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Summary of the IDSA guidelines on the diagnosis of COVID-19
These guidelines were developed using a rigorous evidence-based approach, the GRADE framework, which involved identifying the important questions that need to be addressed ahead of time and, later, integrating the best available evidence into the recommendations.
The Food and Drug Administration’s Emergency Use Authorization is useful for understanding any recommendations related to COVID-19 testing. Under usual FDA approval, a manufacturer has to submit data on the performance of a test in human subjects. Under the Emergency Use Authorization for development and approval of SARS-CoV-2 testing, approval is based on “acceptable analytical accuracy,” meaning that a test is assessed using manufactured reagents. The approved test is not tested in real-world clinical situations prior to FDA approval, and the test’s sensitivity and specificity are not well described.
IDSA formulated 15 recommendations, of which the most relevant to primary care clinicians are described and discussed below. The complete set of recommendations can be viewed on the IDSA website:
Recommendation 1
The IDSA panel recommends a SARS-CoV-2 nucleic acid amplification test in symptomatic individuals in the community suspected of having COVID-19, even when the clinical suspicion is low (strong recommendation, very low certainty of evidence). The panel placed a high value on accurate assessment of COVID-19 with the intent of minimizing overdiagnosis of COVID-19 using clinical diagnosis alone. Without testing, the rate of overdiagnosis ranges from 62% to 98%.
If patients are misdiagnosed as having COVID-19, they may spend unnecessary time in quarantine and then may stop taking appropriate safety precautions to protect themselves from infection.
Recommendation 2
The IDSA panel suggests collecting nasopharyngeal, or mid-turbinate or nasal swabs, rather than oropharyngeal swabs or saliva alone for SARS-CoV-2 RNA testing in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, very low certainty of evidence).
The rationale for this recommendation is that comparative data showed a much lower sensitivity for oral sampling, compared with nasopharyngeal, mid-turbinate, or nasal sampling.
The average sensitivity of oral swabs is 56%, compared with nasopharyngeal at 97%, mid-turbinate at 100%, and nasal sampling at 95%. Given these test characteristics, there are far less false-negative tests with nasopharyngeal, mid-turbinate, and nasal swabs. Fewer false negatives means fewer instances of incorrectly telling COVID-19–positive patients that they do not have the illness. An exciting new area of testing that is being evaluated is saliva, which appears to have a sensitivity of 85%.
Recommendation 3
The IDSA panel suggests that nasal and mid-turbinate swab specimens may be collected for SARS-CoV-2 RNA testing by either patients or health care providers in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, low certainty of evidence).
This recommendation is particularly exciting because patient self-collection provides the potential for health care personnel to avoid exposure to infection, as can occur when health care personnel are swabbing a patient; this is ow testing has been done at most testing centers.
While the data are limited, it appears that patient self-collection of nasal or mid-turbinate swabs results in similar detection rates as occurs with health care personnel–collected nasopharyngeal swabs.
Recommendation 6
The IDSA panel suggests repeating viral RNA testing when the initial test is negative (versus performing a single test) in symptomatic individuals with an intermediate or high clinical suspicion of COVID-19 (conditional recommendation, low certainty of evidence).
Since none of the tests are perfect and any can have false negatives, the panel places a high value on detecting infection when present. If there is a low clinical likelihood of disease, the panel recommends not retesting. When the clinical likelihood of COVID-19 is moderate to high, in the event that the initial test is negative, the panel recommends retesting for COVID-19 1-2 days after the initial test.
Recommendation 8
The IDSA panel suggests SARS-CoV-2 RNA testing in asymptomatic individuals who are either known or suspected to have been exposed to COVID-19 (conditional recommendation, very low certainty of evidence).
For this recommendation, a known contact is defined as someone who has had direct contact with a confirmed case.
A suspected exposure occurs when someone is working or living in a congregate setting such as long-term care, a correctional facility, or a cruise ship in which there is an outbreak. The time frame during which to do post-exposure testing is five to seven days after the exposure.
Recommendation 10
The IDSA panel recommends direct SARS-CoV-2 RNA testing in asymptomatic individuals with no known contact with COVID-19 who are being hospitalized in areas with a high prevalence of COVID-19 in the community (conditional recommendation, very low certainty of evidence).
The idea is to do rapid testing to identify individuals entering the hospital either for other illnesses or for procedures, in order to be able to institute appropriate precautions and decrease the likelihood of nosocomial transmission and/or transmission to health care personnel. It is worth noting that the recommendations do not address testing in areas with a low or intermediate prevalence of COVID-19. In the absence of an official guideline-based-recommendation, the decision about testing needs to made by the local hospital system.
Recommendations 11, 12, and 13
The IDSA panel recommends SARS-CoV-2 RNA testing in immunocompromised asymptomatic individuals who are being admitted to the hospital and in asymptomatic individuals prior to receiving immunosuppressive therapy regardless of exposure to COVID-19. It is also recommended to test asymptomatic individuals planning to undergo major surgery.
The rationale for this recommendation is that patients who are to receive chemotherapy, other immunosuppressive procedures, or surgery are at high risk if they have COVID-19 and may be better off delaying the procedure.
Some additional issues were addressed, though not in the form of additional recommendations. It was clarified that some individuals remain nucleic acid positive after their symptoms resolve, and sometimes even after seroconversion. It is not clear if those individuals remain infectious to others. The recommendations did not address serologic testing for public health surveillance.
Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.
SOURCE: Hanson KE et al. Infectious Diseases Society of America guidelines on the diagnosis of COVID-19.
These guidelines were developed using a rigorous evidence-based approach, the GRADE framework, which involved identifying the important questions that need to be addressed ahead of time and, later, integrating the best available evidence into the recommendations.
The Food and Drug Administration’s Emergency Use Authorization is useful for understanding any recommendations related to COVID-19 testing. Under usual FDA approval, a manufacturer has to submit data on the performance of a test in human subjects. Under the Emergency Use Authorization for development and approval of SARS-CoV-2 testing, approval is based on “acceptable analytical accuracy,” meaning that a test is assessed using manufactured reagents. The approved test is not tested in real-world clinical situations prior to FDA approval, and the test’s sensitivity and specificity are not well described.
IDSA formulated 15 recommendations, of which the most relevant to primary care clinicians are described and discussed below. The complete set of recommendations can be viewed on the IDSA website:
Recommendation 1
The IDSA panel recommends a SARS-CoV-2 nucleic acid amplification test in symptomatic individuals in the community suspected of having COVID-19, even when the clinical suspicion is low (strong recommendation, very low certainty of evidence). The panel placed a high value on accurate assessment of COVID-19 with the intent of minimizing overdiagnosis of COVID-19 using clinical diagnosis alone. Without testing, the rate of overdiagnosis ranges from 62% to 98%.
If patients are misdiagnosed as having COVID-19, they may spend unnecessary time in quarantine and then may stop taking appropriate safety precautions to protect themselves from infection.
Recommendation 2
The IDSA panel suggests collecting nasopharyngeal, or mid-turbinate or nasal swabs, rather than oropharyngeal swabs or saliva alone for SARS-CoV-2 RNA testing in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, very low certainty of evidence).
The rationale for this recommendation is that comparative data showed a much lower sensitivity for oral sampling, compared with nasopharyngeal, mid-turbinate, or nasal sampling.
The average sensitivity of oral swabs is 56%, compared with nasopharyngeal at 97%, mid-turbinate at 100%, and nasal sampling at 95%. Given these test characteristics, there are far less false-negative tests with nasopharyngeal, mid-turbinate, and nasal swabs. Fewer false negatives means fewer instances of incorrectly telling COVID-19–positive patients that they do not have the illness. An exciting new area of testing that is being evaluated is saliva, which appears to have a sensitivity of 85%.
Recommendation 3
The IDSA panel suggests that nasal and mid-turbinate swab specimens may be collected for SARS-CoV-2 RNA testing by either patients or health care providers in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, low certainty of evidence).
This recommendation is particularly exciting because patient self-collection provides the potential for health care personnel to avoid exposure to infection, as can occur when health care personnel are swabbing a patient; this is ow testing has been done at most testing centers.
While the data are limited, it appears that patient self-collection of nasal or mid-turbinate swabs results in similar detection rates as occurs with health care personnel–collected nasopharyngeal swabs.
Recommendation 6
The IDSA panel suggests repeating viral RNA testing when the initial test is negative (versus performing a single test) in symptomatic individuals with an intermediate or high clinical suspicion of COVID-19 (conditional recommendation, low certainty of evidence).
Since none of the tests are perfect and any can have false negatives, the panel places a high value on detecting infection when present. If there is a low clinical likelihood of disease, the panel recommends not retesting. When the clinical likelihood of COVID-19 is moderate to high, in the event that the initial test is negative, the panel recommends retesting for COVID-19 1-2 days after the initial test.
Recommendation 8
The IDSA panel suggests SARS-CoV-2 RNA testing in asymptomatic individuals who are either known or suspected to have been exposed to COVID-19 (conditional recommendation, very low certainty of evidence).
For this recommendation, a known contact is defined as someone who has had direct contact with a confirmed case.
A suspected exposure occurs when someone is working or living in a congregate setting such as long-term care, a correctional facility, or a cruise ship in which there is an outbreak. The time frame during which to do post-exposure testing is five to seven days after the exposure.
Recommendation 10
The IDSA panel recommends direct SARS-CoV-2 RNA testing in asymptomatic individuals with no known contact with COVID-19 who are being hospitalized in areas with a high prevalence of COVID-19 in the community (conditional recommendation, very low certainty of evidence).
The idea is to do rapid testing to identify individuals entering the hospital either for other illnesses or for procedures, in order to be able to institute appropriate precautions and decrease the likelihood of nosocomial transmission and/or transmission to health care personnel. It is worth noting that the recommendations do not address testing in areas with a low or intermediate prevalence of COVID-19. In the absence of an official guideline-based-recommendation, the decision about testing needs to made by the local hospital system.
Recommendations 11, 12, and 13
The IDSA panel recommends SARS-CoV-2 RNA testing in immunocompromised asymptomatic individuals who are being admitted to the hospital and in asymptomatic individuals prior to receiving immunosuppressive therapy regardless of exposure to COVID-19. It is also recommended to test asymptomatic individuals planning to undergo major surgery.
The rationale for this recommendation is that patients who are to receive chemotherapy, other immunosuppressive procedures, or surgery are at high risk if they have COVID-19 and may be better off delaying the procedure.
Some additional issues were addressed, though not in the form of additional recommendations. It was clarified that some individuals remain nucleic acid positive after their symptoms resolve, and sometimes even after seroconversion. It is not clear if those individuals remain infectious to others. The recommendations did not address serologic testing for public health surveillance.
Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.
SOURCE: Hanson KE et al. Infectious Diseases Society of America guidelines on the diagnosis of COVID-19.
These guidelines were developed using a rigorous evidence-based approach, the GRADE framework, which involved identifying the important questions that need to be addressed ahead of time and, later, integrating the best available evidence into the recommendations.
The Food and Drug Administration’s Emergency Use Authorization is useful for understanding any recommendations related to COVID-19 testing. Under usual FDA approval, a manufacturer has to submit data on the performance of a test in human subjects. Under the Emergency Use Authorization for development and approval of SARS-CoV-2 testing, approval is based on “acceptable analytical accuracy,” meaning that a test is assessed using manufactured reagents. The approved test is not tested in real-world clinical situations prior to FDA approval, and the test’s sensitivity and specificity are not well described.
IDSA formulated 15 recommendations, of which the most relevant to primary care clinicians are described and discussed below. The complete set of recommendations can be viewed on the IDSA website:
Recommendation 1
The IDSA panel recommends a SARS-CoV-2 nucleic acid amplification test in symptomatic individuals in the community suspected of having COVID-19, even when the clinical suspicion is low (strong recommendation, very low certainty of evidence). The panel placed a high value on accurate assessment of COVID-19 with the intent of minimizing overdiagnosis of COVID-19 using clinical diagnosis alone. Without testing, the rate of overdiagnosis ranges from 62% to 98%.
If patients are misdiagnosed as having COVID-19, they may spend unnecessary time in quarantine and then may stop taking appropriate safety precautions to protect themselves from infection.
Recommendation 2
The IDSA panel suggests collecting nasopharyngeal, or mid-turbinate or nasal swabs, rather than oropharyngeal swabs or saliva alone for SARS-CoV-2 RNA testing in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, very low certainty of evidence).
The rationale for this recommendation is that comparative data showed a much lower sensitivity for oral sampling, compared with nasopharyngeal, mid-turbinate, or nasal sampling.
The average sensitivity of oral swabs is 56%, compared with nasopharyngeal at 97%, mid-turbinate at 100%, and nasal sampling at 95%. Given these test characteristics, there are far less false-negative tests with nasopharyngeal, mid-turbinate, and nasal swabs. Fewer false negatives means fewer instances of incorrectly telling COVID-19–positive patients that they do not have the illness. An exciting new area of testing that is being evaluated is saliva, which appears to have a sensitivity of 85%.
Recommendation 3
The IDSA panel suggests that nasal and mid-turbinate swab specimens may be collected for SARS-CoV-2 RNA testing by either patients or health care providers in symptomatic individuals with upper respiratory tract infection or influenza-like illness suspected of having COVID-19 (conditional recommendation, low certainty of evidence).
This recommendation is particularly exciting because patient self-collection provides the potential for health care personnel to avoid exposure to infection, as can occur when health care personnel are swabbing a patient; this is ow testing has been done at most testing centers.
While the data are limited, it appears that patient self-collection of nasal or mid-turbinate swabs results in similar detection rates as occurs with health care personnel–collected nasopharyngeal swabs.
Recommendation 6
The IDSA panel suggests repeating viral RNA testing when the initial test is negative (versus performing a single test) in symptomatic individuals with an intermediate or high clinical suspicion of COVID-19 (conditional recommendation, low certainty of evidence).
Since none of the tests are perfect and any can have false negatives, the panel places a high value on detecting infection when present. If there is a low clinical likelihood of disease, the panel recommends not retesting. When the clinical likelihood of COVID-19 is moderate to high, in the event that the initial test is negative, the panel recommends retesting for COVID-19 1-2 days after the initial test.
Recommendation 8
The IDSA panel suggests SARS-CoV-2 RNA testing in asymptomatic individuals who are either known or suspected to have been exposed to COVID-19 (conditional recommendation, very low certainty of evidence).
For this recommendation, a known contact is defined as someone who has had direct contact with a confirmed case.
A suspected exposure occurs when someone is working or living in a congregate setting such as long-term care, a correctional facility, or a cruise ship in which there is an outbreak. The time frame during which to do post-exposure testing is five to seven days after the exposure.
Recommendation 10
The IDSA panel recommends direct SARS-CoV-2 RNA testing in asymptomatic individuals with no known contact with COVID-19 who are being hospitalized in areas with a high prevalence of COVID-19 in the community (conditional recommendation, very low certainty of evidence).
The idea is to do rapid testing to identify individuals entering the hospital either for other illnesses or for procedures, in order to be able to institute appropriate precautions and decrease the likelihood of nosocomial transmission and/or transmission to health care personnel. It is worth noting that the recommendations do not address testing in areas with a low or intermediate prevalence of COVID-19. In the absence of an official guideline-based-recommendation, the decision about testing needs to made by the local hospital system.
Recommendations 11, 12, and 13
The IDSA panel recommends SARS-CoV-2 RNA testing in immunocompromised asymptomatic individuals who are being admitted to the hospital and in asymptomatic individuals prior to receiving immunosuppressive therapy regardless of exposure to COVID-19. It is also recommended to test asymptomatic individuals planning to undergo major surgery.
The rationale for this recommendation is that patients who are to receive chemotherapy, other immunosuppressive procedures, or surgery are at high risk if they have COVID-19 and may be better off delaying the procedure.
Some additional issues were addressed, though not in the form of additional recommendations. It was clarified that some individuals remain nucleic acid positive after their symptoms resolve, and sometimes even after seroconversion. It is not clear if those individuals remain infectious to others. The recommendations did not address serologic testing for public health surveillance.
Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.
SOURCE: Hanson KE et al. Infectious Diseases Society of America guidelines on the diagnosis of COVID-19.
Even with mild COVID-19, athletes need cardiac testing before returning to play
Potential risks of cardiac injury posed by coronavirus disease 2019 (COVID-19) infection warrant a cautious return-to-play for highly active people and competitive athletes who test positive, according to leading sports cardiologists.
To prevent cardiac injury, athletes should rest for at least 2 weeks after symptoms resolve, then undergo cardiac testing before returning high-level competitive sports, reported lead author Dermot Phelan, MD, PhD, of Atrium Health in Charlotte, N.C., and colleagues.
These recommendations, which were published in JAMA Cardiology, are part of a clinical algorithm that sorts athletes based on coronavirus test status and symptom severity. The algorithm offers a clear timeline for resumption of activity, with management decisions for symptomatic individuals based on additional diagnostics, such as high-sensitivity troponin testing and electrocardiogram.
Despite a scarcity of relevant clinical data, Dr. Phelan said that he and his colleagues wanted to offer their best recommendations to the athletic community, who had been reaching out for help.
