

“An important point is that prophylactic TAE of high-risk ulcers after successful endoscopic therapy is not recommended,” the investigators wrote.

Beyond these recommendations, the update includes a comprehensive discussion of relevant literature and strategies for effective clinical decision making. The discussion concludes with global remarks about the evolving role of endoscopy in managing NVUGIB, including a note about cost-effectiveness despite up-front expenses associated with some methods.

“With this expanded endoscopic armamentarium, endoscopic therapy should achieve hemostasis in the majority of patients with NVUGIB,” the investigators wrote. “Despite the increased costs of newer devices or multimodal therapy, effective hemostasis to preventing rebleeding and the need for hospital readmission is likely to be a dominant cost-saving strategy.”

Dr. Mullady disclosed relationships with Boston Scientific, ConMed, and Cook Medical.

This story was updated on 9/9/2020.

SOURCE: Mullady DK et al. Gastro. 2020 Jun 20. doi: 10.1053/j.gastro.2020.05.095.

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The American Gastroenterological Association (AGA) has published a clinical practice update for endoscopic management of nonvariceal upper GI bleeding (NVUGIB).

The update includes 10 best practice recommendations based on clinical experience and a comprehensive literature review, reported lead author Daniel K. Mullady, MD, of Washington University in St. Louis.

“Numerous endoscopic devices have been developed over the past 30 years with demonstrated effectiveness in treating NVUGIB,” Dr. Mullady and colleagues wrote in Gastroenterology. “The purpose of this clinical practice update is to review the key concepts, new devices, and therapeutic strategies in endoscopically combating this age-old clinical dilemma.”

According to the investigators, endoscopy is central to management of NVUGIB, but only after patients are appropriately triaged and stabilized.

“[E]ndoscopy should be performed to determine the source of bleeding, to assess rebleeding risk, and to treat lesions at high risk for rebleeding,” they wrote. “Exactly when the endoscopy should be performed is a clinical judgment made by the gastroenterologist in consultation with the primary service.”

The investigators recommended that endoscopy be performed within 12 hours for emergent cases and within 24 hours for urgent cases, whereas elective cases could wait longer.

They noted that NVUGIB can range from mild and self-limiting, allowing for outpatient management, to severe and life-threatening, necessitating intensive care. Because of this broad range, the investigators recommended familiarity with triage scoring systems, including the Glasgow-Blatchford Score, the Rockall Score, and AIMS-65.

“A common decision is deciding whether or not to wait until the next morning to perform endoscopy on a patient presenting after hours with suspected NVUGIB,” the investigators wrote.

The investigators cautioned that emergent endoscopy may actually be associated with poorer outcomes because of “inadequate resuscitation,” and suggested that “[p]atients who are hemodynamically stable, do not have ongoing hematemesis, and have melena only can generally be deferred to the following morning.”

Concerning hemostatic technique, Dr. Mullady and colleagues recommended familiarity with conventional thermal therapy and placement of hemoclips. If these approaches are unsuccessful, or deemed unlikely to succeed, they recommended an over-the-scope clip.

For ulcers “with a rigid and fibrotic base,” or those that are hard to reach, the investigators recommended monopolar hemostatic forceps with low-voltage coagulation.

According to the update, hemostatic powder should be reserved for scenarios in which bleeding is diffuse and difficult to locate.

“In most instances, hemostatic powder should be preferentially used as a rescue therapy and not for primary hemostasis, except in cases of malignant bleeding or massive bleeding with inability to perform thermal therapy or hemoclip placement,” the investigators wrote.

They noted that hemostatic powder generally dissolves in less than 24 hours, so additional treatment approaches should be considered, particular when there is a high risk of rebleeding.

When deciding between transcatheter arterial embolization (TAE) and surgery after endoscopic failure, the update calls for a comprehensive clinical assessment that incorporates patient factors, such as coagulopathy, hemodynamic instability, and multiorgan failure; bleeding etiology; potential adverse effects; and rebleeding risk.

“An important point is that prophylactic TAE of high-risk ulcers after successful endoscopic therapy is not recommended,” the investigators wrote.

Beyond these recommendations, the update includes a comprehensive discussion of relevant literature and strategies for effective clinical decision making. The discussion concludes with global remarks about the evolving role of endoscopy in managing NVUGIB, including a note about cost-effectiveness despite up-front expenses associated with some methods.

“With this expanded endoscopic armamentarium, endoscopic therapy should achieve hemostasis in the majority of patients with NVUGIB,” the investigators wrote. “Despite the increased costs of newer devices or multimodal therapy, effective hemostasis to preventing rebleeding and the need for hospital readmission is likely to be a dominant cost-saving strategy.”

Dr. Mullady disclosed relationships with Boston Scientific, ConMed, and Cook Medical.

This story was updated on 9/9/2020.

SOURCE: Mullady DK et al. Gastro. 2020 Jun 20. doi: 10.1053/j.gastro.2020.05.095.

The American Gastroenterological Association (AGA) has published a clinical practice update for endoscopic management of nonvariceal upper GI bleeding (NVUGIB).

The update includes 10 best practice recommendations based on clinical experience and a comprehensive literature review, reported lead author Daniel K. Mullady, MD, of Washington University in St. Louis.

“Numerous endoscopic devices have been developed over the past 30 years with demonstrated effectiveness in treating NVUGIB,” Dr. Mullady and colleagues wrote in Gastroenterology. “The purpose of this clinical practice update is to review the key concepts, new devices, and therapeutic strategies in endoscopically combating this age-old clinical dilemma.”

According to the investigators, endoscopy is central to management of NVUGIB, but only after patients are appropriately triaged and stabilized.

“[E]ndoscopy should be performed to determine the source of bleeding, to assess rebleeding risk, and to treat lesions at high risk for rebleeding,” they wrote. “Exactly when the endoscopy should be performed is a clinical judgment made by the gastroenterologist in consultation with the primary service.”

The investigators recommended that endoscopy be performed within 12 hours for emergent cases and within 24 hours for urgent cases, whereas elective cases could wait longer.

They noted that NVUGIB can range from mild and self-limiting, allowing for outpatient management, to severe and life-threatening, necessitating intensive care. Because of this broad range, the investigators recommended familiarity with triage scoring systems, including the Glasgow-Blatchford Score, the Rockall Score, and AIMS-65.

“A common decision is deciding whether or not to wait until the next morning to perform endoscopy on a patient presenting after hours with suspected NVUGIB,” the investigators wrote.

The investigators cautioned that emergent endoscopy may actually be associated with poorer outcomes because of “inadequate resuscitation,” and suggested that “[p]atients who are hemodynamically stable, do not have ongoing hematemesis, and have melena only can generally be deferred to the following morning.”

Concerning hemostatic technique, Dr. Mullady and colleagues recommended familiarity with conventional thermal therapy and placement of hemoclips. If these approaches are unsuccessful, or deemed unlikely to succeed, they recommended an over-the-scope clip.

For ulcers “with a rigid and fibrotic base,” or those that are hard to reach, the investigators recommended monopolar hemostatic forceps with low-voltage coagulation.

According to the update, hemostatic powder should be reserved for scenarios in which bleeding is diffuse and difficult to locate.

“In most instances, hemostatic powder should be preferentially used as a rescue therapy and not for primary hemostasis, except in cases of malignant bleeding or massive bleeding with inability to perform thermal therapy or hemoclip placement,” the investigators wrote.

They noted that hemostatic powder generally dissolves in less than 24 hours, so additional treatment approaches should be considered, particular when there is a high risk of rebleeding.

When deciding between transcatheter arterial embolization (TAE) and surgery after endoscopic failure, the update calls for a comprehensive clinical assessment that incorporates patient factors, such as coagulopathy, hemodynamic instability, and multiorgan failure; bleeding etiology; potential adverse effects; and rebleeding risk.

“An important point is that prophylactic TAE of high-risk ulcers after successful endoscopic therapy is not recommended,” the investigators wrote.

Beyond these recommendations, the update includes a comprehensive discussion of relevant literature and strategies for effective clinical decision making. The discussion concludes with global remarks about the evolving role of endoscopy in managing NVUGIB, including a note about cost-effectiveness despite up-front expenses associated with some methods.

“With this expanded endoscopic armamentarium, endoscopic therapy should achieve hemostasis in the majority of patients with NVUGIB,” the investigators wrote. “Despite the increased costs of newer devices or multimodal therapy, effective hemostasis to preventing rebleeding and the need for hospital readmission is likely to be a dominant cost-saving strategy.”

Dr. Mullady disclosed relationships with Boston Scientific, ConMed, and Cook Medical.

This story was updated on 9/9/2020.

SOURCE: Mullady DK et al. Gastro. 2020 Jun 20. doi: 10.1053/j.gastro.2020.05.095.

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Helping older adults overcome the challenges of technology

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Helping older adults overcome the challenges of technology

Technology is pervasive, and for many people, it is central to their daily activities. Younger people who have been exposed to technology for their entire lives take this for granted, but older individuals often have had much less experience with it. Many technological developments that are now a part of most people’s daily life, such as personal computers, cell phones, and automated teller machines (ATMs), have occurred in the past 4 decades, with the pace accelerating in the last 15 to 20 years.

Such changes have had a substantial impact on older adults who were never exposed to these technologies during their working life. For example, an 85-year-old person who retired at age 65 would probably have not been exposed to wireless internet prior to retirement. Therefore, all of the tasks that they are now required to complete online would have been performed in other ways. Banking, accessing instruction manuals for new devices, and even scheduling and confirming health care appointments and accessing medical records all now require individuals to have a level of technological skills that many older individuals find challenging. At times, this can limit their ability to complete routine daily activities, and also can have clinical implications (Table).

Older adults and technological skills: Clinical implications

Fortunately, there are strategies clinicians can use to help their older patients face these challenges. In this article, we describe the cognitive domains associated with learning technological skills, how aging affects these domains, and what can be done to help older adults improve their technological skills.

 

Limited training on how to use new technology

Technological skills are similar to any other skills in one critical way: they need to be learned. At the same time, technological skills also differ from many other skills, such as playing a musical instrument, because of the constant updating of devices, programs, and applications. When smartphones or computers update their operating systems, the visual appearance of the screen and the way that tasks are performed also can change. Buttons can move and sequences of commands can be altered. Updates often happen with little or no notice, and users may need to navigate a completely different device landscape in order to perform tasks that they had previously mastered.

In addition, the creators/distributors of technology typically provide little training or documentation. Further, institutions such as banks or health care systems frequently do not provide any specific training for using their systems. For example, when patients are required to use technology to refill prescriptions, typically there is no training available on how the system operates.

Cognitive domains associated with technological skills

Because there are minimal opportunities to receive training in how to use most aspects of technology, users have to be able to learn by exposure and experience. This requires several different cognitive abilities to work together. In a recent review, Harvey1 described cognition and cognitive assessment in the general population, with a focus on cognitive domains. Here we discuss several of these domains in terms of the relationship to real-world functional tasks and discuss their importance for mastering technology.

Reasoning and problem solving. Because most technological devices and applications are designed to be “intuitive,” the user needs to be able to adopt a sequential approach to learning the task. For example, using the internet to refill a prescription requires several steps:

  • accessing the internet
  • finding the pharmacy web site
  • establishing a user ID and password
  • navigating the web site to the prescriptions section
  • identifying the correct prescription
  • requesting the refill
  • selecting the pickup date and time.

Continue to: After navigating these steps...

 

 

After navigating these steps, an individual still needs other cognitive abilities to refill other prescriptions later. However, executive functioning is also critical for maintaining organization across different technological demands. For example, web sites have different password rules and require frequent changes without re-using old passwords, so it becomes critical to maintain an organized list of web site addresses and their passwords.

Refilling a prescription with a telephone voice menu also requires a series of steps. Typically, this process is simpler than an internet refill, because no log-in information is necessary. However, it still requires a structured series of tasks.

Working memory refers to the ability to hold information in consciousness long enough to operate on it. At each step of the navigation process, the user needs to remember which steps he/she has already completed, because repeating steps can slow down the process or lead to error messages. Thus, remembering which steps have been completed is as critical for performing tasks as is correctly understanding the anticipated sequence of steps. Further, when a password is forgotten, the user needs to remember the newly provided password.

Working memory can be spatial as well. For example, most web sites do not display a password while it is being entered, which eliminates spatial working memory from the equation. Thus, the ability to remember which characters have been entered and which still need to be entered is necessary.

Episodic memory is the process of learning and retaining newly presented verbal or spatial information as well as recalling it later for adaptive use. After successfully using a new technology, it is critical to be able to remember what to do the next time it is used. This includes both recalling how to access the technology (including the web address, user ID, and password), recalling the steps needed to be performed and their sequence, and recognizing the buttons and instructions presented onscreen.

Continue to: Procedural memory

 

 

Procedural memory is memory for motor acts and sequences. For instance, remembering how to ride a bicycle is a procedural memory, as is the ability to perform motor acts in sequence, such as peeling, cutting, and cooking vegetables. Interestingly, procedural memory can be spared in individuals with major challenges in episodic memory, such as those with amnestic conditions or cortical dementia. Thus, it may be possible for people to continue to perform technology-based skills despite declines in episodic memory. Many current technological functional tasks have fixed sequences of events that, if remembered, can lead to increased efficiency and higher chances of success in performance of functional tasks.

Prospective memory is the ability to remember to perform tasks in the future. This can include event-related tasks (eg, enter your password before trying to make a hotel reservation on a web site) or time-related tasks (eg, refill your prescriptions next Friday). Technology can actually facilitate prospective memory by providing reminders to individuals, such as alarms for appointments. However, prospective memory is required to initially set up such alarms, and setting up confusing or incorrect alarms can impede task performance.

Processing speed is the ability to perform cognitively demanding tasks under time constraints. Traditional processing speed tasks include coding and sorting tasks, which require processing new information and effort for relatively short periods of time. In our research, we discovered that processing speed measured with traditional tests was strongly correlated with the time required to perform functional tasks such as an ATM banking task.2,3 This correlation makes sense in terms of the fact that many real-world functional tasks with technology often have a series of sequential demands that must be accomplished before progression to the next task.

Manual dexterity is also important for using technology. Many electronic devices have small, touch screen-based keyboards. Being able to touch the correct key requires dexterity and can be made more difficult by age-related vision changes, a tremor, or reduced sensation in extremities.

Cognitive changes and aging

It is normal for certain cognitive abilities to change with aging. There are a set of cognitive skills that are generally stable from early adulthood until the early “senescent” period. Some of these skills decline normatively after age 60 to 65, or earlier in some individuals. These include processing new information, solving new problems, and learning and remembering information. Referred to as “fluid intelligence,” these abilities show age-related decline during healthy aging, and even greater decline in individuals with age-related cognitive conditions.

Continue to: On the other hand...

 

 

On the other hand, some cognitive abilities do not decline with aging. These include previously acquired knowledge, such as vocabulary and mathematics skills, as well as factual information, such as academic information and the faces of familiar people. These are referred to as “crystallized intelligence,” and there is limited evidence that they decline with age. In fact, these abilities do not decline until the moderately severe stage of cortical dementias, and are commonly used to index premorbid cognitive functioning and cognitive reserve.

Why is this distinction between fluid intelligence and crystallized intelligence important? As noted above, many older people do not have early-life experience with technology. Thus, their crystallized intelligence, which is not as vulnerable to decline with aging, does not include information about how to perform many technological tasks. In contrast to today’s adolescents and young adults, older adults’ academic history typically does not include using smartphones, doing homework via Google Docs, or having homework and classwork assigned via the internet.

Learning how to use new technology requires fluid intelligence, and these abilities are less efficient in older adults. So for many older people, technological tasks can be complex and unfamiliar, and the skills needed to learn how to perform them are also more limited, even in comparison to older adults’ own ability when younger. Because many technology-based activities require concurrent performance of multiple tasks, older adults are at a disadvantage.4 It is not surprising, therefore, that a subset of older adults rate their technology skills as weak, and technology-based tasks as challenging or anxiety-provoking.

However, studies show most older adults’ attitudes toward technology remain largely positive, and that they are capable of attaining the necessary skills to use information and communication technology.4,5 An individual’s perception of his/her age, age-related beliefs, and self-efficacy are associated not only with attitudes toward technology, but possibly with cognition itself.6

Education level and socioeconomic factors also influence a person’s ability to become proficient in using technology.7-9 In fact, socioeconomic factors are more strongly related to access to the internet than age. Many older adults have internet access, but this access does not always translate into full use of its services.

Continue to: The Box...

 

 

The Box10-22 describes some of the effects of aging on the brain, and how these changes are reflected in cognitive abilities.

Box

The aging brain’s effects on cognitive function

The global baseline intensity of human brain activity, determined by indirectly measuring blood oxygenation, decreases with age.10 Multiple domains of fluid cognition decline with age; these cognitive abilities include processing speed,11,12 working memory,11 episodic memory,11 and executive function.11 Expected neuroanatomic changes of aging include a decrease in cerebral grey matter volume as well as decreased white matter integrity, which is associated with diminished executive function and impaired working memory.13 Processing speed is associated with increased white matter microstructure during neurodevelopment.14 Diminished processing speed in older adults also may predict increased mortality risk.15 Individuals with advanced age may have augmented difficulty with episodic memory, especially when they are required to integrate information from more than one source.11 Diminished hippocampal volume13 and reduced activity of the middle frontal gyrus are associated with age-related decline in episodic memory retrieval.10 Working memory16 is known to share a neurocircuitry overlap with attention processes.17 Working memory capacity also is closely associated with other cognitive functions, such as shifting and inhibition.10 Enhanced cerebellar activity is related to working memory; increased cerebellar activity is likely due to compensatory recruitment of neurons due to reduced activity in the superior frontal gyrus.10 The superior frontal gyrus contributes to both working memory as well as executive processing.10

Although the cognitive decline associated with aging is inevitable, individuals who experience cognitive decline at an increased rate are predisposed to worse outcomes. One longitudinal cohort study found that adults in their 8th and 9th decades of life with preserved cognitive function had a lower risk of disability and death.18

On the other hand, crystallized cognitive functions such as semantic memory,13 shortterm memory,13 and emotion regulation16 remain largely intact throughout the aging process. Semantic memory, a subtype of episodic memory, is related to associated facts or interpretations of previous occurrences.19 This type of memory is detached from an individual’s personal experience.20 Semantic memory loss classically presents with anomia and detectable lesions in the anterior and temporal lobes.20 Emotion regulation deficits are not a part of normal aging; in fact, emotional well-being is known to either improve or remain consistent with age.21 Emotional experiences in patients of advanced age may be more complex and unique in comparison to other cognitive abilities.22

The role of cognitive training

Existing interventions for helping older adults improve their technology proficiency generally focus on improving cognition, and not necessarily on addressing skills learning. Skills learning and cognition are related; however, the brain depends on neural plasticity for skills learning, whereas cognitive declines are a result of gradual and functional worsening of memory, processing speed, executive functioning, and attention.23 Interventions such as cognitive strategy training are capable of altering brain neurocircuitry to improve attention and memory.10,11 Other interventions known to improve cognition include exercise10 and processing speed training.24 On the other hand, skills learning is more effectively targeted by interventions that focus on stimulating realistic environments to mimic activities of daily living that involve technology.

Studies have consistently demonstrated cognitive improvements associated with computerized cognitive training (CCT). The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study was designed to evaluate the efficacy of cognitive training in 2,832 healthy adults age >65 across 6 recruitment sites in the United States.25 Participants were randomized to a control group (no treatment) or to 1 of 3 treatment groups:

  • memory strategy training (instructor-led, not computerized)
  • reasoning training (instructor-led, not computerized)
  • speed training (no instructor, adaptive computerized training).

Each treatment group received 10 sessions of classroom-based training (1 hour each, twice per week for 5 weeks). Following the intervention, participants who had completed ≥8 sessions were randomized to receive 4 booster sessions at 11 and 35 months after the initial training, or no booster sessions.

Each cognitive training program significantly improved performance on within-domain cognitive tests relative to the control group. Effect sizes were large immediately following training; they declined over time, but were still significant at 10-year follow-up. As hypothesized, training effects did not generalize to neuropsychological tests in other training domains. The booster subgroup of speed training showed improved performance on a separate functional speed measure at 2-year26 and 5-year follow-up.27 Each condition showed slower decline in instrumental activities of daily living relative to the control group.

Continue to: The Figure...

 

 

The Figure shows the type of stimuli presented in the speed training, a procedure where individuals are taught high-speed multitasking by having to identify and locate visual information quickly in a divided-attention format. A stimulus appears in the center of the screen—either a car or a truck—and at the same time, a “Route 66” sign appears in the periphery. For every successful response, the next stimulus is presented at a shorter duration after every successful response, and more slowly after errors.

