Much-anticipated results from the National Institute of Allergy and Infectious Diseases’ clinical trial of remdesivir in COVID-19 patients published in the New England Journal of Medicine suggest remdesivir shortens the disease course for hospitalized COVID-19 patients.

The agency reported initial promising results from the study earlier this month, which prompted the Food and Drug Administration to issue an emergency use authorization (EUA) for the drug, but the full data and results have not been widely available until now.

In the study of 1,063 patients, the researchers found patients who received a 10-day course of remdesivir had a reduced recovery time of 11 days, compared with 15 days to recovery in the group that received a placebo. The findings also suggest remdesivir should be started, if possible, before patients have such severe pulmonary disease that they require mechanical ventilation, according to the study authors.

The published results are “completely consistent” with the NIAID’s earlier announcement, H. Clifford Lane, MD, deputy director for clinical research and special projects at the NIAID, said in an interview. “The benefit appeared to be the greatest for the patients who are hospitalized with severe disease who require supplemental oxygen.”

Given the limited supply of remdesivir, physicians have been eager to see the full data to ensure they use the drug most effectively, Daniel Kaul, MD, a professor of infectious diseases at the University of Michigan, Ann Arbor, said in an interview. Hospitals in states across the country, including New York, Michigan, and Washington, have received limited supplies of the drug in the last couple of weeks since the FDA’s authorization.

“I am losing my patience waiting for #remdesivir data. I was willing to give them a week to verify the numbers, triple proof the tables, cautiously frame conclusions. But it’s gone on too long. We are rationing with no rationale. We are floating on whisps [sic] of data, adrift,” Kate Stephenson, MD, an infectious diseases specialist at the Center for Virology and Vaccine Research at Harvard Medical School, Boston, wrote on Twitter May 18. After reading the paper, she tweeted Friday evening that she was “relieved to see convincing benefit – I was starting to worry!”

In the midst of a public health crisis, however, it is not unusual to make an announcement about trial results before the full dataset has been analyzed, said Dr. Lane. The NIAID followed a similar playbook for the PALM trial evaluating possible Ebola treatments in the Democratic Republic of Congo, with the independent monitoring board recommending the trial be terminated early in response to positive results from two of the four candidate drugs.

“When you have a result you think is of public health importance, you don’t wait for it to be published in a peer-reviewed journal,” said Dr. Lane, a coauthor of the study. The lag time from announcement to study publication was a result of the time it took to write up the paper for publication and go through peer review, Dr. Lane added. He also noted that the FDA had access to the data when the agency wrote its guidance for physicians administering the drug to patients under the EUA.

The authors opted not to publish the initial findings on a preprint server because they felt it was important to undergo peer review, said Dr. Lane. “The last thing you want for something this critical is for incomplete data to be out there, or you don’t have everything audited to the level that you want.”

 

Trial details

In the ACTT-1 randomized, placebo-controlled, double-blinded trial, researchers enrolled 1,063 patients from Feb. 21 to April 19, 2020, at 60 trial sites and 13 subsites worldwide (45 sites in the United States). The remdesivir group had 541 patients, and the placebo group had 522. A small number of patients (49 in the remdesivir group and 53 in the placebo group) discontinued treatment before day 10 because of an adverse event or withdrawn consent. When data collection for this preliminary analysis ended in late April, 301 patients had not recovered and had not completed their final follow-up visit.

Most of the patients had one (27%) or more (52.1%) preexisting conditions, including hypertension (49.6%), obesity (37%), and type 2 diabetes mellitus (29.7%). Mean patient age was 58.9 years, and the majority of patients were men (64.3%). The median number of days from symptom onset to randomization was 9, and 53.6% of the patients were white, 20.6% were black, 12.6% were Asian, 23.4% were Hispanic or Latino, and the ethnicity of 13.6% were not reported or reported as other.

Patients received one 200-mg loading dose on the first day of the trial, and then one 100-mg maintenance dose every day for days 2 through 10, or until discharge or death. Patients in the control group of the study received a matching placebo on the same schedule and volume. The clinical status of each patient was assessed every day, from day 1 through day 29 of his or her hospital stay, according to an eight-category ordinal scale.

Time to recovery was defined as the first day during the 28-day enrollment period that a patient’s clinical status met a 1 (not hospitalization, no activity limitations), 2 (not hospitalized, activity limitation, oxygen requirement or both), or 3 (hospitalized, not requiring supplemental oxygen or medical care if hospitalization was extended for infection-control reasons) on the eight-category scale. A score of 4 indicated a patient was hospitalized and needed ongoing medical care, but did not require supplemental oxygen; a score of 8 signified death.

The analysis found remdesivir patients had a median time to recovery of 11 days, compared with the median 15 days for patients on the placebo (rate ratio for recovery, 1.32; 95% confidence interval, 1.12-1.55; P < .001). Mortality was also lower in the remdesivir group (hazard ratio for death, 0.70; 95% CI, 0.47-1.04), but the result was not statistically significant. By 14 days, the Kaplan-Meier estimate of mortality was 7.1 % in the remdesivir group and 11.9% in the placebo group.

Patients receiving oxygen, but not yet requiring high-flow oxygen, mechanical ventilation, or extracorporeal membrane oxygenation, seemed to fare best from treatment with remdesivir (these patients had a baseline ordinal score of 5). That may be a result of the larger sample size of these patients, the researchers note in the study. The study authors were unable to estimate the recovery time for the most severely ill patients (category 7), possibly because the follow-up time was too short to fully evaluate this subgroup.

“There is clear and consistent evidence of clinically significant benefit for those hospitalized on oxygen but not yet requiring mechanical ventilation,” Dr. Kaul, who was not involved in the study, said after seeing the published results. “Surprisingly, early dosing as measured from time to onset of symptoms did not seem to make a difference.”

Dr. Kaul said there is still the possibility that remdesivir could benefit patients on mechanical ventilation, but “clinicians will have to determine if the evidence suggesting no benefit in those who are intubated is strong enough to justify using this currently scarce resource in that population versus limiting use to those requiring oxygen but not on mechanical ventilation.”

Site investigators estimated that just four serious adverse events (two in each group) in enrolled patients were related to remdesivir or placebo. No deaths were attributed to the treatments, although acute respiratory failure, hypotension, acute kidney injury, and viral pneumonia were slightly more common in patients receiving the placebo than those receiving remdesivir.

The researchers plan to publish a follow-up study in the coming weeks or months, after the full cohort has completed 28 days of follow-up, Dr. Lane said. In future studies, the agency will likely focus on comparing remdesivir with combinations of remdesivir with other treatments, like the anti-inflammatory baricitinib.

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

Much-anticipated results from the National Institute of Allergy and Infectious Diseases’ clinical trial of remdesivir in COVID-19 patients published in the New England Journal of Medicine suggest remdesivir shortens the disease course for hospitalized COVID-19 patients.

The agency reported initial promising results from the study earlier this month, which prompted the Food and Drug Administration to issue an emergency use authorization (EUA) for the drug, but the full data and results have not been widely available until now.

In the study of 1,063 patients, the researchers found patients who received a 10-day course of remdesivir had a reduced recovery time of 11 days, compared with 15 days to recovery in the group that received a placebo. The findings also suggest remdesivir should be started, if possible, before patients have such severe pulmonary disease that they require mechanical ventilation, according to the study authors.

The published results are “completely consistent” with the NIAID’s earlier announcement, H. Clifford Lane, MD, deputy director for clinical research and special projects at the NIAID, said in an interview. “The benefit appeared to be the greatest for the patients who are hospitalized with severe disease who require supplemental oxygen.”

Given the limited supply of remdesivir, physicians have been eager to see the full data to ensure they use the drug most effectively, Daniel Kaul, MD, a professor of infectious diseases at the University of Michigan, Ann Arbor, said in an interview. Hospitals in states across the country, including New York, Michigan, and Washington, have received limited supplies of the drug in the last couple of weeks since the FDA’s authorization.

“I am losing my patience waiting for #remdesivir data. I was willing to give them a week to verify the numbers, triple proof the tables, cautiously frame conclusions. But it’s gone on too long. We are rationing with no rationale. We are floating on whisps [sic] of data, adrift,” Kate Stephenson, MD, an infectious diseases specialist at the Center for Virology and Vaccine Research at Harvard Medical School, Boston, wrote on Twitter May 18. After reading the paper, she tweeted Friday evening that she was “relieved to see convincing benefit – I was starting to worry!”

In the midst of a public health crisis, however, it is not unusual to make an announcement about trial results before the full dataset has been analyzed, said Dr. Lane. The NIAID followed a similar playbook for the PALM trial evaluating possible Ebola treatments in the Democratic Republic of Congo, with the independent monitoring board recommending the trial be terminated early in response to positive results from two of the four candidate drugs.

“When you have a result you think is of public health importance, you don’t wait for it to be published in a peer-reviewed journal,” said Dr. Lane, a coauthor of the study. The lag time from announcement to study publication was a result of the time it took to write up the paper for publication and go through peer review, Dr. Lane added. He also noted that the FDA had access to the data when the agency wrote its guidance for physicians administering the drug to patients under the EUA.

The authors opted not to publish the initial findings on a preprint server because they felt it was important to undergo peer review, said Dr. Lane. “The last thing you want for something this critical is for incomplete data to be out there, or you don’t have everything audited to the level that you want.”

 

Trial details

In the ACTT-1 randomized, placebo-controlled, double-blinded trial, researchers enrolled 1,063 patients from Feb. 21 to April 19, 2020, at 60 trial sites and 13 subsites worldwide (45 sites in the United States). The remdesivir group had 541 patients, and the placebo group had 522. A small number of patients (49 in the remdesivir group and 53 in the placebo group) discontinued treatment before day 10 because of an adverse event or withdrawn consent. When data collection for this preliminary analysis ended in late April, 301 patients had not recovered and had not completed their final follow-up visit.

Most of the patients had one (27%) or more (52.1%) preexisting conditions, including hypertension (49.6%), obesity (37%), and type 2 diabetes mellitus (29.7%). Mean patient age was 58.9 years, and the majority of patients were men (64.3%). The median number of days from symptom onset to randomization was 9, and 53.6% of the patients were white, 20.6% were black, 12.6% were Asian, 23.4% were Hispanic or Latino, and the ethnicity of 13.6% were not reported or reported as other.

Patients received one 200-mg loading dose on the first day of the trial, and then one 100-mg maintenance dose every day for days 2 through 10, or until discharge or death. Patients in the control group of the study received a matching placebo on the same schedule and volume. The clinical status of each patient was assessed every day, from day 1 through day 29 of his or her hospital stay, according to an eight-category ordinal scale.

Time to recovery was defined as the first day during the 28-day enrollment period that a patient’s clinical status met a 1 (not hospitalization, no activity limitations), 2 (not hospitalized, activity limitation, oxygen requirement or both), or 3 (hospitalized, not requiring supplemental oxygen or medical care if hospitalization was extended for infection-control reasons) on the eight-category scale. A score of 4 indicated a patient was hospitalized and needed ongoing medical care, but did not require supplemental oxygen; a score of 8 signified death.

The analysis found remdesivir patients had a median time to recovery of 11 days, compared with the median 15 days for patients on the placebo (rate ratio for recovery, 1.32; 95% confidence interval, 1.12-1.55; P < .001). Mortality was also lower in the remdesivir group (hazard ratio for death, 0.70; 95% CI, 0.47-1.04), but the result was not statistically significant. By 14 days, the Kaplan-Meier estimate of mortality was 7.1 % in the remdesivir group and 11.9% in the placebo group.

Patients receiving oxygen, but not yet requiring high-flow oxygen, mechanical ventilation, or extracorporeal membrane oxygenation, seemed to fare best from treatment with remdesivir (these patients had a baseline ordinal score of 5). That may be a result of the larger sample size of these patients, the researchers note in the study. The study authors were unable to estimate the recovery time for the most severely ill patients (category 7), possibly because the follow-up time was too short to fully evaluate this subgroup.

“There is clear and consistent evidence of clinically significant benefit for those hospitalized on oxygen but not yet requiring mechanical ventilation,” Dr. Kaul, who was not involved in the study, said after seeing the published results. “Surprisingly, early dosing as measured from time to onset of symptoms did not seem to make a difference.”

Dr. Kaul said there is still the possibility that remdesivir could benefit patients on mechanical ventilation, but “clinicians will have to determine if the evidence suggesting no benefit in those who are intubated is strong enough to justify using this currently scarce resource in that population versus limiting use to those requiring oxygen but not on mechanical ventilation.”

Site investigators estimated that just four serious adverse events (two in each group) in enrolled patients were related to remdesivir or placebo. No deaths were attributed to the treatments, although acute respiratory failure, hypotension, acute kidney injury, and viral pneumonia were slightly more common in patients receiving the placebo than those receiving remdesivir.

The researchers plan to publish a follow-up study in the coming weeks or months, after the full cohort has completed 28 days of follow-up, Dr. Lane said. In future studies, the agency will likely focus on comparing remdesivir with combinations of remdesivir with other treatments, like the anti-inflammatory baricitinib.

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

Much-anticipated results from the National Institute of Allergy and Infectious Diseases’ clinical trial of remdesivir in COVID-19 patients published in the New England Journal of Medicine suggest remdesivir shortens the disease course for hospitalized COVID-19 patients.

The agency reported initial promising results from the study earlier this month, which prompted the Food and Drug Administration to issue an emergency use authorization (EUA) for the drug, but the full data and results have not been widely available until now.

In the study of 1,063 patients, the researchers found patients who received a 10-day course of remdesivir had a reduced recovery time of 11 days, compared with 15 days to recovery in the group that received a placebo. The findings also suggest remdesivir should be started, if possible, before patients have such severe pulmonary disease that they require mechanical ventilation, according to the study authors.

The published results are “completely consistent” with the NIAID’s earlier announcement, H. Clifford Lane, MD, deputy director for clinical research and special projects at the NIAID, said in an interview. “The benefit appeared to be the greatest for the patients who are hospitalized with severe disease who require supplemental oxygen.”

Given the limited supply of remdesivir, physicians have been eager to see the full data to ensure they use the drug most effectively, Daniel Kaul, MD, a professor of infectious diseases at the University of Michigan, Ann Arbor, said in an interview. Hospitals in states across the country, including New York, Michigan, and Washington, have received limited supplies of the drug in the last couple of weeks since the FDA’s authorization.

“I am losing my patience waiting for #remdesivir data. I was willing to give them a week to verify the numbers, triple proof the tables, cautiously frame conclusions. But it’s gone on too long. We are rationing with no rationale. We are floating on whisps [sic] of data, adrift,” Kate Stephenson, MD, an infectious diseases specialist at the Center for Virology and Vaccine Research at Harvard Medical School, Boston, wrote on Twitter May 18. After reading the paper, she tweeted Friday evening that she was “relieved to see convincing benefit – I was starting to worry!”