“We were getting calls and messages from amateur and professional sporting organizations from around the country asking for guidance about what to do,” Dr. Phelan said. “So a number of us from the American College of Cardiology Sports and Exercise Council decided that we really should provide some guidance even in the absence of good, strong data, for what we feel is a reasonable approach.”
The recommendations were based on what is known of other viral infections, as well as risks posed by COVID-19 that may be worsened by athletic activity.
“We know that, when people have an active infection, vigorous exercise can lower immunity, and that can make the infection worse,” Dr. Phelan said. “That really applies very strongly in people who have had myocarditis. If you exercise when you have myocarditis, it actually increases viral replication and results in increased necrosis of the heart muscle. We really want to avoid exercising during that active infection phase.”
Myocarditis is one of the top causes of sudden cardiac death among young athletes, Dr. Phelan said, “so that’s a major concern for us.”
According to Dr. Phelan, existing data suggest a wide range of incidence of 7%-33% for cardiac injury among patients hospitalized for COVID-19. Even the low end of this range, at 7%, is significantly higher than the incidence rate of 1% found in patients with non–COVID-19 acute viral infections.
“This particular virus appears to cause more cardiac insults than other viruses,” Dr. Phelan said.
The incidence of cardiac injury among nonhospitalized patients remains unknown, leaving a wide knowledge gap that shaped the conservative nature of the present recommendations.
With more information, however, the guidance may “change dramatically,” Dr. Phelan said.
“If the data come back and show that no nonhospitalized patients got cardiac injury, then we would be much more comfortable allowing return to play without the need for cardiac testing,” he said.
Conversely, if cardiac injury is more common than anticipated, then more extensive testing may be needed, he added.
As the algorithm stands, high-sensitivity troponin testing and/or cardiac studies are recommended for all symptomatic athletes; if troponin levels are greater than the 99th percentile or a cardiac study is abnormal, then clinicians should follow return-to-play guidelines for myocarditis. For athletes with normal tests, slow resumption of activity is recommended, including close monitoring for clinical deterioration.
As Dr. Phelan discussed these recommendations in a broader context, he emphasized the need for caution, both preventively, and for cardiologists working with recovering athletes.
“For the early stage of this reentry into normal life while this is still an active pandemic, we need to be cautious,” Dr. Phelan said. “We need to follow the regular CDC guidelines, in terms of social distancing and handwashing, but we also need to consider that those people who have suffered from COVID-19 may have had cardiac injury. We don’t know that yet. But we need to be cautious with these individuals and test them before they return to high-level competitive sports.”
One author disclosed a relationship with the Atlanta Falcons.
SOURCE: Phelan D et al. JAMA Cardiology. 2020 Apr 13. doi: 10.1001/jamacardio.2020.2136.
Potential risks of cardiac injury posed by coronavirus disease 2019 (COVID-19) infection warrant a cautious return-to-play for highly active people and competitive athletes who test positive, according to leading sports cardiologists.
To prevent cardiac injury, athletes should rest for at least 2 weeks after symptoms resolve, then undergo cardiac testing before returning high-level competitive sports, reported lead author Dermot Phelan, MD, PhD, of Atrium Health in Charlotte, N.C., and colleagues.
These recommendations, which were published in JAMA Cardiology, are part of a clinical algorithm that sorts athletes based on coronavirus test status and symptom severity. The algorithm offers a clear timeline for resumption of activity, with management decisions for symptomatic individuals based on additional diagnostics, such as high-sensitivity troponin testing and electrocardiogram.
Despite a scarcity of relevant clinical data, Dr. Phelan said that he and his colleagues wanted to offer their best recommendations to the athletic community, who had been reaching out for help.
“We were getting calls and messages from amateur and professional sporting organizations from around the country asking for guidance about what to do,” Dr. Phelan said. “So a number of us from the American College of Cardiology Sports and Exercise Council decided that we really should provide some guidance even in the absence of good, strong data, for what we feel is a reasonable approach.”
The recommendations were based on what is known of other viral infections, as well as risks posed by COVID-19 that may be worsened by athletic activity.
“We know that, when people have an active infection, vigorous exercise can lower immunity, and that can make the infection worse,” Dr. Phelan said. “That really applies very strongly in people who have had myocarditis. If you exercise when you have myocarditis, it actually increases viral replication and results in increased necrosis of the heart muscle. We really want to avoid exercising during that active infection phase.”
Myocarditis is one of the top causes of sudden cardiac death among young athletes, Dr. Phelan said, “so that’s a major concern for us.”
According to Dr. Phelan, existing data suggest a wide range of incidence of 7%-33% for cardiac injury among patients hospitalized for COVID-19. Even the low end of this range, at 7%, is significantly higher than the incidence rate of 1% found in patients with non–COVID-19 acute viral infections.
“This particular virus appears to cause more cardiac insults than other viruses,” Dr. Phelan said.
The incidence of cardiac injury among nonhospitalized patients remains unknown, leaving a wide knowledge gap that shaped the conservative nature of the present recommendations.
With more information, however, the guidance may “change dramatically,” Dr. Phelan said.
“If the data come back and show that no nonhospitalized patients got cardiac injury, then we would be much more comfortable allowing return to play without the need for cardiac testing,” he said.
Conversely, if cardiac injury is more common than anticipated, then more extensive testing may be needed, he added.
As the algorithm stands, high-sensitivity troponin testing and/or cardiac studies are recommended for all symptomatic athletes; if troponin levels are greater than the 99th percentile or a cardiac study is abnormal, then clinicians should follow return-to-play guidelines for myocarditis. For athletes with normal tests, slow resumption of activity is recommended, including close monitoring for clinical deterioration.
As Dr. Phelan discussed these recommendations in a broader context, he emphasized the need for caution, both preventively, and for cardiologists working with recovering athletes.
“For the early stage of this reentry into normal life while this is still an active pandemic, we need to be cautious,” Dr. Phelan said. “We need to follow the regular CDC guidelines, in terms of social distancing and handwashing, but we also need to consider that those people who have suffered from COVID-19 may have had cardiac injury. We don’t know that yet. But we need to be cautious with these individuals and test them before they return to high-level competitive sports.”
One author disclosed a relationship with the Atlanta Falcons.
SOURCE: Phelan D et al. JAMA Cardiology. 2020 Apr 13. doi: 10.1001/jamacardio.2020.2136.
Potential risks of cardiac injury posed by coronavirus disease 2019 (COVID-19) infection warrant a cautious return-to-play for highly active people and competitive athletes who test positive, according to leading sports cardiologists.
To prevent cardiac injury, athletes should rest for at least 2 weeks after symptoms resolve, then undergo cardiac testing before returning high-level competitive sports, reported lead author Dermot Phelan, MD, PhD, of Atrium Health in Charlotte, N.C., and colleagues.
These recommendations, which were published in JAMA Cardiology, are part of a clinical algorithm that sorts athletes based on coronavirus test status and symptom severity. The algorithm offers a clear timeline for resumption of activity, with management decisions for symptomatic individuals based on additional diagnostics, such as high-sensitivity troponin testing and electrocardiogram.
Despite a scarcity of relevant clinical data, Dr. Phelan said that he and his colleagues wanted to offer their best recommendations to the athletic community, who had been reaching out for help.
“We were getting calls and messages from amateur and professional sporting organizations from around the country asking for guidance about what to do,” Dr. Phelan said. “So a number of us from the American College of Cardiology Sports and Exercise Council decided that we really should provide some guidance even in the absence of good, strong data, for what we feel is a reasonable approach.”
The recommendations were based on what is known of other viral infections, as well as risks posed by COVID-19 that may be worsened by athletic activity.
“We know that, when people have an active infection, vigorous exercise can lower immunity, and that can make the infection worse,” Dr. Phelan said. “That really applies very strongly in people who have had myocarditis. If you exercise when you have myocarditis, it actually increases viral replication and results in increased necrosis of the heart muscle. We really want to avoid exercising during that active infection phase.”
Myocarditis is one of the top causes of sudden cardiac death among young athletes, Dr. Phelan said, “so that’s a major concern for us.”
According to Dr. Phelan, existing data suggest a wide range of incidence of 7%-33% for cardiac injury among patients hospitalized for COVID-19. Even the low end of this range, at 7%, is significantly higher than the incidence rate of 1% found in patients with non–COVID-19 acute viral infections.
“This particular virus appears to cause more cardiac insults than other viruses,” Dr. Phelan said.
The incidence of cardiac injury among nonhospitalized patients remains unknown, leaving a wide knowledge gap that shaped the conservative nature of the present recommendations.
With more information, however, the guidance may “change dramatically,” Dr. Phelan said.
“If the data come back and show that no nonhospitalized patients got cardiac injury, then we would be much more comfortable allowing return to play without the need for cardiac testing,” he said.
Conversely, if cardiac injury is more common than anticipated, then more extensive testing may be needed, he added.
As the algorithm stands, high-sensitivity troponin testing and/or cardiac studies are recommended for all symptomatic athletes; if troponin levels are greater than the 99th percentile or a cardiac study is abnormal, then clinicians should follow return-to-play guidelines for myocarditis. For athletes with normal tests, slow resumption of activity is recommended, including close monitoring for clinical deterioration.
As Dr. Phelan discussed these recommendations in a broader context, he emphasized the need for caution, both preventively, and for cardiologists working with recovering athletes.
“For the early stage of this reentry into normal life while this is still an active pandemic, we need to be cautious,” Dr. Phelan said. “We need to follow the regular CDC guidelines, in terms of social distancing and handwashing, but we also need to consider that those people who have suffered from COVID-19 may have had cardiac injury. We don’t know that yet. But we need to be cautious with these individuals and test them before they return to high-level competitive sports.”
One author disclosed a relationship with the Atlanta Falcons.
SOURCE: Phelan D et al. JAMA Cardiology. 2020 Apr 13. doi: 10.1001/jamacardio.2020.2136.
FROM JAMA CARDIOLOGY
Comparing COVID-19, flu death tolls ‘extremely dangerous’
The number of COVID-19 deaths cannot be directly compared to the number of seasonal influenza deaths because they are calculated differently, researchers say in a report released today.
Whereas COVID-19 death rates are determined from actual counts of people who have died, seasonal influenza death rates are estimated by the Centers for Disease Control and Prevention (CDC) using population modeling algorithms, explains Jeremy Samuel Faust, MD, with Harvard Medical School and Brigham and Women’s Hospital, Division of Health Policy and Public Health in Boston, Massachusetts.
The CDC estimates that between 24,000 and 62,000 people died from influenza during the 2019-2020 season (through April 4). At the time of the analysis (as of April 28), COVID-19 deaths had reached 65,000 in the United States.
But making that comparison “is extremely dangerous,” Faust told Medscape Medical News.
“COVID-19 is far more dangerous and is wreaking far more havoc than seasonal influenza ever has,” he said.
Faust coauthored the perspective article, published online in JAMA Internal Medicine, with Carlos del Rio, MD, Division of Infectious Diseases at Emory University School of Medicine in Atlanta, Georgia.
The message and methodology of Faust’s and del Rio’s article are on target, according to Jonathan L. Temte, MD, PhD, who has been working in influenza surveillance for almost 25 years.
Current flu data draw on limited information from primary care practices and hospitals, said Dr. Temte, associate dean for public health and community engagement at the University of Wisconsin School of Medicine and Public Health in Madison. The estimates help bridge the gaps, he said, but the system is inherently vulnerable to error.
“Comparing them – as so many people in this country have done – to try to diminish the impact of SARS-CoV2 is not fair,” he said.
Estimated versus actual influenza deaths
The authors illustrate the difference in the way rates of death from influenza are calculated: “Between 2013-2014 and 2018-2019, the reported yearly estimated influenza deaths ranged from 23,000 to 61,000. Over that same time period, however, the number of counted influenza deaths was between 3,448 and 15,620 yearly.”
“It’s apparent [the CDC has] been overestimating,” Faust said. “If you publish a number on the higher end of the estimate, people might take your public health messages more seriously, such as, it’s important to get your yearly flu shot.”
He added that until influenza death rates started to be compared with COVID-19 rates, “there was never really a downside” to reporting estimates.
Dr. Temte said he doesn’t regard overestimating flu deaths as intentional but rather the result of a longstanding “bias against the elderly in this country” that the estimates are meant to account for.
For example, he says, reporting influenza deaths is mandatory when such deaths involve persons younger than 18 years but not when they involve adults.
Also, traditionally, influenza has been seen “as a cause of death in people with multiple comorbidities that was just part and parcel of wintertime,” Dr. Temte said.
“The likelihood of being tested for influenza goes down greatly when you’re older,” he said. “This is slowly changing.”
The CDC acknowledges on its website that it “does not know the exact number of people who have been sick and affected by influenza because influenza is not a reportable disease in most areas of the US.”
It adds that the burden is estimated through the US Influenza Surveillance System, which covers approximately 8.5% of the US population.
Comparing recorded deaths
It’s more accurate and meaningful to compare actual numbers of deaths for the diseases, Dr. Faust and Dr. del Rio say in their article.
When the authors made that comparison, they drew a stark contrast.
There were 15,455 recorded COVID-19 deaths in the week that ended April 21. The week before, the number of recorded deaths was 14,478, they found. (Those were the two most recent weeks before they submitted their article for publication.)
In comparison, counted deaths ranged from 351 to 1,626 during the peak week of the seven influenza seasons between 2013-2014 and 2019-2020. The average counted deaths for the peak week of the seven seasons was 752.4 (95% confidence interval, 558.8-946.1).
“These statistics on counted deaths suggest that the number of COVID-19 deaths for the week ending April 21 was 9.5-fold to 44.1-fold greater than the peak week of counted influenza deaths during the past seven influenza seasons in the US, with a 20.5-fold mean increase (95% CI, 16.3-27.7),” the authors write.
However, Natasha Chida, MD, MSPH, an infectious disease physician and assistant professor at the Johns Hopkins University School of Medicine in Baltimore, Maryland, said in an interview that the actual number of deaths doesn’t tell the complete flu story either. That count would miss people who later died from secondary complications associated with influenza, she said.
“There’s just no way to reliably count influenza deaths,” she said. “I think if we required it as a reported illness, that would be the ideal situation, but there’s so much flu every year that that probably would not be practical.”
She said she agrees that rates of influenza deaths and rates of COVID-19 deaths cannot be fairly compared.
What the authors don’t touch on, she said, is that flu season lasts 4 to 6 months a year, and just 3 months into the coronavirus pandemic, US deaths due to COVID-19 are already higher than those for seasonal influenza.
“Even if we look at it in the way that people who think we can compare flu and coronavirus do, it’s still not going to work out in their favor from a numbers standpoint,” she said.
The article clarifies the differences for “people who don’t live in the flu world,” she said.
“It is not accurate to compare the two for the reasons the authors described and also because they are very different diseases,” she added.
Real-life validation
Dr. Faust said in an interview that real-life experiences add external validity to their analysis.
Differences in the way deaths are calculated does not reflect frontline clinical conditions during the COVID-19 crisis, with hospitals stretched past their limits, ventilator shortages, and bodies stacking up in some overwhelmed facilities, the authors say.
Dr. Temte said the external validation of the numbers also rings true in light of his own experience.
He said that, in the past 2 months, he has known two people who have had family members who died of COVID-19.
Conversely, “I would have to search long and hard to come up with people I have known or have been one degree of separation from” who have died from influenza, Dr. Temte said.
The authors, Dr. Temte, and Dr. Chida report no relevant financial relationships.
This article first appeared on Medscape.com.
The number of COVID-19 deaths cannot be directly compared to the number of seasonal influenza deaths because they are calculated differently, researchers say in a report released today.
Whereas COVID-19 death rates are determined from actual counts of people who have died, seasonal influenza death rates are estimated by the Centers for Disease Control and Prevention (CDC) using population modeling algorithms, explains Jeremy Samuel Faust, MD, with Harvard Medical School and Brigham and Women’s Hospital, Division of Health Policy and Public Health in Boston, Massachusetts.
The CDC estimates that between 24,000 and 62,000 people died from influenza during the 2019-2020 season (through April 4). At the time of the analysis (as of April 28), COVID-19 deaths had reached 65,000 in the United States.
But making that comparison “is extremely dangerous,” Faust told Medscape Medical News.
“COVID-19 is far more dangerous and is wreaking far more havoc than seasonal influenza ever has,” he said.
Faust coauthored the perspective article, published online in JAMA Internal Medicine, with Carlos del Rio, MD, Division of Infectious Diseases at Emory University School of Medicine in Atlanta, Georgia.
The message and methodology of Faust’s and del Rio’s article are on target, according to Jonathan L. Temte, MD, PhD, who has been working in influenza surveillance for almost 25 years.
Current flu data draw on limited information from primary care practices and hospitals, said Dr. Temte, associate dean for public health and community engagement at the University of Wisconsin School of Medicine and Public Health in Madison. The estimates help bridge the gaps, he said, but the system is inherently vulnerable to error.
“Comparing them – as so many people in this country have done – to try to diminish the impact of SARS-CoV2 is not fair,” he said.