Example of speed training from the ACTIVE study

Secondary outcome analyses demonstrated that for older adults, speed training reduced rates of driving cessation,27 improved driving habits, and lowered the incidence of at-fault crashes28 (based on motor vehicle records). Speed training also resulted in improvements in health-related quality of life,29,30 depression,31 locus of control,32 and medical expenditures.33 An analysis of 10-year outcomes34 found that speed training was associated with a 29% reduction in risk of developing of dementia, while the other 2 interventions were not. However, despite these multiple areas of benefit, there was no evidence that new functional skills were acquired as a result of the training.26-34

Functional skills training

While there is a long history of using functional skills training to help patients with schizophrenia, for healthy older people, there are considerably more challenges. First, aging is not a disease. Consequently, functional skills training is typically not covered by health insurance. Second, functional skills training delivered by a human trainer can be expensive and is not readily available. Finally, there are no real curricula for training functional skills, particularly those that are device-based (phone, tablet, or computer).

Recently, researchers have developed a functional skills assessment and training program that was originally piloted as a fixed difficulty simulation as described in 2 studies by Czaja et al.2,3 The original assessment was used to compare healthy control individuals with people with mild cognitive impairment (MCI) or schizophrenia. Most recently, training modules for 6 different technology-based functional tasks have been developed and piloted in samples of healthy controls and patients with MCI in a randomized trial.35 Half of the participants in each of the 2 groups were randomized to receive speed training similar to the ACTIVE study, and the other half received skills training alone. All participants were trained for 24 sessions over 12 weeks or until they mastered all 6 simulations.

Both patients with MCI and healthy controls improved in all 6 simulations. Although patients with MCI were considerably less efficient at baseline, their training gains per session were equivalent to that of healthy controls. Finally, concurrent cognitive training increased the efficiency of skills training. At the end of the study, functional gains were the same for people in both groups randomized to either condition, even though individuals in the combined cognitive and skills training interventions received only half as much skills training time.

Continue to: What to tell patients

 

 

What to tell patients

Older patients might ask their clinicians what they can do to “exercise their brain.” Let them know that CCT has been shown to improve cognitive performance in healthy older people, and that there are several evidence-based, commercially available products for this purpose. Two such self-administrable systems with supportive data are BrainHQ (www.brainhq.com) and Happy Neuron (www.happy-neuron.com). Explain that it is likely that the best strategy is a combination of cognitive and functional skills training. One commercially available functional skills training program with supportive data is i-Function (www.i-Function.com). (Editor’s note: One of the authors, PDH, is an employee of i-Function, Inc.)

Bottom Line

Clinicians should ensure older patients that they have the cognitive capacity to learn new technology-related functional skills, and that such patients have the opportunity to learn these skills. Clinicians need to be able to identify people who are at high risk of not being able to adhere to instructions and suggestions that require interactions with technology. Treatment options include computerized cognitive training and functional skills training.

Related Resources

  • Hill NT, Mowszowski L, Naismith SL, et al. Computerized cognitive training in older adults with mild cognitive impairment or dementia: a systematic review and metaanalysis. Am J Psychiatry. 2017;174(4):329-340.
  • Harvey PD, McGurk SR, Mahncke H, et al. Controversies in computerized cognitive training. Biol Psychiatry Cogn Neurosci Neuroimaging. 2018;3(11):907-915.
References

1. Harvey PD. Domains of cognition and their assessment. Dialogues Clin Neuro. 2019;21(3):227-237.
2. Czaja SJ, Loewenstein DA, Sabbag SA, et al. A novel method for direct assessment of everyday competence among older adults. J Alzheimers Dis. 2017;57(4):1229-1238.
3. Czaja SJ, Loewenstein DA, Lee CC, et al. Assessing functional performance using computer-based simulations of everyday activities. Schizophr Res. 2017;183:130-136.
4. Tsai HS, Shillair R, Cotten SR. Social support and “playing around”: an examination of how older adults acquire digital literacy with tablet computers. J Appl Gerontol. 2017;36(1):29-55.
5. Cabrita M, Tabak M, Vollenbroek-Hutten MM. Older adults’ attitudes toward ambulatory technology to support monitoring and coaching of healthy behaviors: qualitative study. JMIR Aging. 2019;2(1):e10476. doi: 10.2196/10476.
6. Lim KY, Chang KJ, Kim HJ, et al. P.5.a.010 association between memory age identity and cognition in the elderly. Eur Neuropsychopharmacol. 2010;20(suppl 3):S555.
7. Moraes C, Pinto JA Jr, Lopes MA, et al. Impact of sociodemographic and health variables on mini-mental state examination in a community-based sample of older people. Eur Arch Psychiatry Clin Neurosci. 2010;260(7):535-542.
8. Freitas S, Simões MR, Alves L, et al. The relevance of sociodemographic and health variables on MMSE normative data. Appl Neuropsychol Adult. 2015;22(4):311-319.
9. Han C, Jo SA, Jo I, et al. An adaptation of the Korean mini-mental state examination (K-MMSE) in elderly Koreans: demographic influence and population-based norms (the AGE study). Arch Gerontol Geriatr. 2008;47(3):302-310.
10. Yin S, Zhu X, Li R, et al. Intervention-induced enhancement in intrinsic brain activity in healthy older adults. Sci Rep. 2014;4:7309.
11. Bender AR, Prindle JJ, Brandmaier AM, et al. White matter and memory in healthy adults: coupled changes over two years. Neuroimage. 2016;131:193-204.
12. Guye S, von Bastian CC. Working memory training in older adults: Bayesian evidence supporting the absence of transfer. Psychol Aging. 2017;32(8):732-746.
13. Taki Y, Kinomura S, Sato K, et al. Correlation between gray/white matter volume and cognition in healthy elderly people. Brain Cogn. 2011;75(2):170-176.
14. Cassidy AR, White MT, DeMaso DR, et al. Processing speed, executive function, and academic achievement in children with dextro-transposition of the great arteries: Testing a longitudinal developmental cascade model. Neuropsychology. 2016;30(7):874-885.
15. Aichele S, Rabbitt P, Ghisletta P. Life span decrements in fluid intelligence and processing speed predict mortality risk. Psychol Aging. 2015;30(3):598-612.
16. Eich TS, Castel AD. The cognitive control of emotional versus value-based information in younger and older adults. Psychol Aging. 2016;31(5):503-512.
17. Rolle CE, Anguera JA, Skinner SN, et al. Enhancing spatial attention and working memory in younger and older adults. J Cogn Neurosci. 2017;29(9):1483-1497.
18. Yaffe K, Lindquist K, Vittinghoff E, et al. The effect of maintaining cognition on risk of disability and death. J Am Geriatr Soc. 2010;58(5):889-894.
19. Madore KP, Schacter DL. An episodic specificity induction enhances means-end problem solving in young and older adults. Psychol Aging. 2014;29(4):913-924.
20. Matthews BR. Memory dysfunction. Continuum (Minneap Minn). 2015;21(3 Behavioral Neurology and Neuropsychiatry):613-626.
21. Mather M. The emotion paradox in the aging brain. Ann N Y Acad Sci. 2012;1251(1):33-49.
22. Gurera JW, Isaacowitz DM. Emotion regulation and emotion perception in aging: A perspective on age-related differences and similarities. Prog Brain Res. 2019;247:329-351.
23. Cai L, Chan JS, Yan JH, et al. Brain plasticity and motor practice in cognitive aging. Front Aging Neurosci. 2014;6:31.
24. Cassetta BD, Tomfohr-Madsen LM, Goghari VM. A randomized controlled trial of working memory and processing speed training in schizophrenia. Psychol Med. 2019;49(12):2009-2019.
25. Ball K, Berch DB, Helmers KF, et al. Effects of cognitive training interventions with older adults: a randomized controlled trial. JAMA. 2002;288(18):2271-2281.
26. Rebok GW, Ball K, Guey LT, et al. Ten-year effects of the advanced cognitive training for independent and vital elderly cognitive training trial on cognition and everyday functioning in older adults. J Am Geriatr Soc. 2014;62(1):16-24.
27. Edwards JD, Delahunt PB, Mahncke HW. Cognitive speed of processing training delays driving cessation. J Gerontol A Biol Sci Med Sci. 2009;64(12):1262-1267.
28. Ball K, Edwards JD, Ross LA, et al. Cognitive training decreases motor vehicle collision involvement of older drivers. J Am Geriatr Soc. 2010;58(11):2107-2113.
29. Wolinsky FD, Unverzagt FW, Smith DM, et al. The effects of the ACTIVE cognitive training trial on clinically relevant declines in health-related quality of life. J Gerontol B Psychol Sci Soc Sci. 2006;61(5):S281-S287.
30. Wolinsky FD, Unverzagt FW, Smith DM, et al. The ACTIVE cognitive training trial and health-related quality of life: protection that lasts for 5 years. J Gerontol A Biol Sci Med Sci. 2006;61(12):1324-1329.
31. Wolinsky FD, Vander Weg MW, Martin R, et al. The effect of speed-of-processing training on depressive symptoms in ACTIVE. J Gerontol A Biol Sci Med Sci. 2009;64(4):468-472.
32. Wolinsky FD, Vander Weg MW, Martin R, et al. Does cognitive training improve internal locus of control among older adults? J Gerontol B Psychol Sci Soc Sci. 2010;65(5):591-598.
33. Wolinsky FD, Mahncke HW, Kosinski M, et al. The ACTIVE cognitive training trial and predicted medical expenditures. BMC Health Serv Res. 2009;9:109.
34. Edwards JD, Xu H, Clark DO, et al. Speed of processing training results in lower risk of dementia. Alzheimers Dement (N Y). 2017;3(4):603-611.
35. Harvey PD, Tibiriçá L, Kallestrup P, et al. A computerized functional skills assessment and training program targeting technology based everyday functional skills. J Vis Exp. 2020;156:e60330. doi: 10.3791/60330.

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Philip D. Harvey, PhD
Leonard M. Miller Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Vanessa Nascimento, MD, MPH
PGY-1 Psychiatry Resident
University of Miami/Jackson Health System Psychiatry Residency Training Program
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Disclosures
Dr. Harvey has received consulting fees or travel reimbursements from Alkermes, Bio Excel, Boehringer Ingelheim, Intra-Cellular Therapies, Mindstrong Health, Minerva Pharma, Regeneron Pharma, Roche Pharma, Sunovion Pharma, Takeda Pharma, and Teva. He receives royalties from the Brief Assessment of Cognition in Schizophrenia. He is Chief Scientific Officer of i-Function, Inc. He has research grants from Takeda and the Stanley Medical Research Foundation. Dr. Nascimento reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Author and Disclosure Information

Philip D. Harvey, PhD
Leonard M. Miller Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Vanessa Nascimento, MD, MPH
PGY-1 Psychiatry Resident
University of Miami/Jackson Health System Psychiatry Residency Training Program
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Disclosures
Dr. Harvey has received consulting fees or travel reimbursements from Alkermes, Bio Excel, Boehringer Ingelheim, Intra-Cellular Therapies, Mindstrong Health, Minerva Pharma, Regeneron Pharma, Roche Pharma, Sunovion Pharma, Takeda Pharma, and Teva. He receives royalties from the Brief Assessment of Cognition in Schizophrenia. He is Chief Scientific Officer of i-Function, Inc. He has research grants from Takeda and the Stanley Medical Research Foundation. Dr. Nascimento reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Author and Disclosure Information

Philip D. Harvey, PhD
Leonard M. Miller Professor of Psychiatry and Behavioral Sciences
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Vanessa Nascimento, MD, MPH
PGY-1 Psychiatry Resident
University of Miami/Jackson Health System Psychiatry Residency Training Program
Department of Psychiatry and Behavioral Sciences
University of Miami Miller School of Medicine
Miami, Florida

Disclosures
Dr. Harvey has received consulting fees or travel reimbursements from Alkermes, Bio Excel, Boehringer Ingelheim, Intra-Cellular Therapies, Mindstrong Health, Minerva Pharma, Regeneron Pharma, Roche Pharma, Sunovion Pharma, Takeda Pharma, and Teva. He receives royalties from the Brief Assessment of Cognition in Schizophrenia. He is Chief Scientific Officer of i-Function, Inc. He has research grants from Takeda and the Stanley Medical Research Foundation. Dr. Nascimento reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Technology is pervasive, and for many people, it is central to their daily activities. Younger people who have been exposed to technology for their entire lives take this for granted, but older individuals often have had much less experience with it. Many technological developments that are now a part of most people’s daily life, such as personal computers, cell phones, and automated teller machines (ATMs), have occurred in the past 4 decades, with the pace accelerating in the last 15 to 20 years.

Such changes have had a substantial impact on older adults who were never exposed to these technologies during their working life. For example, an 85-year-old person who retired at age 65 would probably have not been exposed to wireless internet prior to retirement. Therefore, all of the tasks that they are now required to complete online would have been performed in other ways. Banking, accessing instruction manuals for new devices, and even scheduling and confirming health care appointments and accessing medical records all now require individuals to have a level of technological skills that many older individuals find challenging. At times, this can limit their ability to complete routine daily activities, and also can have clinical implications (Table).

Older adults and technological skills: Clinical implications

Fortunately, there are strategies clinicians can use to help their older patients face these challenges. In this article, we describe the cognitive domains associated with learning technological skills, how aging affects these domains, and what can be done to help older adults improve their technological skills.

 

Limited training on how to use new technology

Technological skills are similar to any other skills in one critical way: they need to be learned. At the same time, technological skills also differ from many other skills, such as playing a musical instrument, because of the constant updating of devices, programs, and applications. When smartphones or computers update their operating systems, the visual appearance of the screen and the way that tasks are performed also can change. Buttons can move and sequences of commands can be altered. Updates often happen with little or no notice, and users may need to navigate a completely different device landscape in order to perform tasks that they had previously mastered.

In addition, the creators/distributors of technology typically provide little training or documentation. Further, institutions such as banks or health care systems frequently do not provide any specific training for using their systems. For example, when patients are required to use technology to refill prescriptions, typically there is no training available on how the system operates.

Cognitive domains associated with technological skills

Because there are minimal opportunities to receive training in how to use most aspects of technology, users have to be able to learn by exposure and experience. This requires several different cognitive abilities to work together. In a recent review, Harvey1 described cognition and cognitive assessment in the general population, with a focus on cognitive domains. Here we discuss several of these domains in terms of the relationship to real-world functional tasks and discuss their importance for mastering technology.

Reasoning and problem solving. Because most technological devices and applications are designed to be “intuitive,” the user needs to be able to adopt a sequential approach to learning the task. For example, using the internet to refill a prescription requires several steps:

  • accessing the internet
  • finding the pharmacy web site
  • establishing a user ID and password
  • navigating the web site to the prescriptions section
  • identifying the correct prescription
  • requesting the refill
  • selecting the pickup date and time.

Continue to: After navigating these steps...

 

 

After navigating these steps, an individual still needs other cognitive abilities to refill other prescriptions later. However, executive functioning is also critical for maintaining organization across different technological demands. For example, web sites have different password rules and require frequent changes without re-using old passwords, so it becomes critical to maintain an organized list of web site addresses and their passwords.

Refilling a prescription with a telephone voice menu also requires a series of steps. Typically, this process is simpler than an internet refill, because no log-in information is necessary. However, it still requires a structured series of tasks.

Working memory refers to the ability to hold information in consciousness long enough to operate on it. At each step of the navigation process, the user needs to remember which steps he/she has already completed, because repeating steps can slow down the process or lead to error messages. Thus, remembering which steps have been completed is as critical for performing tasks as is correctly understanding the anticipated sequence of steps. Further, when a password is forgotten, the user needs to remember the newly provided password.

Working memory can be spatial as well. For example, most web sites do not display a password while it is being entered, which eliminates spatial working memory from the equation. Thus, the ability to remember which characters have been entered and which still need to be entered is necessary.

Episodic memory is the process of learning and retaining newly presented verbal or spatial information as well as recalling it later for adaptive use. After successfully using a new technology, it is critical to be able to remember what to do the next time it is used. This includes both recalling how to access the technology (including the web address, user ID, and password), recalling the steps needed to be performed and their sequence, and recognizing the buttons and instructions presented onscreen.

Continue to: Procedural memory

 

 

Procedural memory is memory for motor acts and sequences. For instance, remembering how to ride a bicycle is a procedural memory, as is the ability to perform motor acts in sequence, such as peeling, cutting, and cooking vegetables. Interestingly, procedural memory can be spared in individuals with major challenges in episodic memory, such as those with amnestic conditions or cortical dementia. Thus, it may be possible for people to continue to perform technology-based skills despite declines in episodic memory. Many current technological functional tasks have fixed sequences of events that, if remembered, can lead to increased efficiency and higher chances of success in performance of functional tasks.

Prospective memory is the ability to remember to perform tasks in the future. This can include event-related tasks (eg, enter your password before trying to make a hotel reservation on a web site) or time-related tasks (eg, refill your prescriptions next Friday). Technology can actually facilitate prospective memory by providing reminders to individuals, such as alarms for appointments. However, prospective memory is required to initially set up such alarms, and setting up confusing or incorrect alarms can impede task performance.

Processing speed is the ability to perform cognitively demanding tasks under time constraints. Traditional processing speed tasks include coding and sorting tasks, which require processing new information and effort for relatively short periods of time. In our research, we discovered that processing speed measured with traditional tests was strongly correlated with the time required to perform functional tasks such as an ATM banking task.2,3 This correlation makes sense in terms of the fact that many real-world functional tasks with technology often have a series of sequential demands that must be accomplished before progression to the next task.

Manual dexterity is also important for using technology. Many electronic devices have small, touch screen-based keyboards. Being able to touch the correct key requires dexterity and can be made more difficult by age-related vision changes, a tremor, or reduced sensation in extremities.

Cognitive changes and aging

It is normal for certain cognitive abilities to change with aging. There are a set of cognitive skills that are generally stable from early adulthood until the early “senescent” period. Some of these skills decline normatively after age 60 to 65, or earlier in some individuals. These include processing new information, solving new problems, and learning and remembering information. Referred to as “fluid intelligence,” these abilities show age-related decline during healthy aging, and even greater decline in individuals with age-related cognitive conditions.

Continue to: On the other hand...

 

 

On the other hand, some cognitive abilities do not decline with aging. These include previously acquired knowledge, such as vocabulary and mathematics skills, as well as factual information, such as academic information and the faces of familiar people. These are referred to as “crystallized intelligence,” and there is limited evidence that they decline with age. In fact, these abilities do not decline until the moderately severe stage of cortical dementias, and are commonly used to index premorbid cognitive functioning and cognitive reserve.

Why is this distinction between fluid intelligence and crystallized intelligence important? As noted above, many older people do not have early-life experience with technology. Thus, their crystallized intelligence, which is not as vulnerable to decline with aging, does not include information about how to perform many technological tasks. In contrast to today’s adolescents and young adults, older adults’ academic history typically does not include using smartphones, doing homework via Google Docs, or having homework and classwork assigned via the internet.

Learning how to use new technology requires fluid intelligence, and these abilities are less efficient in older adults. So for many older people, technological tasks can be complex and unfamiliar, and the skills needed to learn how to perform them are also more limited, even in comparison to older adults’ own ability when younger. Because many technology-based activities require concurrent performance of multiple tasks, older adults are at a disadvantage.4 It is not surprising, therefore, that a subset of older adults rate their technology skills as weak, and technology-based tasks as challenging or anxiety-provoking.

However, studies show most older adults’ attitudes toward technology remain largely positive, and that they are capable of attaining the necessary skills to use information and communication technology.4,5 An individual’s perception of his/her age, age-related beliefs, and self-efficacy are associated not only with attitudes toward technology, but possibly with cognition itself.6

Education level and socioeconomic factors also influence a person’s ability to become proficient in using technology.7-9 In fact, socioeconomic factors are more strongly related to access to the internet than age. Many older adults have internet access, but this access does not always translate into full use of its services.

Continue to: The Box...

 

 

The Box10-22 describes some of the effects of aging on the brain, and how these changes are reflected in cognitive abilities.