In the midst of a public health crisis, however, it is not unusual to make an announcement about trial results before the full dataset has been analyzed, said Dr. Lane. The NIAID followed a similar playbook for the PALM trial evaluating possible Ebola treatments in the Democratic Republic of Congo, with the independent monitoring board recommending the trial be terminated early in response to positive results from two of the four candidate drugs.

“When you have a result you think is of public health importance, you don’t wait for it to be published in a peer-reviewed journal,” said Dr. Lane, a coauthor of the study. The lag time from announcement to study publication was a result of the time it took to write up the paper for publication and go through peer review, Dr. Lane added. He also noted that the FDA had access to the data when the agency wrote its guidance for physicians administering the drug to patients under the EUA.

The authors opted not to publish the initial findings on a preprint server because they felt it was important to undergo peer review, said Dr. Lane. “The last thing you want for something this critical is for incomplete data to be out there, or you don’t have everything audited to the level that you want.”

 

Trial details

In the ACTT-1 randomized, placebo-controlled, double-blinded trial, researchers enrolled 1,063 patients from Feb. 21 to April 19, 2020, at 60 trial sites and 13 subsites worldwide (45 sites in the United States). The remdesivir group had 541 patients, and the placebo group had 522. A small number of patients (49 in the remdesivir group and 53 in the placebo group) discontinued treatment before day 10 because of an adverse event or withdrawn consent. When data collection for this preliminary analysis ended in late April, 301 patients had not recovered and had not completed their final follow-up visit.

Most of the patients had one (27%) or more (52.1%) preexisting conditions, including hypertension (49.6%), obesity (37%), and type 2 diabetes mellitus (29.7%). Mean patient age was 58.9 years, and the majority of patients were men (64.3%). The median number of days from symptom onset to randomization was 9, and 53.6% of the patients were white, 20.6% were black, 12.6% were Asian, 23.4% were Hispanic or Latino, and the ethnicity of 13.6% were not reported or reported as other.

Patients received one 200-mg loading dose on the first day of the trial, and then one 100-mg maintenance dose every day for days 2 through 10, or until discharge or death. Patients in the control group of the study received a matching placebo on the same schedule and volume. The clinical status of each patient was assessed every day, from day 1 through day 29 of his or her hospital stay, according to an eight-category ordinal scale.

Time to recovery was defined as the first day during the 28-day enrollment period that a patient’s clinical status met a 1 (not hospitalization, no activity limitations), 2 (not hospitalized, activity limitation, oxygen requirement or both), or 3 (hospitalized, not requiring supplemental oxygen or medical care if hospitalization was extended for infection-control reasons) on the eight-category scale. A score of 4 indicated a patient was hospitalized and needed ongoing medical care, but did not require supplemental oxygen; a score of 8 signified death.

The analysis found remdesivir patients had a median time to recovery of 11 days, compared with the median 15 days for patients on the placebo (rate ratio for recovery, 1.32; 95% confidence interval, 1.12-1.55; P < .001). Mortality was also lower in the remdesivir group (hazard ratio for death, 0.70; 95% CI, 0.47-1.04), but the result was not statistically significant. By 14 days, the Kaplan-Meier estimate of mortality was 7.1 % in the remdesivir group and 11.9% in the placebo group.

Patients receiving oxygen, but not yet requiring high-flow oxygen, mechanical ventilation, or extracorporeal membrane oxygenation, seemed to fare best from treatment with remdesivir (these patients had a baseline ordinal score of 5). That may be a result of the larger sample size of these patients, the researchers note in the study. The study authors were unable to estimate the recovery time for the most severely ill patients (category 7), possibly because the follow-up time was too short to fully evaluate this subgroup.

“There is clear and consistent evidence of clinically significant benefit for those hospitalized on oxygen but not yet requiring mechanical ventilation,” Dr. Kaul, who was not involved in the study, said after seeing the published results. “Surprisingly, early dosing as measured from time to onset of symptoms did not seem to make a difference.”

Dr. Kaul said there is still the possibility that remdesivir could benefit patients on mechanical ventilation, but “clinicians will have to determine if the evidence suggesting no benefit in those who are intubated is strong enough to justify using this currently scarce resource in that population versus limiting use to those requiring oxygen but not on mechanical ventilation.”

Site investigators estimated that just four serious adverse events (two in each group) in enrolled patients were related to remdesivir or placebo. No deaths were attributed to the treatments, although acute respiratory failure, hypotension, acute kidney injury, and viral pneumonia were slightly more common in patients receiving the placebo than those receiving remdesivir.

The researchers plan to publish a follow-up study in the coming weeks or months, after the full cohort has completed 28 days of follow-up, Dr. Lane said. In future studies, the agency will likely focus on comparing remdesivir with combinations of remdesivir with other treatments, like the anti-inflammatory baricitinib.

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

I agree with Dr. Nasrallah’s clear description of the malign nature of the pre-authorization system, as described in his editorial “Pre-authorization is illegal, unethical, and adversely disrupts patient care” (From the Editor, Current Psychiatry. April 2020, p. 5,10-11). The doctor’s job is not to improve the bottom line of insurance companies by tailoring medication choices based on cost or pill quantity.

As an example of the latter, I was recently told by a pharmacist that I needed to call the insurer to justify why a patient was going from a prescription for #30 citalopram to #45 citalopram. The request had triggered a quantity limit. The pharmacist had explained to the insurer that more pills were required because the dosage was being lowered from 40 to 30 mg/d. Because there are no 30-mg tablets available, it made most sense for the patient to take one and a half 20-mg tablets, which totals 45 pills per month.

The insurer—probably a screener, not a pharmacist—would not accept that explanation and insisted that I call them myself. I bitterly resented how casually the insurer expected busy doctors to interrupt their clinical work to comply with arbitrary micromanagement of pill quantities! I’ve seldom seen such nonsense in more than 40 years of practice.

When doctors call these insurers, they are connected to a screener, but never a pharmacist. The screener asks a series of questions prompted by a computer. We give them verbal answers, but they don’t comprehend what they input into their system. The reasons we give to the screener may not even make it into the report that the screener passes on to the staff member who makes the decision. The doctor is not told what is in the report, or who is reviewing it. So much for transparency in this era that supposedly values it!

In any case, answering all the computer-prompted questions can take a long time. And time, as we know (but they do not), is not elastic.

Serious consequences may ensue if an insurer denies coverage for the doctor’s first choice. Many patients cannot afford to pay hundreds of extra dollars out of pocket. The insurer may ask the doctor to choose a different medication. Aside from the disrespect for the doctor’s decision implied by such a request, another problem is that the patient knows the new medication is his/her doctor’s second (or third) choice. Any positive placebo effect that may have existed before has now been lost. Most doctors would be glad to have a positive placebo effect augmenting the physiologic effects of the medication, especially when the patient is already feeling helpless or hopeless. These negative feelings would likely increase when the patient feels pressured into starting a medication that they know was their doctor’s second choice.

These are just a few reasons pre-authorization is a horrid system; Dr. Nasrallah covered many others in his editorial. The system, as currently structured, needs to be eliminated.

Arthur Mode, MD
Private psychiatric practice
Falls Church, Virginia

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Hooray for...

Hooray for Dr. Nasrallah’s editorial about pre-authorization! I worry, however, that he missed some important considerations.

He writes, “The welfare of the patient is not on the insurance company’s radar screen, perhaps because it is crowded out by dollar signs.” But the welfare of the patient is exactly what is on their radar screens! If the patient dies, the insurance company profits, because it will not have to pay for treatment. This is like having a Red Sox employee manage the Yankees, except we are talking about human lives, not baseball games. Dr. Nasrallah asks (but does not answer), “How did for-profit insurance companies empower themselves to tyrannize clinical practice so that the treatment administered isn’t customized to the patient’s need but instead to fatten the profits of the insurance company?” The answer: Physicians let them. Many physicians are paid by insurers directly or through work for clinics or hospitals. He who pays the piper calls the tune. And because employers often select the insurer, patients have no say.

Honesty is most important. Pre-authorization is a dishonest term, because pre-authorization actually is pre-denial. The term pre-authorization should be replaced by “pre-denial.” It is also fraudulent when insurance companies call themselves health care companies, because they only provide insurance, not health care. Similarly, the term “evidence-based medicine” is typically only an excuse that insurers use to refuse to cover the cost of treatment. In another scenario of Dr. Nasrallah’s patient with treatment-resistant depression who responded to modafinil, what if the evidence for using this medication was based on the patient’s psychiatric history alone, without any evidence from a meta-analysis of randomized controlled trials? That would not be “evidence-based” in the dishonest world of insurance. Evidence to insurers does not include what is evident in the patient’s response to a given treatment. 

What about amnesty, especially for physicians who work in the so-called pre-authorization denial business? Some even claim to be peers (ie, the “peer to peer reviews” they conduct) and insist they cannot be on speakerphone, so that their identity is kept secret from the patient. Not all of these “physicians” are incompetent. Not all of them have criminal minds or lack empathy. Some may have had exceptional circumstances leading them to such a profession, which Dr. Nasrallah correctly notes as felonious behavior. For these physicians, I think some kind of amnesty program would be appropriate, rather than prosecution.

John Jacobs, MD
Private psychiatric practice
Manchester, New Hampshire

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: I have just finished reading...

I have just finished reading Dr. Nasrallah’s editorial about pre-author­ization. I agree with everything he said, but I do have a couple of comments:

1. Many of our colleagues do not accept insurance because their practices operate on a cash basis. This seems to obviate the problem of pre-authorization, and suggests that if we truly want to get rid of pre-authorization, we should get rid of insurance.

2. In practices that do not accept insurance, some patients may be filing their own insurance claims. Do you have any information on this approach? Are patients able to apply pressure to their insurance companies? Do patients get frustrated with their insurance companies and pay cash, rather than trying to negotiate with their insurance companies?

Katherine Hankins, MD
Private psychiatric practice
Omaha, Nebraska

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Why not address...

Why not address the underlying (and actual) cause of the “pre-authorization” scam/scandal: the private health insurance industry.

Other countries in the western world have figured out how to provide guaranteed health care to their citizens without resorting to a costly insurance industry. This parasitic business suborns 10% to 20% of the health care bill while wasting our money on withholding health care deemed “not eligible” for patients who need it. Meanwhile, the executives who manage this insurance racket are paid enormous salaries not to deliver services.

Moreover, we reap a double loss to the health care system because hospitals must employ a building full of clerks to submit (and then, when rejected, re-submit) bills for reimbursement of hospital charges.

Franz Kafka would immediately grasp the despicable workings of this self-serving scheme.

David Link, MD
Associate Professor of Pediatrics
Harvard Medical School

Boston, Massachusetts

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Dr. Nasrallah responds

 

 

Dr. Nasrallah responds

Thanks to all my colleagues who commented on (and unanimously agreed with) my editorial. It is clearly one of the most outrageous hurdles that all psychiatric practitioners face every day.

For the sake of our patients who deserve optimal medical care (laboratory tests, procedures, and medications), insurance companies must be tightly regulated to avoid second-guessing the treating clinicians, and readily cover what is prescribed. Some patients who can afford it resort to paying out of pocket for privacy reasons or for rapid access to psychiatric care, and may or may not file for insurance coverage, but they will certainly receive what their psychiatrist deems appropriate after a direct evaluation.

I hope the American Psychiatric Association and American Medical Asso­ciation will continue to forcefully pursue legislation to eliminate pre-authorization and restore some sanity to the critical process of good clinical care.

Henry A. Nasrallah, MD
Professor of Psychiatry, Neurology, and Neuroscience
Medical Director: Neuropsychiatry
Director, Schizophrenia and Neuropsychiatry Programs
University of Cincinnati College of Medicine
Cincinnati, Ohio
Professor Emeritus, Saint Louis University
St. Louis, Missouri

I agree with Dr. Nasrallah’s clear description of the malign nature of the pre-authorization system, as described in his editorial “Pre-authorization is illegal, unethical, and adversely disrupts patient care” (From the Editor, Current Psychiatry. April 2020, p. 5,10-11). The doctor’s job is not to improve the bottom line of insurance companies by tailoring medication choices based on cost or pill quantity.

As an example of the latter, I was recently told by a pharmacist that I needed to call the insurer to justify why a patient was going from a prescription for #30 citalopram to #45 citalopram. The request had triggered a quantity limit. The pharmacist had explained to the insurer that more pills were required because the dosage was being lowered from 40 to 30 mg/d. Because there are no 30-mg tablets available, it made most sense for the patient to take one and a half 20-mg tablets, which totals 45 pills per month.

The insurer—probably a screener, not a pharmacist—would not accept that explanation and insisted that I call them myself. I bitterly resented how casually the insurer expected busy doctors to interrupt their clinical work to comply with arbitrary micromanagement of pill quantities! I’ve seldom seen such nonsense in more than 40 years of practice.

When doctors call these insurers, they are connected to a screener, but never a pharmacist. The screener asks a series of questions prompted by a computer. We give them verbal answers, but they don’t comprehend what they input into their system. The reasons we give to the screener may not even make it into the report that the screener passes on to the staff member who makes the decision. The doctor is not told what is in the report, or who is reviewing it. So much for transparency in this era that supposedly values it!

In any case, answering all the computer-prompted questions can take a long time. And time, as we know (but they do not), is not elastic.

Serious consequences may ensue if an insurer denies coverage for the doctor’s first choice. Many patients cannot afford to pay hundreds of extra dollars out of pocket. The insurer may ask the doctor to choose a different medication. Aside from the disrespect for the doctor’s decision implied by such a request, another problem is that the patient knows the new medication is his/her doctor’s second (or third) choice. Any positive placebo effect that may have existed before has now been lost. Most doctors would be glad to have a positive placebo effect augmenting the physiologic effects of the medication, especially when the patient is already feeling helpless or hopeless. These negative feelings would likely increase when the patient feels pressured into starting a medication that they know was their doctor’s second choice.

These are just a few reasons pre-authorization is a horrid system; Dr. Nasrallah covered many others in his editorial. The system, as currently structured, needs to be eliminated.

Arthur Mode, MD
Private psychiatric practice
Falls Church, Virginia

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Hooray for...

Hooray for Dr. Nasrallah’s editorial about pre-authorization! I worry, however, that he missed some important considerations.

He writes, “The welfare of the patient is not on the insurance company’s radar screen, perhaps because it is crowded out by dollar signs.” But the welfare of the patient is exactly what is on their radar screens! If the patient dies, the insurance company profits, because it will not have to pay for treatment. This is like having a Red Sox employee manage the Yankees, except we are talking about human lives, not baseball games. Dr. Nasrallah asks (but does not answer), “How did for-profit insurance companies empower themselves to tyrannize clinical practice so that the treatment administered isn’t customized to the patient’s need but instead to fatten the profits of the insurance company?” The answer: Physicians let them. Many physicians are paid by insurers directly or through work for clinics or hospitals. He who pays the piper calls the tune. And because employers often select the insurer, patients have no say.