Estimated versus actual influenza deaths
The authors illustrate the difference in the way rates of death from influenza are calculated: “Between 2013-2014 and 2018-2019, the reported yearly estimated influenza deaths ranged from 23,000 to 61,000. Over that same time period, however, the number of counted influenza deaths was between 3,448 and 15,620 yearly.”
“It’s apparent [the CDC has] been overestimating,” Faust said. “If you publish a number on the higher end of the estimate, people might take your public health messages more seriously, such as, it’s important to get your yearly flu shot.”
He added that until influenza death rates started to be compared with COVID-19 rates, “there was never really a downside” to reporting estimates.
Dr. Temte said he doesn’t regard overestimating flu deaths as intentional but rather the result of a longstanding “bias against the elderly in this country” that the estimates are meant to account for.
For example, he says, reporting influenza deaths is mandatory when such deaths involve persons younger than 18 years but not when they involve adults.
Also, traditionally, influenza has been seen “as a cause of death in people with multiple comorbidities that was just part and parcel of wintertime,” Dr. Temte said.
“The likelihood of being tested for influenza goes down greatly when you’re older,” he said. “This is slowly changing.”
The CDC acknowledges on its website that it “does not know the exact number of people who have been sick and affected by influenza because influenza is not a reportable disease in most areas of the US.”
It adds that the burden is estimated through the US Influenza Surveillance System, which covers approximately 8.5% of the US population.
Comparing recorded deaths
It’s more accurate and meaningful to compare actual numbers of deaths for the diseases, Dr. Faust and Dr. del Rio say in their article.
When the authors made that comparison, they drew a stark contrast.
There were 15,455 recorded COVID-19 deaths in the week that ended April 21. The week before, the number of recorded deaths was 14,478, they found. (Those were the two most recent weeks before they submitted their article for publication.)
In comparison, counted deaths ranged from 351 to 1,626 during the peak week of the seven influenza seasons between 2013-2014 and 2019-2020. The average counted deaths for the peak week of the seven seasons was 752.4 (95% confidence interval, 558.8-946.1).
“These statistics on counted deaths suggest that the number of COVID-19 deaths for the week ending April 21 was 9.5-fold to 44.1-fold greater than the peak week of counted influenza deaths during the past seven influenza seasons in the US, with a 20.5-fold mean increase (95% CI, 16.3-27.7),” the authors write.
However, Natasha Chida, MD, MSPH, an infectious disease physician and assistant professor at the Johns Hopkins University School of Medicine in Baltimore, Maryland, said in an interview that the actual number of deaths doesn’t tell the complete flu story either. That count would miss people who later died from secondary complications associated with influenza, she said.
“There’s just no way to reliably count influenza deaths,” she said. “I think if we required it as a reported illness, that would be the ideal situation, but there’s so much flu every year that that probably would not be practical.”
She said she agrees that rates of influenza deaths and rates of COVID-19 deaths cannot be fairly compared.
What the authors don’t touch on, she said, is that flu season lasts 4 to 6 months a year, and just 3 months into the coronavirus pandemic, US deaths due to COVID-19 are already higher than those for seasonal influenza.
“Even if we look at it in the way that people who think we can compare flu and coronavirus do, it’s still not going to work out in their favor from a numbers standpoint,” she said.
The article clarifies the differences for “people who don’t live in the flu world,” she said.
“It is not accurate to compare the two for the reasons the authors described and also because they are very different diseases,” she added.
Real-life validation
Dr. Faust said in an interview that real-life experiences add external validity to their analysis.
Differences in the way deaths are calculated does not reflect frontline clinical conditions during the COVID-19 crisis, with hospitals stretched past their limits, ventilator shortages, and bodies stacking up in some overwhelmed facilities, the authors say.
Dr. Temte said the external validation of the numbers also rings true in light of his own experience.
He said that, in the past 2 months, he has known two people who have had family members who died of COVID-19.
Conversely, “I would have to search long and hard to come up with people I have known or have been one degree of separation from” who have died from influenza, Dr. Temte said.
The authors, Dr. Temte, and Dr. Chida report no relevant financial relationships.
This article first appeared on Medscape.com.
The number of COVID-19 deaths cannot be directly compared to the number of seasonal influenza deaths because they are calculated differently, researchers say in a report released today.
Whereas COVID-19 death rates are determined from actual counts of people who have died, seasonal influenza death rates are estimated by the Centers for Disease Control and Prevention (CDC) using population modeling algorithms, explains Jeremy Samuel Faust, MD, with Harvard Medical School and Brigham and Women’s Hospital, Division of Health Policy and Public Health in Boston, Massachusetts.
The CDC estimates that between 24,000 and 62,000 people died from influenza during the 2019-2020 season (through April 4). At the time of the analysis (as of April 28), COVID-19 deaths had reached 65,000 in the United States.
But making that comparison “is extremely dangerous,” Faust told Medscape Medical News.
“COVID-19 is far more dangerous and is wreaking far more havoc than seasonal influenza ever has,” he said.
Faust coauthored the perspective article, published online in JAMA Internal Medicine, with Carlos del Rio, MD, Division of Infectious Diseases at Emory University School of Medicine in Atlanta, Georgia.
The message and methodology of Faust’s and del Rio’s article are on target, according to Jonathan L. Temte, MD, PhD, who has been working in influenza surveillance for almost 25 years.
Current flu data draw on limited information from primary care practices and hospitals, said Dr. Temte, associate dean for public health and community engagement at the University of Wisconsin School of Medicine and Public Health in Madison. The estimates help bridge the gaps, he said, but the system is inherently vulnerable to error.
“Comparing them – as so many people in this country have done – to try to diminish the impact of SARS-CoV2 is not fair,” he said.
Estimated versus actual influenza deaths
The authors illustrate the difference in the way rates of death from influenza are calculated: “Between 2013-2014 and 2018-2019, the reported yearly estimated influenza deaths ranged from 23,000 to 61,000. Over that same time period, however, the number of counted influenza deaths was between 3,448 and 15,620 yearly.”
“It’s apparent [the CDC has] been overestimating,” Faust said. “If you publish a number on the higher end of the estimate, people might take your public health messages more seriously, such as, it’s important to get your yearly flu shot.”
He added that until influenza death rates started to be compared with COVID-19 rates, “there was never really a downside” to reporting estimates.
Dr. Temte said he doesn’t regard overestimating flu deaths as intentional but rather the result of a longstanding “bias against the elderly in this country” that the estimates are meant to account for.
For example, he says, reporting influenza deaths is mandatory when such deaths involve persons younger than 18 years but not when they involve adults.
Also, traditionally, influenza has been seen “as a cause of death in people with multiple comorbidities that was just part and parcel of wintertime,” Dr. Temte said.
“The likelihood of being tested for influenza goes down greatly when you’re older,” he said. “This is slowly changing.”
The CDC acknowledges on its website that it “does not know the exact number of people who have been sick and affected by influenza because influenza is not a reportable disease in most areas of the US.”
It adds that the burden is estimated through the US Influenza Surveillance System, which covers approximately 8.5% of the US population.
Comparing recorded deaths
It’s more accurate and meaningful to compare actual numbers of deaths for the diseases, Dr. Faust and Dr. del Rio say in their article.
When the authors made that comparison, they drew a stark contrast.
There were 15,455 recorded COVID-19 deaths in the week that ended April 21. The week before, the number of recorded deaths was 14,478, they found. (Those were the two most recent weeks before they submitted their article for publication.)
In comparison, counted deaths ranged from 351 to 1,626 during the peak week of the seven influenza seasons between 2013-2014 and 2019-2020. The average counted deaths for the peak week of the seven seasons was 752.4 (95% confidence interval, 558.8-946.1).
“These statistics on counted deaths suggest that the number of COVID-19 deaths for the week ending April 21 was 9.5-fold to 44.1-fold greater than the peak week of counted influenza deaths during the past seven influenza seasons in the US, with a 20.5-fold mean increase (95% CI, 16.3-27.7),” the authors write.
However, Natasha Chida, MD, MSPH, an infectious disease physician and assistant professor at the Johns Hopkins University School of Medicine in Baltimore, Maryland, said in an interview that the actual number of deaths doesn’t tell the complete flu story either. That count would miss people who later died from secondary complications associated with influenza, she said.
“There’s just no way to reliably count influenza deaths,” she said. “I think if we required it as a reported illness, that would be the ideal situation, but there’s so much flu every year that that probably would not be practical.”
She said she agrees that rates of influenza deaths and rates of COVID-19 deaths cannot be fairly compared.
What the authors don’t touch on, she said, is that flu season lasts 4 to 6 months a year, and just 3 months into the coronavirus pandemic, US deaths due to COVID-19 are already higher than those for seasonal influenza.
“Even if we look at it in the way that people who think we can compare flu and coronavirus do, it’s still not going to work out in their favor from a numbers standpoint,” she said.
The article clarifies the differences for “people who don’t live in the flu world,” she said.
“It is not accurate to compare the two for the reasons the authors described and also because they are very different diseases,” she added.
Real-life validation
Dr. Faust said in an interview that real-life experiences add external validity to their analysis.
Differences in the way deaths are calculated does not reflect frontline clinical conditions during the COVID-19 crisis, with hospitals stretched past their limits, ventilator shortages, and bodies stacking up in some overwhelmed facilities, the authors say.
Dr. Temte said the external validation of the numbers also rings true in light of his own experience.
He said that, in the past 2 months, he has known two people who have had family members who died of COVID-19.
Conversely, “I would have to search long and hard to come up with people I have known or have been one degree of separation from” who have died from influenza, Dr. Temte said.
The authors, Dr. Temte, and Dr. Chida report no relevant financial relationships.
This article first appeared on Medscape.com.
Masks, fear, and loss of connection in the era of COVID-19
Over the din of the negative pressure machine, I shouted goodbye to my patient and zipped my way out of one of the little plastic enclosures in our ED and carefully shed my gloves, gown, and face shield, leaving on my precious mask. I discarded the rest with disgust and a bit of fear. I thought, “This is a whole new world, and I hate it.”
I feel as if I am constantly battling the fear of dying from COVID-19 but am doing the best I can, given the circumstances at hand. I have the proper equipment and use it well. My work still brings meaning: I serve those in need without hesitation. The problem is that deep feeling of connection with patients, which is such an important part of this work, feels like fraying threads moving further apart because of the havoc this virus has wrought. A few weeks ago, the intricate fabric of what it is to be human connected me to patients through the basics: touch, facial expressions, a physical proximity, and openhearted, honest dialogue. Much of that’s gone, and while I can carry on, I will surely burn out if I can’t figure out how to get at least some of that connection back.
Overwhelmed by the amount of information I need to process daily, I had not been thinking about the interpersonal side of the pandemic for the first weeks. I felt it leaving the ED that morning and later that day, and I felt it again with Ms. Z, who was not even suspected of having COVID. She is a 62-year-old I interviewed with the help of a translator phone. At the end of our encounter, she said “But doctor, will you make my tumor go away?” From across the room, I said, “I will try.” I saw her eyes dampen as I made a hasty exit, following protocol to limit time in the room of all patients.
Typically, leaving a patient’s room, I would feel a fullness associated with a sense of meaning. How did I feel after that? In that moment, mostly ashamed at my lack of compassion during my time with Ms. Z. Then, with further reflection, tense from all things COVID-19! Having an amped-up sympathetic nervous system is understandable, but it’s not where we want to be for our compassion to flow.
We connect best when our parasympathetic nervous system is predominant. So much of the stimuli we need to activate that part of the nervous system is gone. There is a virtuous cycle, much of it unconscious, where something positive leads to more positivity, which is crucial to meaningful patient encounters. We read each other’s facial expressions, hear the tone of voice, and as we pick up subtle cues from our patient, our nervous system is further engaged and our hearts opened.
The specter of COVID-19 has us battling a negative spiral of stress and fear. For the most part, I try to keep that from consuming me, but it clearly saps my energy during encounters. In the same way we need to marshal our resources to battle both the stress and the disease itself, we need to actively engage pro-social elements of providing care to maintain our compassion. Clearly, I needed a more concerted effort to kick start this virtuous cycle of compassion.
My next patient was Ms. J., a 55-year-old with advanced chronic obstructive pulmonary disease (COPD) who came in the night before with shortness of breath. Her slight frame shook from coughing as I entered the room. I did not think she had COVID-19, but we were ruling it out.
We reviewed how she felt since admission, and I performed a hasty exam and stepped back across the room. She coughed again and said, “I feel so weak, and the world feels so crazy; tell it to me straight.” Then looking in my eyes, “I am going to make it, doc?”
I took my cue from her; I walked back to the bedside, placed a gloved hand on her shoulder and with the other, I took her hand. I bent forward just a little. Making eye contact and attempting a comforting tone of voice, I said, “Everyone is a little scared, including me. We need each other more than ever these days. We will do our best for you. That means thoughtful medical care and a whole lot of love! And, truly, I don’t think you are dying; this is just one of your COPD flares.”
“God bless you!” she said, squeezing my hand as a tear rolled down her cheek.
“Bless you, too. We all need blessing with this madness going on,” I replied. Despite the mask, I am sure she saw the smile in my eyes. “Thanks for being the beautiful person you are and opening up to me. That’s the way we will make it through this. I will see you tomorrow.” Backing away, hands together in prayer, I gave a little bow and left the room.
With Ms. J.’s help, I began to figure it out. To tackle the stress of COVID, we need to be very direct – almost to the point of exaggeration – to make sure our words and actions convey what we need to express. William James, the father of psychology, believed that if you force a smile, your emotions would follow. The neural pathways could work backward in that way. He said, “If you want a quality, act as if you have it.” The modern translation would be, “Fake it ’til you make it.’ ” You may be feeling stressed, but with a deep breath and a moment’s reflection on the suffering of that patient you are about to see, you can turn the tide on anxiety and give those under your care what they need.
These are unprecedented times; anxiety abounds. While we can aspire to positivity, there are times when we simply can’t muster showing it. Alternatively, as I experienced with Ms. J., honesty and vulnerability can open the door to meaningful connection. This can be quite powerful when we, as physicians, open up to our patients.
People are yearning for deep connection, and we should attempt to deliver it with:
- Touch (as we can) to convey connection.
- Body language that adds emphasis to our message and our emotions that may go above and beyond what we are used to.
- Tone of voice that enhances our words.
- Talk that emphasizes the big stuff, such as love, fear, connection and community
With gloves, masks, distance, and fear between and us and our patients, we need to actively engage our pro-social tools to turn the negative spiral of fear into the virtuous cycle of positive emotions that promotes healing of our patients and emotional engagement for those providing their care.
Dr. Hass was trained in family medicine at University of California, San Francisco, after receiving his medical degree from the McGill University faculty of medicine, Montreal. He works as a hospitalist with Sutter Health in Oakland, Calif. He is an adviser on health and health care for the Greater Good Science Center at UC Berkeley and clinical faculty at UCSF School of Medicine. This article appeared initially at The Hospital Leader, the official blog of SHM.
Over the din of the negative pressure machine, I shouted goodbye to my patient and zipped my way out of one of the little plastic enclosures in our ED and carefully shed my gloves, gown, and face shield, leaving on my precious mask. I discarded the rest with disgust and a bit of fear. I thought, “This is a whole new world, and I hate it.”
I feel as if I am constantly battling the fear of dying from COVID-19 but am doing the best I can, given the circumstances at hand. I have the proper equipment and use it well. My work still brings meaning: I serve those in need without hesitation. The problem is that deep feeling of connection with patients, which is such an important part of this work, feels like fraying threads moving further apart because of the havoc this virus has wrought. A few weeks ago, the intricate fabric of what it is to be human connected me to patients through the basics: touch, facial expressions, a physical proximity, and openhearted, honest dialogue. Much of that’s gone, and while I can carry on, I will surely burn out if I can’t figure out how to get at least some of that connection back.
Overwhelmed by the amount of information I need to process daily, I had not been thinking about the interpersonal side of the pandemic for the first weeks. I felt it leaving the ED that morning and later that day, and I felt it again with Ms. Z, who was not even suspected of having COVID. She is a 62-year-old I interviewed with the help of a translator phone. At the end of our encounter, she said “But doctor, will you make my tumor go away?” From across the room, I said, “I will try.” I saw her eyes dampen as I made a hasty exit, following protocol to limit time in the room of all patients.
Typically, leaving a patient’s room, I would feel a fullness associated with a sense of meaning. How did I feel after that? In that moment, mostly ashamed at my lack of compassion during my time with Ms. Z. Then, with further reflection, tense from all things COVID-19! Having an amped-up sympathetic nervous system is understandable, but it’s not where we want to be for our compassion to flow.
We connect best when our parasympathetic nervous system is predominant. So much of the stimuli we need to activate that part of the nervous system is gone. There is a virtuous cycle, much of it unconscious, where something positive leads to more positivity, which is crucial to meaningful patient encounters. We read each other’s facial expressions, hear the tone of voice, and as we pick up subtle cues from our patient, our nervous system is further engaged and our hearts opened.
The specter of COVID-19 has us battling a negative spiral of stress and fear. For the most part, I try to keep that from consuming me, but it clearly saps my energy during encounters. In the same way we need to marshal our resources to battle both the stress and the disease itself, we need to actively engage pro-social elements of providing care to maintain our compassion. Clearly, I needed a more concerted effort to kick start this virtuous cycle of compassion.