Box

The aging brain’s effects on cognitive function

The global baseline intensity of human brain activity, determined by indirectly measuring blood oxygenation, decreases with age.10 Multiple domains of fluid cognition decline with age; these cognitive abilities include processing speed,11,12 working memory,11 episodic memory,11 and executive function.11 Expected neuroanatomic changes of aging include a decrease in cerebral grey matter volume as well as decreased white matter integrity, which is associated with diminished executive function and impaired working memory.13 Processing speed is associated with increased white matter microstructure during neurodevelopment.14 Diminished processing speed in older adults also may predict increased mortality risk.15 Individuals with advanced age may have augmented difficulty with episodic memory, especially when they are required to integrate information from more than one source.11 Diminished hippocampal volume13 and reduced activity of the middle frontal gyrus are associated with age-related decline in episodic memory retrieval.10 Working memory16 is known to share a neurocircuitry overlap with attention processes.17 Working memory capacity also is closely associated with other cognitive functions, such as shifting and inhibition.10 Enhanced cerebellar activity is related to working memory; increased cerebellar activity is likely due to compensatory recruitment of neurons due to reduced activity in the superior frontal gyrus.10 The superior frontal gyrus contributes to both working memory as well as executive processing.10

Although the cognitive decline associated with aging is inevitable, individuals who experience cognitive decline at an increased rate are predisposed to worse outcomes. One longitudinal cohort study found that adults in their 8th and 9th decades of life with preserved cognitive function had a lower risk of disability and death.18

On the other hand, crystallized cognitive functions such as semantic memory,13 shortterm memory,13 and emotion regulation16 remain largely intact throughout the aging process. Semantic memory, a subtype of episodic memory, is related to associated facts or interpretations of previous occurrences.19 This type of memory is detached from an individual’s personal experience.20 Semantic memory loss classically presents with anomia and detectable lesions in the anterior and temporal lobes.20 Emotion regulation deficits are not a part of normal aging; in fact, emotional well-being is known to either improve or remain consistent with age.21 Emotional experiences in patients of advanced age may be more complex and unique in comparison to other cognitive abilities.22

The role of cognitive training

Existing interventions for helping older adults improve their technology proficiency generally focus on improving cognition, and not necessarily on addressing skills learning. Skills learning and cognition are related; however, the brain depends on neural plasticity for skills learning, whereas cognitive declines are a result of gradual and functional worsening of memory, processing speed, executive functioning, and attention.23 Interventions such as cognitive strategy training are capable of altering brain neurocircuitry to improve attention and memory.10,11 Other interventions known to improve cognition include exercise10 and processing speed training.24 On the other hand, skills learning is more effectively targeted by interventions that focus on stimulating realistic environments to mimic activities of daily living that involve technology.

Studies have consistently demonstrated cognitive improvements associated with computerized cognitive training (CCT). The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study was designed to evaluate the efficacy of cognitive training in 2,832 healthy adults age >65 across 6 recruitment sites in the United States.25 Participants were randomized to a control group (no treatment) or to 1 of 3 treatment groups:

  • memory strategy training (instructor-led, not computerized)
  • reasoning training (instructor-led, not computerized)
  • speed training (no instructor, adaptive computerized training).

Each treatment group received 10 sessions of classroom-based training (1 hour each, twice per week for 5 weeks). Following the intervention, participants who had completed ≥8 sessions were randomized to receive 4 booster sessions at 11 and 35 months after the initial training, or no booster sessions.

Each cognitive training program significantly improved performance on within-domain cognitive tests relative to the control group. Effect sizes were large immediately following training; they declined over time, but were still significant at 10-year follow-up. As hypothesized, training effects did not generalize to neuropsychological tests in other training domains. The booster subgroup of speed training showed improved performance on a separate functional speed measure at 2-year26 and 5-year follow-up.27 Each condition showed slower decline in instrumental activities of daily living relative to the control group.

Continue to: The Figure...

 

 

The Figure shows the type of stimuli presented in the speed training, a procedure where individuals are taught high-speed multitasking by having to identify and locate visual information quickly in a divided-attention format. A stimulus appears in the center of the screen—either a car or a truck—and at the same time, a “Route 66” sign appears in the periphery. For every successful response, the next stimulus is presented at a shorter duration after every successful response, and more slowly after errors.

Example of speed training from the ACTIVE study

Secondary outcome analyses demonstrated that for older adults, speed training reduced rates of driving cessation,27 improved driving habits, and lowered the incidence of at-fault crashes28 (based on motor vehicle records). Speed training also resulted in improvements in health-related quality of life,29,30 depression,31 locus of control,32 and medical expenditures.33 An analysis of 10-year outcomes34 found that speed training was associated with a 29% reduction in risk of developing of dementia, while the other 2 interventions were not. However, despite these multiple areas of benefit, there was no evidence that new functional skills were acquired as a result of the training.26-34

Functional skills training

While there is a long history of using functional skills training to help patients with schizophrenia, for healthy older people, there are considerably more challenges. First, aging is not a disease. Consequently, functional skills training is typically not covered by health insurance. Second, functional skills training delivered by a human trainer can be expensive and is not readily available. Finally, there are no real curricula for training functional skills, particularly those that are device-based (phone, tablet, or computer).

Recently, researchers have developed a functional skills assessment and training program that was originally piloted as a fixed difficulty simulation as described in 2 studies by Czaja et al.2,3 The original assessment was used to compare healthy control individuals with people with mild cognitive impairment (MCI) or schizophrenia. Most recently, training modules for 6 different technology-based functional tasks have been developed and piloted in samples of healthy controls and patients with MCI in a randomized trial.35 Half of the participants in each of the 2 groups were randomized to receive speed training similar to the ACTIVE study, and the other half received skills training alone. All participants were trained for 24 sessions over 12 weeks or until they mastered all 6 simulations.

Both patients with MCI and healthy controls improved in all 6 simulations. Although patients with MCI were considerably less efficient at baseline, their training gains per session were equivalent to that of healthy controls. Finally, concurrent cognitive training increased the efficiency of skills training. At the end of the study, functional gains were the same for people in both groups randomized to either condition, even though individuals in the combined cognitive and skills training interventions received only half as much skills training time.

Continue to: What to tell patients

 

 

What to tell patients

Older patients might ask their clinicians what they can do to “exercise their brain.” Let them know that CCT has been shown to improve cognitive performance in healthy older people, and that there are several evidence-based, commercially available products for this purpose. Two such self-administrable systems with supportive data are BrainHQ (www.brainhq.com) and Happy Neuron (www.happy-neuron.com). Explain that it is likely that the best strategy is a combination of cognitive and functional skills training. One commercially available functional skills training program with supportive data is i-Function (www.i-Function.com). (Editor’s note: One of the authors, PDH, is an employee of i-Function, Inc.)

Bottom Line

Clinicians should ensure older patients that they have the cognitive capacity to learn new technology-related functional skills, and that such patients have the opportunity to learn these skills. Clinicians need to be able to identify people who are at high risk of not being able to adhere to instructions and suggestions that require interactions with technology. Treatment options include computerized cognitive training and functional skills training.

Related Resources

  • Hill NT, Mowszowski L, Naismith SL, et al. Computerized cognitive training in older adults with mild cognitive impairment or dementia: a systematic review and metaanalysis. Am J Psychiatry. 2017;174(4):329-340.
  • Harvey PD, McGurk SR, Mahncke H, et al. Controversies in computerized cognitive training. Biol Psychiatry Cogn Neurosci Neuroimaging. 2018;3(11):907-915.

Technology is pervasive, and for many people, it is central to their daily activities. Younger people who have been exposed to technology for their entire lives take this for granted, but older individuals often have had much less experience with it. Many technological developments that are now a part of most people’s daily life, such as personal computers, cell phones, and automated teller machines (ATMs), have occurred in the past 4 decades, with the pace accelerating in the last 15 to 20 years.

Such changes have had a substantial impact on older adults who were never exposed to these technologies during their working life. For example, an 85-year-old person who retired at age 65 would probably have not been exposed to wireless internet prior to retirement. Therefore, all of the tasks that they are now required to complete online would have been performed in other ways. Banking, accessing instruction manuals for new devices, and even scheduling and confirming health care appointments and accessing medical records all now require individuals to have a level of technological skills that many older individuals find challenging. At times, this can limit their ability to complete routine daily activities, and also can have clinical implications (Table).

Older adults and technological skills: Clinical implications

Fortunately, there are strategies clinicians can use to help their older patients face these challenges. In this article, we describe the cognitive domains associated with learning technological skills, how aging affects these domains, and what can be done to help older adults improve their technological skills.

 

Limited training on how to use new technology

Technological skills are similar to any other skills in one critical way: they need to be learned. At the same time, technological skills also differ from many other skills, such as playing a musical instrument, because of the constant updating of devices, programs, and applications. When smartphones or computers update their operating systems, the visual appearance of the screen and the way that tasks are performed also can change. Buttons can move and sequences of commands can be altered. Updates often happen with little or no notice, and users may need to navigate a completely different device landscape in order to perform tasks that they had previously mastered.

In addition, the creators/distributors of technology typically provide little training or documentation. Further, institutions such as banks or health care systems frequently do not provide any specific training for using their systems. For example, when patients are required to use technology to refill prescriptions, typically there is no training available on how the system operates.

Cognitive domains associated with technological skills

Because there are minimal opportunities to receive training in how to use most aspects of technology, users have to be able to learn by exposure and experience. This requires several different cognitive abilities to work together. In a recent review, Harvey1 described cognition and cognitive assessment in the general population, with a focus on cognitive domains. Here we discuss several of these domains in terms of the relationship to real-world functional tasks and discuss their importance for mastering technology.

Reasoning and problem solving. Because most technological devices and applications are designed to be “intuitive,” the user needs to be able to adopt a sequential approach to learning the task. For example, using the internet to refill a prescription requires several steps:

  • accessing the internet
  • finding the pharmacy web site
  • establishing a user ID and password
  • navigating the web site to the prescriptions section
  • identifying the correct prescription
  • requesting the refill
  • selecting the pickup date and time.

Continue to: After navigating these steps...

 

 

After navigating these steps, an individual still needs other cognitive abilities to refill other prescriptions later. However, executive functioning is also critical for maintaining organization across different technological demands. For example, web sites have different password rules and require frequent changes without re-using old passwords, so it becomes critical to maintain an organized list of web site addresses and their passwords.

Refilling a prescription with a telephone voice menu also requires a series of steps. Typically, this process is simpler than an internet refill, because no log-in information is necessary. However, it still requires a structured series of tasks.

Working memory refers to the ability to hold information in consciousness long enough to operate on it. At each step of the navigation process, the user needs to remember which steps he/she has already completed, because repeating steps can slow down the process or lead to error messages. Thus, remembering which steps have been completed is as critical for performing tasks as is correctly understanding the anticipated sequence of steps. Further, when a password is forgotten, the user needs to remember the newly provided password.

Working memory can be spatial as well. For example, most web sites do not display a password while it is being entered, which eliminates spatial working memory from the equation. Thus, the ability to remember which characters have been entered and which still need to be entered is necessary.

Episodic memory is the process of learning and retaining newly presented verbal or spatial information as well as recalling it later for adaptive use. After successfully using a new technology, it is critical to be able to remember what to do the next time it is used. This includes both recalling how to access the technology (including the web address, user ID, and password), recalling the steps needed to be performed and their sequence, and recognizing the buttons and instructions presented onscreen.

Continue to: Procedural memory

 

 

Procedural memory is memory for motor acts and sequences. For instance, remembering how to ride a bicycle is a procedural memory, as is the ability to perform motor acts in sequence, such as peeling, cutting, and cooking vegetables. Interestingly, procedural memory can be spared in individuals with major challenges in episodic memory, such as those with amnestic conditions or cortical dementia. Thus, it may be possible for people to continue to perform technology-based skills despite declines in episodic memory. Many current technological functional tasks have fixed sequences of events that, if remembered, can lead to increased efficiency and higher chances of success in performance of functional tasks.

Prospective memory is the ability to remember to perform tasks in the future. This can include event-related tasks (eg, enter your password before trying to make a hotel reservation on a web site) or time-related tasks (eg, refill your prescriptions next Friday). Technology can actually facilitate prospective memory by providing reminders to individuals, such as alarms for appointments. However, prospective memory is required to initially set up such alarms, and setting up confusing or incorrect alarms can impede task performance.

Processing speed is the ability to perform cognitively demanding tasks under time constraints. Traditional processing speed tasks include coding and sorting tasks, which require processing new information and effort for relatively short periods of time. In our research, we discovered that processing speed measured with traditional tests was strongly correlated with the time required to perform functional tasks such as an ATM banking task.2,3 This correlation makes sense in terms of the fact that many real-world functional tasks with technology often have a series of sequential demands that must be accomplished before progression to the next task.

Manual dexterity is also important for using technology. Many electronic devices have small, touch screen-based keyboards. Being able to touch the correct key requires dexterity and can be made more difficult by age-related vision changes, a tremor, or reduced sensation in extremities.

Cognitive changes and aging

It is normal for certain cognitive abilities to change with aging. There are a set of cognitive skills that are generally stable from early adulthood until the early “senescent” period. Some of these skills decline normatively after age 60 to 65, or earlier in some individuals. These include processing new information, solving new problems, and learning and remembering information. Referred to as “fluid intelligence,” these abilities show age-related decline during healthy aging, and even greater decline in individuals with age-related cognitive conditions.

Continue to: On the other hand...

 

 

On the other hand, some cognitive abilities do not decline with aging. These include previously acquired knowledge, such as vocabulary and mathematics skills, as well as factual information, such as academic information and the faces of familiar people. These are referred to as “crystallized intelligence,” and there is limited evidence that they decline with age. In fact, these abilities do not decline until the moderately severe stage of cortical dementias, and are commonly used to index premorbid cognitive functioning and cognitive reserve.

Why is this distinction between fluid intelligence and crystallized intelligence important? As noted above, many older people do not have early-life experience with technology. Thus, their crystallized intelligence, which is not as vulnerable to decline with aging, does not include information about how to perform many technological tasks. In contrast to today’s adolescents and young adults, older adults’ academic history typically does not include using smartphones, doing homework via Google Docs, or having homework and classwork assigned via the internet.

Learning how to use new technology requires fluid intelligence, and these abilities are less efficient in older adults. So for many older people, technological tasks can be complex and unfamiliar, and the skills needed to learn how to perform them are also more limited, even in comparison to older adults’ own ability when younger. Because many technology-based activities require concurrent performance of multiple tasks, older adults are at a disadvantage.4 It is not surprising, therefore, that a subset of older adults rate their technology skills as weak, and technology-based tasks as challenging or anxiety-provoking.

However, studies show most older adults’ attitudes toward technology remain largely positive, and that they are capable of attaining the necessary skills to use information and communication technology.4,5 An individual’s perception of his/her age, age-related beliefs, and self-efficacy are associated not only with attitudes toward technology, but possibly with cognition itself.6

Education level and socioeconomic factors also influence a person’s ability to become proficient in using technology.7-9 In fact, socioeconomic factors are more strongly related to access to the internet than age. Many older adults have internet access, but this access does not always translate into full use of its services.

Continue to: The Box...

 

 

The Box10-22 describes some of the effects of aging on the brain, and how these changes are reflected in cognitive abilities.

Box

The aging brain’s effects on cognitive function

The global baseline intensity of human brain activity, determined by indirectly measuring blood oxygenation, decreases with age.10 Multiple domains of fluid cognition decline with age; these cognitive abilities include processing speed,11,12 working memory,11 episodic memory,11 and executive function.11 Expected neuroanatomic changes of aging include a decrease in cerebral grey matter volume as well as decreased white matter integrity, which is associated with diminished executive function and impaired working memory.13 Processing speed is associated with increased white matter microstructure during neurodevelopment.14 Diminished processing speed in older adults also may predict increased mortality risk.15 Individuals with advanced age may have augmented difficulty with episodic memory, especially when they are required to integrate information from more than one source.11 Diminished hippocampal volume13 and reduced activity of the middle frontal gyrus are associated with age-related decline in episodic memory retrieval.10 Working memory16 is known to share a neurocircuitry overlap with attention processes.17 Working memory capacity also is closely associated with other cognitive functions, such as shifting and inhibition.10 Enhanced cerebellar activity is related to working memory; increased cerebellar activity is likely due to compensatory recruitment of neurons due to reduced activity in the superior frontal gyrus.10 The superior frontal gyrus contributes to both working memory as well as executive processing.10

Although the cognitive decline associated with aging is inevitable, individuals who experience cognitive decline at an increased rate are predisposed to worse outcomes. One longitudinal cohort study found that adults in their 8th and 9th decades of life with preserved cognitive function had a lower risk of disability and death.18

On the other hand, crystallized cognitive functions such as semantic memory,13 shortterm memory,13 and emotion regulation16 remain largely intact throughout the aging process. Semantic memory, a subtype of episodic memory, is related to associated facts or interpretations of previous occurrences.19 This type of memory is detached from an individual’s personal experience.20 Semantic memory loss classically presents with anomia and detectable lesions in the anterior and temporal lobes.20 Emotion regulation deficits are not a part of normal aging; in fact, emotional well-being is known to either improve or remain consistent with age.21 Emotional experiences in patients of advanced age may be more complex and unique in comparison to other cognitive abilities.22

The role of cognitive training

Existing interventions for helping older adults improve their technology proficiency generally focus on improving cognition, and not necessarily on addressing skills learning. Skills learning and cognition are related; however, the brain depends on neural plasticity for skills learning, whereas cognitive declines are a result of gradual and functional worsening of memory, processing speed, executive functioning, and attention.23 Interventions such as cognitive strategy training are capable of altering brain neurocircuitry to improve attention and memory.10,11 Other interventions known to improve cognition include exercise10 and processing speed training.24 On the other hand, skills learning is more effectively targeted by interventions that focus on stimulating realistic environments to mimic activities of daily living that involve technology.

Studies have consistently demonstrated cognitive improvements associated with computerized cognitive training (CCT). The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study was designed to evaluate the efficacy of cognitive training in 2,832 healthy adults age >65 across 6 recruitment sites in the United States.25 Participants were randomized to a control group (no treatment) or to 1 of 3 treatment groups:

  • memory strategy training (instructor-led, not computerized)
  • reasoning training (instructor-led, not computerized)
  • speed training (no instructor, adaptive computerized training).

Each treatment group received 10 sessions of classroom-based training (1 hour each, twice per week for 5 weeks). Following the intervention, participants who had completed ≥8 sessions were randomized to receive 4 booster sessions at 11 and 35 months after the initial training, or no booster sessions.

Each cognitive training program significantly improved performance on within-domain cognitive tests relative to the control group. Effect sizes were large immediately following training; they declined over time, but were still significant at 10-year follow-up. As hypothesized, training effects did not generalize to neuropsychological tests in other training domains. The booster subgroup of speed training showed improved performance on a separate functional speed measure at 2-year26 and 5-year follow-up.27 Each condition showed slower decline in instrumental activities of daily living relative to the control group.

Continue to: The Figure...

 

 

The Figure shows the type of stimuli presented in the speed training, a procedure where individuals are taught high-speed multitasking by having to identify and locate visual information quickly in a divided-attention format. A stimulus appears in the center of the screen—either a car or a truck—and at the same time, a “Route 66” sign appears in the periphery. For every successful response, the next stimulus is presented at a shorter duration after every successful response, and more slowly after errors.

Example of speed training from the ACTIVE study

Secondary outcome analyses demonstrated that for older adults, speed training reduced rates of driving cessation,27 improved driving habits, and lowered the incidence of at-fault crashes28 (based on motor vehicle records). Speed training also resulted in improvements in health-related quality of life,29,30 depression,31 locus of control,32 and medical expenditures.33 An analysis of 10-year outcomes34 found that speed training was associated with a 29% reduction in risk of developing of dementia, while the other 2 interventions were not. However, despite these multiple areas of benefit, there was no evidence that new functional skills were acquired as a result of the training.26-34

Functional skills training

While there is a long history of using functional skills training to help patients with schizophrenia, for healthy older people, there are considerably more challenges. First, aging is not a disease. Consequently, functional skills training is typically not covered by health insurance. Second, functional skills training delivered by a human trainer can be expensive and is not readily available. Finally, there are no real curricula for training functional skills, particularly those that are device-based (phone, tablet, or computer).

Recently, researchers have developed a functional skills assessment and training program that was originally piloted as a fixed difficulty simulation as described in 2 studies by Czaja et al.2,3 The original assessment was used to compare healthy control individuals with people with mild cognitive impairment (MCI) or schizophrenia. Most recently, training modules for 6 different technology-based functional tasks have been developed and piloted in samples of healthy controls and patients with MCI in a randomized trial.35 Half of the participants in each of the 2 groups were randomized to receive speed training similar to the ACTIVE study, and the other half received skills training alone. All participants were trained for 24 sessions over 12 weeks or until they mastered all 6 simulations.

Both patients with MCI and healthy controls improved in all 6 simulations. Although patients with MCI were considerably less efficient at baseline, their training gains per session were equivalent to that of healthy controls. Finally, concurrent cognitive training increased the efficiency of skills training. At the end of the study, functional gains were the same for people in both groups randomized to either condition, even though individuals in the combined cognitive and skills training interventions received only half as much skills training time.