Honesty is most important. Pre-authorization is a dishonest term, because pre-authorization actually is pre-denial. The term pre-authorization should be replaced by “pre-denial.” It is also fraudulent when insurance companies call themselves health care companies, because they only provide insurance, not health care. Similarly, the term “evidence-based medicine” is typically only an excuse that insurers use to refuse to cover the cost of treatment. In another scenario of Dr. Nasrallah’s patient with treatment-resistant depression who responded to modafinil, what if the evidence for using this medication was based on the patient’s psychiatric history alone, without any evidence from a meta-analysis of randomized controlled trials? That would not be “evidence-based” in the dishonest world of insurance. Evidence to insurers does not include what is evident in the patient’s response to a given treatment. 

What about amnesty, especially for physicians who work in the so-called pre-authorization denial business? Some even claim to be peers (ie, the “peer to peer reviews” they conduct) and insist they cannot be on speakerphone, so that their identity is kept secret from the patient. Not all of these “physicians” are incompetent. Not all of them have criminal minds or lack empathy. Some may have had exceptional circumstances leading them to such a profession, which Dr. Nasrallah correctly notes as felonious behavior. For these physicians, I think some kind of amnesty program would be appropriate, rather than prosecution.

John Jacobs, MD
Private psychiatric practice
Manchester, New Hampshire

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: I have just finished reading...

I have just finished reading Dr. Nasrallah’s editorial about pre-author­ization. I agree with everything he said, but I do have a couple of comments:

1. Many of our colleagues do not accept insurance because their practices operate on a cash basis. This seems to obviate the problem of pre-authorization, and suggests that if we truly want to get rid of pre-authorization, we should get rid of insurance.

2. In practices that do not accept insurance, some patients may be filing their own insurance claims. Do you have any information on this approach? Are patients able to apply pressure to their insurance companies? Do patients get frustrated with their insurance companies and pay cash, rather than trying to negotiate with their insurance companies?

Katherine Hankins, MD
Private psychiatric practice
Omaha, Nebraska

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Why not address...

Why not address the underlying (and actual) cause of the “pre-authorization” scam/scandal: the private health insurance industry.

Other countries in the western world have figured out how to provide guaranteed health care to their citizens without resorting to a costly insurance industry. This parasitic business suborns 10% to 20% of the health care bill while wasting our money on withholding health care deemed “not eligible” for patients who need it. Meanwhile, the executives who manage this insurance racket are paid enormous salaries not to deliver services.

Moreover, we reap a double loss to the health care system because hospitals must employ a building full of clerks to submit (and then, when rejected, re-submit) bills for reimbursement of hospital charges.

Franz Kafka would immediately grasp the despicable workings of this self-serving scheme.

David Link, MD
Associate Professor of Pediatrics
Harvard Medical School

Boston, Massachusetts

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Dr. Nasrallah responds

 

 

Dr. Nasrallah responds

Thanks to all my colleagues who commented on (and unanimously agreed with) my editorial. It is clearly one of the most outrageous hurdles that all psychiatric practitioners face every day.

For the sake of our patients who deserve optimal medical care (laboratory tests, procedures, and medications), insurance companies must be tightly regulated to avoid second-guessing the treating clinicians, and readily cover what is prescribed. Some patients who can afford it resort to paying out of pocket for privacy reasons or for rapid access to psychiatric care, and may or may not file for insurance coverage, but they will certainly receive what their psychiatrist deems appropriate after a direct evaluation.

I hope the American Psychiatric Association and American Medical Asso­ciation will continue to forcefully pursue legislation to eliminate pre-authorization and restore some sanity to the critical process of good clinical care.

Henry A. Nasrallah, MD
Professor of Psychiatry, Neurology, and Neuroscience
Medical Director: Neuropsychiatry
Director, Schizophrenia and Neuropsychiatry Programs
University of Cincinnati College of Medicine
Cincinnati, Ohio
Professor Emeritus, Saint Louis University
St. Louis, Missouri

I agree with Dr. Nasrallah’s clear description of the malign nature of the pre-authorization system, as described in his editorial “Pre-authorization is illegal, unethical, and adversely disrupts patient care” (From the Editor, Current Psychiatry. April 2020, p. 5,10-11). The doctor’s job is not to improve the bottom line of insurance companies by tailoring medication choices based on cost or pill quantity.

As an example of the latter, I was recently told by a pharmacist that I needed to call the insurer to justify why a patient was going from a prescription for #30 citalopram to #45 citalopram. The request had triggered a quantity limit. The pharmacist had explained to the insurer that more pills were required because the dosage was being lowered from 40 to 30 mg/d. Because there are no 30-mg tablets available, it made most sense for the patient to take one and a half 20-mg tablets, which totals 45 pills per month.

The insurer—probably a screener, not a pharmacist—would not accept that explanation and insisted that I call them myself. I bitterly resented how casually the insurer expected busy doctors to interrupt their clinical work to comply with arbitrary micromanagement of pill quantities! I’ve seldom seen such nonsense in more than 40 years of practice.

When doctors call these insurers, they are connected to a screener, but never a pharmacist. The screener asks a series of questions prompted by a computer. We give them verbal answers, but they don’t comprehend what they input into their system. The reasons we give to the screener may not even make it into the report that the screener passes on to the staff member who makes the decision. The doctor is not told what is in the report, or who is reviewing it. So much for transparency in this era that supposedly values it!

In any case, answering all the computer-prompted questions can take a long time. And time, as we know (but they do not), is not elastic.

Serious consequences may ensue if an insurer denies coverage for the doctor’s first choice. Many patients cannot afford to pay hundreds of extra dollars out of pocket. The insurer may ask the doctor to choose a different medication. Aside from the disrespect for the doctor’s decision implied by such a request, another problem is that the patient knows the new medication is his/her doctor’s second (or third) choice. Any positive placebo effect that may have existed before has now been lost. Most doctors would be glad to have a positive placebo effect augmenting the physiologic effects of the medication, especially when the patient is already feeling helpless or hopeless. These negative feelings would likely increase when the patient feels pressured into starting a medication that they know was their doctor’s second choice.

These are just a few reasons pre-authorization is a horrid system; Dr. Nasrallah covered many others in his editorial. The system, as currently structured, needs to be eliminated.

Arthur Mode, MD
Private psychiatric practice
Falls Church, Virginia

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Hooray for...

Hooray for Dr. Nasrallah’s editorial about pre-authorization! I worry, however, that he missed some important considerations.

He writes, “The welfare of the patient is not on the insurance company’s radar screen, perhaps because it is crowded out by dollar signs.” But the welfare of the patient is exactly what is on their radar screens! If the patient dies, the insurance company profits, because it will not have to pay for treatment. This is like having a Red Sox employee manage the Yankees, except we are talking about human lives, not baseball games. Dr. Nasrallah asks (but does not answer), “How did for-profit insurance companies empower themselves to tyrannize clinical practice so that the treatment administered isn’t customized to the patient’s need but instead to fatten the profits of the insurance company?” The answer: Physicians let them. Many physicians are paid by insurers directly or through work for clinics or hospitals. He who pays the piper calls the tune. And because employers often select the insurer, patients have no say.

Honesty is most important. Pre-authorization is a dishonest term, because pre-authorization actually is pre-denial. The term pre-authorization should be replaced by “pre-denial.” It is also fraudulent when insurance companies call themselves health care companies, because they only provide insurance, not health care. Similarly, the term “evidence-based medicine” is typically only an excuse that insurers use to refuse to cover the cost of treatment. In another scenario of Dr. Nasrallah’s patient with treatment-resistant depression who responded to modafinil, what if the evidence for using this medication was based on the patient’s psychiatric history alone, without any evidence from a meta-analysis of randomized controlled trials? That would not be “evidence-based” in the dishonest world of insurance. Evidence to insurers does not include what is evident in the patient’s response to a given treatment. 

What about amnesty, especially for physicians who work in the so-called pre-authorization denial business? Some even claim to be peers (ie, the “peer to peer reviews” they conduct) and insist they cannot be on speakerphone, so that their identity is kept secret from the patient. Not all of these “physicians” are incompetent. Not all of them have criminal minds or lack empathy. Some may have had exceptional circumstances leading them to such a profession, which Dr. Nasrallah correctly notes as felonious behavior. For these physicians, I think some kind of amnesty program would be appropriate, rather than prosecution.

John Jacobs, MD
Private psychiatric practice
Manchester, New Hampshire

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: I have just finished reading...

I have just finished reading Dr. Nasrallah’s editorial about pre-author­ization. I agree with everything he said, but I do have a couple of comments:

1. Many of our colleagues do not accept insurance because their practices operate on a cash basis. This seems to obviate the problem of pre-authorization, and suggests that if we truly want to get rid of pre-authorization, we should get rid of insurance.

2. In practices that do not accept insurance, some patients may be filing their own insurance claims. Do you have any information on this approach? Are patients able to apply pressure to their insurance companies? Do patients get frustrated with their insurance companies and pay cash, rather than trying to negotiate with their insurance companies?

Katherine Hankins, MD
Private psychiatric practice
Omaha, Nebraska

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Why not address...

Why not address the underlying (and actual) cause of the “pre-authorization” scam/scandal: the private health insurance industry.

Other countries in the western world have figured out how to provide guaranteed health care to their citizens without resorting to a costly insurance industry. This parasitic business suborns 10% to 20% of the health care bill while wasting our money on withholding health care deemed “not eligible” for patients who need it. Meanwhile, the executives who manage this insurance racket are paid enormous salaries not to deliver services.

Moreover, we reap a double loss to the health care system because hospitals must employ a building full of clerks to submit (and then, when rejected, re-submit) bills for reimbursement of hospital charges.

Franz Kafka would immediately grasp the despicable workings of this self-serving scheme.

David Link, MD
Associate Professor of Pediatrics
Harvard Medical School

Boston, Massachusetts

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Continue to: Dr. Nasrallah responds

 

 

Dr. Nasrallah responds

Thanks to all my colleagues who commented on (and unanimously agreed with) my editorial. It is clearly one of the most outrageous hurdles that all psychiatric practitioners face every day.

For the sake of our patients who deserve optimal medical care (laboratory tests, procedures, and medications), insurance companies must be tightly regulated to avoid second-guessing the treating clinicians, and readily cover what is prescribed. Some patients who can afford it resort to paying out of pocket for privacy reasons or for rapid access to psychiatric care, and may or may not file for insurance coverage, but they will certainly receive what their psychiatrist deems appropriate after a direct evaluation.

I hope the American Psychiatric Association and American Medical Asso­ciation will continue to forcefully pursue legislation to eliminate pre-authorization and restore some sanity to the critical process of good clinical care.

Henry A. Nasrallah, MD
Professor of Psychiatry, Neurology, and Neuroscience
Medical Director: Neuropsychiatry
Director, Schizophrenia and Neuropsychiatry Programs
University of Cincinnati College of Medicine
Cincinnati, Ohio
Professor Emeritus, Saint Louis University
St. Louis, Missouri

Real epidemiologists are out knocking on doors, chasing down contacts, or hunched over their computers trying to make sense out of screens full of data and maps. A few are trying valiantly to talk some sense into our elected officials.

konradlew/Thinkstock

This leaves the rest of us with time on our hands to fabricate our own less-than-scientific explanations for the behavior of the SARS-CoV-2 virus. So I have decided to put on hold my current mental challenge of choosing which pasta shape to pair with the sauce I’ve prepared from an online recipe. Here is my educated guess based on what I can glean from media sources that may have been filtered through a variety politically biased lenses. Remember, I did go to medical school; however, when I was in college the DNA helix was still just theoretical.

From those halcyon days of mid-February when our attention was focused on the Diamond Princess quarantined in Yokohama Harbor, it didn’t take a board-certified epidemiologist to suspect that the virus was spreading through the ventilating system in the ship’s tight quarters. Subsequent outbreaks on U.S. and French military ships suggests a similar explanation.

While still not proven, it sounds like SARS-CoV-2 jumped to humans from bats. It should not surprise us that having evolved in a dense population of mammals it would thrive in other high-density populations such as New York and nursing homes. Because we have lacked a robust testing capability, it has been less obvious until recently that, while it is easily transmitted, the virus has infected many who are asymptomatic (“Antibody surveys suggesting vast undercount of coronavirus infections may be unreliable,” Gretchen Vogel, Science, April 21, 2020). Subsequent surveys seem to confirm this higher level carrier state; it suggests that the virus is far less deadly than was previously suggested. However, it seems to be a crafty little bug attacking just about any organ system it lands on.

I don’t think any of us are surprised that the elderly population with weakened immune systems, particularly those in congregate housing, has been much more vulnerable. However, many of the deaths among younger apparently healthy people have defied explanation. The anecdotal observations that physicians, particularly those who practice in-your-face medicine (e.g., ophthalmologists and otolaryngologists) may be more vulnerable raises the issue of viral load. It may be that, although it can be extremely contagious, the virus is not terribly dangerous for most people until the inoculum dose of the virus reaches a certain level. To my knowledge this dose is unknown.

A published survey of more than 300 outbreaks from 120 Chinese cities also may support my suspicion that viral load is of critical importance. The researchers found that all the “identified outbreaks of three or more cases occurred in an indoor environment, which confirms that sharing indoor space is a major SARS-CoV-2 infection risk” (Huan Qian et al. “Indoor transmission of SARS-CoV-2,” MedRxiv. 2020 Apr 7. doi: 10.1101/2020.04.04.20053058). Again, this data shouldn’t surprise us when we look back at what little we know about the outbreaks in the confined spaces on cruise ships and in nursing homes.

I’m not sure that we have any data that helps us determine whether wearing a mask in an outdoor space has any more than symbolic value when we are talking about this particular virus. We may read that the virus in a droplet can survive on the surface it lands on for 8 minutes, and we can see those slow motion videos of the impressive plume of snot spray released by a sneeze. It would seem obvious that even outside someone within 10 feet of the sneeze has a good chance of being infected. However, how much of a threat is the asymptomatic carrier who passes within three feet of you while you are out on lovely summer day stroll? This armchair epidemiologist suspects that, when we are talking about an outside space, the 6-foot guideline for small groups of a dozen or less is overly restrictive. But until we know, I’m staying put in my armchair ... outside on the porch overlooking Casco Bay.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” He has no disclosures. Email him at pdnews@mdedge.com.

Real epidemiologists are out knocking on doors, chasing down contacts, or hunched over their computers trying to make sense out of screens full of data and maps. A few are trying valiantly to talk some sense into our elected officials.

konradlew/Thinkstock

This leaves the rest of us with time on our hands to fabricate our own less-than-scientific explanations for the behavior of the SARS-CoV-2 virus. So I have decided to put on hold my current mental challenge of choosing which pasta shape to pair with the sauce I’ve prepared from an online recipe. Here is my educated guess based on what I can glean from media sources that may have been filtered through a variety politically biased lenses. Remember, I did go to medical school; however, when I was in college the DNA helix was still just theoretical.