My next patient was Ms. J., a 55-year-old with advanced chronic obstructive pulmonary disease (COPD) who came in the night before with shortness of breath. Her slight frame shook from coughing as I entered the room. I did not think she had COVID-19, but we were ruling it out.
We reviewed how she felt since admission, and I performed a hasty exam and stepped back across the room. She coughed again and said, “I feel so weak, and the world feels so crazy; tell it to me straight.” Then looking in my eyes, “I am going to make it, doc?”
I took my cue from her; I walked back to the bedside, placed a gloved hand on her shoulder and with the other, I took her hand. I bent forward just a little. Making eye contact and attempting a comforting tone of voice, I said, “Everyone is a little scared, including me. We need each other more than ever these days. We will do our best for you. That means thoughtful medical care and a whole lot of love! And, truly, I don’t think you are dying; this is just one of your COPD flares.”
“God bless you!” she said, squeezing my hand as a tear rolled down her cheek.
“Bless you, too. We all need blessing with this madness going on,” I replied. Despite the mask, I am sure she saw the smile in my eyes. “Thanks for being the beautiful person you are and opening up to me. That’s the way we will make it through this. I will see you tomorrow.” Backing away, hands together in prayer, I gave a little bow and left the room.
With Ms. J.’s help, I began to figure it out. To tackle the stress of COVID, we need to be very direct – almost to the point of exaggeration – to make sure our words and actions convey what we need to express. William James, the father of psychology, believed that if you force a smile, your emotions would follow. The neural pathways could work backward in that way. He said, “If you want a quality, act as if you have it.” The modern translation would be, “Fake it ’til you make it.’ ” You may be feeling stressed, but with a deep breath and a moment’s reflection on the suffering of that patient you are about to see, you can turn the tide on anxiety and give those under your care what they need.
These are unprecedented times; anxiety abounds. While we can aspire to positivity, there are times when we simply can’t muster showing it. Alternatively, as I experienced with Ms. J., honesty and vulnerability can open the door to meaningful connection. This can be quite powerful when we, as physicians, open up to our patients.
People are yearning for deep connection, and we should attempt to deliver it with:
- Touch (as we can) to convey connection.
- Body language that adds emphasis to our message and our emotions that may go above and beyond what we are used to.
- Tone of voice that enhances our words.
- Talk that emphasizes the big stuff, such as love, fear, connection and community
With gloves, masks, distance, and fear between and us and our patients, we need to actively engage our pro-social tools to turn the negative spiral of fear into the virtuous cycle of positive emotions that promotes healing of our patients and emotional engagement for those providing their care.
Dr. Hass was trained in family medicine at University of California, San Francisco, after receiving his medical degree from the McGill University faculty of medicine, Montreal. He works as a hospitalist with Sutter Health in Oakland, Calif. He is an adviser on health and health care for the Greater Good Science Center at UC Berkeley and clinical faculty at UCSF School of Medicine. This article appeared initially at The Hospital Leader, the official blog of SHM.
Over the din of the negative pressure machine, I shouted goodbye to my patient and zipped my way out of one of the little plastic enclosures in our ED and carefully shed my gloves, gown, and face shield, leaving on my precious mask. I discarded the rest with disgust and a bit of fear. I thought, “This is a whole new world, and I hate it.”
I feel as if I am constantly battling the fear of dying from COVID-19 but am doing the best I can, given the circumstances at hand. I have the proper equipment and use it well. My work still brings meaning: I serve those in need without hesitation. The problem is that deep feeling of connection with patients, which is such an important part of this work, feels like fraying threads moving further apart because of the havoc this virus has wrought. A few weeks ago, the intricate fabric of what it is to be human connected me to patients through the basics: touch, facial expressions, a physical proximity, and openhearted, honest dialogue. Much of that’s gone, and while I can carry on, I will surely burn out if I can’t figure out how to get at least some of that connection back.
Overwhelmed by the amount of information I need to process daily, I had not been thinking about the interpersonal side of the pandemic for the first weeks. I felt it leaving the ED that morning and later that day, and I felt it again with Ms. Z, who was not even suspected of having COVID. She is a 62-year-old I interviewed with the help of a translator phone. At the end of our encounter, she said “But doctor, will you make my tumor go away?” From across the room, I said, “I will try.” I saw her eyes dampen as I made a hasty exit, following protocol to limit time in the room of all patients.
Typically, leaving a patient’s room, I would feel a fullness associated with a sense of meaning. How did I feel after that? In that moment, mostly ashamed at my lack of compassion during my time with Ms. Z. Then, with further reflection, tense from all things COVID-19! Having an amped-up sympathetic nervous system is understandable, but it’s not where we want to be for our compassion to flow.
We connect best when our parasympathetic nervous system is predominant. So much of the stimuli we need to activate that part of the nervous system is gone. There is a virtuous cycle, much of it unconscious, where something positive leads to more positivity, which is crucial to meaningful patient encounters. We read each other’s facial expressions, hear the tone of voice, and as we pick up subtle cues from our patient, our nervous system is further engaged and our hearts opened.
The specter of COVID-19 has us battling a negative spiral of stress and fear. For the most part, I try to keep that from consuming me, but it clearly saps my energy during encounters. In the same way we need to marshal our resources to battle both the stress and the disease itself, we need to actively engage pro-social elements of providing care to maintain our compassion. Clearly, I needed a more concerted effort to kick start this virtuous cycle of compassion.
My next patient was Ms. J., a 55-year-old with advanced chronic obstructive pulmonary disease (COPD) who came in the night before with shortness of breath. Her slight frame shook from coughing as I entered the room. I did not think she had COVID-19, but we were ruling it out.
We reviewed how she felt since admission, and I performed a hasty exam and stepped back across the room. She coughed again and said, “I feel so weak, and the world feels so crazy; tell it to me straight.” Then looking in my eyes, “I am going to make it, doc?”
I took my cue from her; I walked back to the bedside, placed a gloved hand on her shoulder and with the other, I took her hand. I bent forward just a little. Making eye contact and attempting a comforting tone of voice, I said, “Everyone is a little scared, including me. We need each other more than ever these days. We will do our best for you. That means thoughtful medical care and a whole lot of love! And, truly, I don’t think you are dying; this is just one of your COPD flares.”
“God bless you!” she said, squeezing my hand as a tear rolled down her cheek.
“Bless you, too. We all need blessing with this madness going on,” I replied. Despite the mask, I am sure she saw the smile in my eyes. “Thanks for being the beautiful person you are and opening up to me. That’s the way we will make it through this. I will see you tomorrow.” Backing away, hands together in prayer, I gave a little bow and left the room.
With Ms. J.’s help, I began to figure it out. To tackle the stress of COVID, we need to be very direct – almost to the point of exaggeration – to make sure our words and actions convey what we need to express. William James, the father of psychology, believed that if you force a smile, your emotions would follow. The neural pathways could work backward in that way. He said, “If you want a quality, act as if you have it.” The modern translation would be, “Fake it ’til you make it.’ ” You may be feeling stressed, but with a deep breath and a moment’s reflection on the suffering of that patient you are about to see, you can turn the tide on anxiety and give those under your care what they need.
These are unprecedented times; anxiety abounds. While we can aspire to positivity, there are times when we simply can’t muster showing it. Alternatively, as I experienced with Ms. J., honesty and vulnerability can open the door to meaningful connection. This can be quite powerful when we, as physicians, open up to our patients.
People are yearning for deep connection, and we should attempt to deliver it with:
- Touch (as we can) to convey connection.
- Body language that adds emphasis to our message and our emotions that may go above and beyond what we are used to.
- Tone of voice that enhances our words.
- Talk that emphasizes the big stuff, such as love, fear, connection and community
With gloves, masks, distance, and fear between and us and our patients, we need to actively engage our pro-social tools to turn the negative spiral of fear into the virtuous cycle of positive emotions that promotes healing of our patients and emotional engagement for those providing their care.
Dr. Hass was trained in family medicine at University of California, San Francisco, after receiving his medical degree from the McGill University faculty of medicine, Montreal. He works as a hospitalist with Sutter Health in Oakland, Calif. He is an adviser on health and health care for the Greater Good Science Center at UC Berkeley and clinical faculty at UCSF School of Medicine. This article appeared initially at The Hospital Leader, the official blog of SHM.
Doctors advise asthmatics to continue therapy during pandemic
“In fact, there’s no data to support this at this time. Maintaining adequate asthma control is the current CDC recommendation,” said pediatric pulmonologist John Carl, MD, of Cleveland Clinic Children’s Hospital. Patients, he said, should be advised to “follow your asthma action plan as outlined by your primary care or specialty clinician and communicate about evolving symptoms, such as fever rather than just congestion, wheezing, and coughing, etc.”
Dr. Carl spoke in a May 7 webinar about asthma and COVID-19 with Lakiea Wright, M.D., a physician specializing in internal medicine and allergy and immunology at Brigham and Women’s Hospital in Boston and medical director of clinical affairs for Thermo Fisher Scientific’s ImmunoDiagnostics division. The webinar, sponsored by Thermo Fisher Scientific, included discussion of COVID-19 risks, disease management, and distinguishing between the virus and asthma.
In a follow-up interview, Dr. Wright said she’s hearing from patients and parents who are concerned about whether people with asthma face a higher risk of COVID-19 infection. There’s no evidence that they do, she said, but “the CDC states that individuals with moderate to severe asthma may be higher risk for moderate to severe disease from COVID-19 if they were to become infected.”
Indeed, she said, “it is well established that viruses can trigger asthma.” But, as she also noted, early research about the risk in patients with asthma is conflicting.
“Some studies suggest asthma may be a risk factor for hospitalization while other data suggests asthma is not a common risk factor for those hospitalized,” Dr. Wright said.
She highlighted a recent study that suggests people with allergic asthma have “a reduced ACE2 gene expression in airway cells and thus decreased susceptibility to infection” by the novel coronavirus (J Allergy Clin Immunol. 2020 Apr 22. doi: 10.1016/j.jaci.2020.04.009).
Dr. Wright cautioned, however, that “this is a hypothesis and will need to be studied more.”
For now, she said, patients “should follow their asthma action plan and take their inhalers, including inhaled corticosteroids, as prescribed by their health care providers.”
Most patients are reasonable and do comply when their physicians explain why they should take a medication,” she noted.
Dr. Carl agreed, and added that a short course of oral corticosteroids are also recommended to manage minor exacerbations and “prevent patients from having to arrive as inpatients in more acute settings and risk health system–related exposures to the current pandemic.”
He cautioned, however, that metered-dose inhalers are preferable to nebulizers, and side vent ports should be avoided since they can aerosolize infectious agents and put health care providers and family members at risk.
Unfortunately, he said, there’s been a shortage of short-acting beta agonist albuterol inhalers. This has been linked to hospitals trying to avoid the use of nebulizers.
Dr. Wright advised colleagues to focus on unique symptoms first, then address overlapping symptoms and other symptoms to differentiate between COVID-19 and asthma/allergy.
She noted that environmental allergy symptoms alone do not cause fever, a hallmark of COVID-19. Shortness of breath can be a distinguishing symptom for the virus, because this is not a common symptom of environmental allergies unless the patient has asthma, Dr. Wright said.
Cough can be an overlapping symptom because in environmental allergies, postnasal drip from allergic rhinitis can trigger cough, she explained. Nasal congestion and/or runny nose can develop with viral illnesses in general, but these are symptoms not included in the CDC’s list of the most common COVID-19 symptoms. Severe fatigue and body aches aren’t symptoms consistent with environmental allergies, Dr. Wright said.
Both Dr. Carl and Dr. Wright emphasized the importance of continuing routine asthma therapy during the pandemic.
“When discussing the importance of taking their inhaled steroids with patients, I also remind patients that asthma management is comprehensive,” Dr. Wright said. “I want them to take their medications, but I also want them avoid or minimize exposure to triggers. Allergic and nonallergic triggers such as environmental tobacco smoke can exacerbate asthma.”
In addition, she said, “it’s important to take a detailed medical history to identify triggers. And it’s important to conduct allergy testing to common environmental allergens to help identify allergic triggers and tailor environmental allergen control strategies based on the results. All of these strategies help patients keep their asthma well-controlled.”
Dr. Carl and Dr. Wright report having no relevant disclosures.
“In fact, there’s no data to support this at this time. Maintaining adequate asthma control is the current CDC recommendation,” said pediatric pulmonologist John Carl, MD, of Cleveland Clinic Children’s Hospital. Patients, he said, should be advised to “follow your asthma action plan as outlined by your primary care or specialty clinician and communicate about evolving symptoms, such as fever rather than just congestion, wheezing, and coughing, etc.”
Dr. Carl spoke in a May 7 webinar about asthma and COVID-19 with Lakiea Wright, M.D., a physician specializing in internal medicine and allergy and immunology at Brigham and Women’s Hospital in Boston and medical director of clinical affairs for Thermo Fisher Scientific’s ImmunoDiagnostics division. The webinar, sponsored by Thermo Fisher Scientific, included discussion of COVID-19 risks, disease management, and distinguishing between the virus and asthma.
In a follow-up interview, Dr. Wright said she’s hearing from patients and parents who are concerned about whether people with asthma face a higher risk of COVID-19 infection. There’s no evidence that they do, she said, but “the CDC states that individuals with moderate to severe asthma may be higher risk for moderate to severe disease from COVID-19 if they were to become infected.”
Indeed, she said, “it is well established that viruses can trigger asthma.” But, as she also noted, early research about the risk in patients with asthma is conflicting.
“Some studies suggest asthma may be a risk factor for hospitalization while other data suggests asthma is not a common risk factor for those hospitalized,” Dr. Wright said.
She highlighted a recent study that suggests people with allergic asthma have “a reduced ACE2 gene expression in airway cells and thus decreased susceptibility to infection” by the novel coronavirus (J Allergy Clin Immunol. 2020 Apr 22. doi: 10.1016/j.jaci.2020.04.009).
Dr. Wright cautioned, however, that “this is a hypothesis and will need to be studied more.”
For now, she said, patients “should follow their asthma action plan and take their inhalers, including inhaled corticosteroids, as prescribed by their health care providers.”
Most patients are reasonable and do comply when their physicians explain why they should take a medication,” she noted.
Dr. Carl agreed, and added that a short course of oral corticosteroids are also recommended to manage minor exacerbations and “prevent patients from having to arrive as inpatients in more acute settings and risk health system–related exposures to the current pandemic.”
He cautioned, however, that metered-dose inhalers are preferable to nebulizers, and side vent ports should be avoided since they can aerosolize infectious agents and put health care providers and family members at risk.
Unfortunately, he said, there’s been a shortage of short-acting beta agonist albuterol inhalers. This has been linked to hospitals trying to avoid the use of nebulizers.
Dr. Wright advised colleagues to focus on unique symptoms first, then address overlapping symptoms and other symptoms to differentiate between COVID-19 and asthma/allergy.
She noted that environmental allergy symptoms alone do not cause fever, a hallmark of COVID-19. Shortness of breath can be a distinguishing symptom for the virus, because this is not a common symptom of environmental allergies unless the patient has asthma, Dr. Wright said.
Cough can be an overlapping symptom because in environmental allergies, postnasal drip from allergic rhinitis can trigger cough, she explained. Nasal congestion and/or runny nose can develop with viral illnesses in general, but these are symptoms not included in the CDC’s list of the most common COVID-19 symptoms. Severe fatigue and body aches aren’t symptoms consistent with environmental allergies, Dr. Wright said.
Both Dr. Carl and Dr. Wright emphasized the importance of continuing routine asthma therapy during the pandemic.
“When discussing the importance of taking their inhaled steroids with patients, I also remind patients that asthma management is comprehensive,” Dr. Wright said. “I want them to take their medications, but I also want them avoid or minimize exposure to triggers. Allergic and nonallergic triggers such as environmental tobacco smoke can exacerbate asthma.”
In addition, she said, “it’s important to take a detailed medical history to identify triggers. And it’s important to conduct allergy testing to common environmental allergens to help identify allergic triggers and tailor environmental allergen control strategies based on the results. All of these strategies help patients keep their asthma well-controlled.”
Dr. Carl and Dr. Wright report having no relevant disclosures.
“In fact, there’s no data to support this at this time. Maintaining adequate asthma control is the current CDC recommendation,” said pediatric pulmonologist John Carl, MD, of Cleveland Clinic Children’s Hospital. Patients, he said, should be advised to “follow your asthma action plan as outlined by your primary care or specialty clinician and communicate about evolving symptoms, such as fever rather than just congestion, wheezing, and coughing, etc.”
Dr. Carl spoke in a May 7 webinar about asthma and COVID-19 with Lakiea Wright, M.D., a physician specializing in internal medicine and allergy and immunology at Brigham and Women’s Hospital in Boston and medical director of clinical affairs for Thermo Fisher Scientific’s ImmunoDiagnostics division. The webinar, sponsored by Thermo Fisher Scientific, included discussion of COVID-19 risks, disease management, and distinguishing between the virus and asthma.