Continue to: What to tell patients

 

 

What to tell patients

Older patients might ask their clinicians what they can do to “exercise their brain.” Let them know that CCT has been shown to improve cognitive performance in healthy older people, and that there are several evidence-based, commercially available products for this purpose. Two such self-administrable systems with supportive data are BrainHQ (www.brainhq.com) and Happy Neuron (www.happy-neuron.com). Explain that it is likely that the best strategy is a combination of cognitive and functional skills training. One commercially available functional skills training program with supportive data is i-Function (www.i-Function.com). (Editor’s note: One of the authors, PDH, is an employee of i-Function, Inc.)

Bottom Line

Clinicians should ensure older patients that they have the cognitive capacity to learn new technology-related functional skills, and that such patients have the opportunity to learn these skills. Clinicians need to be able to identify people who are at high risk of not being able to adhere to instructions and suggestions that require interactions with technology. Treatment options include computerized cognitive training and functional skills training.

Related Resources

  • Hill NT, Mowszowski L, Naismith SL, et al. Computerized cognitive training in older adults with mild cognitive impairment or dementia: a systematic review and metaanalysis. Am J Psychiatry. 2017;174(4):329-340.
  • Harvey PD, McGurk SR, Mahncke H, et al. Controversies in computerized cognitive training. Biol Psychiatry Cogn Neurosci Neuroimaging. 2018;3(11):907-915.
References

1. Harvey PD. Domains of cognition and their assessment. Dialogues Clin Neuro. 2019;21(3):227-237.
2. Czaja SJ, Loewenstein DA, Sabbag SA, et al. A novel method for direct assessment of everyday competence among older adults. J Alzheimers Dis. 2017;57(4):1229-1238.
3. Czaja SJ, Loewenstein DA, Lee CC, et al. Assessing functional performance using computer-based simulations of everyday activities. Schizophr Res. 2017;183:130-136.
4. Tsai HS, Shillair R, Cotten SR. Social support and “playing around”: an examination of how older adults acquire digital literacy with tablet computers. J Appl Gerontol. 2017;36(1):29-55.
5. Cabrita M, Tabak M, Vollenbroek-Hutten MM. Older adults’ attitudes toward ambulatory technology to support monitoring and coaching of healthy behaviors: qualitative study. JMIR Aging. 2019;2(1):e10476. doi: 10.2196/10476.
6. Lim KY, Chang KJ, Kim HJ, et al. P.5.a.010 association between memory age identity and cognition in the elderly. Eur Neuropsychopharmacol. 2010;20(suppl 3):S555.
7. Moraes C, Pinto JA Jr, Lopes MA, et al. Impact of sociodemographic and health variables on mini-mental state examination in a community-based sample of older people. Eur Arch Psychiatry Clin Neurosci. 2010;260(7):535-542.
8. Freitas S, Simões MR, Alves L, et al. The relevance of sociodemographic and health variables on MMSE normative data. Appl Neuropsychol Adult. 2015;22(4):311-319.
9. Han C, Jo SA, Jo I, et al. An adaptation of the Korean mini-mental state examination (K-MMSE) in elderly Koreans: demographic influence and population-based norms (the AGE study). Arch Gerontol Geriatr. 2008;47(3):302-310.
10. Yin S, Zhu X, Li R, et al. Intervention-induced enhancement in intrinsic brain activity in healthy older adults. Sci Rep. 2014;4:7309.
11. Bender AR, Prindle JJ, Brandmaier AM, et al. White matter and memory in healthy adults: coupled changes over two years. Neuroimage. 2016;131:193-204.
12. Guye S, von Bastian CC. Working memory training in older adults: Bayesian evidence supporting the absence of transfer. Psychol Aging. 2017;32(8):732-746.
13. Taki Y, Kinomura S, Sato K, et al. Correlation between gray/white matter volume and cognition in healthy elderly people. Brain Cogn. 2011;75(2):170-176.
14. Cassidy AR, White MT, DeMaso DR, et al. Processing speed, executive function, and academic achievement in children with dextro-transposition of the great arteries: Testing a longitudinal developmental cascade model. Neuropsychology. 2016;30(7):874-885.
15. Aichele S, Rabbitt P, Ghisletta P. Life span decrements in fluid intelligence and processing speed predict mortality risk. Psychol Aging. 2015;30(3):598-612.
16. Eich TS, Castel AD. The cognitive control of emotional versus value-based information in younger and older adults. Psychol Aging. 2016;31(5):503-512.
17. Rolle CE, Anguera JA, Skinner SN, et al. Enhancing spatial attention and working memory in younger and older adults. J Cogn Neurosci. 2017;29(9):1483-1497.
18. Yaffe K, Lindquist K, Vittinghoff E, et al. The effect of maintaining cognition on risk of disability and death. J Am Geriatr Soc. 2010;58(5):889-894.
19. Madore KP, Schacter DL. An episodic specificity induction enhances means-end problem solving in young and older adults. Psychol Aging. 2014;29(4):913-924.
20. Matthews BR. Memory dysfunction. Continuum (Minneap Minn). 2015;21(3 Behavioral Neurology and Neuropsychiatry):613-626.
21. Mather M. The emotion paradox in the aging brain. Ann N Y Acad Sci. 2012;1251(1):33-49.
22. Gurera JW, Isaacowitz DM. Emotion regulation and emotion perception in aging: A perspective on age-related differences and similarities. Prog Brain Res. 2019;247:329-351.
23. Cai L, Chan JS, Yan JH, et al. Brain plasticity and motor practice in cognitive aging. Front Aging Neurosci. 2014;6:31.
24. Cassetta BD, Tomfohr-Madsen LM, Goghari VM. A randomized controlled trial of working memory and processing speed training in schizophrenia. Psychol Med. 2019;49(12):2009-2019.
25. Ball K, Berch DB, Helmers KF, et al. Effects of cognitive training interventions with older adults: a randomized controlled trial. JAMA. 2002;288(18):2271-2281.
26. Rebok GW, Ball K, Guey LT, et al. Ten-year effects of the advanced cognitive training for independent and vital elderly cognitive training trial on cognition and everyday functioning in older adults. J Am Geriatr Soc. 2014;62(1):16-24.
27. Edwards JD, Delahunt PB, Mahncke HW. Cognitive speed of processing training delays driving cessation. J Gerontol A Biol Sci Med Sci. 2009;64(12):1262-1267.
28. Ball K, Edwards JD, Ross LA, et al. Cognitive training decreases motor vehicle collision involvement of older drivers. J Am Geriatr Soc. 2010;58(11):2107-2113.
29. Wolinsky FD, Unverzagt FW, Smith DM, et al. The effects of the ACTIVE cognitive training trial on clinically relevant declines in health-related quality of life. J Gerontol B Psychol Sci Soc Sci. 2006;61(5):S281-S287.
30. Wolinsky FD, Unverzagt FW, Smith DM, et al. The ACTIVE cognitive training trial and health-related quality of life: protection that lasts for 5 years. J Gerontol A Biol Sci Med Sci. 2006;61(12):1324-1329.
31. Wolinsky FD, Vander Weg MW, Martin R, et al. The effect of speed-of-processing training on depressive symptoms in ACTIVE. J Gerontol A Biol Sci Med Sci. 2009;64(4):468-472.
32. Wolinsky FD, Vander Weg MW, Martin R, et al. Does cognitive training improve internal locus of control among older adults? J Gerontol B Psychol Sci Soc Sci. 2010;65(5):591-598.
33. Wolinsky FD, Mahncke HW, Kosinski M, et al. The ACTIVE cognitive training trial and predicted medical expenditures. BMC Health Serv Res. 2009;9:109.
34. Edwards JD, Xu H, Clark DO, et al. Speed of processing training results in lower risk of dementia. Alzheimers Dement (N Y). 2017;3(4):603-611.
35. Harvey PD, Tibiriçá L, Kallestrup P, et al. A computerized functional skills assessment and training program targeting technology based everyday functional skills. J Vis Exp. 2020;156:e60330. doi: 10.3791/60330.

References

1. Harvey PD. Domains of cognition and their assessment. Dialogues Clin Neuro. 2019;21(3):227-237.
2. Czaja SJ, Loewenstein DA, Sabbag SA, et al. A novel method for direct assessment of everyday competence among older adults. J Alzheimers Dis. 2017;57(4):1229-1238.
3. Czaja SJ, Loewenstein DA, Lee CC, et al. Assessing functional performance using computer-based simulations of everyday activities. Schizophr Res. 2017;183:130-136.
4. Tsai HS, Shillair R, Cotten SR. Social support and “playing around”: an examination of how older adults acquire digital literacy with tablet computers. J Appl Gerontol. 2017;36(1):29-55.
5. Cabrita M, Tabak M, Vollenbroek-Hutten MM. Older adults’ attitudes toward ambulatory technology to support monitoring and coaching of healthy behaviors: qualitative study. JMIR Aging. 2019;2(1):e10476. doi: 10.2196/10476.
6. Lim KY, Chang KJ, Kim HJ, et al. P.5.a.010 association between memory age identity and cognition in the elderly. Eur Neuropsychopharmacol. 2010;20(suppl 3):S555.
7. Moraes C, Pinto JA Jr, Lopes MA, et al. Impact of sociodemographic and health variables on mini-mental state examination in a community-based sample of older people. Eur Arch Psychiatry Clin Neurosci. 2010;260(7):535-542.
8. Freitas S, Simões MR, Alves L, et al. The relevance of sociodemographic and health variables on MMSE normative data. Appl Neuropsychol Adult. 2015;22(4):311-319.
9. Han C, Jo SA, Jo I, et al. An adaptation of the Korean mini-mental state examination (K-MMSE) in elderly Koreans: demographic influence and population-based norms (the AGE study). Arch Gerontol Geriatr. 2008;47(3):302-310.
10. Yin S, Zhu X, Li R, et al. Intervention-induced enhancement in intrinsic brain activity in healthy older adults. Sci Rep. 2014;4:7309.
11. Bender AR, Prindle JJ, Brandmaier AM, et al. White matter and memory in healthy adults: coupled changes over two years. Neuroimage. 2016;131:193-204.
12. Guye S, von Bastian CC. Working memory training in older adults: Bayesian evidence supporting the absence of transfer. Psychol Aging. 2017;32(8):732-746.
13. Taki Y, Kinomura S, Sato K, et al. Correlation between gray/white matter volume and cognition in healthy elderly people. Brain Cogn. 2011;75(2):170-176.
14. Cassidy AR, White MT, DeMaso DR, et al. Processing speed, executive function, and academic achievement in children with dextro-transposition of the great arteries: Testing a longitudinal developmental cascade model. Neuropsychology. 2016;30(7):874-885.
15. Aichele S, Rabbitt P, Ghisletta P. Life span decrements in fluid intelligence and processing speed predict mortality risk. Psychol Aging. 2015;30(3):598-612.
16. Eich TS, Castel AD. The cognitive control of emotional versus value-based information in younger and older adults. Psychol Aging. 2016;31(5):503-512.
17. Rolle CE, Anguera JA, Skinner SN, et al. Enhancing spatial attention and working memory in younger and older adults. J Cogn Neurosci. 2017;29(9):1483-1497.
18. Yaffe K, Lindquist K, Vittinghoff E, et al. The effect of maintaining cognition on risk of disability and death. J Am Geriatr Soc. 2010;58(5):889-894.
19. Madore KP, Schacter DL. An episodic specificity induction enhances means-end problem solving in young and older adults. Psychol Aging. 2014;29(4):913-924.
20. Matthews BR. Memory dysfunction. Continuum (Minneap Minn). 2015;21(3 Behavioral Neurology and Neuropsychiatry):613-626.
21. Mather M. The emotion paradox in the aging brain. Ann N Y Acad Sci. 2012;1251(1):33-49.
22. Gurera JW, Isaacowitz DM. Emotion regulation and emotion perception in aging: A perspective on age-related differences and similarities. Prog Brain Res. 2019;247:329-351.
23. Cai L, Chan JS, Yan JH, et al. Brain plasticity and motor practice in cognitive aging. Front Aging Neurosci. 2014;6:31.
24. Cassetta BD, Tomfohr-Madsen LM, Goghari VM. A randomized controlled trial of working memory and processing speed training in schizophrenia. Psychol Med. 2019;49(12):2009-2019.
25. Ball K, Berch DB, Helmers KF, et al. Effects of cognitive training interventions with older adults: a randomized controlled trial. JAMA. 2002;288(18):2271-2281.
26. Rebok GW, Ball K, Guey LT, et al. Ten-year effects of the advanced cognitive training for independent and vital elderly cognitive training trial on cognition and everyday functioning in older adults. J Am Geriatr Soc. 2014;62(1):16-24.
27. Edwards JD, Delahunt PB, Mahncke HW. Cognitive speed of processing training delays driving cessation. J Gerontol A Biol Sci Med Sci. 2009;64(12):1262-1267.
28. Ball K, Edwards JD, Ross LA, et al. Cognitive training decreases motor vehicle collision involvement of older drivers. J Am Geriatr Soc. 2010;58(11):2107-2113.
29. Wolinsky FD, Unverzagt FW, Smith DM, et al. The effects of the ACTIVE cognitive training trial on clinically relevant declines in health-related quality of life. J Gerontol B Psychol Sci Soc Sci. 2006;61(5):S281-S287.
30. Wolinsky FD, Unverzagt FW, Smith DM, et al. The ACTIVE cognitive training trial and health-related quality of life: protection that lasts for 5 years. J Gerontol A Biol Sci Med Sci. 2006;61(12):1324-1329.
31. Wolinsky FD, Vander Weg MW, Martin R, et al. The effect of speed-of-processing training on depressive symptoms in ACTIVE. J Gerontol A Biol Sci Med Sci. 2009;64(4):468-472.
32. Wolinsky FD, Vander Weg MW, Martin R, et al. Does cognitive training improve internal locus of control among older adults? J Gerontol B Psychol Sci Soc Sci. 2010;65(5):591-598.
33. Wolinsky FD, Mahncke HW, Kosinski M, et al. The ACTIVE cognitive training trial and predicted medical expenditures. BMC Health Serv Res. 2009;9:109.
34. Edwards JD, Xu H, Clark DO, et al. Speed of processing training results in lower risk of dementia. Alzheimers Dement (N Y). 2017;3(4):603-611.
35. Harvey PD, Tibiriçá L, Kallestrup P, et al. A computerized functional skills assessment and training program targeting technology based everyday functional skills. J Vis Exp. 2020;156:e60330. doi: 10.3791/60330.

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COVID-19 and patients with serious mental illness

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COVID-19 and patients with serious mental illness

“This whole thing is not about heroism. It’s about decency. It may seem a ridiculous idea, but the only way to fight the plague is with decency . ”

– Albert Camus, La Peste (1947)1

Severe acute respiratory syndrome (SARS), H1N1 swine flu, Ebola, Zika, and Middle East respiratory syndrome (MERS): the 21st century has already been witness to several serious infectious outbreaks and pandemics,2 but none has been as deadly and consequential as the current one. The ongoing SARS-coronavirus-2 (SARS-CoV-2) pandemic is shaping not only current psychiatric care but the future of psychiatry. Now that we are beyond the initial stages of the coronavirus disease 2019 (COVID-19) pandemic, when psychiatrists had a crash course in disaster psychiatry, our attention must shift to rebuilding and managing disillusionment and other psychological fallout of the intense early days.3

In this article, we offer guidance to psychiatrists caring for patients with serious mental illness (SMI) during the SARS-CoV-2 pandemic. Patients with SMI are easily forgotten as other issues (eg, preserving ICU capacity) overshadow the already historically neglected needs of this impoverished group.4 From both human and public-health perspectives, this inattention is a mistake. Assuring psychiatric stability is critically important to prevent the spread of COVID-19 in marginalized communities comprised of individuals who are poor, members of racial minorities, and others who already experience health disparities.5 Without controlling transmission in these groups, the pandemic will not be sufficiently contained.

We begin by highlighting general principles of pandemic management because caring for patients with SMI does not occur in a vacuum. Infectious outbreaks require not only helping those who need direct medical care because they are infected, but also managing populations that are at risk of getting infected, including health care and other essential workers.

Principles of pandemic management

Delivery of medical care during a pandemic differs from routine care. An effective disaster response requires collaboration and coordination among public-health, treatment, and emergency systems. Many institutions shift to an incident management system and crisis leadership, with clear lines of authority to coordinate responders and build medical surge capacity. Such a top-down leadership approach must plan and allow for the emergence of other credible leaders and for the restoration of people’s agency.

Unfortunately, adaptive capacity may be limited, especially in the public sector and psychiatric care system, where resources are already poor. Particularly early in a pandemic, services considered non-essential—which includes most psychiatric outpatient care—can become unavailable. A major effort is needed to prevent the psychiatric care system from contracting further, as happened during 9/11.6 Additionally, “essential” cannot be conflated with “emergent,” as can easily occur in extreme circumstances. Early and sustained efforts are required to ensure that patients with SMI who may be teetering on the edge of emergency status do not slip off that edge, especially when the emergency medical system is operating over capacity.

A comprehensive outbreak response must consider that a pandemic is not only a medical crisis but a mental health crisis and a communication emergency.7 Mental health clinicians need to provide accurate information and help patients cope with their fears.

Continue to: Psychological aspects of pandemics

 

 

Psychological aspects of pandemics. Previous infectious outbreaks have reaffirmed that mental health plays an outsized role during epidemics. Chaos, uncertainty, fear of death, and loss of income and housing cause prolonged stress and exact a psychological toll.

Adverse psychological impacts include expectable, normal reactions such as stress-induced anxiety or insomnia. In addition, new-onset psychiatric illnesses or exacerbations of existing ones may emerge.8 As disillusionment and demoralization appear in the wake of the acute phase, with persistently high unemployment, suicide prevention becomes an important goal.9

Pandemics lead to expectable behavioral responses (eg, increases in substance use and interpersonal conflict). Fear-based decisions may result in unhelpful behavior, such as hoarding medications (which may result in shortages) or dangerous, unsupervised use of unproven medications (eg, hydroxychloroquine). Trust is needed to accept public-health measures, and recommendations (eg, wearing masks) must be culturally informed to be credible and effective.

Because people are affected differently, at individual, cultural, and socioeconomic levels, they will view the situation differently. For many people, secondary stressors (eg, job loss) may be more disastrous than the primary medical event (ie, the pandemic). This distinction is critical because concrete financial help, not psychiatric care, is needed. Sometimes, even when a psychiatric disorder such as SMI or major neurocognitive disorder is present, the illusion of an acute decompensation can be created by the loss of social and structural supports that previously scaffolded a person’s life.

Mental illness prevention. Community mental-health surveillance is important to monitor for distress, psychiatric symptoms, health-risk behaviors, risk and safety perception, and preparedness. Clinicians must be ready to normalize expectable and temporary distress, while recognizing when that distress becomes pathological. This may be difficult in patients with SMI who often already have reduced stress tolerance or problem-based coping skills.10

Continue to: Psychological first aid...

 

 

Psychological first aid (PFA) is a standard intervention recommended by the World Health Organization for most individuals following a disaster; it is evidence-informed and has face validity.11 Intended to relieve distress by creating an environment that is safe, calm, and connected, PFA fosters self-efficacy and hope. While PFA is a form of universal prevention, it is not designed for patients with SMI, is not a psychiatric intervention, and is not provided by clinicians. Its principles, however, can easily be applied to patients with SMI to prevent distressing symptoms from becoming a relapse.

Communication. Good risk and crisis communication are critical because individual and population behavior will be governed by the perception of risk and fear, and not by facts. Failure to manage the “infodemic”7—with its misinformation, contradictory messages, and rumors—jeopardizes infection control if patients become paralyzed by uncertainty and fear. Scapegoating occurs easily during times of threat, and society must contain the parallel epidemic of xenophobia based on stigma and misinformation.12

Decision-making under uncertainty is not perfect and subject to revision as better information becomes available. Pointing this out to the public is delicate but essential to curtail skepticism and mistrust when policies are adjusted in response to new circumstances and knowledge.

Mistrust of an authority’s legitimacy and fear-based decisions lead to lack of cooperation with public-health measures, which can undermine an effective response to the pandemic. Travel restrictions or quarantine measures will not be followed if individuals question their importance. Like the general public, patients need education and clear communication to address their fear of contagion, dangers posed to family (and pets), and mistrust of authority and government. A lack of appreciation of the seriousness of the pandemic and individual responsibility may need to be addressed. Two important measures to accomplish this are steering patients to reputable sources of information and advising that they limit media exposure.