From those halcyon days of mid-February when our attention was focused on the Diamond Princess quarantined in Yokohama Harbor, it didn’t take a board-certified epidemiologist to suspect that the virus was spreading through the ventilating system in the ship’s tight quarters. Subsequent outbreaks on U.S. and French military ships suggests a similar explanation.

While still not proven, it sounds like SARS-CoV-2 jumped to humans from bats. It should not surprise us that having evolved in a dense population of mammals it would thrive in other high-density populations such as New York and nursing homes. Because we have lacked a robust testing capability, it has been less obvious until recently that, while it is easily transmitted, the virus has infected many who are asymptomatic (“Antibody surveys suggesting vast undercount of coronavirus infections may be unreliable,” Gretchen Vogel, Science, April 21, 2020). Subsequent surveys seem to confirm this higher level carrier state; it suggests that the virus is far less deadly than was previously suggested. However, it seems to be a crafty little bug attacking just about any organ system it lands on.

I don’t think any of us are surprised that the elderly population with weakened immune systems, particularly those in congregate housing, has been much more vulnerable. However, many of the deaths among younger apparently healthy people have defied explanation. The anecdotal observations that physicians, particularly those who practice in-your-face medicine (e.g., ophthalmologists and otolaryngologists) may be more vulnerable raises the issue of viral load. It may be that, although it can be extremely contagious, the virus is not terribly dangerous for most people until the inoculum dose of the virus reaches a certain level. To my knowledge this dose is unknown.

A published survey of more than 300 outbreaks from 120 Chinese cities also may support my suspicion that viral load is of critical importance. The researchers found that all the “identified outbreaks of three or more cases occurred in an indoor environment, which confirms that sharing indoor space is a major SARS-CoV-2 infection risk” (Huan Qian et al. “Indoor transmission of SARS-CoV-2,” MedRxiv. 2020 Apr 7. doi: 10.1101/2020.04.04.20053058). Again, this data shouldn’t surprise us when we look back at what little we know about the outbreaks in the confined spaces on cruise ships and in nursing homes.

I’m not sure that we have any data that helps us determine whether wearing a mask in an outdoor space has any more than symbolic value when we are talking about this particular virus. We may read that the virus in a droplet can survive on the surface it lands on for 8 minutes, and we can see those slow motion videos of the impressive plume of snot spray released by a sneeze. It would seem obvious that even outside someone within 10 feet of the sneeze has a good chance of being infected. However, how much of a threat is the asymptomatic carrier who passes within three feet of you while you are out on lovely summer day stroll? This armchair epidemiologist suspects that, when we are talking about an outside space, the 6-foot guideline for small groups of a dozen or less is overly restrictive. But until we know, I’m staying put in my armchair ... outside on the porch overlooking Casco Bay.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” He has no disclosures. Email him at pdnews@mdedge.com.

Real epidemiologists are out knocking on doors, chasing down contacts, or hunched over their computers trying to make sense out of screens full of data and maps. A few are trying valiantly to talk some sense into our elected officials.

konradlew/Thinkstock

This leaves the rest of us with time on our hands to fabricate our own less-than-scientific explanations for the behavior of the SARS-CoV-2 virus. So I have decided to put on hold my current mental challenge of choosing which pasta shape to pair with the sauce I’ve prepared from an online recipe. Here is my educated guess based on what I can glean from media sources that may have been filtered through a variety politically biased lenses. Remember, I did go to medical school; however, when I was in college the DNA helix was still just theoretical.

From those halcyon days of mid-February when our attention was focused on the Diamond Princess quarantined in Yokohama Harbor, it didn’t take a board-certified epidemiologist to suspect that the virus was spreading through the ventilating system in the ship’s tight quarters. Subsequent outbreaks on U.S. and French military ships suggests a similar explanation.

While still not proven, it sounds like SARS-CoV-2 jumped to humans from bats. It should not surprise us that having evolved in a dense population of mammals it would thrive in other high-density populations such as New York and nursing homes. Because we have lacked a robust testing capability, it has been less obvious until recently that, while it is easily transmitted, the virus has infected many who are asymptomatic (“Antibody surveys suggesting vast undercount of coronavirus infections may be unreliable,” Gretchen Vogel, Science, April 21, 2020). Subsequent surveys seem to confirm this higher level carrier state; it suggests that the virus is far less deadly than was previously suggested. However, it seems to be a crafty little bug attacking just about any organ system it lands on.

I don’t think any of us are surprised that the elderly population with weakened immune systems, particularly those in congregate housing, has been much more vulnerable. However, many of the deaths among younger apparently healthy people have defied explanation. The anecdotal observations that physicians, particularly those who practice in-your-face medicine (e.g., ophthalmologists and otolaryngologists) may be more vulnerable raises the issue of viral load. It may be that, although it can be extremely contagious, the virus is not terribly dangerous for most people until the inoculum dose of the virus reaches a certain level. To my knowledge this dose is unknown.

A published survey of more than 300 outbreaks from 120 Chinese cities also may support my suspicion that viral load is of critical importance. The researchers found that all the “identified outbreaks of three or more cases occurred in an indoor environment, which confirms that sharing indoor space is a major SARS-CoV-2 infection risk” (Huan Qian et al. “Indoor transmission of SARS-CoV-2,” MedRxiv. 2020 Apr 7. doi: 10.1101/2020.04.04.20053058). Again, this data shouldn’t surprise us when we look back at what little we know about the outbreaks in the confined spaces on cruise ships and in nursing homes.

I’m not sure that we have any data that helps us determine whether wearing a mask in an outdoor space has any more than symbolic value when we are talking about this particular virus. We may read that the virus in a droplet can survive on the surface it lands on for 8 minutes, and we can see those slow motion videos of the impressive plume of snot spray released by a sneeze. It would seem obvious that even outside someone within 10 feet of the sneeze has a good chance of being infected. However, how much of a threat is the asymptomatic carrier who passes within three feet of you while you are out on lovely summer day stroll? This armchair epidemiologist suspects that, when we are talking about an outside space, the 6-foot guideline for small groups of a dozen or less is overly restrictive. But until we know, I’m staying put in my armchair ... outside on the porch overlooking Casco Bay.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” He has no disclosures. Email him at pdnews@mdedge.com.

The US Poison Control Centers’ National Poison Data System (NPDS) publishes annual reports describing exposures to various substances among the general population.¹ Table 22B of each NPDS report shows the number of outcomes from exposures to different pharmacologic treatments in the United States, including psychotropic medications.² In this Table, the relative morbidity (RM) of a medication is calculated as the ratio of serious outcomes (SO) to single exposures (SE), where SO = moderate + major + death. In this article, I use the NPDS data to demonstrate how time series analysis of the RM ratios for hypertension and psychiatric medications can help predict SO associated with these agents, which may help guide clinicians’ prescribing decisions.^2,3

Time series analysis of hypertension medications

Due to the high prevalence of hypertension, it is not surprising that more suicide deaths occur each year from calcium channel blockers (CCB) than from lithium (37 vs 2, according to 2017 NPDS data).³ I used time series analysis to compare SO during 2006-2017 for 5 classes of hypertension medications: CCB, beta blockers (BB), angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), and diuretics (Figure 1).

Time series analysis of 2006-2017 data predicted the following number of deaths for 2018: CCB ≥33, BB ≥17, ACEI ≤2, ARB 0, and diuretics ≤1. The observed deaths in 2018 were 41, 23, 0, 0, and 1, respectively.² The 2018 predicted RM were CCB 10.66%, BB 11.10%, ACEI 3.51%, ARB 2.04%, and diuretics 3.38%. The 2018 observed RM for these medications were 11.01%, 11.37%, 3.02%, 2.40%, and 2.88%, respectively.²

Because the NPDS data for hyper­tension medications was only provided by class, in order to detect differences within each class, I used the relative lethality (RL) equation: RL = 310x / LD50, where x is the maximum daily dose of a medication prescribed for 30 days, and LD50 is the rat oral lethal dose 50. The RL equation represents the ratio of a 30-day supply of medication to the human equivalent LD50 for a 60-kg person.⁴ The RL equation is useful for comparing the safety of various medications, and can help clinicians avoid prescribing a lethal amount of a given medication (Figure 2). For example, the equation shows that among CCB, felodipine is 466 times safer than verapamil and 101 times safer than diltiazem. Not surprisingly, 2006-2018 data shows many deaths via intentional verapamil or diltiazem overdose vs only 1 reference to felodipine. A regression model shows significant correlation and causality between RL and SO over time.⁵ Integrating all 3 mathematical models suggests that the higher RM of CCB and BB may be caused by the high RL of verapamil, diltiazem, nicardipine, propranolol, and labetalol.

These mathematical models can help physicians consider whether to switch the patient’s current medication to another class with a lower RM. For patients who need a BB or CCB, prescribing a medication with a lower RL within the same class may be another option. The data suggest that avoiding hypertension medications with RL >100% may significantly decrease morbidity and mortality.

Predicting serious outcomes of psychiatric medications

The 2018 NPDS data for psychiatric medications show similarly important results.² For example, the lithium RM is predictable over time (Figure 3) and has been consistently the highest among psychiatric medications. Using 2006-2017 NPDS data,³ I predicted that the 2018 lithium RM would be 41.56%. The 2018 observed lithium RM was 41.45%.² I created a linear regression model for each NPDS report from 2013 to 2018 to illustrate the correlation between RL and adjusted SO for 13 psychiatric medications.^2,3,6,7 To account for different sample sizes among medications, the lithium SE for each respective year was used for all medications (adjusted SO = SE × RM). A time series analysis of these regression models shows that SO data points hover in the same y-axis region from year to year, with a corresponding RL on the x-axis: escitalopram 6.33%, citalopram 15.50%, mirtazapine 28.47%, paroxetine 37.35%, sertraline 46.72%, fluoxetine 54.87%, venlafaxine 99.64%, duloxetine 133.33%, trazodone 269.57%, bupropion 289.42%, amitriptyline 387.50%, doxepin 632.65%, and lithium 1062.86% (Figure 4). Every year, the scatter plot shape remains approximately the same, which suggests that both SO and RM can be predicted over time. Medications with RL >300% have SO ≈ 1500 (RM ≈ 40%), and those with RL <100% have SO ≈ 500 (RM ≈ 13%).

Time series analysis of NPDS data sheds light on hidden patterns. It may help clinicians discern patterns of potential SO associated with various hypertension and psychiatric medications. RL based on rat experimental data is highly correlated to RM based on human observational data, and the causality is self-evident. On a global scale, data-driven prescribing of medications with RL <100% could potentially help prevent millions of SO every year.

The US Poison Control Centers’ National Poison Data System (NPDS) publishes annual reports describing exposures to various substances among the general population.¹ Table 22B of each NPDS report shows the number of outcomes from exposures to different pharmacologic treatments in the United States, including psychotropic medications.² In this Table, the relative morbidity (RM) of a medication is calculated as the ratio of serious outcomes (SO) to single exposures (SE), where SO = moderate + major + death. In this article, I use the NPDS data to demonstrate how time series analysis of the RM ratios for hypertension and psychiatric medications can help predict SO associated with these agents, which may help guide clinicians’ prescribing decisions.^2,3

Time series analysis of hypertension medications

Due to the high prevalence of hypertension, it is not surprising that more suicide deaths occur each year from calcium channel blockers (CCB) than from lithium (37 vs 2, according to 2017 NPDS data).³ I used time series analysis to compare SO during 2006-2017 for 5 classes of hypertension medications: CCB, beta blockers (BB), angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), and diuretics (Figure 1).

Time series analysis of 2006-2017 data predicted the following number of deaths for 2018: CCB ≥33, BB ≥17, ACEI ≤2, ARB 0, and diuretics ≤1. The observed deaths in 2018 were 41, 23, 0, 0, and 1, respectively.² The 2018 predicted RM were CCB 10.66%, BB 11.10%, ACEI 3.51%, ARB 2.04%, and diuretics 3.38%. The 2018 observed RM for these medications were 11.01%, 11.37%, 3.02%, 2.40%, and 2.88%, respectively.²

Because the NPDS data for hyper­tension medications was only provided by class, in order to detect differences within each class, I used the relative lethality (RL) equation: RL = 310x / LD50, where x is the maximum daily dose of a medication prescribed for 30 days, and LD50 is the rat oral lethal dose 50. The RL equation represents the ratio of a 30-day supply of medication to the human equivalent LD50 for a 60-kg person.⁴ The RL equation is useful for comparing the safety of various medications, and can help clinicians avoid prescribing a lethal amount of a given medication (Figure 2). For example, the equation shows that among CCB, felodipine is 466 times safer than verapamil and 101 times safer than diltiazem. Not surprisingly, 2006-2018 data shows many deaths via intentional verapamil or diltiazem overdose vs only 1 reference to felodipine. A regression model shows significant correlation and causality between RL and SO over time.⁵ Integrating all 3 mathematical models suggests that the higher RM of CCB and BB may be caused by the high RL of verapamil, diltiazem, nicardipine, propranolol, and labetalol.

These mathematical models can help physicians consider whether to switch the patient’s current medication to another class with a lower RM. For patients who need a BB or CCB, prescribing a medication with a lower RL within the same class may be another option. The data suggest that avoiding hypertension medications with RL >100% may significantly decrease morbidity and mortality.

Predicting serious outcomes of psychiatric medications

The 2018 NPDS data for psychiatric medications show similarly important results.² For example, the lithium RM is predictable over time (Figure 3) and has been consistently the highest among psychiatric medications. Using 2006-2017 NPDS data,³ I predicted that the 2018 lithium RM would be 41.56%. The 2018 observed lithium RM was 41.45%.² I created a linear regression model for each NPDS report from 2013 to 2018 to illustrate the correlation between RL and adjusted SO for 13 psychiatric medications.^2,3,6,7 To account for different sample sizes among medications, the lithium SE for each respective year was used for all medications (adjusted SO = SE × RM). A time series analysis of these regression models shows that SO data points hover in the same y-axis region from year to year, with a corresponding RL on the x-axis: escitalopram 6.33%, citalopram 15.50%, mirtazapine 28.47%, paroxetine 37.35%, sertraline 46.72%, fluoxetine 54.87%, venlafaxine 99.64%, duloxetine 133.33%, trazodone 269.57%, bupropion 289.42%, amitriptyline 387.50%, doxepin 632.65%, and lithium 1062.86% (Figure 4). Every year, the scatter plot shape remains approximately the same, which suggests that both SO and RM can be predicted over time. Medications with RL >300% have SO ≈ 1500 (RM ≈ 40%), and those with RL <100% have SO ≈ 500 (RM ≈ 13%).