In a follow-up interview, Dr. Wright said she’s hearing from patients and parents who are concerned about whether people with asthma face a higher risk of COVID-19 infection. There’s no evidence that they do, she said, but “the CDC states that individuals with moderate to severe asthma may be higher risk for moderate to severe disease from COVID-19 if they were to become infected.”
Indeed, she said, “it is well established that viruses can trigger asthma.” But, as she also noted, early research about the risk in patients with asthma is conflicting.
“Some studies suggest asthma may be a risk factor for hospitalization while other data suggests asthma is not a common risk factor for those hospitalized,” Dr. Wright said.
She highlighted a recent study that suggests people with allergic asthma have “a reduced ACE2 gene expression in airway cells and thus decreased susceptibility to infection” by the novel coronavirus (J Allergy Clin Immunol. 2020 Apr 22. doi: 10.1016/j.jaci.2020.04.009).
Dr. Wright cautioned, however, that “this is a hypothesis and will need to be studied more.”
For now, she said, patients “should follow their asthma action plan and take their inhalers, including inhaled corticosteroids, as prescribed by their health care providers.”
Most patients are reasonable and do comply when their physicians explain why they should take a medication,” she noted.
Dr. Carl agreed, and added that a short course of oral corticosteroids are also recommended to manage minor exacerbations and “prevent patients from having to arrive as inpatients in more acute settings and risk health system–related exposures to the current pandemic.”
He cautioned, however, that metered-dose inhalers are preferable to nebulizers, and side vent ports should be avoided since they can aerosolize infectious agents and put health care providers and family members at risk.
Unfortunately, he said, there’s been a shortage of short-acting beta agonist albuterol inhalers. This has been linked to hospitals trying to avoid the use of nebulizers.
Dr. Wright advised colleagues to focus on unique symptoms first, then address overlapping symptoms and other symptoms to differentiate between COVID-19 and asthma/allergy.
She noted that environmental allergy symptoms alone do not cause fever, a hallmark of COVID-19. Shortness of breath can be a distinguishing symptom for the virus, because this is not a common symptom of environmental allergies unless the patient has asthma, Dr. Wright said.
Cough can be an overlapping symptom because in environmental allergies, postnasal drip from allergic rhinitis can trigger cough, she explained. Nasal congestion and/or runny nose can develop with viral illnesses in general, but these are symptoms not included in the CDC’s list of the most common COVID-19 symptoms. Severe fatigue and body aches aren’t symptoms consistent with environmental allergies, Dr. Wright said.
Both Dr. Carl and Dr. Wright emphasized the importance of continuing routine asthma therapy during the pandemic.
“When discussing the importance of taking their inhaled steroids with patients, I also remind patients that asthma management is comprehensive,” Dr. Wright said. “I want them to take their medications, but I also want them avoid or minimize exposure to triggers. Allergic and nonallergic triggers such as environmental tobacco smoke can exacerbate asthma.”
In addition, she said, “it’s important to take a detailed medical history to identify triggers. And it’s important to conduct allergy testing to common environmental allergens to help identify allergic triggers and tailor environmental allergen control strategies based on the results. All of these strategies help patients keep their asthma well-controlled.”
Dr. Carl and Dr. Wright report having no relevant disclosures.
Consider COVID-19–associated multisystem hyperinflammatory syndrome
A 21-year-old young adult presented to the ED with a 1-week history of high fever, vomiting, diarrhea, and abdominal pain. His mother was SARS-CoV-2 positive by polymerase chain reaction approximately 3 weeks prior; his PCR was negative for SARS-CoV-2.
Following admission, he became hypotensive and tachycardic with evidence of myocarditis. His chest x-ray was normal and his O2 saturation was 100% on room air. His clinical presentation was initially suggestive of toxic shock syndrome without a rash, but despite aggressive fluid resuscitation and broad-spectrum antibiotics, he continued to clinically deteriorate with persistent high fever and increasing cardiac stress. Echocardiography revealed biventricular dysfunction. His laboratory abnormalities included rising inflammatory markers and troponin I and B-type natriuretic peptide (BNP). A repeat PCR for SARS-CoV-2 was negative on day 2 of illness. He was diagnosed as likely having macrophage-activation syndrome (MAS) despite the atypical features (myocarditis), and he received Anakinra with no apparent response. He also was given intravenous immunoglobulin (IVIg) for his myocarditis and subsequently high-dose steroids. He became afebrile, his blood pressure stabilized, his inflammatory markers declined, and over several days he returned to normal. His COVID-19 antibody test IgG was positive on day 4 of illness.
This case challenged us for several reasons. First, the PCR from his nasopharynx was negative on two occasions, which raises the issue of how sensitive and accurate these PCR tests are for SARS-CoV-2 or are patients with COVID-19–associated hyperinflammatory syndrome still PCR positive? Second, although we have seen many adult cases with a cytokine storm picture similar to this patient, nearly all of the prior cases had chest x-ray abnormalities and hypoxia. Third, the severity of the myocardial dysfunction and rising troponin and BNP also was unusual in our experience with COVID-19 infection. Lastly, the use of antibody detection to SARS-CoV-2 enabled us to confirm recent COIVD-19 disease and see his illness as part of the likely spectrum of clinical syndromes seen with this virus.
The Lancet reported eight children, aged 4-14 years, with a hyperinflammatory shock-like syndrome in early May.1 The cases had features similar to atypical Kawasaki disease, KD shock syndrome, and toxic shock syndrome. Each case had high fever for multiple days; diarrhea and abdominal pain was present in even children; elevated ferritin, C-reactive protein, d-dimer, increased troponins, and ventricular dysfunction also was present in seven. Most patients had no pulmonary involvement, and most tested negative for SARS-CoV-2 despite four of the eight having direct contact with a COVID-positive family member. All received IVIg and antibiotics; six received aspirin. Seven of the eight made a full recovery; one child died from a large cerebrovascular infarct.
Also in early May, the New York Times described a “mysterious” hyperinflammatory syndrome in children thought to be linked to COVID-19. A total of 76 suspected cases in children had been reported in New York state, three of whom died. The syndrome has been given the name pediatric multisystem inflammatory syndrome. The syndrome can resemble KD shock syndrome with rash; fever; conjunctivitis; hypotension; and redness in the lips, tongue and mucous membranes . It also can resemble toxic shock syndrome with abdominal pain, vomiting, and diarrhea. However, the degree of cardiac inflammation and dysfunction is substantial in many cases and usually beyond that seen in KD or toxic shock.
The syndrome is not limited to the United States. The Royal College of Pediatrics and Child Health has created a case definition:2
- A child presenting with persistent fever, inflammation (elevated C-reactive protein, neutrophilia, and lymphopenia) and evidence of single or multiorgan dysfunction (shock, cardiac, respiratory, renal, gastrointestinal, or neurologic) with additional features.
- Exclusion of any other microbial causes such as bacterial sepsis or staphylococcal or streptococcal shock syndromes, infections known to be associated with myocarditis (such as enterovirus).
- SARS-CoV-2 testing may or may not be positive.
As with our young adult, treatment is supportive, nonspecific, and aimed at quieting the inflammatory response. The current thinking is the syndrome is seen as antibody to SARS-CoV-2 appears and frequently the nasopharyngeal PCR is negative. It is hypothesized that the syndrome occurs in genetically predisposed hosts and potentially is a late-onset inflammatory process or potentially an antibody-triggered inflammatory process. The negative PCR from nasopharyngeal specimens reflects that the onset is later in the course of disease; whether fecal samples would be COVID positive is unknown. As with our case, antibody testing for IgG against SARS-CoV-2 is appropriate to confirm COVID-19 disease and may be positive as early as day 7.
The approach needs to be team oriented and include cardiology, rheumatology, infectious diseases, and intensive care specialists working collaboratively. Such cases should be considered COVID positive despite negative PCR tests, and full personal protective equipment should be used as we do not as yet know if live virus could be found in stool. We initiated treatment with Anakinra (an interleukin-1 type-1 receptor inhibitor) as part of our treatment protocol for MAS; we did not appreciate a response. He then received IVIg and high-dose steroids, and he recovered over several days with improved cardiac function and stable blood pressure.
What is the pathogenesis? Is SARS-CoV-2 causative or just an associated finding? Who are the at-risk children, adolescents, and adults? Is there a genetic predisposition? What therapies work best? The eight cases described in London all received IVIg, as did our case, and all but one improved and survived. In adults we have seen substantial inflammation with elevated C-reactive protein (often as high as 300), ferritin, lactate dehydrogenase, triglycerides, fibrinogen, and d-dimers, but nearly all have extensive pulmonary disease, hypoxia, and are SARS-CoV-2 positive by PCR. Influenza is also associated with a cytokine storm syndrome in adolescents and young adults.3 The mechanisms influenza virus uses to initiate a cytokine storm and strategies for immunomodulatory treatment may provide insights into COVID-19–associated multisystem hyperinflammatory syndrome.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician in pediatric infectious diseases at Boston Medical Center. Dr. Camelo is a senior fellow in pediatric infectious diseases at Boston Medical Center. They have no relevant financial disclosures. Email them at [email protected].
References
1. Riphagen S et al. Lancet. 2020 May 6. doi: 10.1016/S0140-6736(20)31094-1.
2. Royal College of Paediatrics and Child Health Guidance: Paediatric multisystem inflammatory syndrome temporally associated with COVID-19.
3. Liu Q et al.Cell Mol Immunol. 2016 Jan;13(1):3-10.
A 21-year-old young adult presented to the ED with a 1-week history of high fever, vomiting, diarrhea, and abdominal pain. His mother was SARS-CoV-2 positive by polymerase chain reaction approximately 3 weeks prior; his PCR was negative for SARS-CoV-2.
Following admission, he became hypotensive and tachycardic with evidence of myocarditis. His chest x-ray was normal and his O2 saturation was 100% on room air. His clinical presentation was initially suggestive of toxic shock syndrome without a rash, but despite aggressive fluid resuscitation and broad-spectrum antibiotics, he continued to clinically deteriorate with persistent high fever and increasing cardiac stress. Echocardiography revealed biventricular dysfunction. His laboratory abnormalities included rising inflammatory markers and troponin I and B-type natriuretic peptide (BNP). A repeat PCR for SARS-CoV-2 was negative on day 2 of illness. He was diagnosed as likely having macrophage-activation syndrome (MAS) despite the atypical features (myocarditis), and he received Anakinra with no apparent response. He also was given intravenous immunoglobulin (IVIg) for his myocarditis and subsequently high-dose steroids. He became afebrile, his blood pressure stabilized, his inflammatory markers declined, and over several days he returned to normal. His COVID-19 antibody test IgG was positive on day 4 of illness.
This case challenged us for several reasons. First, the PCR from his nasopharynx was negative on two occasions, which raises the issue of how sensitive and accurate these PCR tests are for SARS-CoV-2 or are patients with COVID-19–associated hyperinflammatory syndrome still PCR positive? Second, although we have seen many adult cases with a cytokine storm picture similar to this patient, nearly all of the prior cases had chest x-ray abnormalities and hypoxia. Third, the severity of the myocardial dysfunction and rising troponin and BNP also was unusual in our experience with COVID-19 infection. Lastly, the use of antibody detection to SARS-CoV-2 enabled us to confirm recent COIVD-19 disease and see his illness as part of the likely spectrum of clinical syndromes seen with this virus.
The Lancet reported eight children, aged 4-14 years, with a hyperinflammatory shock-like syndrome in early May.1 The cases had features similar to atypical Kawasaki disease, KD shock syndrome, and toxic shock syndrome. Each case had high fever for multiple days; diarrhea and abdominal pain was present in even children; elevated ferritin, C-reactive protein, d-dimer, increased troponins, and ventricular dysfunction also was present in seven. Most patients had no pulmonary involvement, and most tested negative for SARS-CoV-2 despite four of the eight having direct contact with a COVID-positive family member. All received IVIg and antibiotics; six received aspirin. Seven of the eight made a full recovery; one child died from a large cerebrovascular infarct.
Also in early May, the New York Times described a “mysterious” hyperinflammatory syndrome in children thought to be linked to COVID-19. A total of 76 suspected cases in children had been reported in New York state, three of whom died. The syndrome has been given the name pediatric multisystem inflammatory syndrome. The syndrome can resemble KD shock syndrome with rash; fever; conjunctivitis; hypotension; and redness in the lips, tongue and mucous membranes . It also can resemble toxic shock syndrome with abdominal pain, vomiting, and diarrhea. However, the degree of cardiac inflammation and dysfunction is substantial in many cases and usually beyond that seen in KD or toxic shock.
The syndrome is not limited to the United States. The Royal College of Pediatrics and Child Health has created a case definition:2
- A child presenting with persistent fever, inflammation (elevated C-reactive protein, neutrophilia, and lymphopenia) and evidence of single or multiorgan dysfunction (shock, cardiac, respiratory, renal, gastrointestinal, or neurologic) with additional features.
- Exclusion of any other microbial causes such as bacterial sepsis or staphylococcal or streptococcal shock syndromes, infections known to be associated with myocarditis (such as enterovirus).
- SARS-CoV-2 testing may or may not be positive.
As with our young adult, treatment is supportive, nonspecific, and aimed at quieting the inflammatory response. The current thinking is the syndrome is seen as antibody to SARS-CoV-2 appears and frequently the nasopharyngeal PCR is negative. It is hypothesized that the syndrome occurs in genetically predisposed hosts and potentially is a late-onset inflammatory process or potentially an antibody-triggered inflammatory process. The negative PCR from nasopharyngeal specimens reflects that the onset is later in the course of disease; whether fecal samples would be COVID positive is unknown. As with our case, antibody testing for IgG against SARS-CoV-2 is appropriate to confirm COVID-19 disease and may be positive as early as day 7.
The approach needs to be team oriented and include cardiology, rheumatology, infectious diseases, and intensive care specialists working collaboratively. Such cases should be considered COVID positive despite negative PCR tests, and full personal protective equipment should be used as we do not as yet know if live virus could be found in stool. We initiated treatment with Anakinra (an interleukin-1 type-1 receptor inhibitor) as part of our treatment protocol for MAS; we did not appreciate a response. He then received IVIg and high-dose steroids, and he recovered over several days with improved cardiac function and stable blood pressure.
What is the pathogenesis? Is SARS-CoV-2 causative or just an associated finding? Who are the at-risk children, adolescents, and adults? Is there a genetic predisposition? What therapies work best? The eight cases described in London all received IVIg, as did our case, and all but one improved and survived. In adults we have seen substantial inflammation with elevated C-reactive protein (often as high as 300), ferritin, lactate dehydrogenase, triglycerides, fibrinogen, and d-dimers, but nearly all have extensive pulmonary disease, hypoxia, and are SARS-CoV-2 positive by PCR. Influenza is also associated with a cytokine storm syndrome in adolescents and young adults.3 The mechanisms influenza virus uses to initiate a cytokine storm and strategies for immunomodulatory treatment may provide insights into COVID-19–associated multisystem hyperinflammatory syndrome.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician in pediatric infectious diseases at Boston Medical Center. Dr. Camelo is a senior fellow in pediatric infectious diseases at Boston Medical Center. They have no relevant financial disclosures. Email them at [email protected].
References
1. Riphagen S et al. Lancet. 2020 May 6. doi: 10.1016/S0140-6736(20)31094-1.
2. Royal College of Paediatrics and Child Health Guidance: Paediatric multisystem inflammatory syndrome temporally associated with COVID-19.
3. Liu Q et al.Cell Mol Immunol. 2016 Jan;13(1):3-10.
A 21-year-old young adult presented to the ED with a 1-week history of high fever, vomiting, diarrhea, and abdominal pain. His mother was SARS-CoV-2 positive by polymerase chain reaction approximately 3 weeks prior; his PCR was negative for SARS-CoV-2.
Following admission, he became hypotensive and tachycardic with evidence of myocarditis. His chest x-ray was normal and his O2 saturation was 100% on room air. His clinical presentation was initially suggestive of toxic shock syndrome without a rash, but despite aggressive fluid resuscitation and broad-spectrum antibiotics, he continued to clinically deteriorate with persistent high fever and increasing cardiac stress. Echocardiography revealed biventricular dysfunction. His laboratory abnormalities included rising inflammatory markers and troponin I and B-type natriuretic peptide (BNP). A repeat PCR for SARS-CoV-2 was negative on day 2 of illness. He was diagnosed as likely having macrophage-activation syndrome (MAS) despite the atypical features (myocarditis), and he received Anakinra with no apparent response. He also was given intravenous immunoglobulin (IVIg) for his myocarditis and subsequently high-dose steroids. He became afebrile, his blood pressure stabilized, his inflammatory markers declined, and over several days he returned to normal. His COVID-19 antibody test IgG was positive on day 4 of illness.
This case challenged us for several reasons. First, the PCR from his nasopharynx was negative on two occasions, which raises the issue of how sensitive and accurate these PCR tests are for SARS-CoV-2 or are patients with COVID-19–associated hyperinflammatory syndrome still PCR positive? Second, although we have seen many adult cases with a cytokine storm picture similar to this patient, nearly all of the prior cases had chest x-ray abnormalities and hypoxia. Third, the severity of the myocardial dysfunction and rising troponin and BNP also was unusual in our experience with COVID-19 infection. Lastly, the use of antibody detection to SARS-CoV-2 enabled us to confirm recent COIVD-19 disease and see his illness as part of the likely spectrum of clinical syndromes seen with this virus.