Resilience-building. Community and workplace resilience are important aspects of making it through a disaster as best as possible. Resilience is not innate and fixed; it must be deliberately built.13 Choosing an attitude of post-traumatic growth over the victim narrative is a helpful stance. Practicing self-care (rest, nutrition, exercise) and self-compassion (self-kindness, common humanity, mindfulness) is good advice for patients and caregivers alike.

Continue to: Workforce protection

 

 

Workforce protection. Compared to other disasters, infectious outbreaks disproportionally affect the medical community, and care delivery is at stake. While psychological and psychiatric needs may increase during a pandemic, services often contract, day programs and clinics close, teams are reduced to skeleton crews, and only emergency psychiatric care is available. Workforce protection is critical to avoid illness or simple absenteeism due to mistrust of protective measures.

Only a well-briefed, well-led, well-supported, and adequately resourced workforce is going to be effective in managing this public-health emergency. Burnout and moral injury are feared long-term consequences for health care workers that need to be proactively addressed.14 As opposed to other forms of disasters, managing your own fears about safety is important. Clinicians and their patients sit in the proverbial same boat.

Ethics. The anticipated need to ration life-saving care (eg, ventilators) has been at the forefront of ethical concerns.15 In psychiatry, the question of involuntary public-health interventions for uncooperative psychiatric patients sits uncomfortably between public-health ethics and human rights, and is an opportunity for collaboration with public-health and infectious-disease colleagues.

Redeployed clinicians and those working under substandard conditions may be concerned about civil liability due to a modified standard of care during a crisis. Some clinicians may ask if their duty to care must override their natural instinct to protect themselves. There is a lot of room for resentment in these circumstances. Redeployed or otherwise “conscripted” clinicians may resent administrators, especially those administering from the safety of their homes. Those “left behind” to work in potentially precarious circumstances may resent their absent colleagues. Moreover, these front-line clinicians may have been forced to make ethical decisions for which they were not prepared.16 Maintaining morale is far from trivial, not just during the pandemic, but afterward, when (and if) the entire workforce is reunited. All parties need to be mindful of how their actions and decisions impact and are perceived by others, both in the hospital and at home.

Managing patients with SMI during COVID-19

Patients with SMI are potentially hard hit by COVID-19 due to a “tragic” epidemiologic triad of agent-host-environment: SARS-CoV-2 is a highly infectious agent affecting patients with SMI who are vulnerable hosts in permissive environments (Figure).

‘Tragic’ epidemiologic triad for patients with SMI

Continue to: While not as infectious as measles...

 

 

While not as infectious as measles, COVID-19 is more infectious than the seasonal flu virus.17 It can lead to uncontrolled infection within a short period of time, particularly in enclosed settings. Outbreaks have occurred readily on cruise ships and aircraft carriers as well as in nursing homes, homeless shelters, prisons, and group homes.

Patients with SMI are vulnerable hosts because they have many of the medical risk factors18 that portend a poor prognosis if they become infected, including pre-existing lung conditions and heart disease19 as well as diabetes and obesity.20 Obesity likely creates a hyperinflammatory state and a decrease in vital capacity. Patient-related behavioral factors include poor early-symptom reporting and ineffective infection control.

Unfavorable social determinants of health include not only poverty but crowded housing that is a perfect incubator for COVID-19.

Priority treatment goals. The overarching goal during a pandemic is to keep patients with SMI in psychiatric treatment and prevent them from disengaging from care in the service of infection control. Urgent tasks include infection control, relapse prevention, and preventing treatment disengagement and loneliness.

Infection control. As trusted sources of information, psychiatrists can play an important role in infection control in several important ways:

  • educating patients about infection-control measures and public-health recommendations
  • helping patients understand what testing can accomplish and when to pursue it
  • encouraging protective health behaviors (eg, hand washing, mask wearing, physical distancing)
  • assessing patients’ risk appreciation
  • assessing for and addressing obstacles to implementing and complying with infection-control measures
  • explaining contact tracing
  • providing reassurance.

Continue to: Materials and explanations...

 

 

Materials and explanations must be adapted for patient understanding.

Patients with disorganization or cognitive disturbances may have difficulties cooperating or problem-solving. Patients with negative symptoms may be inappropriately unconcerned and also inaccurately report symptoms that suggest COVID-19. Acute psychosis or mania can prevent patients from complying with public-health efforts. Some measures may be difficult to implement if the means are simply not there (eg, physical distancing in a crowded apartment). Previously open settings (eg, group homes) have had to develop new mechanisms under the primacy of infection control. Inpatient units—traditionally places where community, shared healing, and group therapy are prized—have had to decrease maximum occupancy, limit the number of patients attending groups, and discourage or outrightly prohibit social interaction (eg, dining together).

Relapse prevention. Patients who take maintenance medications need to be supported. A manic or psychotic relapse during a pandemic puts patients at risk of acquiring and spreading COVID-19. “Treatment as prevention” is a slogan from human immunodeficiency virus (HIV) care that captures the importance of antiretroviral treatment to prevent medical complications from HIV, and also to reduce infecting other people. By analogy, psychiatric treatment for patients with SMI can prevent psychiatric instability and thereby control viral transmission. Avoiding sending psychiatric patients to a potentially stressed acute-care system is important.

Psychosocial support. Clinics need to ensure that patients continue to engage in care beyond medication-taking to proactively prevent psychiatric exacerbations. Healthful, resilience-building behaviors should be encouraged while monitoring and counseling against maladaptive ones (eg, increased substance use). Supporting patients emotionally and helping them solve problems are critical, particularly for those who are subjected to quarantine or isolation. Obviously, in these latter situations, outreach will be necessary and may require creative delivery systems and dedicated clinicians for patients who lack access to the technology necessary for virtual visits. Havens and Ghaemi21 have suggested that a good therapeutic alliance can be viewed as a mood stabilizer. Helping patients grieve losses (loved ones, jobs, sense of safety) may be an important part of support.

Even before COVID-19, loneliness was a major factor for patients with schizophrenia.22 A psychiatric clinic is one aspect of a person with SMI’s social network; during the initial phase of the pandemic, many clinics and treatment programs closed. Patients for whom clinics structure and anchor their activities are at high risk of disconnecting from treatment, staying at home, and becoming lonely.

Continue to: Caregivers are always important...

 

 

Caregivers are always important to SMI patients, but they may assume an even bigger role during this pandemic. Some patients may have moved in with a relative, after years of living on their own. In other cases, stable caregiver relationships may be disrupted due to COVID-19–related sickness in the caregiver; if not addressed, this can result in a patient’s clinical decompensation. Clinicians should take the opportunity to understand who a patient’s caregivers are (group home staff, families) and rekindle clinical contact with them. Relationships with caregivers that may have been on “autopilot” during normal times are opportunities for welcome support and guidance, to the benefit of both patients and caregivers.

Table 1 summarizes clinical tasks that need to be kept in mind when conducting clinic visits during COVID-19 in order to achieve the high-priority treatment goals of infection control, relapse prevention, and psychosocial support.

Clinical tasks for patients with SMI during the COVID-19 pandemic

Differential diagnosis. Neuropsychiatric syndromes have long been observed in influenza pandemics,23 due both to direct viral effects and to the effects of critical illness on the brain. Two core symptoms of COVID-19—anosmia and ageusia—suggest that COVID-19 can directly affect the brain. While neurologic manifestations are common,24 it remains unclear to what extent COVID-19 can directly “cause” psychiatric symptoms, or if such symptoms are the result of cytokines25 or other medical processes (eg, thromboembolism).26 Psychosis due to COVID-19 may, in some cases, represent a stress-related brief psychotic disorder.27

Hospitalized patients who have recovered from COVID-19 may have experienced prolonged sedation and severe delirium in an ICU.28 Complications such as posttraumatic stress disorder,29 hypoperfusion-related brain injuries, or other long-term cognitive difficulties may result. In previous flu epidemics, patients developed serious neurologic complications such as post-encephalitic Parkinson’s disease.30

Any person subjected to isolation or quarantine is at risk for psychiatric complications.31 Patients with SMI who live in group homes may be particularly susceptible to new rules, including no-visitor policies.

Continue to: Outpatients whose primary disorder...

 

 

Outpatients whose primary disorder is well controlled may, like anyone else, struggle with the effects of the pandemic. It is necessary to carefully differentiate non-specific symptoms associated with stress from the emergence of a new disorder resulting from stress.32 For some patients, grief or adjustment disorders should be considered. Prolonged stress and uncertainty may eventually lead to an exacerbation of a primary disorder, particularly if the situation (eg, financial loss) does not improve or worsens. Demoralization and suicidal thinking need to be monitored. Relapse or increased use of alcohol or other substances as a response to stress may also complicate the clinical picture.33 Last, smoking cessation as a major treatment goal in general should be re-emphasized and not ignored during the ongoing pandemic.34

Psychiatric symptoms in patients with SMI during the COVID-19 pandemic

Table 2 summarizes psychiatric symptoms that need to be considered when managing a patient with SMI during this pandemic.

Treatment tools

Psychopharmacology. Even though crisis-mode prescribing may be necessary, the safe use of psychotropics remains the goal of psychiatric prescribing. Access to medications becomes a larger consideration; for many patients, a 90-day supply may be indicated. Review of polypharmacy, including for pneumonia risk, should be undertaken. Preventing drooling (eg, from sedation, clozapine, extrapyramidal symptoms [EPS]) will decrease aspiration risk.

 

In general, treatment of psychiatric symptoms in a patient with COVID-19 follows usual guidelines. The best treatment for COVID-19 patients with delirium, however, remains to be established, particularly how to manage severe agitation.28 Pharmacodynamic and pharmacokinetic drug–drug interactions between psychotropics and antiviral treatments for COVID-19 (eg, QTc prolongation) can be expected and need to be reviewed.35 For stress-related anxiety, judicious pharmacotherapy can be helpful. Diazepam given at the earliest signs of a psychotic relapse may stave off a relapse for patients with schizophrenia.36 Even if permitted under relaxed prescribing rules during a public-health emergency, prescribing controlled substances without seeing patients in person requires additional thought. In some cases, adjusting the primary medication to buffer against stress may be preferred (eg, adjusting an antipsychotic in a patient on maintenance treatment for schizophrenia, particularly if a low-dose strategy is pursued).

Consensus statement on the use of clozapine during the COVID-19 pandemic

Clozapine requires registry-based prescribing and bloodwork (“no blood, no drug”). The use of clozapine during this public-health emergency has been made easier because of FDA guidance that allows clozapine to be dispensed without blood work if obtaining blood work is not possible (eg, a patient is quarantined) or can be accomplished only at substantial risk to patients and the population at large. Under certain conditions, clozapine can be dispensed safely and in a way that is consistent with infection prevention. Clozapine-treated patients admitted with COVID-19 should be monitored for clozapine toxicity and the clozapine dose adjusted.37 A consensus statement consistent with the FDA and clinical considerations for using clozapine during COVID-19 is summarized in Table 3.38

Continue to: Long-acting injectable antipsychotics...

 

 

Long-acting injectable antipsychotics (LAIs) pose a problem because they require in-person visits. Ideally, during a pandemic, patients should be seen in person as frequently as medically necessary but as infrequently as possible to limit exposure of both patients and staff. Table 4 provides some clinical recommendations on how to use LAIs during the pandemic.39

Use of long-acting injectable antipsychotics during the COVID-19 pandemic

Supportive psychotherapy may be the most important tool we have in helping patients with loss and uncertainty during these challenging months.40 Simply staying in contact with patients plays a major role in preventing care discontinuity. Even routine interactions have become stressful, with everyone wearing a mask that partially obscures the face. People with impaired hearing may find it even more difficult to understand you.

Education, problem-solving, and a directive, encouraging style are major tools of supportive psychotherapy to reduce symptoms and increase adaptive skills. Clarify that social distancing refers to physical, not emotional, distancing. The judicious and temporary use of anxiolytics is appropriate to reduce anxiety. Concrete help and problem-solving (eg, filling out forms) are examples of proactive crisis intervention.

Telepsychiatry emerged in the pandemic’s early days as the default mode of practice in order to limit in-person contacts.41 Like all new technology, telepsychiatry brings progress and peril.42 While it has gone surprisingly well for most, the “digital divide” does not afford all patients access to the needed technology. The long-term effectiveness and acceptance of telehealth remain to be seen. (Editor’s Note: For more about this topic, see “Telepsychiatry: What you need to know.” Current Psychiatry. 2020;19[6]:16-23.)

Lessons learned and outlook

Infectious outbreaks have historically inflicted long-term disruptions on societies and altered the course of history. However, each disaster is unique, and lessons from previous disasters may only partially apply.43 We do not yet know how this one will end, including how long it will take for the world’s economies to recover. If nothing else, the current public-health emergency has brought to the forefront what psychiatrists have always known: health disparities are partially responsible for different disease risks (in this case, the risk of getting infected with SARS-CoV-2).5 It may not be a coincidence that the Black Lives Matter movement is becoming a major impetus for social change at a time when the pandemic is exposing health-care inequalities.

Continue to: Some areas of the country...

 

 

Some areas of the country succeeded in reducing infections and limiting community spread, which ushered in an uneasy sense of normalcy even while the pandemic continues. At least for now, these locales can focus on rebuilding and preparing for expectable fluctuations in disease activity, including the arrival of the annual flu season on top of COVID-19.44 Recovery is not a return to the status quo ante but building stronger communities—“building back better.”45 Unless there is a continuum of care, shortcomings in one sector will have ripple effects through the entire system, particularly for psychiatric care for patients with SMI, which was inadequate before the pandemic.

Ensuring access to critical care was a priority during the pandemic’s early phase but came at the price of deferring other types of care, such as routine primary care; the coming months will see the downstream consequences of this approach,46 including for patients with SMI.

In the meantime, doing our job as clinicians, as Camus’s fictitious Dr. Bernard Rieux from the epigraph responds when asked how to define decency, may be the best we can do in these times. This includes contributing to and molding our field’s future and fostering a sense of agency in our patients and in ourselves. Major goals will be to preserve lessons learned, maintain flexibility, and avoid a return to unhelpful overregulation and payment models that do not reflect the flexible, person-centered care so important for patients with SMI.47

Bottom Line

During a pandemic, patients with serious mental illness may be easily forgotten as other issues overshadow the needs of this impoverished group. During a pandemic, the priority treatment goals for these patients are infection control, relapse prevention, and preventing treatment disengagement and loneliness. A pandemic requires changes in how patients with serious mental illness will receive psychopharmacology and psychotherapy.

Related Resources

Drug Brand Names

Clozapine • Clozaril
Diazepam • Valium
Hydroxychloroquine • Plaquenil

References

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2. Huremovic´ D. Brief history of pandemics (pandemics throughout history). In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019:7-35.
3. Substance Abuse and Mental Health Services Administration. Phases of disaster. https://www.samhsa.gov/dtac/recovering-disasters/phases-disaster. Updated June 17, 2020. Accessed August 7, 2020.
4. Geller J. COVID-19 and advocacy—the good and the unacceptable. Psychiatric News. https://psychnews.psychiatryonline.org/doi/10.1176/appi.pn.2020.5b13. Published May 7, 2020. Accessed August 7, 2020.
5. Webb Hooper M, Nápoles AM, Perez-Stable EJ. COVID-19 and racial/ethnic disparities. JAMA. 2020;323(24):2466-2467.
6. Sederer LI, Lanzara CB, Essock SM, et al. Lessons learned from the New York State mental health response to the September 11, 2001, attacks. Psychiatr Serv. 2011;62(9):1085-1089.
7. World Health Organization. Infodemic management – infodemiology. https://www.who.int/teams/risk-communication/infodemic-management. Accessed August 7, 2020.
8. Zhou J, Liu L, Xue P, et al. Mental health response to the COVID-19 outbreak in China. Am J Psychiatry. 2020;117(7):574-575.
9. Kawohl W, Nordt C. COVID-19, unemployment, and suicide. Lancet Psychiatry. 2020;7(5):389-390.
10. Yao H, Chen JH, Xu YF. Patients with mental health disorders in the COVID-19 epidemic. Lancet Psychiatry. 2020;7(4):e21. doi: 10.1016/S2215-0366(20)30090-0.
11. Minihan E, Gavin B, Kelly BD, et al. Covid-19, mental health and psychological first aid. Ir J Psychol Med. 2020:1-12.
12. Adja KYC, Golinelli D, Lenzi J, et al. Pandemics and social stigma: who’s next? Italy’s experience with COVID-19. Public Health. 2020;185:39-41.
13. Rosenberg AR. Cultivating deliberate resilience during the coronavirus disease 2019 pandemic [published online April 14, 2020]. JAMA Pediatr. doi: 10.1001/jamapediatrics.2020.1436.
14. Dean W, Talbot SG, Caplan A. Clarifying the language of clinician distress [published online January 31, 2020]. JAMA. doi: 10.1001/jama.2019.21576.
15. Emanuel EJ, Persad G, Upshur R, et al. Fair allocation of scarce medical resources in the time of Covid-19. N Engl J Med. 2020;382(21):2049-2055.
16. Rosenbaum L. Facing Covid-19 in Italy - ethics, logistics, and therapeutics on the epidemic’s front line. N Engl J Med. 2020;382(20):1873-1875.
17. Viceconte G, Petrosillo N. COVID-19 R0: magic number or conundrum? Infect Dis Rep. 2020;12(1):8516.
18. de Hert M, Schreurs V, Vancampfort D, van Winkel R. Metabolic syndrome in people with schizophrenia: a review. World Psychiatry. 2009;8(1):15-22.
19. Chen R, Liang W, Jiang M, et al. Risk factors of fatal outcome in hospitalized subjects with coronavirus disease 2019 from a nationwide analysis in China. Chest. 2020;158(1):97-105.
20. Finer N, Garnett SP, Bruun JM. COVID-19 and obesity. Clin Obes. 2020;10(3):e12365. doi: 10.1111/cob.12365.
21. Havens LL, Ghaemi SN. Existential despair and bipolar disorder: the therapeutic alliance as a mood stabilizer. Am J Psychother. 2005;59(2):137-147.
22. Trémeau F, Antonius D, Malaspina D, et al. Loneliness in schizophrenia and its possible correlates. An exploratory study. Psychiatry Res. 2016;246:211-217.
23. Menninger KA. Psychoses associated with influenza: I. General data: statistical analysis. JAMA. 1919;72(4):235-241.
24. Asadi-Pooya AA, Simani L. Central nervous system manifestations of COVID-19: a systematic review. J Neurol Sci. 2020;413:116832. doi: 10.1016/j.jns.2020.116832.
25. Ferrando SJ, Klepacz L, Lynch S, et al. COVID-19 psychosis: a potential new neuropsychiatric condition triggered by novel coronavirus infection and the inflammatory response? [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.012.
26. Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;87:34-39.
27. Martin Jr. EB. Brief psychotic disorder triggered by fear of coronavirus? Psychiatric Times. https://www.psychiatrictimes.com/view/brief-psychotic-disorder-triggered-fear-coronavirus-small-case-series. Published May 8, 2020. Accessed August 7, 2020.
28. Sher Y, Rabkin B, Maldonado JR, et al. COVID-19-associated hyperactive intensive care unit delirium with proposed pathophysiology and treatment: a case report [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.007.
29. Wolters AE, Peelen LM, Welling MC, et al. Long-term mental health problems after delirium in the ICU. Crit Care Med. 2016;44(10):1808-1813.
30. Toovey S. Influenza-associated central nervous system dysfunction: a literature review. Travel Med Infect Dis. 2008;6(3):114-124.
31. Brooks SK, Webster RK, Smith LE, et al. The psychological impact of quarantine and how to reduce it: rapid review of the evidence. Lancet. 2020;395(10227):912-920.
32. Maercker A, Brewin CR, Bryant RA, et al. Diagnosis and classification of disorders specifically associated with stress: proposals for ICD-11. World Psychiatry. 2013;12(3):198-206.
33. Ornell F, Moura HF, Scherer JN, et al. The COVID-19 pandemic and its impact on substance use: implications for prevention and treatment. Psychiatry Res. 2020;289:113096. doi: 10.1016/j.psychres.2020.113096.
34. Berlin I, Thomas D, Le Faou AL, Cornuz J. COVID-19 and smoking [published online April 3, 2020]. Nicotine Tob Res. https://doi.org/10.1093/ntr/ntaa059.
35. Back D, Marzolini C, Hodge C, et al. COVID-19 treatment in patients with comorbidities: awareness of drug-drug interactions [published online May 8, 2020]. Br J Clin Pharmacol. doi: 10.1111/bcp.14358.
36. Carpenter WT Jr., Buchanan RW, Kirkpatrick B, et al. Diazepam treatment of early signs of exacerbation in schizophrenia. Am J Psychiatry. 1999;156(2):299-303.
37. Dotson S, Hartvigsen N, Wesner T, et al. Clozapine toxicity in the setting of COVID-19 [published online May 30, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.025.
38. Siskind D, Honer WG, Clark S, et al. Consensus statement on the use of clozapine during the COVID-19 pandemic. J Psychiatry Neurosci. 2020;45(3):222-223.
39. Schnitzer K, MacLaurin S, Freudenreich O. Long-acting injectable antipsychotics during the COVID-19 pandemic. Current Psychiatry. In press.
40. Winston A, Rosenthal RN, Pinsker H. Learning supportive psychotherapy: an illustrated guide. Washington, DC: American Psychiatric Publishing; 2012.
41. Hollander JE, Carr BG. Virtually perfect? Telemedicine for Covid-19. N Engl J Med. 2020;382(18):1679-1681.
42. Jordan A, Dixon LB. Considerations for telepsychiatry service implementation in the era of COVID-19. Psychiatr Serv. 2020;71(6):643-644.
43. DePierro J, Lowe S, Katz C. Lessons learned from 9/11: mental health perspectives on the COVID-19 pandemic. Psychiatry Res. 2020;288:113024.
44. Hussain S. Immunization and vaccination. In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019.
45. Epping-Jordan JE, van Ommeren M, Ashour HN, et al. Beyond the crisis: building back better mental health care in 10 emergency-affected areas using a longer-term perspective. Int J Ment Health Syst. 2015;9:15.
46. Rosenbaum L. The untold toll - the pandemic’s effects on patients without Covid-19. N Engl J Med. 2020;382(24):2368-2371.
47. Bartels SJ, Baggett TP, Freudenreich O, et al. COVID-19 emergency reforms in Massachusetts to support behavioral health care and reduce mortality of people with serious mental illness [published online June 3, 2020]. Psychiatr Serv. doi: 10.1176/appi.ps.202000244.