Time series analysis of NPDS data sheds light on hidden patterns. It may help clinicians discern patterns of potential SO associated with various hypertension and psychiatric medications. RL based on rat experimental data is highly correlated to RM based on human observational data, and the causality is self-evident. On a global scale, data-driven prescribing of medications with RL <100% could potentially help prevent millions of SO every year.

The US Poison Control Centers’ National Poison Data System (NPDS) publishes annual reports describing exposures to various substances among the general population.¹ Table 22B of each NPDS report shows the number of outcomes from exposures to different pharmacologic treatments in the United States, including psychotropic medications.² In this Table, the relative morbidity (RM) of a medication is calculated as the ratio of serious outcomes (SO) to single exposures (SE), where SO = moderate + major + death. In this article, I use the NPDS data to demonstrate how time series analysis of the RM ratios for hypertension and psychiatric medications can help predict SO associated with these agents, which may help guide clinicians’ prescribing decisions.^2,3

Time series analysis of hypertension medications

Due to the high prevalence of hypertension, it is not surprising that more suicide deaths occur each year from calcium channel blockers (CCB) than from lithium (37 vs 2, according to 2017 NPDS data).³ I used time series analysis to compare SO during 2006-2017 for 5 classes of hypertension medications: CCB, beta blockers (BB), angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), and diuretics (Figure 1).

Time series analysis of 2006-2017 data predicted the following number of deaths for 2018: CCB ≥33, BB ≥17, ACEI ≤2, ARB 0, and diuretics ≤1. The observed deaths in 2018 were 41, 23, 0, 0, and 1, respectively.² The 2018 predicted RM were CCB 10.66%, BB 11.10%, ACEI 3.51%, ARB 2.04%, and diuretics 3.38%. The 2018 observed RM for these medications were 11.01%, 11.37%, 3.02%, 2.40%, and 2.88%, respectively.²

Because the NPDS data for hyper­tension medications was only provided by class, in order to detect differences within each class, I used the relative lethality (RL) equation: RL = 310x / LD50, where x is the maximum daily dose of a medication prescribed for 30 days, and LD50 is the rat oral lethal dose 50. The RL equation represents the ratio of a 30-day supply of medication to the human equivalent LD50 for a 60-kg person.⁴ The RL equation is useful for comparing the safety of various medications, and can help clinicians avoid prescribing a lethal amount of a given medication (Figure 2). For example, the equation shows that among CCB, felodipine is 466 times safer than verapamil and 101 times safer than diltiazem. Not surprisingly, 2006-2018 data shows many deaths via intentional verapamil or diltiazem overdose vs only 1 reference to felodipine. A regression model shows significant correlation and causality between RL and SO over time.⁵ Integrating all 3 mathematical models suggests that the higher RM of CCB and BB may be caused by the high RL of verapamil, diltiazem, nicardipine, propranolol, and labetalol.

These mathematical models can help physicians consider whether to switch the patient’s current medication to another class with a lower RM. For patients who need a BB or CCB, prescribing a medication with a lower RL within the same class may be another option. The data suggest that avoiding hypertension medications with RL >100% may significantly decrease morbidity and mortality.

Predicting serious outcomes of psychiatric medications

The 2018 NPDS data for psychiatric medications show similarly important results.² For example, the lithium RM is predictable over time (Figure 3) and has been consistently the highest among psychiatric medications. Using 2006-2017 NPDS data,³ I predicted that the 2018 lithium RM would be 41.56%. The 2018 observed lithium RM was 41.45%.² I created a linear regression model for each NPDS report from 2013 to 2018 to illustrate the correlation between RL and adjusted SO for 13 psychiatric medications.^2,3,6,7 To account for different sample sizes among medications, the lithium SE for each respective year was used for all medications (adjusted SO = SE × RM). A time series analysis of these regression models shows that SO data points hover in the same y-axis region from year to year, with a corresponding RL on the x-axis: escitalopram 6.33%, citalopram 15.50%, mirtazapine 28.47%, paroxetine 37.35%, sertraline 46.72%, fluoxetine 54.87%, venlafaxine 99.64%, duloxetine 133.33%, trazodone 269.57%, bupropion 289.42%, amitriptyline 387.50%, doxepin 632.65%, and lithium 1062.86% (Figure 4). Every year, the scatter plot shape remains approximately the same, which suggests that both SO and RM can be predicted over time. Medications with RL >300% have SO ≈ 1500 (RM ≈ 40%), and those with RL <100% have SO ≈ 500 (RM ≈ 13%).

Time series analysis of NPDS data sheds light on hidden patterns. It may help clinicians discern patterns of potential SO associated with various hypertension and psychiatric medications. RL based on rat experimental data is highly correlated to RM based on human observational data, and the causality is self-evident. On a global scale, data-driven prescribing of medications with RL <100% could potentially help prevent millions of SO every year.

In addition to affecting our personal lives, coronavirus disease 2019 (COVID-19) has altered the way we practice psychiatry. Telepsychiatry—the delivery of mental health services via remote communication—is being used to replace face-to-face outpatient encounters. Several rules and regulations governing the provision of care and prescribing have been temporarily modified or suspended to allow clinicians to more easily use telepsychiatry to care for their patients. Although these requirements are continually changing, here I review some of the telepsychiatry rules and regulations clinicians need to understand to minimize their risk for liability.

Changes in light of COVID-19

In March 2020, the Centers for Medicare & Medicaid Services (CMS) released guidance that allows Medicare beneficiaries to receive various services at home through telehealth without having to travel to a doctor’s office or hospital.¹ Many commercial insurers also are allowing patients to receive telehealth services in their home. The US Department of Health & Human Services Office for Civil Rights, which enforces the Health Insurance Portability and Accountability Act (HIPAA), reported in March 2020 that it will not impose penalties for not complying with HIPAA requirements on clinicians who provide good-faith telepsychiatry during the COVID-19 crisis.²

Clinicians who want to use audio or video remote communication to provide any type of telehealth services (not just those related to COVID-19) should use “non-public facing” products.² Non-public facing products (eg, Skype, WhatsApp video call, Zoom) allow only the intended parties to participate in the communication.³ Usually, these products employ end-to-end encryption, which allows only those engaging in communication to see and hear what is transmitted.³ To limit access and verify the participants, these products also support individual user accounts, login names, and passwords.³ In addition, these products usually allow participants and/or “the host” to exert some degree of control over particular features, such as choosing to record the communication, mute, or turn off the video or audio signal.³ When using these products, clinicians should enable all available encryption and privacy modes.²

“Public-facing” products (eg, Facebook Live, TikTok, Twitch) should not be used to provide telepsychiatry services because they are designed to be open to the public or allow for wide or indiscriminate access to the communication.^2,3 Clinicians who desire additional privacy protections (and a more permanent solution) should choose a HIPAA-compliant telehealth vendor (eg, Doxy.me, VSee, Zoom for Healthcare) and obtain a Business Associate Agreement with the vendor to ensure data protection and security.^2,4

Regardless of the product, obtain informed consent from your patients that authorizes the use of remote communication.⁴ Inform your patients of any potential privacy or security breaches, the need for interactions to be conducted in a location that provides privacy, and whether the specific technology used is HIPAA-compliant.⁴ Document that your patients understand these issues before using remote communication.⁴

How licensing requirements have changed

As of March 31, 2020, the CMS temporarily waived the requirement that out-of-state clinicians be licensed in the state where they are providing services to Medicare beneficiaries.⁵ The CMS waived this requirement for clinicians who meet the following 4 conditions^5,6:

• must be enrolled in Medicare
• must possess a valid license to practice in the state that relates to his/her Medicare enrollment
• are furnishing services—whether in person or via telepsychiatry—in a state where the emergency is occurring to contribute to relief efforts in his/her professional capacity
• are not excluded from practicing in any state that is part of the nationally declared emergency area.

Note that individual state licensure requirements continue to apply unless waived by the state.⁶ Therefore, in order for clinicians to see Medicare patients via remote communication under the 4 conditions described above, the state also would have to waive its licensure requirements for the type of practice for which the clinicians are licensed in their own state.⁶ Regarding commercial payers, in general, clinicians providing telepsychiatry services need a license to practice in the state where the patient is located at the time services are provided.⁶ During the COVID-19 pandemic, many governors issued executive orders waiving licensure requirements, and many have accelerated granting temporary licenses to out-of-state clinicians who wish to provide telepsychiatry services to the residents of their state.⁴

Continue to: Prescribing via telepsychiatry

 

 

Prescribing via telepsychiatry

Effective March 31, 2020 and lasting for the duration of COVID-19 emergency declaration, the Drug Enforcement Agency (DEA) suspended the Ryan Haight Online Pharmacy Consumer Protection Act of 2008, which requires clinicians to conduct initial, in-person examinations of patients before they can prescribe controlled substances electronically.^6,7 The DEA suspension allows clinicians to prescribe controlled substances after conducting an initial evaluation via remote communication. In addition, the DEA waived the requirement that a clinician needs to hold a DEA license in the state where the patient is located to be able to prescribe a controlled substance electronically.^4,6 However, you still must comply with all other state laws and regulations for prescribing controlled substances.⁴

Staying informed

Although several telepsychiatry rules and regulations have been modified or suspended during the COVID-19 pandemic, the standard of care for services rendered via telepsychiatry remains the same as services provided via face-to-face encounters, including patient evaluation and assessment, treatment plans, medication, and documentation.⁴ Clinicians can keep up-to-date on how practicing telepsychiatry may evolve during these times by using the following resources from the American Psychiatric Association:

• Telepsychiatry Toolkit: www.psychiatry.org/psychiatrists/practice/telepsychiatry
• Practice Guidance for COVID-19: www.psychiatry.org/psychiatrists/covid-19-coronavirus/practice-guidance-for-covid-19.

In addition to affecting our personal lives, coronavirus disease 2019 (COVID-19) has altered the way we practice psychiatry. Telepsychiatry—the delivery of mental health services via remote communication—is being used to replace face-to-face outpatient encounters. Several rules and regulations governing the provision of care and prescribing have been temporarily modified or suspended to allow clinicians to more easily use telepsychiatry to care for their patients. Although these requirements are continually changing, here I review some of the telepsychiatry rules and regulations clinicians need to understand to minimize their risk for liability.

Changes in light of COVID-19

In March 2020, the Centers for Medicare & Medicaid Services (CMS) released guidance that allows Medicare beneficiaries to receive various services at home through telehealth without having to travel to a doctor’s office or hospital.¹ Many commercial insurers also are allowing patients to receive telehealth services in their home. The US Department of Health & Human Services Office for Civil Rights, which enforces the Health Insurance Portability and Accountability Act (HIPAA), reported in March 2020 that it will not impose penalties for not complying with HIPAA requirements on clinicians who provide good-faith telepsychiatry during the COVID-19 crisis.²

Clinicians who want to use audio or video remote communication to provide any type of telehealth services (not just those related to COVID-19) should use “non-public facing” products.² Non-public facing products (eg, Skype, WhatsApp video call, Zoom) allow only the intended parties to participate in the communication.³ Usually, these products employ end-to-end encryption, which allows only those engaging in communication to see and hear what is transmitted.³ To limit access and verify the participants, these products also support individual user accounts, login names, and passwords.³ In addition, these products usually allow participants and/or “the host” to exert some degree of control over particular features, such as choosing to record the communication, mute, or turn off the video or audio signal.³ When using these products, clinicians should enable all available encryption and privacy modes.²

“Public-facing” products (eg, Facebook Live, TikTok, Twitch) should not be used to provide telepsychiatry services because they are designed to be open to the public or allow for wide or indiscriminate access to the communication.^2,3 Clinicians who desire additional privacy protections (and a more permanent solution) should choose a HIPAA-compliant telehealth vendor (eg, Doxy.me, VSee, Zoom for Healthcare) and obtain a Business Associate Agreement with the vendor to ensure data protection and security.^2,4

Regardless of the product, obtain informed consent from your patients that authorizes the use of remote communication.⁴ Inform your patients of any potential privacy or security breaches, the need for interactions to be conducted in a location that provides privacy, and whether the specific technology used is HIPAA-compliant.⁴ Document that your patients understand these issues before using remote communication.⁴

How licensing requirements have changed

As of March 31, 2020, the CMS temporarily waived the requirement that out-of-state clinicians be licensed in the state where they are providing services to Medicare beneficiaries.⁵ The CMS waived this requirement for clinicians who meet the following 4 conditions^5,6:

• must be enrolled in Medicare
• must possess a valid license to practice in the state that relates to his/her Medicare enrollment
• are furnishing services—whether in person or via telepsychiatry—in a state where the emergency is occurring to contribute to relief efforts in his/her professional capacity
• are not excluded from practicing in any state that is part of the nationally declared emergency area.

Note that individual state licensure requirements continue to apply unless waived by the state.⁶ Therefore, in order for clinicians to see Medicare patients via remote communication under the 4 conditions described above, the state also would have to waive its licensure requirements for the type of practice for which the clinicians are licensed in their own state.⁶ Regarding commercial payers, in general, clinicians providing telepsychiatry services need a license to practice in the state where the patient is located at the time services are provided.⁶ During the COVID-19 pandemic, many governors issued executive orders waiving licensure requirements, and many have accelerated granting temporary licenses to out-of-state clinicians who wish to provide telepsychiatry services to the residents of their state.⁴

Continue to: Prescribing via telepsychiatry

 

 

Prescribing via telepsychiatry

Effective March 31, 2020 and lasting for the duration of COVID-19 emergency declaration, the Drug Enforcement Agency (DEA) suspended the Ryan Haight Online Pharmacy Consumer Protection Act of 2008, which requires clinicians to conduct initial, in-person examinations of patients before they can prescribe controlled substances electronically.^6,7 The DEA suspension allows clinicians to prescribe controlled substances after conducting an initial evaluation via remote communication. In addition, the DEA waived the requirement that a clinician needs to hold a DEA license in the state where the patient is located to be able to prescribe a controlled substance electronically.^4,6 However, you still must comply with all other state laws and regulations for prescribing controlled substances.⁴

Staying informed

Although several telepsychiatry rules and regulations have been modified or suspended during the COVID-19 pandemic, the standard of care for services rendered via telepsychiatry remains the same as services provided via face-to-face encounters, including patient evaluation and assessment, treatment plans, medication, and documentation.⁴ Clinicians can keep up-to-date on how practicing telepsychiatry may evolve during these times by using the following resources from the American Psychiatric Association:

• Telepsychiatry Toolkit: www.psychiatry.org/psychiatrists/practice/telepsychiatry
• Practice Guidance for COVID-19: www.psychiatry.org/psychiatrists/covid-19-coronavirus/practice-guidance-for-covid-19.

In addition to affecting our personal lives, coronavirus disease 2019 (COVID-19) has altered the way we practice psychiatry. Telepsychiatry—the delivery of mental health services via remote communication—is being used to replace face-to-face outpatient encounters. Several rules and regulations governing the provision of care and prescribing have been temporarily modified or suspended to allow clinicians to more easily use telepsychiatry to care for their patients. Although these requirements are continually changing, here I review some of the telepsychiatry rules and regulations clinicians need to understand to minimize their risk for liability.