The Lancet reported eight children, aged 4-14 years, with a hyperinflammatory shock-like syndrome in early May.1 The cases had features similar to atypical Kawasaki disease, KD shock syndrome, and toxic shock syndrome. Each case had high fever for multiple days; diarrhea and abdominal pain was present in even children; elevated ferritin, C-reactive protein, d-dimer, increased troponins, and ventricular dysfunction also was present in seven. Most patients had no pulmonary involvement, and most tested negative for SARS-CoV-2 despite four of the eight having direct contact with a COVID-positive family member. All received IVIg and antibiotics; six received aspirin. Seven of the eight made a full recovery; one child died from a large cerebrovascular infarct.
Also in early May, the New York Times described a “mysterious” hyperinflammatory syndrome in children thought to be linked to COVID-19. A total of 76 suspected cases in children had been reported in New York state, three of whom died. The syndrome has been given the name pediatric multisystem inflammatory syndrome. The syndrome can resemble KD shock syndrome with rash; fever; conjunctivitis; hypotension; and redness in the lips, tongue and mucous membranes . It also can resemble toxic shock syndrome with abdominal pain, vomiting, and diarrhea. However, the degree of cardiac inflammation and dysfunction is substantial in many cases and usually beyond that seen in KD or toxic shock.
The syndrome is not limited to the United States. The Royal College of Pediatrics and Child Health has created a case definition:2
- A child presenting with persistent fever, inflammation (elevated C-reactive protein, neutrophilia, and lymphopenia) and evidence of single or multiorgan dysfunction (shock, cardiac, respiratory, renal, gastrointestinal, or neurologic) with additional features.
- Exclusion of any other microbial causes such as bacterial sepsis or staphylococcal or streptococcal shock syndromes, infections known to be associated with myocarditis (such as enterovirus).
- SARS-CoV-2 testing may or may not be positive.
As with our young adult, treatment is supportive, nonspecific, and aimed at quieting the inflammatory response. The current thinking is the syndrome is seen as antibody to SARS-CoV-2 appears and frequently the nasopharyngeal PCR is negative. It is hypothesized that the syndrome occurs in genetically predisposed hosts and potentially is a late-onset inflammatory process or potentially an antibody-triggered inflammatory process. The negative PCR from nasopharyngeal specimens reflects that the onset is later in the course of disease; whether fecal samples would be COVID positive is unknown. As with our case, antibody testing for IgG against SARS-CoV-2 is appropriate to confirm COVID-19 disease and may be positive as early as day 7.
The approach needs to be team oriented and include cardiology, rheumatology, infectious diseases, and intensive care specialists working collaboratively. Such cases should be considered COVID positive despite negative PCR tests, and full personal protective equipment should be used as we do not as yet know if live virus could be found in stool. We initiated treatment with Anakinra (an interleukin-1 type-1 receptor inhibitor) as part of our treatment protocol for MAS; we did not appreciate a response. He then received IVIg and high-dose steroids, and he recovered over several days with improved cardiac function and stable blood pressure.
What is the pathogenesis? Is SARS-CoV-2 causative or just an associated finding? Who are the at-risk children, adolescents, and adults? Is there a genetic predisposition? What therapies work best? The eight cases described in London all received IVIg, as did our case, and all but one improved and survived. In adults we have seen substantial inflammation with elevated C-reactive protein (often as high as 300), ferritin, lactate dehydrogenase, triglycerides, fibrinogen, and d-dimers, but nearly all have extensive pulmonary disease, hypoxia, and are SARS-CoV-2 positive by PCR. Influenza is also associated with a cytokine storm syndrome in adolescents and young adults.3 The mechanisms influenza virus uses to initiate a cytokine storm and strategies for immunomodulatory treatment may provide insights into COVID-19–associated multisystem hyperinflammatory syndrome.
Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician in pediatric infectious diseases at Boston Medical Center. Dr. Camelo is a senior fellow in pediatric infectious diseases at Boston Medical Center. They have no relevant financial disclosures. Email them at [email protected].
References
1. Riphagen S et al. Lancet. 2020 May 6. doi: 10.1016/S0140-6736(20)31094-1.
2. Royal College of Paediatrics and Child Health Guidance: Paediatric multisystem inflammatory syndrome temporally associated with COVID-19.
3. Liu Q et al.Cell Mol Immunol. 2016 Jan;13(1):3-10.
COVID-19 fears tied to dangerous drop in child vaccinations
The social distancing and sheltering in place mandated because of the COVID-19 pandemic are keeping parents and kids out of their doctors’ offices, and that has prompted a steep decline in recommended routine vaccinations for U.S. children, according to Centers for Disease Control and Prevention researchers.
Pediatric vaccinations dropped sharply after the national emergency was declared on March 13, suggesting that some children may be at increased risk for other serious infectious diseases, such as measles.
The researchers compared weekly orders for federally funded vaccines from Jan. 6 to April 19, 2020, with those during the same period in 2019.
They noted that, by the end of the study period, there was a cumulative COVID-19–related decline of 2.5 million doses in orders for routine noninfluenza pediatric childhood vaccines recommended by the Advisory Committee on Immunization Practices, as well as a cumulative decline in orders of 250,000 doses of measles vaccines.
Although the overall decrease in vaccinations during the study period was larger, according to CDC spokesperson Richard Quartarone, the above figures represent declines clearly associated with the pandemic.
The weekly number of measles vaccines ordered for children aged 24 months or older fell dramatically to about 500 during the week beginning March 16, 2020, and fell further to approximately 250 during the week beginning March 23. It stayed at that level until the week beginning April 13. By comparison, more than 2,500 were ordered during the week starting March 2, before the emergency was declared.
The decline was notably less for children younger than 2 years. For those children, orders dropped to about 750 during the week starting March 23 and climbed slightly for 3 weeks. By comparison, during the week of March 2, about 2,000 vaccines were ordered.
The findings, which were published in the CDC’s Morbidity and Mortality Weekly Report, stem from an analysis of ordering data from the federal Vaccines for Children (VFC) Program, as well as from vaccine administration data from the CDC’s Vaccine Tracking System and the collaborative Vaccine Safety Datalink (VSD).
The VFC provides federally purchased vaccines at no cost to about half of persons aged 18 years or younger. The VSD collaborates on vaccine coverage with the CDC’s Immunization Safety Office and eight large health care organizations across the country. Vaccination coverage is the usual metric for assessing vaccine usage; providers’ orders and the number of doses administered are two proxy measures, the authors explained.
“The substantial reduction in VFC-funded pediatric vaccine ordering after the COVID-19 emergency declaration is consistent with changes in vaccine administration among children in the VSD population receiving care through eight large U.S. health care organizations,” wrote Jeanne M. Santoli, MD, and colleagues, of the immunization services division at the National Center for Immunization and Respiratory Diseases. “The smaller decline in measles-containing vaccine administration among children aged ≤24 months suggests that system-level strategies to prioritize well child care and immunization for this age group are being implemented.”
Dr. Santoli, who is an Atlanta-based pediatrician, and associates stressed the importance of maintaining regular vaccinations during the pandemic. “The identified declines in routine pediatric vaccine ordering and doses administered might indicate that U.S. children and their communities face increased risks for outbreaks of vaccine-preventable diseases,” they wrote. “Parental concerns about potentially exposing their children to COVID-19 during well child visits might contribute to the declines observed.” Parents should therefore be reminded of the necessity of protecting their children against vaccine-preventable diseases.
In 2019, a Gallup survey reported that overall support for vaccination continued to decline in the United States.
The researchers predicted that, as social distancing relaxes, unvaccinated children will be more susceptible to other serious diseases. “In response, continued coordinated efforts between health care providers and public health officials at the local, state, and federal levels will be necessary to achieve rapid catch-up vaccination,” they concluded.
The authors disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The social distancing and sheltering in place mandated because of the COVID-19 pandemic are keeping parents and kids out of their doctors’ offices, and that has prompted a steep decline in recommended routine vaccinations for U.S. children, according to Centers for Disease Control and Prevention researchers.
Pediatric vaccinations dropped sharply after the national emergency was declared on March 13, suggesting that some children may be at increased risk for other serious infectious diseases, such as measles.
The researchers compared weekly orders for federally funded vaccines from Jan. 6 to April 19, 2020, with those during the same period in 2019.
They noted that, by the end of the study period, there was a cumulative COVID-19–related decline of 2.5 million doses in orders for routine noninfluenza pediatric childhood vaccines recommended by the Advisory Committee on Immunization Practices, as well as a cumulative decline in orders of 250,000 doses of measles vaccines.
Although the overall decrease in vaccinations during the study period was larger, according to CDC spokesperson Richard Quartarone, the above figures represent declines clearly associated with the pandemic.
The weekly number of measles vaccines ordered for children aged 24 months or older fell dramatically to about 500 during the week beginning March 16, 2020, and fell further to approximately 250 during the week beginning March 23. It stayed at that level until the week beginning April 13. By comparison, more than 2,500 were ordered during the week starting March 2, before the emergency was declared.
The decline was notably less for children younger than 2 years. For those children, orders dropped to about 750 during the week starting March 23 and climbed slightly for 3 weeks. By comparison, during the week of March 2, about 2,000 vaccines were ordered.
The findings, which were published in the CDC’s Morbidity and Mortality Weekly Report, stem from an analysis of ordering data from the federal Vaccines for Children (VFC) Program, as well as from vaccine administration data from the CDC’s Vaccine Tracking System and the collaborative Vaccine Safety Datalink (VSD).
The VFC provides federally purchased vaccines at no cost to about half of persons aged 18 years or younger. The VSD collaborates on vaccine coverage with the CDC’s Immunization Safety Office and eight large health care organizations across the country. Vaccination coverage is the usual metric for assessing vaccine usage; providers’ orders and the number of doses administered are two proxy measures, the authors explained.
“The substantial reduction in VFC-funded pediatric vaccine ordering after the COVID-19 emergency declaration is consistent with changes in vaccine administration among children in the VSD population receiving care through eight large U.S. health care organizations,” wrote Jeanne M. Santoli, MD, and colleagues, of the immunization services division at the National Center for Immunization and Respiratory Diseases. “The smaller decline in measles-containing vaccine administration among children aged ≤24 months suggests that system-level strategies to prioritize well child care and immunization for this age group are being implemented.”
Dr. Santoli, who is an Atlanta-based pediatrician, and associates stressed the importance of maintaining regular vaccinations during the pandemic. “The identified declines in routine pediatric vaccine ordering and doses administered might indicate that U.S. children and their communities face increased risks for outbreaks of vaccine-preventable diseases,” they wrote. “Parental concerns about potentially exposing their children to COVID-19 during well child visits might contribute to the declines observed.” Parents should therefore be reminded of the necessity of protecting their children against vaccine-preventable diseases.
In 2019, a Gallup survey reported that overall support for vaccination continued to decline in the United States.
The researchers predicted that, as social distancing relaxes, unvaccinated children will be more susceptible to other serious diseases. “In response, continued coordinated efforts between health care providers and public health officials at the local, state, and federal levels will be necessary to achieve rapid catch-up vaccination,” they concluded.
The authors disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The social distancing and sheltering in place mandated because of the COVID-19 pandemic are keeping parents and kids out of their doctors’ offices, and that has prompted a steep decline in recommended routine vaccinations for U.S. children, according to Centers for Disease Control and Prevention researchers.
Pediatric vaccinations dropped sharply after the national emergency was declared on March 13, suggesting that some children may be at increased risk for other serious infectious diseases, such as measles.
The researchers compared weekly orders for federally funded vaccines from Jan. 6 to April 19, 2020, with those during the same period in 2019.
They noted that, by the end of the study period, there was a cumulative COVID-19–related decline of 2.5 million doses in orders for routine noninfluenza pediatric childhood vaccines recommended by the Advisory Committee on Immunization Practices, as well as a cumulative decline in orders of 250,000 doses of measles vaccines.
Although the overall decrease in vaccinations during the study period was larger, according to CDC spokesperson Richard Quartarone, the above figures represent declines clearly associated with the pandemic.
The weekly number of measles vaccines ordered for children aged 24 months or older fell dramatically to about 500 during the week beginning March 16, 2020, and fell further to approximately 250 during the week beginning March 23. It stayed at that level until the week beginning April 13. By comparison, more than 2,500 were ordered during the week starting March 2, before the emergency was declared.
The decline was notably less for children younger than 2 years. For those children, orders dropped to about 750 during the week starting March 23 and climbed slightly for 3 weeks. By comparison, during the week of March 2, about 2,000 vaccines were ordered.
The findings, which were published in the CDC’s Morbidity and Mortality Weekly Report, stem from an analysis of ordering data from the federal Vaccines for Children (VFC) Program, as well as from vaccine administration data from the CDC’s Vaccine Tracking System and the collaborative Vaccine Safety Datalink (VSD).
The VFC provides federally purchased vaccines at no cost to about half of persons aged 18 years or younger. The VSD collaborates on vaccine coverage with the CDC’s Immunization Safety Office and eight large health care organizations across the country. Vaccination coverage is the usual metric for assessing vaccine usage; providers’ orders and the number of doses administered are two proxy measures, the authors explained.
“The substantial reduction in VFC-funded pediatric vaccine ordering after the COVID-19 emergency declaration is consistent with changes in vaccine administration among children in the VSD population receiving care through eight large U.S. health care organizations,” wrote Jeanne M. Santoli, MD, and colleagues, of the immunization services division at the National Center for Immunization and Respiratory Diseases. “The smaller decline in measles-containing vaccine administration among children aged ≤24 months suggests that system-level strategies to prioritize well child care and immunization for this age group are being implemented.”
Dr. Santoli, who is an Atlanta-based pediatrician, and associates stressed the importance of maintaining regular vaccinations during the pandemic. “The identified declines in routine pediatric vaccine ordering and doses administered might indicate that U.S. children and their communities face increased risks for outbreaks of vaccine-preventable diseases,” they wrote. “Parental concerns about potentially exposing their children to COVID-19 during well child visits might contribute to the declines observed.” Parents should therefore be reminded of the necessity of protecting their children against vaccine-preventable diseases.
In 2019, a Gallup survey reported that overall support for vaccination continued to decline in the United States.
The researchers predicted that, as social distancing relaxes, unvaccinated children will be more susceptible to other serious diseases. “In response, continued coordinated efforts between health care providers and public health officials at the local, state, and federal levels will be necessary to achieve rapid catch-up vaccination,” they concluded.
The authors disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Nucleoside polymers show early promise in HBV
For patients with chronic hepatitis B virus (HBV) infection, triple-combination therapy with tenofovir disoproxil fumarate, pegylated interferon alfa-2a (TDF-pegIFN), and either of two investigational nucleic acid polymers was tolerable and led to long-term functional cures in an open-label phase 2 trial.
The addition of either REP 2139 or REP 2165 to backbone TDF-pegIFN therapy produced functional cures in 39% of patients without lessening HBV DNA control or exacerbating treatment-induced neutropenia or thrombocytopenia, said Michel Bazinet, MD, of Replicor in Montreal and his associates. “Increases in levels of transaminases were significantly more frequent (P < .001 vs. controls) and greater (P = .002 vs. controls) in the nucleic acid polymer groups but did not produce symptoms, correlated with [an] initial decrease in hepatitis B surface antigen [HBsAg], and normalized during therapy and follow-up,” the investigators wrote in Gastroenterology.
Nucleic acid polymers (NAPs) suppress the assembly and secretion of HBV subviral particles. NAP monotherapy is active against HBV but usually does not provide long-term virologic control. In a small study, adding pegIFN or thymosin alpha-1 to an investigational NAP achieved functional control (HBsAg positive, HBV DNA ≤ 2000 IU/mL, and normal alanine aminotransferase levels) in eight of nine patients.
Building on these findings, two triple-combination NAP regimens were evaluated in 40 noncirrhotic HB envelope antigen–negative adults with chronic HBV infection. After 24 weeks of TDF monotherapy, participants were randomly assigned to either 48 weeks of REP 2139 or REP 2165 plus backbone therapy with TDF and pegIFN, or 24 weeks of backbone therapy followed by 48 weeks of triple-combination treatment. Patients were then followed without treatment for 24-48 weeks.
Backbone TDF-pegIFN therapy produced no HBsAg seroconversions, and HBsAg levels dropped by more than 1 log10 IU/mL in only three patients. In contrast, triple-combination NAP therapy produced undetectable HBsAg and HBsAg seroconversions (up to 233,055 mIU/mL) for 60% of patients. Among 36 patients followed for 24-48 weeks after completing treatment, 78% maintained virologic control and 39% showed functional cures (HBsAg < 0.05 IU/mL, undetectable HBV DNA, and normal ALT). “Additional follow-up is planned to confirm the long-term stability of [these] outcomes,” the researchers said.
Both NAPs were formulated with chelated magnesium to improve their tolerability. Although 95% of patients experienced transaminase flares, these “self-resolved or declined during continuing NAP therapy and normalized in 32 of 34 (94%) of participants completing 48 weeks of follow-up,” the researchers said. In keeping with prior studies, transaminase flares were associated with early declines in HBsAg but not with altered liver function or liver disease symptoms.