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Author and Disclosure Information

Oliver Freudenreich, MD, FACLP
Co-Director, MGH Schizophrenia Clinical and Research Program
Associate Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

Nicholas Kontos, MD, FACLP
Director, Fellowship in Consultation-Liaison Psychiatry
Assistant Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

John Querques, MD
Vice Chairman for Hospital Services
Department of Psychiatry
Tufts Medical Center
Associate Professor of Psychiatry
Tufts University School of Medicine
Boston, Massachusetts

Disclosures
Dr. Freudenreich has received grant or research support from Alkermes, Avanir, Janssen, and Otsuka, and has served as a consultant to American Psychiatric Association, Alkermes, Janssen, Neurocrine, Novartis, and Roche. Dr. Kontos and Dr. Querques report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Author and Disclosure Information

Oliver Freudenreich, MD, FACLP
Co-Director, MGH Schizophrenia Clinical and Research Program
Associate Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

Nicholas Kontos, MD, FACLP
Director, Fellowship in Consultation-Liaison Psychiatry
Assistant Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

John Querques, MD
Vice Chairman for Hospital Services
Department of Psychiatry
Tufts Medical Center
Associate Professor of Psychiatry
Tufts University School of Medicine
Boston, Massachusetts

Disclosures
Dr. Freudenreich has received grant or research support from Alkermes, Avanir, Janssen, and Otsuka, and has served as a consultant to American Psychiatric Association, Alkermes, Janssen, Neurocrine, Novartis, and Roche. Dr. Kontos and Dr. Querques report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Author and Disclosure Information

Oliver Freudenreich, MD, FACLP
Co-Director, MGH Schizophrenia Clinical and Research Program
Associate Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

Nicholas Kontos, MD, FACLP
Director, Fellowship in Consultation-Liaison Psychiatry
Assistant Professor of Psychiatry
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

John Querques, MD
Vice Chairman for Hospital Services
Department of Psychiatry
Tufts Medical Center
Associate Professor of Psychiatry
Tufts University School of Medicine
Boston, Massachusetts

Disclosures
Dr. Freudenreich has received grant or research support from Alkermes, Avanir, Janssen, and Otsuka, and has served as a consultant to American Psychiatric Association, Alkermes, Janssen, Neurocrine, Novartis, and Roche. Dr. Kontos and Dr. Querques report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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“This whole thing is not about heroism. It’s about decency. It may seem a ridiculous idea, but the only way to fight the plague is with decency . ”

– Albert Camus, La Peste (1947)1

Severe acute respiratory syndrome (SARS), H1N1 swine flu, Ebola, Zika, and Middle East respiratory syndrome (MERS): the 21st century has already been witness to several serious infectious outbreaks and pandemics,2 but none has been as deadly and consequential as the current one. The ongoing SARS-coronavirus-2 (SARS-CoV-2) pandemic is shaping not only current psychiatric care but the future of psychiatry. Now that we are beyond the initial stages of the coronavirus disease 2019 (COVID-19) pandemic, when psychiatrists had a crash course in disaster psychiatry, our attention must shift to rebuilding and managing disillusionment and other psychological fallout of the intense early days.3

In this article, we offer guidance to psychiatrists caring for patients with serious mental illness (SMI) during the SARS-CoV-2 pandemic. Patients with SMI are easily forgotten as other issues (eg, preserving ICU capacity) overshadow the already historically neglected needs of this impoverished group.4 From both human and public-health perspectives, this inattention is a mistake. Assuring psychiatric stability is critically important to prevent the spread of COVID-19 in marginalized communities comprised of individuals who are poor, members of racial minorities, and others who already experience health disparities.5 Without controlling transmission in these groups, the pandemic will not be sufficiently contained.

We begin by highlighting general principles of pandemic management because caring for patients with SMI does not occur in a vacuum. Infectious outbreaks require not only helping those who need direct medical care because they are infected, but also managing populations that are at risk of getting infected, including health care and other essential workers.

Principles of pandemic management

Delivery of medical care during a pandemic differs from routine care. An effective disaster response requires collaboration and coordination among public-health, treatment, and emergency systems. Many institutions shift to an incident management system and crisis leadership, with clear lines of authority to coordinate responders and build medical surge capacity. Such a top-down leadership approach must plan and allow for the emergence of other credible leaders and for the restoration of people’s agency.

Unfortunately, adaptive capacity may be limited, especially in the public sector and psychiatric care system, where resources are already poor. Particularly early in a pandemic, services considered non-essential—which includes most psychiatric outpatient care—can become unavailable. A major effort is needed to prevent the psychiatric care system from contracting further, as happened during 9/11.6 Additionally, “essential” cannot be conflated with “emergent,” as can easily occur in extreme circumstances. Early and sustained efforts are required to ensure that patients with SMI who may be teetering on the edge of emergency status do not slip off that edge, especially when the emergency medical system is operating over capacity.

A comprehensive outbreak response must consider that a pandemic is not only a medical crisis but a mental health crisis and a communication emergency.7 Mental health clinicians need to provide accurate information and help patients cope with their fears.

Continue to: Psychological aspects of pandemics

 

 

Psychological aspects of pandemics. Previous infectious outbreaks have reaffirmed that mental health plays an outsized role during epidemics. Chaos, uncertainty, fear of death, and loss of income and housing cause prolonged stress and exact a psychological toll.

Adverse psychological impacts include expectable, normal reactions such as stress-induced anxiety or insomnia. In addition, new-onset psychiatric illnesses or exacerbations of existing ones may emerge.8 As disillusionment and demoralization appear in the wake of the acute phase, with persistently high unemployment, suicide prevention becomes an important goal.9

Pandemics lead to expectable behavioral responses (eg, increases in substance use and interpersonal conflict). Fear-based decisions may result in unhelpful behavior, such as hoarding medications (which may result in shortages) or dangerous, unsupervised use of unproven medications (eg, hydroxychloroquine). Trust is needed to accept public-health measures, and recommendations (eg, wearing masks) must be culturally informed to be credible and effective.

Because people are affected differently, at individual, cultural, and socioeconomic levels, they will view the situation differently. For many people, secondary stressors (eg, job loss) may be more disastrous than the primary medical event (ie, the pandemic). This distinction is critical because concrete financial help, not psychiatric care, is needed. Sometimes, even when a psychiatric disorder such as SMI or major neurocognitive disorder is present, the illusion of an acute decompensation can be created by the loss of social and structural supports that previously scaffolded a person’s life.

Mental illness prevention. Community mental-health surveillance is important to monitor for distress, psychiatric symptoms, health-risk behaviors, risk and safety perception, and preparedness. Clinicians must be ready to normalize expectable and temporary distress, while recognizing when that distress becomes pathological. This may be difficult in patients with SMI who often already have reduced stress tolerance or problem-based coping skills.10

Continue to: Psychological first aid...

 

 

Psychological first aid (PFA) is a standard intervention recommended by the World Health Organization for most individuals following a disaster; it is evidence-informed and has face validity.11 Intended to relieve distress by creating an environment that is safe, calm, and connected, PFA fosters self-efficacy and hope. While PFA is a form of universal prevention, it is not designed for patients with SMI, is not a psychiatric intervention, and is not provided by clinicians. Its principles, however, can easily be applied to patients with SMI to prevent distressing symptoms from becoming a relapse.

Communication. Good risk and crisis communication are critical because individual and population behavior will be governed by the perception of risk and fear, and not by facts. Failure to manage the “infodemic”7—with its misinformation, contradictory messages, and rumors—jeopardizes infection control if patients become paralyzed by uncertainty and fear. Scapegoating occurs easily during times of threat, and society must contain the parallel epidemic of xenophobia based on stigma and misinformation.12

Decision-making under uncertainty is not perfect and subject to revision as better information becomes available. Pointing this out to the public is delicate but essential to curtail skepticism and mistrust when policies are adjusted in response to new circumstances and knowledge.

Mistrust of an authority’s legitimacy and fear-based decisions lead to lack of cooperation with public-health measures, which can undermine an effective response to the pandemic. Travel restrictions or quarantine measures will not be followed if individuals question their importance. Like the general public, patients need education and clear communication to address their fear of contagion, dangers posed to family (and pets), and mistrust of authority and government. A lack of appreciation of the seriousness of the pandemic and individual responsibility may need to be addressed. Two important measures to accomplish this are steering patients to reputable sources of information and advising that they limit media exposure.

Resilience-building. Community and workplace resilience are important aspects of making it through a disaster as best as possible. Resilience is not innate and fixed; it must be deliberately built.13 Choosing an attitude of post-traumatic growth over the victim narrative is a helpful stance. Practicing self-care (rest, nutrition, exercise) and self-compassion (self-kindness, common humanity, mindfulness) is good advice for patients and caregivers alike.

Continue to: Workforce protection

 

 

Workforce protection. Compared to other disasters, infectious outbreaks disproportionally affect the medical community, and care delivery is at stake. While psychological and psychiatric needs may increase during a pandemic, services often contract, day programs and clinics close, teams are reduced to skeleton crews, and only emergency psychiatric care is available. Workforce protection is critical to avoid illness or simple absenteeism due to mistrust of protective measures.

Only a well-briefed, well-led, well-supported, and adequately resourced workforce is going to be effective in managing this public-health emergency. Burnout and moral injury are feared long-term consequences for health care workers that need to be proactively addressed.14 As opposed to other forms of disasters, managing your own fears about safety is important. Clinicians and their patients sit in the proverbial same boat.

Ethics. The anticipated need to ration life-saving care (eg, ventilators) has been at the forefront of ethical concerns.15 In psychiatry, the question of involuntary public-health interventions for uncooperative psychiatric patients sits uncomfortably between public-health ethics and human rights, and is an opportunity for collaboration with public-health and infectious-disease colleagues.

Redeployed clinicians and those working under substandard conditions may be concerned about civil liability due to a modified standard of care during a crisis. Some clinicians may ask if their duty to care must override their natural instinct to protect themselves. There is a lot of room for resentment in these circumstances. Redeployed or otherwise “conscripted” clinicians may resent administrators, especially those administering from the safety of their homes. Those “left behind” to work in potentially precarious circumstances may resent their absent colleagues. Moreover, these front-line clinicians may have been forced to make ethical decisions for which they were not prepared.16 Maintaining morale is far from trivial, not just during the pandemic, but afterward, when (and if) the entire workforce is reunited. All parties need to be mindful of how their actions and decisions impact and are perceived by others, both in the hospital and at home.

Managing patients with SMI during COVID-19

Patients with SMI are potentially hard hit by COVID-19 due to a “tragic” epidemiologic triad of agent-host-environment: SARS-CoV-2 is a highly infectious agent affecting patients with SMI who are vulnerable hosts in permissive environments (Figure).

‘Tragic’ epidemiologic triad for patients with SMI

Continue to: While not as infectious as measles...

 

 

While not as infectious as measles, COVID-19 is more infectious than the seasonal flu virus.17 It can lead to uncontrolled infection within a short period of time, particularly in enclosed settings. Outbreaks have occurred readily on cruise ships and aircraft carriers as well as in nursing homes, homeless shelters, prisons, and group homes.

Patients with SMI are vulnerable hosts because they have many of the medical risk factors18 that portend a poor prognosis if they become infected, including pre-existing lung conditions and heart disease19 as well as diabetes and obesity.20 Obesity likely creates a hyperinflammatory state and a decrease in vital capacity. Patient-related behavioral factors include poor early-symptom reporting and ineffective infection control.

Unfavorable social determinants of health include not only poverty but crowded housing that is a perfect incubator for COVID-19.

Priority treatment goals. The overarching goal during a pandemic is to keep patients with SMI in psychiatric treatment and prevent them from disengaging from care in the service of infection control. Urgent tasks include infection control, relapse prevention, and preventing treatment disengagement and loneliness.

Infection control. As trusted sources of information, psychiatrists can play an important role in infection control in several important ways:

  • educating patients about infection-control measures and public-health recommendations
  • helping patients understand what testing can accomplish and when to pursue it
  • encouraging protective health behaviors (eg, hand washing, mask wearing, physical distancing)
  • assessing patients’ risk appreciation
  • assessing for and addressing obstacles to implementing and complying with infection-control measures
  • explaining contact tracing
  • providing reassurance.

Continue to: Materials and explanations...

 

 

Materials and explanations must be adapted for patient understanding.

Patients with disorganization or cognitive disturbances may have difficulties cooperating or problem-solving. Patients with negative symptoms may be inappropriately unconcerned and also inaccurately report symptoms that suggest COVID-19. Acute psychosis or mania can prevent patients from complying with public-health efforts. Some measures may be difficult to implement if the means are simply not there (eg, physical distancing in a crowded apartment). Previously open settings (eg, group homes) have had to develop new mechanisms under the primacy of infection control. Inpatient units—traditionally places where community, shared healing, and group therapy are prized—have had to decrease maximum occupancy, limit the number of patients attending groups, and discourage or outrightly prohibit social interaction (eg, dining together).

Relapse prevention. Patients who take maintenance medications need to be supported. A manic or psychotic relapse during a pandemic puts patients at risk of acquiring and spreading COVID-19. “Treatment as prevention” is a slogan from human immunodeficiency virus (HIV) care that captures the importance of antiretroviral treatment to prevent medical complications from HIV, and also to reduce infecting other people. By analogy, psychiatric treatment for patients with SMI can prevent psychiatric instability and thereby control viral transmission. Avoiding sending psychiatric patients to a potentially stressed acute-care system is important.

Psychosocial support. Clinics need to ensure that patients continue to engage in care beyond medication-taking to proactively prevent psychiatric exacerbations. Healthful, resilience-building behaviors should be encouraged while monitoring and counseling against maladaptive ones (eg, increased substance use). Supporting patients emotionally and helping them solve problems are critical, particularly for those who are subjected to quarantine or isolation. Obviously, in these latter situations, outreach will be necessary and may require creative delivery systems and dedicated clinicians for patients who lack access to the technology necessary for virtual visits. Havens and Ghaemi21 have suggested that a good therapeutic alliance can be viewed as a mood stabilizer. Helping patients grieve losses (loved ones, jobs, sense of safety) may be an important part of support.

Even before COVID-19, loneliness was a major factor for patients with schizophrenia.22 A psychiatric clinic is one aspect of a person with SMI’s social network; during the initial phase of the pandemic, many clinics and treatment programs closed. Patients for whom clinics structure and anchor their activities are at high risk of disconnecting from treatment, staying at home, and becoming lonely.

Continue to: Caregivers are always important...

 

 

Caregivers are always important to SMI patients, but they may assume an even bigger role during this pandemic. Some patients may have moved in with a relative, after years of living on their own. In other cases, stable caregiver relationships may be disrupted due to COVID-19–related sickness in the caregiver; if not addressed, this can result in a patient’s clinical decompensation. Clinicians should take the opportunity to understand who a patient’s caregivers are (group home staff, families) and rekindle clinical contact with them. Relationships with caregivers that may have been on “autopilot” during normal times are opportunities for welcome support and guidance, to the benefit of both patients and caregivers.

Table 1 summarizes clinical tasks that need to be kept in mind when conducting clinic visits during COVID-19 in order to achieve the high-priority treatment goals of infection control, relapse prevention, and psychosocial support.

Clinical tasks for patients with SMI during the COVID-19 pandemic

Differential diagnosis. Neuropsychiatric syndromes have long been observed in influenza pandemics,23 due both to direct viral effects and to the effects of critical illness on the brain. Two core symptoms of COVID-19—anosmia and ageusia—suggest that COVID-19 can directly affect the brain. While neurologic manifestations are common,24 it remains unclear to what extent COVID-19 can directly “cause” psychiatric symptoms, or if such symptoms are the result of cytokines25 or other medical processes (eg, thromboembolism).26 Psychosis due to COVID-19 may, in some cases, represent a stress-related brief psychotic disorder.27

Hospitalized patients who have recovered from COVID-19 may have experienced prolonged sedation and severe delirium in an ICU.28 Complications such as posttraumatic stress disorder,29 hypoperfusion-related brain injuries, or other long-term cognitive difficulties may result. In previous flu epidemics, patients developed serious neurologic complications such as post-encephalitic Parkinson’s disease.30

Any person subjected to isolation or quarantine is at risk for psychiatric complications.31 Patients with SMI who live in group homes may be particularly susceptible to new rules, including no-visitor policies.

Continue to: Outpatients whose primary disorder...

 

 

Outpatients whose primary disorder is well controlled may, like anyone else, struggle with the effects of the pandemic. It is necessary to carefully differentiate non-specific symptoms associated with stress from the emergence of a new disorder resulting from stress.32 For some patients, grief or adjustment disorders should be considered. Prolonged stress and uncertainty may eventually lead to an exacerbation of a primary disorder, particularly if the situation (eg, financial loss) does not improve or worsens. Demoralization and suicidal thinking need to be monitored. Relapse or increased use of alcohol or other substances as a response to stress may also complicate the clinical picture.33 Last, smoking cessation as a major treatment goal in general should be re-emphasized and not ignored during the ongoing pandemic.34

Psychiatric symptoms in patients with SMI during the COVID-19 pandemic

Table 2 summarizes psychiatric symptoms that need to be considered when managing a patient with SMI during this pandemic.

Treatment tools

Psychopharmacology. Even though crisis-mode prescribing may be necessary, the safe use of psychotropics remains the goal of psychiatric prescribing. Access to medications becomes a larger consideration; for many patients, a 90-day supply may be indicated. Review of polypharmacy, including for pneumonia risk, should be undertaken. Preventing drooling (eg, from sedation, clozapine, extrapyramidal symptoms [EPS]) will decrease aspiration risk.

 

In general, treatment of psychiatric symptoms in a patient with COVID-19 follows usual guidelines. The best treatment for COVID-19 patients with delirium, however, remains to be established, particularly how to manage severe agitation.28 Pharmacodynamic and pharmacokinetic drug–drug interactions between psychotropics and antiviral treatments for COVID-19 (eg, QTc prolongation) can be expected and need to be reviewed.35 For stress-related anxiety, judicious pharmacotherapy can be helpful. Diazepam given at the earliest signs of a psychotic relapse may stave off a relapse for patients with schizophrenia.36 Even if permitted under relaxed prescribing rules during a public-health emergency, prescribing controlled substances without seeing patients in person requires additional thought. In some cases, adjusting the primary medication to buffer against stress may be preferred (eg, adjusting an antipsychotic in a patient on maintenance treatment for schizophrenia, particularly if a low-dose strategy is pursued).