Changes in light of COVID-19

In March 2020, the Centers for Medicare & Medicaid Services (CMS) released guidance that allows Medicare beneficiaries to receive various services at home through telehealth without having to travel to a doctor’s office or hospital.¹ Many commercial insurers also are allowing patients to receive telehealth services in their home. The US Department of Health & Human Services Office for Civil Rights, which enforces the Health Insurance Portability and Accountability Act (HIPAA), reported in March 2020 that it will not impose penalties for not complying with HIPAA requirements on clinicians who provide good-faith telepsychiatry during the COVID-19 crisis.²

Clinicians who want to use audio or video remote communication to provide any type of telehealth services (not just those related to COVID-19) should use “non-public facing” products.² Non-public facing products (eg, Skype, WhatsApp video call, Zoom) allow only the intended parties to participate in the communication.³ Usually, these products employ end-to-end encryption, which allows only those engaging in communication to see and hear what is transmitted.³ To limit access and verify the participants, these products also support individual user accounts, login names, and passwords.³ In addition, these products usually allow participants and/or “the host” to exert some degree of control over particular features, such as choosing to record the communication, mute, or turn off the video or audio signal.³ When using these products, clinicians should enable all available encryption and privacy modes.²

“Public-facing” products (eg, Facebook Live, TikTok, Twitch) should not be used to provide telepsychiatry services because they are designed to be open to the public or allow for wide or indiscriminate access to the communication.^2,3 Clinicians who desire additional privacy protections (and a more permanent solution) should choose a HIPAA-compliant telehealth vendor (eg, Doxy.me, VSee, Zoom for Healthcare) and obtain a Business Associate Agreement with the vendor to ensure data protection and security.^2,4

Regardless of the product, obtain informed consent from your patients that authorizes the use of remote communication.⁴ Inform your patients of any potential privacy or security breaches, the need for interactions to be conducted in a location that provides privacy, and whether the specific technology used is HIPAA-compliant.⁴ Document that your patients understand these issues before using remote communication.⁴

How licensing requirements have changed

As of March 31, 2020, the CMS temporarily waived the requirement that out-of-state clinicians be licensed in the state where they are providing services to Medicare beneficiaries.⁵ The CMS waived this requirement for clinicians who meet the following 4 conditions^5,6:

• must be enrolled in Medicare
• must possess a valid license to practice in the state that relates to his/her Medicare enrollment
• are furnishing services—whether in person or via telepsychiatry—in a state where the emergency is occurring to contribute to relief efforts in his/her professional capacity
• are not excluded from practicing in any state that is part of the nationally declared emergency area.

Note that individual state licensure requirements continue to apply unless waived by the state.⁶ Therefore, in order for clinicians to see Medicare patients via remote communication under the 4 conditions described above, the state also would have to waive its licensure requirements for the type of practice for which the clinicians are licensed in their own state.⁶ Regarding commercial payers, in general, clinicians providing telepsychiatry services need a license to practice in the state where the patient is located at the time services are provided.⁶ During the COVID-19 pandemic, many governors issued executive orders waiving licensure requirements, and many have accelerated granting temporary licenses to out-of-state clinicians who wish to provide telepsychiatry services to the residents of their state.⁴

Continue to: Prescribing via telepsychiatry

 

 

Prescribing via telepsychiatry

Effective March 31, 2020 and lasting for the duration of COVID-19 emergency declaration, the Drug Enforcement Agency (DEA) suspended the Ryan Haight Online Pharmacy Consumer Protection Act of 2008, which requires clinicians to conduct initial, in-person examinations of patients before they can prescribe controlled substances electronically.^6,7 The DEA suspension allows clinicians to prescribe controlled substances after conducting an initial evaluation via remote communication. In addition, the DEA waived the requirement that a clinician needs to hold a DEA license in the state where the patient is located to be able to prescribe a controlled substance electronically.^4,6 However, you still must comply with all other state laws and regulations for prescribing controlled substances.⁴

Staying informed

Although several telepsychiatry rules and regulations have been modified or suspended during the COVID-19 pandemic, the standard of care for services rendered via telepsychiatry remains the same as services provided via face-to-face encounters, including patient evaluation and assessment, treatment plans, medication, and documentation.⁴ Clinicians can keep up-to-date on how practicing telepsychiatry may evolve during these times by using the following resources from the American Psychiatric Association:

• Telepsychiatry Toolkit: www.psychiatry.org/psychiatrists/practice/telepsychiatry
• Practice Guidance for COVID-19: www.psychiatry.org/psychiatrists/covid-19-coronavirus/practice-guidance-for-covid-19.

Daily low-dose aspirin for primary disease prevention in apparently healthy older people increased their risk of serious gastrointestinal bleeding by 60% in a new analysis from the large randomized ASPREE trial released as part of the annual Digestive Disease Week^.

David Sucsy/iStockphoto

The analysis identified several independent risk factors for major GI bleeding – advanced age, hypertension, obesity, smoking, and chronic kidney disease – according to Suzanne E. Mahady, MBBS, PhD, a gastroenterologist and clinical epidemiologist at Monash University in Melbourne.

“To date, there [are] no comparable data assessing aspirin-related bleeding in older healthy people from a large randomized, controlled trial. Previous data [have] been observational, with variable definitions of significant bleeding, and retrospective. We derived a standard definition for bleeding, used physicians to adjudicate bleeding endpoints, and followed older people for 5 years,” she explained in an interview.

“Our data on bleeding [are] novel,” Dr. Mahady added. “It will help clinicians assess who is most at risk of bleeding with aspirin and target modifiable bleeding risk factors where possible.”

ASPREE was a double-blind trial including 19,114 apparently healthy Australian and American adults age 70 or older, or age 65-plus for blacks and Hispanics in the United States. Participants were randomized to 100 mg/day of enteric-coated aspirin or placebo. At a median 4.7 years of follow-up, there was no between-group difference in major adverse cardiovascular events, a lack of benefit accompanied by a 38% greater risk of major hemorrhage risk and a statistically significant 14% increase in all-cause mortality in the aspirin group. (N Engl J Med. 2018 Oct 18;379[16]:1509-18). The chief contributor to the excess mortality in the aspirin group was their 31% greater risk of cancer-related death (N Engl J Med. 2018 Oct 18;379[16]:1519-28).

The new analysis of severe GI bleeding documented an absolute 5-year risk of 0.2% for 70-year-olds and 0.4% in 80-year-olds on aspirin. In 80-year-olds with additional GI bleeding risk factors as identified in the study, the rate reached up to 5.5%. The risk of major upper GI bleeding events was 87% greater in the aspirin group, compared with placebo-treated controls, and the risk of serious lower GI bleeding was increased 36%.

ASPREE coinvestigator Andrew T. Chan, MD, said that the bleeding data should prove useful in future efforts to appropriately weight the risks and benefits of low-dose aspirin treatment.

“We need to better understand how to incorporate bleeding risk in clinical decision making about how to use aspirin among older adults because aspirin has many potential benefits, including prevention of colorectal cancer,” said Dr. Chan, a gastroenterologist and professor of medicine at Harvard Medical School and director for cancer epidemiology at Massachusetts General Hospital, both in Boston.

However, ASPREE has soured cardiologists on the decades-long practice of recommending aspirin for primary prevention of cardiovascular disease in older individuals. In response to the publication of primary outcomes in ASPREE, which was closely bracketed by publication of the largely negative results of the randomized ARRIVE and ASCEND trials in a collective 47,000-plus randomized patients, the American College of Cardiology/American Heart Association clipped aspirin’s role for primary prevention of atherosclerotic cardiovascular disease. The current recommendation is that low-dose aspirin should not be administered on a routine basis for primary cardiovascular prevention in people above age 70, nor in adults at any age at increased bleeding risk, although the practice “might be considered” for primary prevention in select higher atherosclerotic cardiovascular disease–risk 40- to 70-year-olds, provided they are not at increased bleeding risk (J Am Coll Cardiol. 2019 Sep. doi: 10.1016/j.jacc.2019.03.010).

Dr. Mahady reported having no financial conflicts of interest. Dr. Chan serves as a consultant to Bayer Pharma, Janssen, and Pfizer.

bjancin@mdedge.com

Daily low-dose aspirin for primary disease prevention in apparently healthy older people increased their risk of serious gastrointestinal bleeding by 60% in a new analysis from the large randomized ASPREE trial released as part of the annual Digestive Disease Week^.

David Sucsy/iStockphoto

The analysis identified several independent risk factors for major GI bleeding – advanced age, hypertension, obesity, smoking, and chronic kidney disease – according to Suzanne E. Mahady, MBBS, PhD, a gastroenterologist and clinical epidemiologist at Monash University in Melbourne.

“To date, there [are] no comparable data assessing aspirin-related bleeding in older healthy people from a large randomized, controlled trial. Previous data [have] been observational, with variable definitions of significant bleeding, and retrospective. We derived a standard definition for bleeding, used physicians to adjudicate bleeding endpoints, and followed older people for 5 years,” she explained in an interview.

“Our data on bleeding [are] novel,” Dr. Mahady added. “It will help clinicians assess who is most at risk of bleeding with aspirin and target modifiable bleeding risk factors where possible.”

ASPREE was a double-blind trial including 19,114 apparently healthy Australian and American adults age 70 or older, or age 65-plus for blacks and Hispanics in the United States. Participants were randomized to 100 mg/day of enteric-coated aspirin or placebo. At a median 4.7 years of follow-up, there was no between-group difference in major adverse cardiovascular events, a lack of benefit accompanied by a 38% greater risk of major hemorrhage risk and a statistically significant 14% increase in all-cause mortality in the aspirin group. (N Engl J Med. 2018 Oct 18;379[16]:1509-18). The chief contributor to the excess mortality in the aspirin group was their 31% greater risk of cancer-related death (N Engl J Med. 2018 Oct 18;379[16]:1519-28).

The new analysis of severe GI bleeding documented an absolute 5-year risk of 0.2% for 70-year-olds and 0.4% in 80-year-olds on aspirin. In 80-year-olds with additional GI bleeding risk factors as identified in the study, the rate reached up to 5.5%. The risk of major upper GI bleeding events was 87% greater in the aspirin group, compared with placebo-treated controls, and the risk of serious lower GI bleeding was increased 36%.

ASPREE coinvestigator Andrew T. Chan, MD, said that the bleeding data should prove useful in future efforts to appropriately weight the risks and benefits of low-dose aspirin treatment.

“We need to better understand how to incorporate bleeding risk in clinical decision making about how to use aspirin among older adults because aspirin has many potential benefits, including prevention of colorectal cancer,” said Dr. Chan, a gastroenterologist and professor of medicine at Harvard Medical School and director for cancer epidemiology at Massachusetts General Hospital, both in Boston.

However, ASPREE has soured cardiologists on the decades-long practice of recommending aspirin for primary prevention of cardiovascular disease in older individuals. In response to the publication of primary outcomes in ASPREE, which was closely bracketed by publication of the largely negative results of the randomized ARRIVE and ASCEND trials in a collective 47,000-plus randomized patients, the American College of Cardiology/American Heart Association clipped aspirin’s role for primary prevention of atherosclerotic cardiovascular disease. The current recommendation is that low-dose aspirin should not be administered on a routine basis for primary cardiovascular prevention in people above age 70, nor in adults at any age at increased bleeding risk, although the practice “might be considered” for primary prevention in select higher atherosclerotic cardiovascular disease–risk 40- to 70-year-olds, provided they are not at increased bleeding risk (J Am Coll Cardiol. 2019 Sep. doi: 10.1016/j.jacc.2019.03.010).

Dr. Mahady reported having no financial conflicts of interest. Dr. Chan serves as a consultant to Bayer Pharma, Janssen, and Pfizer.

bjancin@mdedge.com

Daily low-dose aspirin for primary disease prevention in apparently healthy older people increased their risk of serious gastrointestinal bleeding by 60% in a new analysis from the large randomized ASPREE trial released as part of the annual Digestive Disease Week^.

David Sucsy/iStockphoto

The analysis identified several independent risk factors for major GI bleeding – advanced age, hypertension, obesity, smoking, and chronic kidney disease – according to Suzanne E. Mahady, MBBS, PhD, a gastroenterologist and clinical epidemiologist at Monash University in Melbourne.

“To date, there [are] no comparable data assessing aspirin-related bleeding in older healthy people from a large randomized, controlled trial. Previous data [have] been observational, with variable definitions of significant bleeding, and retrospective. We derived a standard definition for bleeding, used physicians to adjudicate bleeding endpoints, and followed older people for 5 years,” she explained in an interview.

“Our data on bleeding [are] novel,” Dr. Mahady added. “It will help clinicians assess who is most at risk of bleeding with aspirin and target modifiable bleeding risk factors where possible.”

ASPREE was a double-blind trial including 19,114 apparently healthy Australian and American adults age 70 or older, or age 65-plus for blacks and Hispanics in the United States. Participants were randomized to 100 mg/day of enteric-coated aspirin or placebo. At a median 4.7 years of follow-up, there was no between-group difference in major adverse cardiovascular events, a lack of benefit accompanied by a 38% greater risk of major hemorrhage risk and a statistically significant 14% increase in all-cause mortality in the aspirin group. (N Engl J Med. 2018 Oct 18;379[16]:1509-18). The chief contributor to the excess mortality in the aspirin group was their 31% greater risk of cancer-related death (N Engl J Med. 2018 Oct 18;379[16]:1519-28).

The new analysis of severe GI bleeding documented an absolute 5-year risk of 0.2% for 70-year-olds and 0.4% in 80-year-olds on aspirin. In 80-year-olds with additional GI bleeding risk factors as identified in the study, the rate reached up to 5.5%. The risk of major upper GI bleeding events was 87% greater in the aspirin group, compared with placebo-treated controls, and the risk of serious lower GI bleeding was increased 36%.

ASPREE coinvestigator Andrew T. Chan, MD, said that the bleeding data should prove useful in future efforts to appropriately weight the risks and benefits of low-dose aspirin treatment.

“We need to better understand how to incorporate bleeding risk in clinical decision making about how to use aspirin among older adults because aspirin has many potential benefits, including prevention of colorectal cancer,” said Dr. Chan, a gastroenterologist and professor of medicine at Harvard Medical School and director for cancer epidemiology at Massachusetts General Hospital, both in Boston.