The study was conducted at three sites in Maldova. Most participants were men with HBV genotype D infection. “During follow-up, viral rebound occurred in participants [in whom] HBsAg was still detectable at the end of 48 weeks of combination therapy (≥ 57.9 IU/mL), who did not complete therapy, or [for whom] HBsAg clearance occurred very late in therapy,” the researchers wrote. Thus, “persistent exposure to pegIFN while HBsAg is cleared may be important for the establishment of virologic control and functional cure.” They recommended evaluating NAP plus nucleos(t)ide analogue (NUC) therapy to assess response in the absence of pegIFN. Such studies should enroll “NUC-experienced participants with well-controlled HBV DNA.”
Replicor provided funding. Dr. Bazinet and the senior investigator reported that they are employees and shareholders of Replicor and have invented patents that Replicor holds. One coinvestigator reported compensation from Replicor to his institution. The remaining 11 coinvestigators reported having no relevant disclosures.
SOURCE: Bazinet M et al. Gastroenterology. 2020 Mar 5. doi: 0.1053/j.gastro.2020.02.058.
Manhal Izzy, MD, is assistant professor of medicine, Vanderbilt University Medical Center, division of gastroenterology, hepatology, and nutrition, and transplant hepatology at the Vanderbilt Clinic, Nashville, Tenn. He has no conflicts.
Manhal Izzy, MD, is assistant professor of medicine, Vanderbilt University Medical Center, division of gastroenterology, hepatology, and nutrition, and transplant hepatology at the Vanderbilt Clinic, Nashville, Tenn. He has no conflicts.
Manhal Izzy, MD, is assistant professor of medicine, Vanderbilt University Medical Center, division of gastroenterology, hepatology, and nutrition, and transplant hepatology at the Vanderbilt Clinic, Nashville, Tenn. He has no conflicts.
For patients with chronic hepatitis B virus (HBV) infection, triple-combination therapy with tenofovir disoproxil fumarate, pegylated interferon alfa-2a (TDF-pegIFN), and either of two investigational nucleic acid polymers was tolerable and led to long-term functional cures in an open-label phase 2 trial.
The addition of either REP 2139 or REP 2165 to backbone TDF-pegIFN therapy produced functional cures in 39% of patients without lessening HBV DNA control or exacerbating treatment-induced neutropenia or thrombocytopenia, said Michel Bazinet, MD, of Replicor in Montreal and his associates. “Increases in levels of transaminases were significantly more frequent (P < .001 vs. controls) and greater (P = .002 vs. controls) in the nucleic acid polymer groups but did not produce symptoms, correlated with [an] initial decrease in hepatitis B surface antigen [HBsAg], and normalized during therapy and follow-up,” the investigators wrote in Gastroenterology.
Nucleic acid polymers (NAPs) suppress the assembly and secretion of HBV subviral particles. NAP monotherapy is active against HBV but usually does not provide long-term virologic control. In a small study, adding pegIFN or thymosin alpha-1 to an investigational NAP achieved functional control (HBsAg positive, HBV DNA ≤ 2000 IU/mL, and normal alanine aminotransferase levels) in eight of nine patients.
Building on these findings, two triple-combination NAP regimens were evaluated in 40 noncirrhotic HB envelope antigen–negative adults with chronic HBV infection. After 24 weeks of TDF monotherapy, participants were randomly assigned to either 48 weeks of REP 2139 or REP 2165 plus backbone therapy with TDF and pegIFN, or 24 weeks of backbone therapy followed by 48 weeks of triple-combination treatment. Patients were then followed without treatment for 24-48 weeks.
Backbone TDF-pegIFN therapy produced no HBsAg seroconversions, and HBsAg levels dropped by more than 1 log10 IU/mL in only three patients. In contrast, triple-combination NAP therapy produced undetectable HBsAg and HBsAg seroconversions (up to 233,055 mIU/mL) for 60% of patients. Among 36 patients followed for 24-48 weeks after completing treatment, 78% maintained virologic control and 39% showed functional cures (HBsAg < 0.05 IU/mL, undetectable HBV DNA, and normal ALT). “Additional follow-up is planned to confirm the long-term stability of [these] outcomes,” the researchers said.
Both NAPs were formulated with chelated magnesium to improve their tolerability. Although 95% of patients experienced transaminase flares, these “self-resolved or declined during continuing NAP therapy and normalized in 32 of 34 (94%) of participants completing 48 weeks of follow-up,” the researchers said. In keeping with prior studies, transaminase flares were associated with early declines in HBsAg but not with altered liver function or liver disease symptoms.
The study was conducted at three sites in Maldova. Most participants were men with HBV genotype D infection. “During follow-up, viral rebound occurred in participants [in whom] HBsAg was still detectable at the end of 48 weeks of combination therapy (≥ 57.9 IU/mL), who did not complete therapy, or [for whom] HBsAg clearance occurred very late in therapy,” the researchers wrote. Thus, “persistent exposure to pegIFN while HBsAg is cleared may be important for the establishment of virologic control and functional cure.” They recommended evaluating NAP plus nucleos(t)ide analogue (NUC) therapy to assess response in the absence of pegIFN. Such studies should enroll “NUC-experienced participants with well-controlled HBV DNA.”
Replicor provided funding. Dr. Bazinet and the senior investigator reported that they are employees and shareholders of Replicor and have invented patents that Replicor holds. One coinvestigator reported compensation from Replicor to his institution. The remaining 11 coinvestigators reported having no relevant disclosures.
SOURCE: Bazinet M et al. Gastroenterology. 2020 Mar 5. doi: 0.1053/j.gastro.2020.02.058.
For patients with chronic hepatitis B virus (HBV) infection, triple-combination therapy with tenofovir disoproxil fumarate, pegylated interferon alfa-2a (TDF-pegIFN), and either of two investigational nucleic acid polymers was tolerable and led to long-term functional cures in an open-label phase 2 trial.
The addition of either REP 2139 or REP 2165 to backbone TDF-pegIFN therapy produced functional cures in 39% of patients without lessening HBV DNA control or exacerbating treatment-induced neutropenia or thrombocytopenia, said Michel Bazinet, MD, of Replicor in Montreal and his associates. “Increases in levels of transaminases were significantly more frequent (P < .001 vs. controls) and greater (P = .002 vs. controls) in the nucleic acid polymer groups but did not produce symptoms, correlated with [an] initial decrease in hepatitis B surface antigen [HBsAg], and normalized during therapy and follow-up,” the investigators wrote in Gastroenterology.
Nucleic acid polymers (NAPs) suppress the assembly and secretion of HBV subviral particles. NAP monotherapy is active against HBV but usually does not provide long-term virologic control. In a small study, adding pegIFN or thymosin alpha-1 to an investigational NAP achieved functional control (HBsAg positive, HBV DNA ≤ 2000 IU/mL, and normal alanine aminotransferase levels) in eight of nine patients.
Building on these findings, two triple-combination NAP regimens were evaluated in 40 noncirrhotic HB envelope antigen–negative adults with chronic HBV infection. After 24 weeks of TDF monotherapy, participants were randomly assigned to either 48 weeks of REP 2139 or REP 2165 plus backbone therapy with TDF and pegIFN, or 24 weeks of backbone therapy followed by 48 weeks of triple-combination treatment. Patients were then followed without treatment for 24-48 weeks.
Backbone TDF-pegIFN therapy produced no HBsAg seroconversions, and HBsAg levels dropped by more than 1 log10 IU/mL in only three patients. In contrast, triple-combination NAP therapy produced undetectable HBsAg and HBsAg seroconversions (up to 233,055 mIU/mL) for 60% of patients. Among 36 patients followed for 24-48 weeks after completing treatment, 78% maintained virologic control and 39% showed functional cures (HBsAg < 0.05 IU/mL, undetectable HBV DNA, and normal ALT). “Additional follow-up is planned to confirm the long-term stability of [these] outcomes,” the researchers said.
Both NAPs were formulated with chelated magnesium to improve their tolerability. Although 95% of patients experienced transaminase flares, these “self-resolved or declined during continuing NAP therapy and normalized in 32 of 34 (94%) of participants completing 48 weeks of follow-up,” the researchers said. In keeping with prior studies, transaminase flares were associated with early declines in HBsAg but not with altered liver function or liver disease symptoms.
The study was conducted at three sites in Maldova. Most participants were men with HBV genotype D infection. “During follow-up, viral rebound occurred in participants [in whom] HBsAg was still detectable at the end of 48 weeks of combination therapy (≥ 57.9 IU/mL), who did not complete therapy, or [for whom] HBsAg clearance occurred very late in therapy,” the researchers wrote. Thus, “persistent exposure to pegIFN while HBsAg is cleared may be important for the establishment of virologic control and functional cure.” They recommended evaluating NAP plus nucleos(t)ide analogue (NUC) therapy to assess response in the absence of pegIFN. Such studies should enroll “NUC-experienced participants with well-controlled HBV DNA.”
Replicor provided funding. Dr. Bazinet and the senior investigator reported that they are employees and shareholders of Replicor and have invented patents that Replicor holds. One coinvestigator reported compensation from Replicor to his institution. The remaining 11 coinvestigators reported having no relevant disclosures.
SOURCE: Bazinet M et al. Gastroenterology. 2020 Mar 5. doi: 0.1053/j.gastro.2020.02.058.
FROM GASTROENTEROLOGY
Modify risk factors to manage ICU delirium in patients with COVID-19
, and a bedside risk management strategy based on modifiable risk factors can help prevent lingering effects on cognition, according to an article published in Critical Care.
Several factors can contribute to an increased risk of ICU delirium in COVID-19 patients, wrote Katarzyna Kotfis, MD, of Pomeranian Medical University, Szczecin, Poland, and colleagues.
“In patients with COVID-19, delirium may be a manifestation of direct central nervous system invasion, induction of CNS inflammatory mediators, a secondary effect of other organ system failure, an effect of sedative strategies, prolonged mechanical ventilation time, or environmental factors, including social isolation,” they said.
Delirium in the context of COVID-19 can mean an early sign of infection, so patients should be screened using dedicated psychometric tools, the researchers wrote. Also, COVID-19 has been shown to cause pneumonia in elderly patients, who are at high risk for severe pulmonary disease related to COVID-19 and for ICU delirium generally, they said.
In addition, don’t underestimate the impact of social isolation created by quarantines, the researchers said.
“What is needed now, is not only high-quality ICU care, concentrated on providing adequate respiratory support to critically ill patients, but an identification of the source and degree of mental and spiritual suffering of patients as well as their families to provide the most ethical and person-centered care during this humanitarian crisis,” they emphasized. However, they acknowledged that nonpharmacologic interventions such as mobility outside the ICU room and interactions with family members are limited by the COVID-19 situation.
The researchers noted several mechanisms by which the COVID-19 virus may cause brain damage, including through the dysfunction of the renin-angiotensin system.
“Inflammatory response of the CNS to viral infection seems to be another important reason for poor neurological outcome and occurrence of delirium,” in COVID-19 patients, they said.
As for risk-reduction strategies, the researchers noted that “delirium in mechanically ventilated patients can be reduced dramatically to 50% using a culture of lighter sedation and mobilization via the implementation of the safety bundle called the ABCDEFs promoted by the Society of Critical Care Medicine in their ICU Liberation Collaborative,” although COVID-19 isolation is a barrier, they said.
The ABCDEF bundle consists of Assessment of pain, Both spontaneous awakening trials and spontaneous breathing trials, Choice of sedation, Delirium (hyperactive or hypoactive), Early mobility, and Family presence; all of which are challenging in the COVID-19 environment, the researchers said.
They advised implementing easy screening methods for delirium to reduce the burden on medical staff, and emphasized the importance of regular patient orientation, despite social separation from family and caregivers.
“No drugs can be recommended for the prevention or treatment of ICU delirium other than avoidance of overuse of potent psychoactive agents like sedatives and neuromuscular blockers (NMB) unless patients absolutely require such management,” they added.
“Delirium is so common and so hard to manage in the COVID-19 population,” Mangala Narasimhan, DO, of Northwell Health in New Hyde Park, N.Y., said in an interview. Delirium is impacted by many sources including a viral encephalopathy, the amount and duration of sedation medications, and prolonged intubation and hypoxemia, she said. “Managing the delirium allows you to wake the patient up successfully and without a lot of discoordination. This will help with weaning,” she noted. Barriers to delirium management for COVID-19 patients include the length of time on a ventilator, as well as amount of sedatives and paralytics, and the added issues of renal insufficiency, she noted. “How they can be addressed is thoughtful plans on the addition of long-term sedation for withdrawal symptoms, and anxiolytics for the profound anxiety associated with arousal from this type of sedation on ventilators, she said. The take-home message for clinicians is the need to perform weaning trials to manage delirium in the ICU. “We have to combat this delirium in order to be successful in taking these patients off of ventilators,” she said. Dr. Narasimhan added that more research is needed on areas including drug-to-drug interactions, duration of efficacy of various drugs, and how the virus affects the brain.
“Adherence to the ABCDEF bundle can reduce the incidence of delirium, from approximately 75% of mechanically ventilated patients to 50% or less,” David L. Bowton, MD, of Wake Forest Baptist Health in Winston-Salem, N.C., said in an interview.
“Importantly, in most studies, bundle adherence reduces mortality and ICU length of stay and lowers the total cost of care. However, isolation of patients and protection of staff, visitor restrictions, and potentially stressed staffing will likely alter how most institutions approach bundle compliance,” he said. “Gathering input from infection control clinicians and bedside providers from multiple disciplines that consider these factors to critically examine current bundle procedures and workflow will be essential to the creation and/or revision of bundle processes of care that maintain the integrity of the ABCDEF bundle yet preserve staff, patient, and family safety,” he said.
“We did not have strong evidence to suggest an optimal approach to treating delirium before the advent of the COVID-19 pandemic, so I do not believe we know what the best approach is in the current environment,” Dr. Bowton added. “Further, vigilance will be necessary to ensure that altered consciousness or cognition is ICU delirium and not attributable to another cause such as drug withdrawal, drug adverse effect, or primary central nervous system infection or immune response that mandates specific therapy,” he emphasized.
For clinicians, “this study reminds us of the importance of the ABCDEF bundle to improve outcomes of critical illness,” said Dr. Bowton. “It highlights the difficulties of providing frequent reassessment of pain, comfort, reassurance, and reorientation to critically ill patients. To me, it underscores the importance of each institution critically examining staffing needs and staffing roles to mitigate these difficulties and to explore novel methods of maintaining staff-patient and family-patient interactions to enhance compliance with all elements of the ABCDEF bundle while maintaining the safety of staff and families.”
Dr. Bowton added, “When necessary, explicit modifications to existing ABCDEF bundles should be developed and disseminated to provide realistic, readily understood guidance to achieve the best possible compliance with each bundle element. One potentially underrecognized issue will be the large, hopefully temporary, number of people requiring post–critical illness rehabilitation and mental health services,” he said. “In many regions these services are already underfunded and ill-equipped to handle an increased demand for these services,” he noted.
Additional research is needed in many areas, said Dr. Bowton. “While compliance with the ABCDEF bundle decreases the incidence and duration of delirium, decreases ICU length of stay, decreases duration of mechanical ventilation, and improves mortality, many questions remain. Individual elements of the bundle have been inconsistently associated with improved outcomes,” he said. “What is the relative importance of specific elements and what are the mechanisms by which they improve outcomes?” he asked. “We still do not know how to best achieve physical/functional recovery following critical illness, which, in light of these authors’ studies relating persisting physical debility to depression (Lancet Respir Med. 2014; 2[5]:369-79), may be a key component to improving long-term outcomes,” he said.
The study received no specific funding, although several coauthors disclosed grants from agencies including the National Center for Advancing Translational Sciences, National Institute of General Medical Sciences, National Heart, Lung, and Blood Institute, and National Institute on Aging. Dr. Narasimhan and Dr. Bowton had no financial conflicts to disclose.
SOURCE: Kotfis K et al. Critical Care. 2020 Apr 28. doi: 10.1186/s13054-020-02882-x.
, and a bedside risk management strategy based on modifiable risk factors can help prevent lingering effects on cognition, according to an article published in Critical Care.
Several factors can contribute to an increased risk of ICU delirium in COVID-19 patients, wrote Katarzyna Kotfis, MD, of Pomeranian Medical University, Szczecin, Poland, and colleagues.
“In patients with COVID-19, delirium may be a manifestation of direct central nervous system invasion, induction of CNS inflammatory mediators, a secondary effect of other organ system failure, an effect of sedative strategies, prolonged mechanical ventilation time, or environmental factors, including social isolation,” they said.
Delirium in the context of COVID-19 can mean an early sign of infection, so patients should be screened using dedicated psychometric tools, the researchers wrote. Also, COVID-19 has been shown to cause pneumonia in elderly patients, who are at high risk for severe pulmonary disease related to COVID-19 and for ICU delirium generally, they said.
In addition, don’t underestimate the impact of social isolation created by quarantines, the researchers said.