Consensus statement on the use of clozapine during the COVID-19 pandemic

Clozapine requires registry-based prescribing and bloodwork (“no blood, no drug”). The use of clozapine during this public-health emergency has been made easier because of FDA guidance that allows clozapine to be dispensed without blood work if obtaining blood work is not possible (eg, a patient is quarantined) or can be accomplished only at substantial risk to patients and the population at large. Under certain conditions, clozapine can be dispensed safely and in a way that is consistent with infection prevention. Clozapine-treated patients admitted with COVID-19 should be monitored for clozapine toxicity and the clozapine dose adjusted.37 A consensus statement consistent with the FDA and clinical considerations for using clozapine during COVID-19 is summarized in Table 3.38

Continue to: Long-acting injectable antipsychotics...

 

 

Long-acting injectable antipsychotics (LAIs) pose a problem because they require in-person visits. Ideally, during a pandemic, patients should be seen in person as frequently as medically necessary but as infrequently as possible to limit exposure of both patients and staff. Table 4 provides some clinical recommendations on how to use LAIs during the pandemic.39

Use of long-acting injectable antipsychotics during the COVID-19 pandemic

Supportive psychotherapy may be the most important tool we have in helping patients with loss and uncertainty during these challenging months.40 Simply staying in contact with patients plays a major role in preventing care discontinuity. Even routine interactions have become stressful, with everyone wearing a mask that partially obscures the face. People with impaired hearing may find it even more difficult to understand you.

Education, problem-solving, and a directive, encouraging style are major tools of supportive psychotherapy to reduce symptoms and increase adaptive skills. Clarify that social distancing refers to physical, not emotional, distancing. The judicious and temporary use of anxiolytics is appropriate to reduce anxiety. Concrete help and problem-solving (eg, filling out forms) are examples of proactive crisis intervention.

Telepsychiatry emerged in the pandemic’s early days as the default mode of practice in order to limit in-person contacts.41 Like all new technology, telepsychiatry brings progress and peril.42 While it has gone surprisingly well for most, the “digital divide” does not afford all patients access to the needed technology. The long-term effectiveness and acceptance of telehealth remain to be seen. (Editor’s Note: For more about this topic, see “Telepsychiatry: What you need to know.” Current Psychiatry. 2020;19[6]:16-23.)

Lessons learned and outlook

Infectious outbreaks have historically inflicted long-term disruptions on societies and altered the course of history. However, each disaster is unique, and lessons from previous disasters may only partially apply.43 We do not yet know how this one will end, including how long it will take for the world’s economies to recover. If nothing else, the current public-health emergency has brought to the forefront what psychiatrists have always known: health disparities are partially responsible for different disease risks (in this case, the risk of getting infected with SARS-CoV-2).5 It may not be a coincidence that the Black Lives Matter movement is becoming a major impetus for social change at a time when the pandemic is exposing health-care inequalities.

Continue to: Some areas of the country...

 

 

Some areas of the country succeeded in reducing infections and limiting community spread, which ushered in an uneasy sense of normalcy even while the pandemic continues. At least for now, these locales can focus on rebuilding and preparing for expectable fluctuations in disease activity, including the arrival of the annual flu season on top of COVID-19.44 Recovery is not a return to the status quo ante but building stronger communities—“building back better.”45 Unless there is a continuum of care, shortcomings in one sector will have ripple effects through the entire system, particularly for psychiatric care for patients with SMI, which was inadequate before the pandemic.

Ensuring access to critical care was a priority during the pandemic’s early phase but came at the price of deferring other types of care, such as routine primary care; the coming months will see the downstream consequences of this approach,46 including for patients with SMI.

In the meantime, doing our job as clinicians, as Camus’s fictitious Dr. Bernard Rieux from the epigraph responds when asked how to define decency, may be the best we can do in these times. This includes contributing to and molding our field’s future and fostering a sense of agency in our patients and in ourselves. Major goals will be to preserve lessons learned, maintain flexibility, and avoid a return to unhelpful overregulation and payment models that do not reflect the flexible, person-centered care so important for patients with SMI.47

Bottom Line

During a pandemic, patients with serious mental illness may be easily forgotten as other issues overshadow the needs of this impoverished group. During a pandemic, the priority treatment goals for these patients are infection control, relapse prevention, and preventing treatment disengagement and loneliness. A pandemic requires changes in how patients with serious mental illness will receive psychopharmacology and psychotherapy.

Related Resources

Drug Brand Names

Clozapine • Clozaril
Diazepam • Valium
Hydroxychloroquine • Plaquenil

“This whole thing is not about heroism. It’s about decency. It may seem a ridiculous idea, but the only way to fight the plague is with decency . ”

– Albert Camus, La Peste (1947)1

Severe acute respiratory syndrome (SARS), H1N1 swine flu, Ebola, Zika, and Middle East respiratory syndrome (MERS): the 21st century has already been witness to several serious infectious outbreaks and pandemics,2 but none has been as deadly and consequential as the current one. The ongoing SARS-coronavirus-2 (SARS-CoV-2) pandemic is shaping not only current psychiatric care but the future of psychiatry. Now that we are beyond the initial stages of the coronavirus disease 2019 (COVID-19) pandemic, when psychiatrists had a crash course in disaster psychiatry, our attention must shift to rebuilding and managing disillusionment and other psychological fallout of the intense early days.3

In this article, we offer guidance to psychiatrists caring for patients with serious mental illness (SMI) during the SARS-CoV-2 pandemic. Patients with SMI are easily forgotten as other issues (eg, preserving ICU capacity) overshadow the already historically neglected needs of this impoverished group.4 From both human and public-health perspectives, this inattention is a mistake. Assuring psychiatric stability is critically important to prevent the spread of COVID-19 in marginalized communities comprised of individuals who are poor, members of racial minorities, and others who already experience health disparities.5 Without controlling transmission in these groups, the pandemic will not be sufficiently contained.

We begin by highlighting general principles of pandemic management because caring for patients with SMI does not occur in a vacuum. Infectious outbreaks require not only helping those who need direct medical care because they are infected, but also managing populations that are at risk of getting infected, including health care and other essential workers.

Principles of pandemic management

Delivery of medical care during a pandemic differs from routine care. An effective disaster response requires collaboration and coordination among public-health, treatment, and emergency systems. Many institutions shift to an incident management system and crisis leadership, with clear lines of authority to coordinate responders and build medical surge capacity. Such a top-down leadership approach must plan and allow for the emergence of other credible leaders and for the restoration of people’s agency.

Unfortunately, adaptive capacity may be limited, especially in the public sector and psychiatric care system, where resources are already poor. Particularly early in a pandemic, services considered non-essential—which includes most psychiatric outpatient care—can become unavailable. A major effort is needed to prevent the psychiatric care system from contracting further, as happened during 9/11.6 Additionally, “essential” cannot be conflated with “emergent,” as can easily occur in extreme circumstances. Early and sustained efforts are required to ensure that patients with SMI who may be teetering on the edge of emergency status do not slip off that edge, especially when the emergency medical system is operating over capacity.

A comprehensive outbreak response must consider that a pandemic is not only a medical crisis but a mental health crisis and a communication emergency.7 Mental health clinicians need to provide accurate information and help patients cope with their fears.

Continue to: Psychological aspects of pandemics

 

 

Psychological aspects of pandemics. Previous infectious outbreaks have reaffirmed that mental health plays an outsized role during epidemics. Chaos, uncertainty, fear of death, and loss of income and housing cause prolonged stress and exact a psychological toll.

Adverse psychological impacts include expectable, normal reactions such as stress-induced anxiety or insomnia. In addition, new-onset psychiatric illnesses or exacerbations of existing ones may emerge.8 As disillusionment and demoralization appear in the wake of the acute phase, with persistently high unemployment, suicide prevention becomes an important goal.9

Pandemics lead to expectable behavioral responses (eg, increases in substance use and interpersonal conflict). Fear-based decisions may result in unhelpful behavior, such as hoarding medications (which may result in shortages) or dangerous, unsupervised use of unproven medications (eg, hydroxychloroquine). Trust is needed to accept public-health measures, and recommendations (eg, wearing masks) must be culturally informed to be credible and effective.

Because people are affected differently, at individual, cultural, and socioeconomic levels, they will view the situation differently. For many people, secondary stressors (eg, job loss) may be more disastrous than the primary medical event (ie, the pandemic). This distinction is critical because concrete financial help, not psychiatric care, is needed. Sometimes, even when a psychiatric disorder such as SMI or major neurocognitive disorder is present, the illusion of an acute decompensation can be created by the loss of social and structural supports that previously scaffolded a person’s life.

Mental illness prevention. Community mental-health surveillance is important to monitor for distress, psychiatric symptoms, health-risk behaviors, risk and safety perception, and preparedness. Clinicians must be ready to normalize expectable and temporary distress, while recognizing when that distress becomes pathological. This may be difficult in patients with SMI who often already have reduced stress tolerance or problem-based coping skills.10

Continue to: Psychological first aid...

 

 

Psychological first aid (PFA) is a standard intervention recommended by the World Health Organization for most individuals following a disaster; it is evidence-informed and has face validity.11 Intended to relieve distress by creating an environment that is safe, calm, and connected, PFA fosters self-efficacy and hope. While PFA is a form of universal prevention, it is not designed for patients with SMI, is not a psychiatric intervention, and is not provided by clinicians. Its principles, however, can easily be applied to patients with SMI to prevent distressing symptoms from becoming a relapse.

Communication. Good risk and crisis communication are critical because individual and population behavior will be governed by the perception of risk and fear, and not by facts. Failure to manage the “infodemic”7—with its misinformation, contradictory messages, and rumors—jeopardizes infection control if patients become paralyzed by uncertainty and fear. Scapegoating occurs easily during times of threat, and society must contain the parallel epidemic of xenophobia based on stigma and misinformation.12

Decision-making under uncertainty is not perfect and subject to revision as better information becomes available. Pointing this out to the public is delicate but essential to curtail skepticism and mistrust when policies are adjusted in response to new circumstances and knowledge.

Mistrust of an authority’s legitimacy and fear-based decisions lead to lack of cooperation with public-health measures, which can undermine an effective response to the pandemic. Travel restrictions or quarantine measures will not be followed if individuals question their importance. Like the general public, patients need education and clear communication to address their fear of contagion, dangers posed to family (and pets), and mistrust of authority and government. A lack of appreciation of the seriousness of the pandemic and individual responsibility may need to be addressed. Two important measures to accomplish this are steering patients to reputable sources of information and advising that they limit media exposure.

Resilience-building. Community and workplace resilience are important aspects of making it through a disaster as best as possible. Resilience is not innate and fixed; it must be deliberately built.13 Choosing an attitude of post-traumatic growth over the victim narrative is a helpful stance. Practicing self-care (rest, nutrition, exercise) and self-compassion (self-kindness, common humanity, mindfulness) is good advice for patients and caregivers alike.

Continue to: Workforce protection

 

 

Workforce protection. Compared to other disasters, infectious outbreaks disproportionally affect the medical community, and care delivery is at stake. While psychological and psychiatric needs may increase during a pandemic, services often contract, day programs and clinics close, teams are reduced to skeleton crews, and only emergency psychiatric care is available. Workforce protection is critical to avoid illness or simple absenteeism due to mistrust of protective measures.

Only a well-briefed, well-led, well-supported, and adequately resourced workforce is going to be effective in managing this public-health emergency. Burnout and moral injury are feared long-term consequences for health care workers that need to be proactively addressed.14 As opposed to other forms of disasters, managing your own fears about safety is important. Clinicians and their patients sit in the proverbial same boat.

Ethics. The anticipated need to ration life-saving care (eg, ventilators) has been at the forefront of ethical concerns.15 In psychiatry, the question of involuntary public-health interventions for uncooperative psychiatric patients sits uncomfortably between public-health ethics and human rights, and is an opportunity for collaboration with public-health and infectious-disease colleagues.

Redeployed clinicians and those working under substandard conditions may be concerned about civil liability due to a modified standard of care during a crisis. Some clinicians may ask if their duty to care must override their natural instinct to protect themselves. There is a lot of room for resentment in these circumstances. Redeployed or otherwise “conscripted” clinicians may resent administrators, especially those administering from the safety of their homes. Those “left behind” to work in potentially precarious circumstances may resent their absent colleagues. Moreover, these front-line clinicians may have been forced to make ethical decisions for which they were not prepared.16 Maintaining morale is far from trivial, not just during the pandemic, but afterward, when (and if) the entire workforce is reunited. All parties need to be mindful of how their actions and decisions impact and are perceived by others, both in the hospital and at home.

Managing patients with SMI during COVID-19

Patients with SMI are potentially hard hit by COVID-19 due to a “tragic” epidemiologic triad of agent-host-environment: SARS-CoV-2 is a highly infectious agent affecting patients with SMI who are vulnerable hosts in permissive environments (Figure).

‘Tragic’ epidemiologic triad for patients with SMI

Continue to: While not as infectious as measles...

 

 

While not as infectious as measles, COVID-19 is more infectious than the seasonal flu virus.17 It can lead to uncontrolled infection within a short period of time, particularly in enclosed settings. Outbreaks have occurred readily on cruise ships and aircraft carriers as well as in nursing homes, homeless shelters, prisons, and group homes.

Patients with SMI are vulnerable hosts because they have many of the medical risk factors18 that portend a poor prognosis if they become infected, including pre-existing lung conditions and heart disease19 as well as diabetes and obesity.20 Obesity likely creates a hyperinflammatory state and a decrease in vital capacity. Patient-related behavioral factors include poor early-symptom reporting and ineffective infection control.

Unfavorable social determinants of health include not only poverty but crowded housing that is a perfect incubator for COVID-19.

Priority treatment goals. The overarching goal during a pandemic is to keep patients with SMI in psychiatric treatment and prevent them from disengaging from care in the service of infection control. Urgent tasks include infection control, relapse prevention, and preventing treatment disengagement and loneliness.

Infection control. As trusted sources of information, psychiatrists can play an important role in infection control in several important ways:

  • educating patients about infection-control measures and public-health recommendations
  • helping patients understand what testing can accomplish and when to pursue it
  • encouraging protective health behaviors (eg, hand washing, mask wearing, physical distancing)
  • assessing patients’ risk appreciation
  • assessing for and addressing obstacles to implementing and complying with infection-control measures
  • explaining contact tracing
  • providing reassurance.

Continue to: Materials and explanations...

 

 

Materials and explanations must be adapted for patient understanding.

Patients with disorganization or cognitive disturbances may have difficulties cooperating or problem-solving. Patients with negative symptoms may be inappropriately unconcerned and also inaccurately report symptoms that suggest COVID-19. Acute psychosis or mania can prevent patients from complying with public-health efforts. Some measures may be difficult to implement if the means are simply not there (eg, physical distancing in a crowded apartment). Previously open settings (eg, group homes) have had to develop new mechanisms under the primacy of infection control. Inpatient units—traditionally places where community, shared healing, and group therapy are prized—have had to decrease maximum occupancy, limit the number of patients attending groups, and discourage or outrightly prohibit social interaction (eg, dining together).

Relapse prevention. Patients who take maintenance medications need to be supported. A manic or psychotic relapse during a pandemic puts patients at risk of acquiring and spreading COVID-19. “Treatment as prevention” is a slogan from human immunodeficiency virus (HIV) care that captures the importance of antiretroviral treatment to prevent medical complications from HIV, and also to reduce infecting other people. By analogy, psychiatric treatment for patients with SMI can prevent psychiatric instability and thereby control viral transmission. Avoiding sending psychiatric patients to a potentially stressed acute-care system is important.

Psychosocial support. Clinics need to ensure that patients continue to engage in care beyond medication-taking to proactively prevent psychiatric exacerbations. Healthful, resilience-building behaviors should be encouraged while monitoring and counseling against maladaptive ones (eg, increased substance use). Supporting patients emotionally and helping them solve problems are critical, particularly for those who are subjected to quarantine or isolation. Obviously, in these latter situations, outreach will be necessary and may require creative delivery systems and dedicated clinicians for patients who lack access to the technology necessary for virtual visits. Havens and Ghaemi21 have suggested that a good therapeutic alliance can be viewed as a mood stabilizer. Helping patients grieve losses (loved ones, jobs, sense of safety) may be an important part of support.

Even before COVID-19, loneliness was a major factor for patients with schizophrenia.22 A psychiatric clinic is one aspect of a person with SMI’s social network; during the initial phase of the pandemic, many clinics and treatment programs closed. Patients for whom clinics structure and anchor their activities are at high risk of disconnecting from treatment, staying at home, and becoming lonely.

Continue to: Caregivers are always important...

 

 

Caregivers are always important to SMI patients, but they may assume an even bigger role during this pandemic. Some patients may have moved in with a relative, after years of living on their own. In other cases, stable caregiver relationships may be disrupted due to COVID-19–related sickness in the caregiver; if not addressed, this can result in a patient’s clinical decompensation. Clinicians should take the opportunity to understand who a patient’s caregivers are (group home staff, families) and rekindle clinical contact with them. Relationships with caregivers that may have been on “autopilot” during normal times are opportunities for welcome support and guidance, to the benefit of both patients and caregivers.

Table 1 summarizes clinical tasks that need to be kept in mind when conducting clinic visits during COVID-19 in order to achieve the high-priority treatment goals of infection control, relapse prevention, and psychosocial support.

Clinical tasks for patients with SMI during the COVID-19 pandemic

Differential diagnosis. Neuropsychiatric syndromes have long been observed in influenza pandemics,23 due both to direct viral effects and to the effects of critical illness on the brain. Two core symptoms of COVID-19—anosmia and ageusia—suggest that COVID-19 can directly affect the brain. While neurologic manifestations are common,24 it remains unclear to what extent COVID-19 can directly “cause” psychiatric symptoms, or if such symptoms are the result of cytokines25 or other medical processes (eg, thromboembolism).26 Psychosis due to COVID-19 may, in some cases, represent a stress-related brief psychotic disorder.27

Hospitalized patients who have recovered from COVID-19 may have experienced prolonged sedation and severe delirium in an ICU.28 Complications such as posttraumatic stress disorder,29 hypoperfusion-related brain injuries, or other long-term cognitive difficulties may result. In previous flu epidemics, patients developed serious neurologic complications such as post-encephalitic Parkinson’s disease.30

Any person subjected to isolation or quarantine is at risk for psychiatric complications.31 Patients with SMI who live in group homes may be particularly susceptible to new rules, including no-visitor policies.

Continue to: Outpatients whose primary disorder...

 

 

Outpatients whose primary disorder is well controlled may, like anyone else, struggle with the effects of the pandemic. It is necessary to carefully differentiate non-specific symptoms associated with stress from the emergence of a new disorder resulting from stress.32 For some patients, grief or adjustment disorders should be considered. Prolonged stress and uncertainty may eventually lead to an exacerbation of a primary disorder, particularly if the situation (eg, financial loss) does not improve or worsens. Demoralization and suicidal thinking need to be monitored. Relapse or increased use of alcohol or other substances as a response to stress may also complicate the clinical picture.33 Last, smoking cessation as a major treatment goal in general should be re-emphasized and not ignored during the ongoing pandemic.34

Psychiatric symptoms in patients with SMI during the COVID-19 pandemic

Table 2 summarizes psychiatric symptoms that need to be considered when managing a patient with SMI during this pandemic.

Treatment tools

Psychopharmacology. Even though crisis-mode prescribing may be necessary, the safe use of psychotropics remains the goal of psychiatric prescribing. Access to medications becomes a larger consideration; for many patients, a 90-day supply may be indicated. Review of polypharmacy, including for pneumonia risk, should be undertaken. Preventing drooling (eg, from sedation, clozapine, extrapyramidal symptoms [EPS]) will decrease aspiration risk.

 

In general, treatment of psychiatric symptoms in a patient with COVID-19 follows usual guidelines. The best treatment for COVID-19 patients with delirium, however, remains to be established, particularly how to manage severe agitation.28 Pharmacodynamic and pharmacokinetic drug–drug interactions between psychotropics and antiviral treatments for COVID-19 (eg, QTc prolongation) can be expected and need to be reviewed.35 For stress-related anxiety, judicious pharmacotherapy can be helpful. Diazepam given at the earliest signs of a psychotic relapse may stave off a relapse for patients with schizophrenia.36 Even if permitted under relaxed prescribing rules during a public-health emergency, prescribing controlled substances without seeing patients in person requires additional thought. In some cases, adjusting the primary medication to buffer against stress may be preferred (eg, adjusting an antipsychotic in a patient on maintenance treatment for schizophrenia, particularly if a low-dose strategy is pursued).