However, ASPREE has soured cardiologists on the decades-long practice of recommending aspirin for primary prevention of cardiovascular disease in older individuals. In response to the publication of primary outcomes in ASPREE, which was closely bracketed by publication of the largely negative results of the randomized ARRIVE and ASCEND trials in a collective 47,000-plus randomized patients, the American College of Cardiology/American Heart Association clipped aspirin’s role for primary prevention of atherosclerotic cardiovascular disease. The current recommendation is that low-dose aspirin should not be administered on a routine basis for primary cardiovascular prevention in people above age 70, nor in adults at any age at increased bleeding risk, although the practice “might be considered” for primary prevention in select higher atherosclerotic cardiovascular disease–risk 40- to 70-year-olds, provided they are not at increased bleeding risk (J Am Coll Cardiol. 2019 Sep. doi: 10.1016/j.jacc.2019.03.010).

Dr. Mahady reported having no financial conflicts of interest. Dr. Chan serves as a consultant to Bayer Pharma, Janssen, and Pfizer.

bjancin@mdedge.com

Burnout among health care professionals has been increasingly recognized by the medical community over the past several years. The concern for burnout among medical students is equally serious. In this article, I review the prevalence of burnout among medical students, and the personal and clinical effects they experience. I also discuss how as psychiatry residents we can be more effective in preventing and identifying medical student burnout.

An underappreciated problem

Burnout has been defined as long-term unresolvable job stress that leads to exhaustion and feeling overwhelmed, cynical, and detached from work, and lacking a sense of personal accomplishment. It can lead to depression, anxiety, and suicidal ideation—one survey found that 5.8% of medical students had experienced suicidal ideation at some point in the previous 12 months.¹ Burnout affects not only the individual, but also his/her team and patients. One study found that compared to medical students who didn’t report burnout, medical students who did had lower scores on measures of empathy and professionalism.²

While burnout among physicians and residents has received increasing attention, it often may go unrecognized and unreported in medical students. A literature review that included 51 studies found 28% to 45% of medical students report burnout.³ In a survey at one institution, 60% of medical students reported burnout.⁴ It is evident that medical schools have an important role in helping to minimize burnout rates in their students, and many schools are working toward this goal. However, what happens when students leave the classroom setting for clinical rotations?

A recent study found burnout among medical students peaks during the third year of medical school.⁵ This is when students are on their clinical rotations, new to the hospital environment, and without the inherent structure and support of being at school.

How residents can help

Like most medical students, while on my clinical rotations, I spent most of my day with residents, and I believe residents can help to both recognize burnout in medical students and prevent it.

The first step in addressing this problem is to understand why it occurs. A survey of medical students showed that inadequate sleep and decreased exercise play a significant role in burnout rates.⁶ Another study found a correlation between burnout and feeling emotionally exhausted and a decreased perceived quality of life.⁷ A medical student I recently worked with stated, “How can you not feel burnt out? Juggling work hours, studying, debt, health, and trying to have a life… something always gets dropped.”

So as residents, what can we do to identify and assist medical students who are experiencing burnout, or are at risk of getting there? When needed, we can utilize our psychiatry training to assess our students for depression and substance use disorders, and connect them with appropriate resources. When identifying a medical student with burnout, I believe it can become necessary to notify the attending, the site director responsible for the student, and often the school, so that the student has access to all available resources.

Continue to: It's as important to be proactive...

It’s as important to be proactive as it is to be reactive. Engaging in regular check-ins with our students about self-care and workload, as well as asking about how they are feeling, can offer them opportunities to talk about issues that they might not be getting anywhere else. One medical student I worked with told me, “It’s easy to fade into the background as the student, or to feel like I can’t complain because this is just how medical school is supposed to be.” We have the ability to change this notion with each student we work with.

It is likely that as residents we have worked with a student struggling with burnout without even realizing it. I believe we can play an important role in helping to prevent burnout by identifying at-risk students, offering assistance, and encouraging them to seek professional help. Someone’s life may depend on it.

Burnout among health care professionals has been increasingly recognized by the medical community over the past several years. The concern for burnout among medical students is equally serious. In this article, I review the prevalence of burnout among medical students, and the personal and clinical effects they experience. I also discuss how as psychiatry residents we can be more effective in preventing and identifying medical student burnout.

An underappreciated problem

Burnout has been defined as long-term unresolvable job stress that leads to exhaustion and feeling overwhelmed, cynical, and detached from work, and lacking a sense of personal accomplishment. It can lead to depression, anxiety, and suicidal ideation—one survey found that 5.8% of medical students had experienced suicidal ideation at some point in the previous 12 months.¹ Burnout affects not only the individual, but also his/her team and patients. One study found that compared to medical students who didn’t report burnout, medical students who did had lower scores on measures of empathy and professionalism.²

While burnout among physicians and residents has received increasing attention, it often may go unrecognized and unreported in medical students. A literature review that included 51 studies found 28% to 45% of medical students report burnout.³ In a survey at one institution, 60% of medical students reported burnout.⁴ It is evident that medical schools have an important role in helping to minimize burnout rates in their students, and many schools are working toward this goal. However, what happens when students leave the classroom setting for clinical rotations?

A recent study found burnout among medical students peaks during the third year of medical school.⁵ This is when students are on their clinical rotations, new to the hospital environment, and without the inherent structure and support of being at school.

How residents can help

Like most medical students, while on my clinical rotations, I spent most of my day with residents, and I believe residents can help to both recognize burnout in medical students and prevent it.

The first step in addressing this problem is to understand why it occurs. A survey of medical students showed that inadequate sleep and decreased exercise play a significant role in burnout rates.⁶ Another study found a correlation between burnout and feeling emotionally exhausted and a decreased perceived quality of life.⁷ A medical student I recently worked with stated, “How can you not feel burnt out? Juggling work hours, studying, debt, health, and trying to have a life… something always gets dropped.”

So as residents, what can we do to identify and assist medical students who are experiencing burnout, or are at risk of getting there? When needed, we can utilize our psychiatry training to assess our students for depression and substance use disorders, and connect them with appropriate resources. When identifying a medical student with burnout, I believe it can become necessary to notify the attending, the site director responsible for the student, and often the school, so that the student has access to all available resources.

Continue to: It's as important to be proactive...

It’s as important to be proactive as it is to be reactive. Engaging in regular check-ins with our students about self-care and workload, as well as asking about how they are feeling, can offer them opportunities to talk about issues that they might not be getting anywhere else. One medical student I worked with told me, “It’s easy to fade into the background as the student, or to feel like I can’t complain because this is just how medical school is supposed to be.” We have the ability to change this notion with each student we work with.

It is likely that as residents we have worked with a student struggling with burnout without even realizing it. I believe we can play an important role in helping to prevent burnout by identifying at-risk students, offering assistance, and encouraging them to seek professional help. Someone’s life may depend on it.

Burnout among health care professionals has been increasingly recognized by the medical community over the past several years. The concern for burnout among medical students is equally serious. In this article, I review the prevalence of burnout among medical students, and the personal and clinical effects they experience. I also discuss how as psychiatry residents we can be more effective in preventing and identifying medical student burnout.

An underappreciated problem

Burnout has been defined as long-term unresolvable job stress that leads to exhaustion and feeling overwhelmed, cynical, and detached from work, and lacking a sense of personal accomplishment. It can lead to depression, anxiety, and suicidal ideation—one survey found that 5.8% of medical students had experienced suicidal ideation at some point in the previous 12 months.¹ Burnout affects not only the individual, but also his/her team and patients. One study found that compared to medical students who didn’t report burnout, medical students who did had lower scores on measures of empathy and professionalism.²

While burnout among physicians and residents has received increasing attention, it often may go unrecognized and unreported in medical students. A literature review that included 51 studies found 28% to 45% of medical students report burnout.³ In a survey at one institution, 60% of medical students reported burnout.⁴ It is evident that medical schools have an important role in helping to minimize burnout rates in their students, and many schools are working toward this goal. However, what happens when students leave the classroom setting for clinical rotations?

A recent study found burnout among medical students peaks during the third year of medical school.⁵ This is when students are on their clinical rotations, new to the hospital environment, and without the inherent structure and support of being at school.

How residents can help

Like most medical students, while on my clinical rotations, I spent most of my day with residents, and I believe residents can help to both recognize burnout in medical students and prevent it.

The first step in addressing this problem is to understand why it occurs. A survey of medical students showed that inadequate sleep and decreased exercise play a significant role in burnout rates.⁶ Another study found a correlation between burnout and feeling emotionally exhausted and a decreased perceived quality of life.⁷ A medical student I recently worked with stated, “How can you not feel burnt out? Juggling work hours, studying, debt, health, and trying to have a life… something always gets dropped.”

So as residents, what can we do to identify and assist medical students who are experiencing burnout, or are at risk of getting there? When needed, we can utilize our psychiatry training to assess our students for depression and substance use disorders, and connect them with appropriate resources. When identifying a medical student with burnout, I believe it can become necessary to notify the attending, the site director responsible for the student, and often the school, so that the student has access to all available resources.

Continue to: It's as important to be proactive...

It’s as important to be proactive as it is to be reactive. Engaging in regular check-ins with our students about self-care and workload, as well as asking about how they are feeling, can offer them opportunities to talk about issues that they might not be getting anywhere else. One medical student I worked with told me, “It’s easy to fade into the background as the student, or to feel like I can’t complain because this is just how medical school is supposed to be.” We have the ability to change this notion with each student we work with.

It is likely that as residents we have worked with a student struggling with burnout without even realizing it. I believe we can play an important role in helping to prevent burnout by identifying at-risk students, offering assistance, and encouraging them to seek professional help. Someone’s life may depend on it.

Our world has radically changed during the coronavirus disease 2019 (COVID-19) crisis, and this impact has quickly transformed many lives. Whether you’re on the front lines of the COVID-19 pandemic or waiting in eager anticipation to return to practice, there is no denying that a few months ago we could never have imagined the health care and humanitarian crisis that is now before us. While we are united in our longing for a better time, we couldn’t be further apart socially and emotionally … and I’m not just talking about 6 feet.

One thing that has been truly striking to me is the silence. While experts have suggested there is a “silent pandemic” of mental illness on the horizon,¹ I’ve been struck by the actual silence that exists as we walk through our stores and neighborhoods. We’re not speaking to each other anymore; it’s almost as if we’re afraid to make eye contact with one another.

Humans are social creatures, and the isolation that many people are experiencing during this pandemic could have detrimental and lasting effects if we don’t take action. While I highly encourage and support efforts to employ social distancing and mitigate the spread of this illness, I’m increasingly concerned about another kind of truly silent pandemic brewing beneath the surface of the COVID-19 crisis. Even under the best conditions, many individuals with posttraumatic stress disorder, depression, anxiety, bipolar disorder, schizophrenia, and other psychiatric disorders may lack adequate social interaction and experience feelings of isolation. These individuals need connection—not silence.

What happens to people who already felt intense isolation before COVID-19 and may have had invaluable lifelines cut off during this time of social distancing? What about individuals with alcohol or substance use disorders, or families who are sheltered in place in unsafe or violent home conditions? How can they reach out in silence? How can we help?

Fostering human connection

To address this, we must actively work to engage our patients and communities. One simple way to help is to acknowledge the people you encounter. Yes, stay 6 feet apart, and wear appropriate personal protective equipment. However, it is still OK to smile and greet someone with a nod, a smile, or a “hello.” A genuine smile can still be seen in someone’s eyes. We need these types of human connection, perhaps now more than ever before. We need each other.

Most importantly, during this time, we need to be aware of individuals who are most at risk in this silent pandemic. We can offer our patients appointments via video conferencing. We can use texting, e-mail, social media, phone calls, and video conferencing to check in with our families, friends, and neighbors. We’re at war with a terrible foe, but let’s not let the human connection become collateral damage.

Our world has radically changed during the coronavirus disease 2019 (COVID-19) crisis, and this impact has quickly transformed many lives. Whether you’re on the front lines of the COVID-19 pandemic or waiting in eager anticipation to return to practice, there is no denying that a few months ago we could never have imagined the health care and humanitarian crisis that is now before us. While we are united in our longing for a better time, we couldn’t be further apart socially and emotionally … and I’m not just talking about 6 feet.

One thing that has been truly striking to me is the silence. While experts have suggested there is a “silent pandemic” of mental illness on the horizon,¹ I’ve been struck by the actual silence that exists as we walk through our stores and neighborhoods. We’re not speaking to each other anymore; it’s almost as if we’re afraid to make eye contact with one another.

Humans are social creatures, and the isolation that many people are experiencing during this pandemic could have detrimental and lasting effects if we don’t take action. While I highly encourage and support efforts to employ social distancing and mitigate the spread of this illness, I’m increasingly concerned about another kind of truly silent pandemic brewing beneath the surface of the COVID-19 crisis. Even under the best conditions, many individuals with posttraumatic stress disorder, depression, anxiety, bipolar disorder, schizophrenia, and other psychiatric disorders may lack adequate social interaction and experience feelings of isolation. These individuals need connection—not silence.

What happens to people who already felt intense isolation before COVID-19 and may have had invaluable lifelines cut off during this time of social distancing? What about individuals with alcohol or substance use disorders, or families who are sheltered in place in unsafe or violent home conditions? How can they reach out in silence? How can we help?

Fostering human connection

To address this, we must actively work to engage our patients and communities. One simple way to help is to acknowledge the people you encounter. Yes, stay 6 feet apart, and wear appropriate personal protective equipment. However, it is still OK to smile and greet someone with a nod, a smile, or a “hello.” A genuine smile can still be seen in someone’s eyes. We need these types of human connection, perhaps now more than ever before. We need each other.

Most importantly, during this time, we need to be aware of individuals who are most at risk in this silent pandemic. We can offer our patients appointments via video conferencing. We can use texting, e-mail, social media, phone calls, and video conferencing to check in with our families, friends, and neighbors. We’re at war with a terrible foe, but let’s not let the human connection become collateral damage.

Our world has radically changed during the coronavirus disease 2019 (COVID-19) crisis, and this impact has quickly transformed many lives. Whether you’re on the front lines of the COVID-19 pandemic or waiting in eager anticipation to return to practice, there is no denying that a few months ago we could never have imagined the health care and humanitarian crisis that is now before us. While we are united in our longing for a better time, we couldn’t be further apart socially and emotionally … and I’m not just talking about 6 feet.

One thing that has been truly striking to me is the silence. While experts have suggested there is a “silent pandemic” of mental illness on the horizon,¹ I’ve been struck by the actual silence that exists as we walk through our stores and neighborhoods. We’re not speaking to each other anymore; it’s almost as if we’re afraid to make eye contact with one another.

Humans are social creatures, and the isolation that many people are experiencing during this pandemic could have detrimental and lasting effects if we don’t take action. While I highly encourage and support efforts to employ social distancing and mitigate the spread of this illness, I’m increasingly concerned about another kind of truly silent pandemic brewing beneath the surface of the COVID-19 crisis. Even under the best conditions, many individuals with posttraumatic stress disorder, depression, anxiety, bipolar disorder, schizophrenia, and other psychiatric disorders may lack adequate social interaction and experience feelings of isolation. These individuals need connection—not silence.