“What is needed now, is not only high-quality ICU care, concentrated on providing adequate respiratory support to critically ill patients, but an identification of the source and degree of mental and spiritual suffering of patients as well as their families to provide the most ethical and person-centered care during this humanitarian crisis,” they emphasized. However, they acknowledged that nonpharmacologic interventions such as mobility outside the ICU room and interactions with family members are limited by the COVID-19 situation.
The researchers noted several mechanisms by which the COVID-19 virus may cause brain damage, including through the dysfunction of the renin-angiotensin system.
“Inflammatory response of the CNS to viral infection seems to be another important reason for poor neurological outcome and occurrence of delirium,” in COVID-19 patients, they said.
As for risk-reduction strategies, the researchers noted that “delirium in mechanically ventilated patients can be reduced dramatically to 50% using a culture of lighter sedation and mobilization via the implementation of the safety bundle called the ABCDEFs promoted by the Society of Critical Care Medicine in their ICU Liberation Collaborative,” although COVID-19 isolation is a barrier, they said.
The ABCDEF bundle consists of Assessment of pain, Both spontaneous awakening trials and spontaneous breathing trials, Choice of sedation, Delirium (hyperactive or hypoactive), Early mobility, and Family presence; all of which are challenging in the COVID-19 environment, the researchers said.
They advised implementing easy screening methods for delirium to reduce the burden on medical staff, and emphasized the importance of regular patient orientation, despite social separation from family and caregivers.
“No drugs can be recommended for the prevention or treatment of ICU delirium other than avoidance of overuse of potent psychoactive agents like sedatives and neuromuscular blockers (NMB) unless patients absolutely require such management,” they added.
“Delirium is so common and so hard to manage in the COVID-19 population,” Mangala Narasimhan, DO, of Northwell Health in New Hyde Park, N.Y., said in an interview. Delirium is impacted by many sources including a viral encephalopathy, the amount and duration of sedation medications, and prolonged intubation and hypoxemia, she said. “Managing the delirium allows you to wake the patient up successfully and without a lot of discoordination. This will help with weaning,” she noted. Barriers to delirium management for COVID-19 patients include the length of time on a ventilator, as well as amount of sedatives and paralytics, and the added issues of renal insufficiency, she noted. “How they can be addressed is thoughtful plans on the addition of long-term sedation for withdrawal symptoms, and anxiolytics for the profound anxiety associated with arousal from this type of sedation on ventilators, she said. The take-home message for clinicians is the need to perform weaning trials to manage delirium in the ICU. “We have to combat this delirium in order to be successful in taking these patients off of ventilators,” she said. Dr. Narasimhan added that more research is needed on areas including drug-to-drug interactions, duration of efficacy of various drugs, and how the virus affects the brain.
“Adherence to the ABCDEF bundle can reduce the incidence of delirium, from approximately 75% of mechanically ventilated patients to 50% or less,” David L. Bowton, MD, of Wake Forest Baptist Health in Winston-Salem, N.C., said in an interview.
“Importantly, in most studies, bundle adherence reduces mortality and ICU length of stay and lowers the total cost of care. However, isolation of patients and protection of staff, visitor restrictions, and potentially stressed staffing will likely alter how most institutions approach bundle compliance,” he said. “Gathering input from infection control clinicians and bedside providers from multiple disciplines that consider these factors to critically examine current bundle procedures and workflow will be essential to the creation and/or revision of bundle processes of care that maintain the integrity of the ABCDEF bundle yet preserve staff, patient, and family safety,” he said.
“We did not have strong evidence to suggest an optimal approach to treating delirium before the advent of the COVID-19 pandemic, so I do not believe we know what the best approach is in the current environment,” Dr. Bowton added. “Further, vigilance will be necessary to ensure that altered consciousness or cognition is ICU delirium and not attributable to another cause such as drug withdrawal, drug adverse effect, or primary central nervous system infection or immune response that mandates specific therapy,” he emphasized.
For clinicians, “this study reminds us of the importance of the ABCDEF bundle to improve outcomes of critical illness,” said Dr. Bowton. “It highlights the difficulties of providing frequent reassessment of pain, comfort, reassurance, and reorientation to critically ill patients. To me, it underscores the importance of each institution critically examining staffing needs and staffing roles to mitigate these difficulties and to explore novel methods of maintaining staff-patient and family-patient interactions to enhance compliance with all elements of the ABCDEF bundle while maintaining the safety of staff and families.”
Dr. Bowton added, “When necessary, explicit modifications to existing ABCDEF bundles should be developed and disseminated to provide realistic, readily understood guidance to achieve the best possible compliance with each bundle element. One potentially underrecognized issue will be the large, hopefully temporary, number of people requiring post–critical illness rehabilitation and mental health services,” he said. “In many regions these services are already underfunded and ill-equipped to handle an increased demand for these services,” he noted.
Additional research is needed in many areas, said Dr. Bowton. “While compliance with the ABCDEF bundle decreases the incidence and duration of delirium, decreases ICU length of stay, decreases duration of mechanical ventilation, and improves mortality, many questions remain. Individual elements of the bundle have been inconsistently associated with improved outcomes,” he said. “What is the relative importance of specific elements and what are the mechanisms by which they improve outcomes?” he asked. “We still do not know how to best achieve physical/functional recovery following critical illness, which, in light of these authors’ studies relating persisting physical debility to depression (Lancet Respir Med. 2014; 2[5]:369-79), may be a key component to improving long-term outcomes,” he said.
The study received no specific funding, although several coauthors disclosed grants from agencies including the National Center for Advancing Translational Sciences, National Institute of General Medical Sciences, National Heart, Lung, and Blood Institute, and National Institute on Aging. Dr. Narasimhan and Dr. Bowton had no financial conflicts to disclose.
SOURCE: Kotfis K et al. Critical Care. 2020 Apr 28. doi: 10.1186/s13054-020-02882-x.
, and a bedside risk management strategy based on modifiable risk factors can help prevent lingering effects on cognition, according to an article published in Critical Care.
Several factors can contribute to an increased risk of ICU delirium in COVID-19 patients, wrote Katarzyna Kotfis, MD, of Pomeranian Medical University, Szczecin, Poland, and colleagues.
“In patients with COVID-19, delirium may be a manifestation of direct central nervous system invasion, induction of CNS inflammatory mediators, a secondary effect of other organ system failure, an effect of sedative strategies, prolonged mechanical ventilation time, or environmental factors, including social isolation,” they said.
Delirium in the context of COVID-19 can mean an early sign of infection, so patients should be screened using dedicated psychometric tools, the researchers wrote. Also, COVID-19 has been shown to cause pneumonia in elderly patients, who are at high risk for severe pulmonary disease related to COVID-19 and for ICU delirium generally, they said.
In addition, don’t underestimate the impact of social isolation created by quarantines, the researchers said.
“What is needed now, is not only high-quality ICU care, concentrated on providing adequate respiratory support to critically ill patients, but an identification of the source and degree of mental and spiritual suffering of patients as well as their families to provide the most ethical and person-centered care during this humanitarian crisis,” they emphasized. However, they acknowledged that nonpharmacologic interventions such as mobility outside the ICU room and interactions with family members are limited by the COVID-19 situation.
The researchers noted several mechanisms by which the COVID-19 virus may cause brain damage, including through the dysfunction of the renin-angiotensin system.
“Inflammatory response of the CNS to viral infection seems to be another important reason for poor neurological outcome and occurrence of delirium,” in COVID-19 patients, they said.
As for risk-reduction strategies, the researchers noted that “delirium in mechanically ventilated patients can be reduced dramatically to 50% using a culture of lighter sedation and mobilization via the implementation of the safety bundle called the ABCDEFs promoted by the Society of Critical Care Medicine in their ICU Liberation Collaborative,” although COVID-19 isolation is a barrier, they said.
The ABCDEF bundle consists of Assessment of pain, Both spontaneous awakening trials and spontaneous breathing trials, Choice of sedation, Delirium (hyperactive or hypoactive), Early mobility, and Family presence; all of which are challenging in the COVID-19 environment, the researchers said.
They advised implementing easy screening methods for delirium to reduce the burden on medical staff, and emphasized the importance of regular patient orientation, despite social separation from family and caregivers.
“No drugs can be recommended for the prevention or treatment of ICU delirium other than avoidance of overuse of potent psychoactive agents like sedatives and neuromuscular blockers (NMB) unless patients absolutely require such management,” they added.
“Delirium is so common and so hard to manage in the COVID-19 population,” Mangala Narasimhan, DO, of Northwell Health in New Hyde Park, N.Y., said in an interview. Delirium is impacted by many sources including a viral encephalopathy, the amount and duration of sedation medications, and prolonged intubation and hypoxemia, she said. “Managing the delirium allows you to wake the patient up successfully and without a lot of discoordination. This will help with weaning,” she noted. Barriers to delirium management for COVID-19 patients include the length of time on a ventilator, as well as amount of sedatives and paralytics, and the added issues of renal insufficiency, she noted. “How they can be addressed is thoughtful plans on the addition of long-term sedation for withdrawal symptoms, and anxiolytics for the profound anxiety associated with arousal from this type of sedation on ventilators, she said. The take-home message for clinicians is the need to perform weaning trials to manage delirium in the ICU. “We have to combat this delirium in order to be successful in taking these patients off of ventilators,” she said. Dr. Narasimhan added that more research is needed on areas including drug-to-drug interactions, duration of efficacy of various drugs, and how the virus affects the brain.
“Adherence to the ABCDEF bundle can reduce the incidence of delirium, from approximately 75% of mechanically ventilated patients to 50% or less,” David L. Bowton, MD, of Wake Forest Baptist Health in Winston-Salem, N.C., said in an interview.
“Importantly, in most studies, bundle adherence reduces mortality and ICU length of stay and lowers the total cost of care. However, isolation of patients and protection of staff, visitor restrictions, and potentially stressed staffing will likely alter how most institutions approach bundle compliance,” he said. “Gathering input from infection control clinicians and bedside providers from multiple disciplines that consider these factors to critically examine current bundle procedures and workflow will be essential to the creation and/or revision of bundle processes of care that maintain the integrity of the ABCDEF bundle yet preserve staff, patient, and family safety,” he said.
“We did not have strong evidence to suggest an optimal approach to treating delirium before the advent of the COVID-19 pandemic, so I do not believe we know what the best approach is in the current environment,” Dr. Bowton added. “Further, vigilance will be necessary to ensure that altered consciousness or cognition is ICU delirium and not attributable to another cause such as drug withdrawal, drug adverse effect, or primary central nervous system infection or immune response that mandates specific therapy,” he emphasized.
For clinicians, “this study reminds us of the importance of the ABCDEF bundle to improve outcomes of critical illness,” said Dr. Bowton. “It highlights the difficulties of providing frequent reassessment of pain, comfort, reassurance, and reorientation to critically ill patients. To me, it underscores the importance of each institution critically examining staffing needs and staffing roles to mitigate these difficulties and to explore novel methods of maintaining staff-patient and family-patient interactions to enhance compliance with all elements of the ABCDEF bundle while maintaining the safety of staff and families.”
Dr. Bowton added, “When necessary, explicit modifications to existing ABCDEF bundles should be developed and disseminated to provide realistic, readily understood guidance to achieve the best possible compliance with each bundle element. One potentially underrecognized issue will be the large, hopefully temporary, number of people requiring post–critical illness rehabilitation and mental health services,” he said. “In many regions these services are already underfunded and ill-equipped to handle an increased demand for these services,” he noted.
Additional research is needed in many areas, said Dr. Bowton. “While compliance with the ABCDEF bundle decreases the incidence and duration of delirium, decreases ICU length of stay, decreases duration of mechanical ventilation, and improves mortality, many questions remain. Individual elements of the bundle have been inconsistently associated with improved outcomes,” he said. “What is the relative importance of specific elements and what are the mechanisms by which they improve outcomes?” he asked. “We still do not know how to best achieve physical/functional recovery following critical illness, which, in light of these authors’ studies relating persisting physical debility to depression (Lancet Respir Med. 2014; 2[5]:369-79), may be a key component to improving long-term outcomes,” he said.
The study received no specific funding, although several coauthors disclosed grants from agencies including the National Center for Advancing Translational Sciences, National Institute of General Medical Sciences, National Heart, Lung, and Blood Institute, and National Institute on Aging. Dr. Narasimhan and Dr. Bowton had no financial conflicts to disclose.
SOURCE: Kotfis K et al. Critical Care. 2020 Apr 28. doi: 10.1186/s13054-020-02882-x.
FROM CRITICAL CARE
U.S. is poised to produce a COVID-19 vaccine, but don’t expect it soon
Manufacturers will begin producing COVID-19 vaccine doses in anticipation of approval so that if a product gets the okay for usage, distribution can begin quickly, according to Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases.
“We will be producing vaccine at risk, which means we’ll be [investing] considerable resources in developing doses even before we know any given candidate or candidates work,” he testified during a May 12, 2020, hearing of the Senate Health, Education, Labor, and Pensions Committee.
During the hearing, Dr. Fauci did not elaborate on how the production at risk would be undertaken, what criteria would be in place for selecting which candidates would be in the pipeline, or how much would be spent on the advanced production of these vaccines.
And while Dr. Fauci, a member of the White House coronavirus task force, remained optimistic that one or more vaccine candidates would ultimately be viable, he cautioned that there remain many unknowns that could slow the development of a vaccine for COVID-19.
“I must warn that there’s also the possibility of negative consequences that certain vaccines can actually enhance the negative effect of the infection,” he said. “The big unknown is efficacy. Will it be present or absent and how durable will it be?”
It’s unlikely that either a vaccine or an effective treatment will be available in the next 3 months, Dr. Fauci told the committee.
Sen. Lamar Alexander (R-Tenn.), the committee chairman, asked Dr. Fauci what he would say to college, primary, and secondary school administrators about how the availability of treatments and vaccines could influence the ability to reopen campuses to students. Dr. Fauci replied that the idea of having treatments or a vaccine available to facilitate the reentry of students in the fall term would be “a bit of a bridge too far.”
The emphasis in the coming months should be on testing, contact tracing, and isolation of those infected with the virus, Dr. Fauci said.
Manufacturers will begin producing COVID-19 vaccine doses in anticipation of approval so that if a product gets the okay for usage, distribution can begin quickly, according to Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases.
“We will be producing vaccine at risk, which means we’ll be [investing] considerable resources in developing doses even before we know any given candidate or candidates work,” he testified during a May 12, 2020, hearing of the Senate Health, Education, Labor, and Pensions Committee.
During the hearing, Dr. Fauci did not elaborate on how the production at risk would be undertaken, what criteria would be in place for selecting which candidates would be in the pipeline, or how much would be spent on the advanced production of these vaccines.
And while Dr. Fauci, a member of the White House coronavirus task force, remained optimistic that one or more vaccine candidates would ultimately be viable, he cautioned that there remain many unknowns that could slow the development of a vaccine for COVID-19.
“I must warn that there’s also the possibility of negative consequences that certain vaccines can actually enhance the negative effect of the infection,” he said. “The big unknown is efficacy. Will it be present or absent and how durable will it be?”
It’s unlikely that either a vaccine or an effective treatment will be available in the next 3 months, Dr. Fauci told the committee.
Sen. Lamar Alexander (R-Tenn.), the committee chairman, asked Dr. Fauci what he would say to college, primary, and secondary school administrators about how the availability of treatments and vaccines could influence the ability to reopen campuses to students. Dr. Fauci replied that the idea of having treatments or a vaccine available to facilitate the reentry of students in the fall term would be “a bit of a bridge too far.”
The emphasis in the coming months should be on testing, contact tracing, and isolation of those infected with the virus, Dr. Fauci said.
Manufacturers will begin producing COVID-19 vaccine doses in anticipation of approval so that if a product gets the okay for usage, distribution can begin quickly, according to Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases.
“We will be producing vaccine at risk, which means we’ll be [investing] considerable resources in developing doses even before we know any given candidate or candidates work,” he testified during a May 12, 2020, hearing of the Senate Health, Education, Labor, and Pensions Committee.
During the hearing, Dr. Fauci did not elaborate on how the production at risk would be undertaken, what criteria would be in place for selecting which candidates would be in the pipeline, or how much would be spent on the advanced production of these vaccines.
And while Dr. Fauci, a member of the White House coronavirus task force, remained optimistic that one or more vaccine candidates would ultimately be viable, he cautioned that there remain many unknowns that could slow the development of a vaccine for COVID-19.
“I must warn that there’s also the possibility of negative consequences that certain vaccines can actually enhance the negative effect of the infection,” he said. “The big unknown is efficacy. Will it be present or absent and how durable will it be?”
It’s unlikely that either a vaccine or an effective treatment will be available in the next 3 months, Dr. Fauci told the committee.
Sen. Lamar Alexander (R-Tenn.), the committee chairman, asked Dr. Fauci what he would say to college, primary, and secondary school administrators about how the availability of treatments and vaccines could influence the ability to reopen campuses to students. Dr. Fauci replied that the idea of having treatments or a vaccine available to facilitate the reentry of students in the fall term would be “a bit of a bridge too far.”
The emphasis in the coming months should be on testing, contact tracing, and isolation of those infected with the virus, Dr. Fauci said.