Consensus statement on the use of clozapine during the COVID-19 pandemic

Clozapine requires registry-based prescribing and bloodwork (“no blood, no drug”). The use of clozapine during this public-health emergency has been made easier because of FDA guidance that allows clozapine to be dispensed without blood work if obtaining blood work is not possible (eg, a patient is quarantined) or can be accomplished only at substantial risk to patients and the population at large. Under certain conditions, clozapine can be dispensed safely and in a way that is consistent with infection prevention. Clozapine-treated patients admitted with COVID-19 should be monitored for clozapine toxicity and the clozapine dose adjusted.37 A consensus statement consistent with the FDA and clinical considerations for using clozapine during COVID-19 is summarized in Table 3.38

Continue to: Long-acting injectable antipsychotics...

 

 

Long-acting injectable antipsychotics (LAIs) pose a problem because they require in-person visits. Ideally, during a pandemic, patients should be seen in person as frequently as medically necessary but as infrequently as possible to limit exposure of both patients and staff. Table 4 provides some clinical recommendations on how to use LAIs during the pandemic.39

Use of long-acting injectable antipsychotics during the COVID-19 pandemic

Supportive psychotherapy may be the most important tool we have in helping patients with loss and uncertainty during these challenging months.40 Simply staying in contact with patients plays a major role in preventing care discontinuity. Even routine interactions have become stressful, with everyone wearing a mask that partially obscures the face. People with impaired hearing may find it even more difficult to understand you.

Education, problem-solving, and a directive, encouraging style are major tools of supportive psychotherapy to reduce symptoms and increase adaptive skills. Clarify that social distancing refers to physical, not emotional, distancing. The judicious and temporary use of anxiolytics is appropriate to reduce anxiety. Concrete help and problem-solving (eg, filling out forms) are examples of proactive crisis intervention.

Telepsychiatry emerged in the pandemic’s early days as the default mode of practice in order to limit in-person contacts.41 Like all new technology, telepsychiatry brings progress and peril.42 While it has gone surprisingly well for most, the “digital divide” does not afford all patients access to the needed technology. The long-term effectiveness and acceptance of telehealth remain to be seen. (Editor’s Note: For more about this topic, see “Telepsychiatry: What you need to know.” Current Psychiatry. 2020;19[6]:16-23.)

Lessons learned and outlook

Infectious outbreaks have historically inflicted long-term disruptions on societies and altered the course of history. However, each disaster is unique, and lessons from previous disasters may only partially apply.43 We do not yet know how this one will end, including how long it will take for the world’s economies to recover. If nothing else, the current public-health emergency has brought to the forefront what psychiatrists have always known: health disparities are partially responsible for different disease risks (in this case, the risk of getting infected with SARS-CoV-2).5 It may not be a coincidence that the Black Lives Matter movement is becoming a major impetus for social change at a time when the pandemic is exposing health-care inequalities.

Continue to: Some areas of the country...

 

 

Some areas of the country succeeded in reducing infections and limiting community spread, which ushered in an uneasy sense of normalcy even while the pandemic continues. At least for now, these locales can focus on rebuilding and preparing for expectable fluctuations in disease activity, including the arrival of the annual flu season on top of COVID-19.44 Recovery is not a return to the status quo ante but building stronger communities—“building back better.”45 Unless there is a continuum of care, shortcomings in one sector will have ripple effects through the entire system, particularly for psychiatric care for patients with SMI, which was inadequate before the pandemic.

Ensuring access to critical care was a priority during the pandemic’s early phase but came at the price of deferring other types of care, such as routine primary care; the coming months will see the downstream consequences of this approach,46 including for patients with SMI.

In the meantime, doing our job as clinicians, as Camus’s fictitious Dr. Bernard Rieux from the epigraph responds when asked how to define decency, may be the best we can do in these times. This includes contributing to and molding our field’s future and fostering a sense of agency in our patients and in ourselves. Major goals will be to preserve lessons learned, maintain flexibility, and avoid a return to unhelpful overregulation and payment models that do not reflect the flexible, person-centered care so important for patients with SMI.47

Bottom Line

During a pandemic, patients with serious mental illness may be easily forgotten as other issues overshadow the needs of this impoverished group. During a pandemic, the priority treatment goals for these patients are infection control, relapse prevention, and preventing treatment disengagement and loneliness. A pandemic requires changes in how patients with serious mental illness will receive psychopharmacology and psychotherapy.

Related Resources

Drug Brand Names

Clozapine • Clozaril
Diazepam • Valium
Hydroxychloroquine • Plaquenil

References

1. Camus A. La peste. Paris, France: Éditions Gallimard; 1947.
2. Huremovic´ D. Brief history of pandemics (pandemics throughout history). In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019:7-35.
3. Substance Abuse and Mental Health Services Administration. Phases of disaster. https://www.samhsa.gov/dtac/recovering-disasters/phases-disaster. Updated June 17, 2020. Accessed August 7, 2020.
4. Geller J. COVID-19 and advocacy—the good and the unacceptable. Psychiatric News. https://psychnews.psychiatryonline.org/doi/10.1176/appi.pn.2020.5b13. Published May 7, 2020. Accessed August 7, 2020.
5. Webb Hooper M, Nápoles AM, Perez-Stable EJ. COVID-19 and racial/ethnic disparities. JAMA. 2020;323(24):2466-2467.
6. Sederer LI, Lanzara CB, Essock SM, et al. Lessons learned from the New York State mental health response to the September 11, 2001, attacks. Psychiatr Serv. 2011;62(9):1085-1089.
7. World Health Organization. Infodemic management – infodemiology. https://www.who.int/teams/risk-communication/infodemic-management. Accessed August 7, 2020.
8. Zhou J, Liu L, Xue P, et al. Mental health response to the COVID-19 outbreak in China. Am J Psychiatry. 2020;117(7):574-575.
9. Kawohl W, Nordt C. COVID-19, unemployment, and suicide. Lancet Psychiatry. 2020;7(5):389-390.
10. Yao H, Chen JH, Xu YF. Patients with mental health disorders in the COVID-19 epidemic. Lancet Psychiatry. 2020;7(4):e21. doi: 10.1016/S2215-0366(20)30090-0.
11. Minihan E, Gavin B, Kelly BD, et al. Covid-19, mental health and psychological first aid. Ir J Psychol Med. 2020:1-12.
12. Adja KYC, Golinelli D, Lenzi J, et al. Pandemics and social stigma: who’s next? Italy’s experience with COVID-19. Public Health. 2020;185:39-41.
13. Rosenberg AR. Cultivating deliberate resilience during the coronavirus disease 2019 pandemic [published online April 14, 2020]. JAMA Pediatr. doi: 10.1001/jamapediatrics.2020.1436.
14. Dean W, Talbot SG, Caplan A. Clarifying the language of clinician distress [published online January 31, 2020]. JAMA. doi: 10.1001/jama.2019.21576.
15. Emanuel EJ, Persad G, Upshur R, et al. Fair allocation of scarce medical resources in the time of Covid-19. N Engl J Med. 2020;382(21):2049-2055.
16. Rosenbaum L. Facing Covid-19 in Italy - ethics, logistics, and therapeutics on the epidemic’s front line. N Engl J Med. 2020;382(20):1873-1875.
17. Viceconte G, Petrosillo N. COVID-19 R0: magic number or conundrum? Infect Dis Rep. 2020;12(1):8516.
18. de Hert M, Schreurs V, Vancampfort D, van Winkel R. Metabolic syndrome in people with schizophrenia: a review. World Psychiatry. 2009;8(1):15-22.
19. Chen R, Liang W, Jiang M, et al. Risk factors of fatal outcome in hospitalized subjects with coronavirus disease 2019 from a nationwide analysis in China. Chest. 2020;158(1):97-105.
20. Finer N, Garnett SP, Bruun JM. COVID-19 and obesity. Clin Obes. 2020;10(3):e12365. doi: 10.1111/cob.12365.
21. Havens LL, Ghaemi SN. Existential despair and bipolar disorder: the therapeutic alliance as a mood stabilizer. Am J Psychother. 2005;59(2):137-147.
22. Trémeau F, Antonius D, Malaspina D, et al. Loneliness in schizophrenia and its possible correlates. An exploratory study. Psychiatry Res. 2016;246:211-217.
23. Menninger KA. Psychoses associated with influenza: I. General data: statistical analysis. JAMA. 1919;72(4):235-241.
24. Asadi-Pooya AA, Simani L. Central nervous system manifestations of COVID-19: a systematic review. J Neurol Sci. 2020;413:116832. doi: 10.1016/j.jns.2020.116832.
25. Ferrando SJ, Klepacz L, Lynch S, et al. COVID-19 psychosis: a potential new neuropsychiatric condition triggered by novel coronavirus infection and the inflammatory response? [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.012.
26. Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;87:34-39.
27. Martin Jr. EB. Brief psychotic disorder triggered by fear of coronavirus? Psychiatric Times. https://www.psychiatrictimes.com/view/brief-psychotic-disorder-triggered-fear-coronavirus-small-case-series. Published May 8, 2020. Accessed August 7, 2020.
28. Sher Y, Rabkin B, Maldonado JR, et al. COVID-19-associated hyperactive intensive care unit delirium with proposed pathophysiology and treatment: a case report [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.007.
29. Wolters AE, Peelen LM, Welling MC, et al. Long-term mental health problems after delirium in the ICU. Crit Care Med. 2016;44(10):1808-1813.
30. Toovey S. Influenza-associated central nervous system dysfunction: a literature review. Travel Med Infect Dis. 2008;6(3):114-124.
31. Brooks SK, Webster RK, Smith LE, et al. The psychological impact of quarantine and how to reduce it: rapid review of the evidence. Lancet. 2020;395(10227):912-920.
32. Maercker A, Brewin CR, Bryant RA, et al. Diagnosis and classification of disorders specifically associated with stress: proposals for ICD-11. World Psychiatry. 2013;12(3):198-206.
33. Ornell F, Moura HF, Scherer JN, et al. The COVID-19 pandemic and its impact on substance use: implications for prevention and treatment. Psychiatry Res. 2020;289:113096. doi: 10.1016/j.psychres.2020.113096.
34. Berlin I, Thomas D, Le Faou AL, Cornuz J. COVID-19 and smoking [published online April 3, 2020]. Nicotine Tob Res. https://doi.org/10.1093/ntr/ntaa059.
35. Back D, Marzolini C, Hodge C, et al. COVID-19 treatment in patients with comorbidities: awareness of drug-drug interactions [published online May 8, 2020]. Br J Clin Pharmacol. doi: 10.1111/bcp.14358.
36. Carpenter WT Jr., Buchanan RW, Kirkpatrick B, et al. Diazepam treatment of early signs of exacerbation in schizophrenia. Am J Psychiatry. 1999;156(2):299-303.
37. Dotson S, Hartvigsen N, Wesner T, et al. Clozapine toxicity in the setting of COVID-19 [published online May 30, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.025.
38. Siskind D, Honer WG, Clark S, et al. Consensus statement on the use of clozapine during the COVID-19 pandemic. J Psychiatry Neurosci. 2020;45(3):222-223.
39. Schnitzer K, MacLaurin S, Freudenreich O. Long-acting injectable antipsychotics during the COVID-19 pandemic. Current Psychiatry. In press.
40. Winston A, Rosenthal RN, Pinsker H. Learning supportive psychotherapy: an illustrated guide. Washington, DC: American Psychiatric Publishing; 2012.
41. Hollander JE, Carr BG. Virtually perfect? Telemedicine for Covid-19. N Engl J Med. 2020;382(18):1679-1681.
42. Jordan A, Dixon LB. Considerations for telepsychiatry service implementation in the era of COVID-19. Psychiatr Serv. 2020;71(6):643-644.
43. DePierro J, Lowe S, Katz C. Lessons learned from 9/11: mental health perspectives on the COVID-19 pandemic. Psychiatry Res. 2020;288:113024.
44. Hussain S. Immunization and vaccination. In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019.
45. Epping-Jordan JE, van Ommeren M, Ashour HN, et al. Beyond the crisis: building back better mental health care in 10 emergency-affected areas using a longer-term perspective. Int J Ment Health Syst. 2015;9:15.
46. Rosenbaum L. The untold toll - the pandemic’s effects on patients without Covid-19. N Engl J Med. 2020;382(24):2368-2371.
47. Bartels SJ, Baggett TP, Freudenreich O, et al. COVID-19 emergency reforms in Massachusetts to support behavioral health care and reduce mortality of people with serious mental illness [published online June 3, 2020]. Psychiatr Serv. doi: 10.1176/appi.ps.202000244.

References

1. Camus A. La peste. Paris, France: Éditions Gallimard; 1947.
2. Huremovic´ D. Brief history of pandemics (pandemics throughout history). In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019:7-35.
3. Substance Abuse and Mental Health Services Administration. Phases of disaster. https://www.samhsa.gov/dtac/recovering-disasters/phases-disaster. Updated June 17, 2020. Accessed August 7, 2020.
4. Geller J. COVID-19 and advocacy—the good and the unacceptable. Psychiatric News. https://psychnews.psychiatryonline.org/doi/10.1176/appi.pn.2020.5b13. Published May 7, 2020. Accessed August 7, 2020.
5. Webb Hooper M, Nápoles AM, Perez-Stable EJ. COVID-19 and racial/ethnic disparities. JAMA. 2020;323(24):2466-2467.
6. Sederer LI, Lanzara CB, Essock SM, et al. Lessons learned from the New York State mental health response to the September 11, 2001, attacks. Psychiatr Serv. 2011;62(9):1085-1089.
7. World Health Organization. Infodemic management – infodemiology. https://www.who.int/teams/risk-communication/infodemic-management. Accessed August 7, 2020.
8. Zhou J, Liu L, Xue P, et al. Mental health response to the COVID-19 outbreak in China. Am J Psychiatry. 2020;117(7):574-575.
9. Kawohl W, Nordt C. COVID-19, unemployment, and suicide. Lancet Psychiatry. 2020;7(5):389-390.
10. Yao H, Chen JH, Xu YF. Patients with mental health disorders in the COVID-19 epidemic. Lancet Psychiatry. 2020;7(4):e21. doi: 10.1016/S2215-0366(20)30090-0.
11. Minihan E, Gavin B, Kelly BD, et al. Covid-19, mental health and psychological first aid. Ir J Psychol Med. 2020:1-12.
12. Adja KYC, Golinelli D, Lenzi J, et al. Pandemics and social stigma: who’s next? Italy’s experience with COVID-19. Public Health. 2020;185:39-41.
13. Rosenberg AR. Cultivating deliberate resilience during the coronavirus disease 2019 pandemic [published online April 14, 2020]. JAMA Pediatr. doi: 10.1001/jamapediatrics.2020.1436.
14. Dean W, Talbot SG, Caplan A. Clarifying the language of clinician distress [published online January 31, 2020]. JAMA. doi: 10.1001/jama.2019.21576.
15. Emanuel EJ, Persad G, Upshur R, et al. Fair allocation of scarce medical resources in the time of Covid-19. N Engl J Med. 2020;382(21):2049-2055.
16. Rosenbaum L. Facing Covid-19 in Italy - ethics, logistics, and therapeutics on the epidemic’s front line. N Engl J Med. 2020;382(20):1873-1875.
17. Viceconte G, Petrosillo N. COVID-19 R0: magic number or conundrum? Infect Dis Rep. 2020;12(1):8516.
18. de Hert M, Schreurs V, Vancampfort D, van Winkel R. Metabolic syndrome in people with schizophrenia: a review. World Psychiatry. 2009;8(1):15-22.
19. Chen R, Liang W, Jiang M, et al. Risk factors of fatal outcome in hospitalized subjects with coronavirus disease 2019 from a nationwide analysis in China. Chest. 2020;158(1):97-105.
20. Finer N, Garnett SP, Bruun JM. COVID-19 and obesity. Clin Obes. 2020;10(3):e12365. doi: 10.1111/cob.12365.
21. Havens LL, Ghaemi SN. Existential despair and bipolar disorder: the therapeutic alliance as a mood stabilizer. Am J Psychother. 2005;59(2):137-147.
22. Trémeau F, Antonius D, Malaspina D, et al. Loneliness in schizophrenia and its possible correlates. An exploratory study. Psychiatry Res. 2016;246:211-217.
23. Menninger KA. Psychoses associated with influenza: I. General data: statistical analysis. JAMA. 1919;72(4):235-241.
24. Asadi-Pooya AA, Simani L. Central nervous system manifestations of COVID-19: a systematic review. J Neurol Sci. 2020;413:116832. doi: 10.1016/j.jns.2020.116832.
25. Ferrando SJ, Klepacz L, Lynch S, et al. COVID-19 psychosis: a potential new neuropsychiatric condition triggered by novel coronavirus infection and the inflammatory response? [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.012.
26. Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;87:34-39.
27. Martin Jr. EB. Brief psychotic disorder triggered by fear of coronavirus? Psychiatric Times. https://www.psychiatrictimes.com/view/brief-psychotic-disorder-triggered-fear-coronavirus-small-case-series. Published May 8, 2020. Accessed August 7, 2020.
28. Sher Y, Rabkin B, Maldonado JR, et al. COVID-19-associated hyperactive intensive care unit delirium with proposed pathophysiology and treatment: a case report [published online May 19, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.007.
29. Wolters AE, Peelen LM, Welling MC, et al. Long-term mental health problems after delirium in the ICU. Crit Care Med. 2016;44(10):1808-1813.
30. Toovey S. Influenza-associated central nervous system dysfunction: a literature review. Travel Med Infect Dis. 2008;6(3):114-124.
31. Brooks SK, Webster RK, Smith LE, et al. The psychological impact of quarantine and how to reduce it: rapid review of the evidence. Lancet. 2020;395(10227):912-920.
32. Maercker A, Brewin CR, Bryant RA, et al. Diagnosis and classification of disorders specifically associated with stress: proposals for ICD-11. World Psychiatry. 2013;12(3):198-206.
33. Ornell F, Moura HF, Scherer JN, et al. The COVID-19 pandemic and its impact on substance use: implications for prevention and treatment. Psychiatry Res. 2020;289:113096. doi: 10.1016/j.psychres.2020.113096.
34. Berlin I, Thomas D, Le Faou AL, Cornuz J. COVID-19 and smoking [published online April 3, 2020]. Nicotine Tob Res. https://doi.org/10.1093/ntr/ntaa059.
35. Back D, Marzolini C, Hodge C, et al. COVID-19 treatment in patients with comorbidities: awareness of drug-drug interactions [published online May 8, 2020]. Br J Clin Pharmacol. doi: 10.1111/bcp.14358.
36. Carpenter WT Jr., Buchanan RW, Kirkpatrick B, et al. Diazepam treatment of early signs of exacerbation in schizophrenia. Am J Psychiatry. 1999;156(2):299-303.
37. Dotson S, Hartvigsen N, Wesner T, et al. Clozapine toxicity in the setting of COVID-19 [published online May 30, 2020]. Psychosomatics. doi: 10.1016/j.psym.2020.05.025.
38. Siskind D, Honer WG, Clark S, et al. Consensus statement on the use of clozapine during the COVID-19 pandemic. J Psychiatry Neurosci. 2020;45(3):222-223.
39. Schnitzer K, MacLaurin S, Freudenreich O. Long-acting injectable antipsychotics during the COVID-19 pandemic. Current Psychiatry. In press.
40. Winston A, Rosenthal RN, Pinsker H. Learning supportive psychotherapy: an illustrated guide. Washington, DC: American Psychiatric Publishing; 2012.
41. Hollander JE, Carr BG. Virtually perfect? Telemedicine for Covid-19. N Engl J Med. 2020;382(18):1679-1681.
42. Jordan A, Dixon LB. Considerations for telepsychiatry service implementation in the era of COVID-19. Psychiatr Serv. 2020;71(6):643-644.
43. DePierro J, Lowe S, Katz C. Lessons learned from 9/11: mental health perspectives on the COVID-19 pandemic. Psychiatry Res. 2020;288:113024.
44. Hussain S. Immunization and vaccination. In: Huremovic´ D (ed). Psychiatry of pandemics: a mental health response to infection outbreak. Cham, Switzerland: Springer Nature Switzerland AG; 2019.
45. Epping-Jordan JE, van Ommeren M, Ashour HN, et al. Beyond the crisis: building back better mental health care in 10 emergency-affected areas using a longer-term perspective. Int J Ment Health Syst. 2015;9:15.
46. Rosenbaum L. The untold toll - the pandemic’s effects on patients without Covid-19. N Engl J Med. 2020;382(24):2368-2371.
47. Bartels SJ, Baggett TP, Freudenreich O, et al. COVID-19 emergency reforms in Massachusetts to support behavioral health care and reduce mortality of people with serious mental illness [published online June 3, 2020]. Psychiatr Serv. doi: 10.1176/appi.ps.202000244.

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