What happens to people who already felt intense isolation before COVID-19 and may have had invaluable lifelines cut off during this time of social distancing? What about individuals with alcohol or substance use disorders, or families who are sheltered in place in unsafe or violent home conditions? How can they reach out in silence? How can we help?

Fostering human connection

To address this, we must actively work to engage our patients and communities. One simple way to help is to acknowledge the people you encounter. Yes, stay 6 feet apart, and wear appropriate personal protective equipment. However, it is still OK to smile and greet someone with a nod, a smile, or a “hello.” A genuine smile can still be seen in someone’s eyes. We need these types of human connection, perhaps now more than ever before. We need each other.

Most importantly, during this time, we need to be aware of individuals who are most at risk in this silent pandemic. We can offer our patients appointments via video conferencing. We can use texting, e-mail, social media, phone calls, and video conferencing to check in with our families, friends, and neighbors. We’re at war with a terrible foe, but let’s not let the human connection become collateral damage.

On March 11, 2020, the World Health Organization declared that coronavirus disease 2019 (COVID-19) was a pandemic.¹ As of mid-May 2020, the illness had claimed more than 316,000 lives worldwide.² The main symptoms of the respiratory illness caused by COVID-19 are fever, dry cough, and shortness of breath. However, disorders of consciousness also have been reported, especially in patients who succumb to the illness.³ In fact, approximately one-third of hospitalized COVID-19 patients experience neurologic symptoms.⁴ Although the most common of these symptoms are dizziness, headache, and loss of smell and taste, patients with more severe cases can experience acute cerebrovascular diseases and impaired consciousness.⁴ As such, psychiatrists assessing confusion should include COVID-19 in their differential diagnosis as a potential cause of altered mental status.

How COVID-19 might affect the CNS

Although primarily considered a respiratory illness, COVID-19 also may have neurotropic potential. The virus that causes COVID-19, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), is a beta-coronavirus. Two other highly pathogenic coronaviruses—SARS-CoV-1 and Middle East respiratory syndrome–related coronavirus (MERS-CoV)—are also beta-coronaviruses, and both have been reported to invade the CNS in some patients.⁵ These viruses are thought to invade cells via angiotensin-converting enzyme 2 (ACE2) receptors.⁶ These receptors are located on the epithelial cells of the respiratory and gastrointestinal (GI) tracts, but also are expressed in certain areas of the brain.⁷ Transmission to the brain could occur through various routes. However, the clinical symptom of loss of smell and taste hints to possible transmission of the virus from nasal cells to the olfactory bulb via trans-synaptic transmission in olfactory neurons.^5,8,9

Immune injury via systemic inflammation is another proposed mechanism for nervous system damage.^8,9 This has been described as “cytokine storm syndrome” and provides support to the role of immuno­therapy in COVID-19 patients.¹⁰ Such inflammation has been long hypothesized as a contributor to psychiatric illnesses, especially neurocognitive disorders.^11,12

Neuropsychiatric complications of COVID-19

Disorders of consciousness were identified early as a symptom of COVID-19.³ Subsequent studies and case reports have confirmed impaired consciousness as a possible symptom of COVID-19.⁴ The first case of encephalitis secondary to COVID-19 was reported by Chinese media on March 5, 2020 in Beijing, China.¹³ Subsequently, cases of encephalopathy secondary to COVID-19 have been reported in the United States. A 74-year-old man in Boca Raton, Florida who had recently returned from the Netherlands presented with altered mental status and was confirmed positive for COVID-19.¹⁴ A female airline worker in her late 50s who presented with altered mental status and tested positive for COVID-19 was found on imaging to have acute hemorrhagic necrotizing encephalopathy.¹⁵ There also have been cases of patients with confirmed COVID-19 who initially presented with complaints of seizures¹⁶ and Guillain-Barré syndrome.¹⁷ As such, neuro­psychiatric complications of COVID-19 are being increasingly recognized and are important to consider during psychiatric assessments.

Consider COVID-19 when assessing altered mental status

Psychiatrists are often consulted to assess patients with impaired consciousness, mental status changes, or confusion. Acute changes to mentation raise concern for delirium. In fact, delirium should always be ruled out when assessing new psychiatric symptoms. The astute psychiatrist is aware of the myriad of medical contributors to delirium. However, because knowledge of COVID-19 is in its infancy, it can be easy to overlook this virus as a potential contributor to delirium. Even patients whose confusion seems to be more in line with a major neurocognitive disorder should be evaluated for COVID-19, because the sudden onset of cognitive impairment may be due to hypoxia, inflammatory damage, or cerebrovascular changes secondary to infection with the virus or its respiratory complications, such as acute respiratory distress syndrome (ARDS).¹⁸

The most obvious clues to the possible presence of COVID-19 in a patient who is confused would be fever, dry cough, and shortness of breath. Because ACE2 receptors are also located in the GI tract, nausea, vomiting, and diarrhea also are possible. However, patients who are confused may be poor historians, demonstrating behavioral symptoms that might make physical assessments challenging, or simply may be pre- or asymptomatic carriers of the virus. Hence, a thorough review of the patient’s history and collateral information is invaluable. A recent history of travel or contact with COVID-19–positive individuals should raise suspicion for viral infection. A patient who mentions a loss of taste or smell would also alert the psychiatrist to the possibility of COVID-19. A patient might not directly state this information, but may mention that he/she has been eating less or has not been disturbed by odors. Neuroimaging can be useful because patients with severe cases are at increased risk for acute cerebrovascular diseases.⁴ Also, ordering a chest CT may prove helpful because this testing is highly sensitive for COVID-19.¹⁹ If there is sufficient clinical evidence to suspect viral infection, testing for COVID-19 should be performed immediately.

It is important to be vigilant for the possibility of COVID-19 infection in patients who present with confusion. Because the virus is highly contagious, the threshold for COVID-19 testing should be low. Viral infection in patients can manifest in ways other than classic respiratory symptoms. Psychiatrists should be aware of COVID-19’s potential to invade the CNS and cause neuropsychiatric symptoms. When assessing confusion in any setting, the clinical and historical clues for COVID-19 should be kept in mind. This will allow patients with COVID-19 to be quickly diagnosed to initiate appropriate management and minimize progression of the illness. Additionally, this will allow for efficient quarantine of the patient to prevent the spread of the virus to others. As such, psychiatrists can play an important role in containing this virus and resolving the COVID-19 pandemic.

Continue to: Bottom Line

 

 

Bottom Line

Although primarily considered a respiratory illness, coronavirus disease 2019 (COVID-19) also may have the potential to invade the CNS and cause neuropsychiatric symptoms, such as impaired consciousness, encephalitis, or a loss of taste or smell. When assessing a patient who presents with confusion, be vigilant for the possibility of COVID-19.

Related Resources

• American Psychiatry Association. APA coronavirus resources. https://www.psychiatry.org/psychiatrists/covid-19-coronavirus#psych.
• Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;S0889-1591(20)30489-X. doi: 10.1016/j.bbi.2020.04.027.

On March 11, 2020, the World Health Organization declared that coronavirus disease 2019 (COVID-19) was a pandemic.¹ As of mid-May 2020, the illness had claimed more than 316,000 lives worldwide.² The main symptoms of the respiratory illness caused by COVID-19 are fever, dry cough, and shortness of breath. However, disorders of consciousness also have been reported, especially in patients who succumb to the illness.³ In fact, approximately one-third of hospitalized COVID-19 patients experience neurologic symptoms.⁴ Although the most common of these symptoms are dizziness, headache, and loss of smell and taste, patients with more severe cases can experience acute cerebrovascular diseases and impaired consciousness.⁴ As such, psychiatrists assessing confusion should include COVID-19 in their differential diagnosis as a potential cause of altered mental status.

How COVID-19 might affect the CNS

Although primarily considered a respiratory illness, COVID-19 also may have neurotropic potential. The virus that causes COVID-19, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), is a beta-coronavirus. Two other highly pathogenic coronaviruses—SARS-CoV-1 and Middle East respiratory syndrome–related coronavirus (MERS-CoV)—are also beta-coronaviruses, and both have been reported to invade the CNS in some patients.⁵ These viruses are thought to invade cells via angiotensin-converting enzyme 2 (ACE2) receptors.⁶ These receptors are located on the epithelial cells of the respiratory and gastrointestinal (GI) tracts, but also are expressed in certain areas of the brain.⁷ Transmission to the brain could occur through various routes. However, the clinical symptom of loss of smell and taste hints to possible transmission of the virus from nasal cells to the olfactory bulb via trans-synaptic transmission in olfactory neurons.^5,8,9

Immune injury via systemic inflammation is another proposed mechanism for nervous system damage.^8,9 This has been described as “cytokine storm syndrome” and provides support to the role of immuno­therapy in COVID-19 patients.¹⁰ Such inflammation has been long hypothesized as a contributor to psychiatric illnesses, especially neurocognitive disorders.^11,12

Neuropsychiatric complications of COVID-19

Disorders of consciousness were identified early as a symptom of COVID-19.³ Subsequent studies and case reports have confirmed impaired consciousness as a possible symptom of COVID-19.⁴ The first case of encephalitis secondary to COVID-19 was reported by Chinese media on March 5, 2020 in Beijing, China.¹³ Subsequently, cases of encephalopathy secondary to COVID-19 have been reported in the United States. A 74-year-old man in Boca Raton, Florida who had recently returned from the Netherlands presented with altered mental status and was confirmed positive for COVID-19.¹⁴ A female airline worker in her late 50s who presented with altered mental status and tested positive for COVID-19 was found on imaging to have acute hemorrhagic necrotizing encephalopathy.¹⁵ There also have been cases of patients with confirmed COVID-19 who initially presented with complaints of seizures¹⁶ and Guillain-Barré syndrome.¹⁷ As such, neuro­psychiatric complications of COVID-19 are being increasingly recognized and are important to consider during psychiatric assessments.

Consider COVID-19 when assessing altered mental status

Psychiatrists are often consulted to assess patients with impaired consciousness, mental status changes, or confusion. Acute changes to mentation raise concern for delirium. In fact, delirium should always be ruled out when assessing new psychiatric symptoms. The astute psychiatrist is aware of the myriad of medical contributors to delirium. However, because knowledge of COVID-19 is in its infancy, it can be easy to overlook this virus as a potential contributor to delirium. Even patients whose confusion seems to be more in line with a major neurocognitive disorder should be evaluated for COVID-19, because the sudden onset of cognitive impairment may be due to hypoxia, inflammatory damage, or cerebrovascular changes secondary to infection with the virus or its respiratory complications, such as acute respiratory distress syndrome (ARDS).¹⁸

The most obvious clues to the possible presence of COVID-19 in a patient who is confused would be fever, dry cough, and shortness of breath. Because ACE2 receptors are also located in the GI tract, nausea, vomiting, and diarrhea also are possible. However, patients who are confused may be poor historians, demonstrating behavioral symptoms that might make physical assessments challenging, or simply may be pre- or asymptomatic carriers of the virus. Hence, a thorough review of the patient’s history and collateral information is invaluable. A recent history of travel or contact with COVID-19–positive individuals should raise suspicion for viral infection. A patient who mentions a loss of taste or smell would also alert the psychiatrist to the possibility of COVID-19. A patient might not directly state this information, but may mention that he/she has been eating less or has not been disturbed by odors. Neuroimaging can be useful because patients with severe cases are at increased risk for acute cerebrovascular diseases.⁴ Also, ordering a chest CT may prove helpful because this testing is highly sensitive for COVID-19.¹⁹ If there is sufficient clinical evidence to suspect viral infection, testing for COVID-19 should be performed immediately.

It is important to be vigilant for the possibility of COVID-19 infection in patients who present with confusion. Because the virus is highly contagious, the threshold for COVID-19 testing should be low. Viral infection in patients can manifest in ways other than classic respiratory symptoms. Psychiatrists should be aware of COVID-19’s potential to invade the CNS and cause neuropsychiatric symptoms. When assessing confusion in any setting, the clinical and historical clues for COVID-19 should be kept in mind. This will allow patients with COVID-19 to be quickly diagnosed to initiate appropriate management and minimize progression of the illness. Additionally, this will allow for efficient quarantine of the patient to prevent the spread of the virus to others. As such, psychiatrists can play an important role in containing this virus and resolving the COVID-19 pandemic.

Continue to: Bottom Line

 

 

Bottom Line

Although primarily considered a respiratory illness, coronavirus disease 2019 (COVID-19) also may have the potential to invade the CNS and cause neuropsychiatric symptoms, such as impaired consciousness, encephalitis, or a loss of taste or smell. When assessing a patient who presents with confusion, be vigilant for the possibility of COVID-19.

Related Resources

• American Psychiatry Association. APA coronavirus resources. https://www.psychiatry.org/psychiatrists/covid-19-coronavirus#psych.
• Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;S0889-1591(20)30489-X. doi: 10.1016/j.bbi.2020.04.027.

On March 11, 2020, the World Health Organization declared that coronavirus disease 2019 (COVID-19) was a pandemic.¹ As of mid-May 2020, the illness had claimed more than 316,000 lives worldwide.² The main symptoms of the respiratory illness caused by COVID-19 are fever, dry cough, and shortness of breath. However, disorders of consciousness also have been reported, especially in patients who succumb to the illness.³ In fact, approximately one-third of hospitalized COVID-19 patients experience neurologic symptoms.⁴ Although the most common of these symptoms are dizziness, headache, and loss of smell and taste, patients with more severe cases can experience acute cerebrovascular diseases and impaired consciousness.⁴ As such, psychiatrists assessing confusion should include COVID-19 in their differential diagnosis as a potential cause of altered mental status.

How COVID-19 might affect the CNS

Although primarily considered a respiratory illness, COVID-19 also may have neurotropic potential. The virus that causes COVID-19, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), is a beta-coronavirus. Two other highly pathogenic coronaviruses—SARS-CoV-1 and Middle East respiratory syndrome–related coronavirus (MERS-CoV)—are also beta-coronaviruses, and both have been reported to invade the CNS in some patients.⁵ These viruses are thought to invade cells via angiotensin-converting enzyme 2 (ACE2) receptors.⁶ These receptors are located on the epithelial cells of the respiratory and gastrointestinal (GI) tracts, but also are expressed in certain areas of the brain.⁷ Transmission to the brain could occur through various routes. However, the clinical symptom of loss of smell and taste hints to possible transmission of the virus from nasal cells to the olfactory bulb via trans-synaptic transmission in olfactory neurons.^5,8,9

Immune injury via systemic inflammation is another proposed mechanism for nervous system damage.^8,9 This has been described as “cytokine storm syndrome” and provides support to the role of immuno­therapy in COVID-19 patients.¹⁰ Such inflammation has been long hypothesized as a contributor to psychiatric illnesses, especially neurocognitive disorders.^11,12

Neuropsychiatric complications of COVID-19

Disorders of consciousness were identified early as a symptom of COVID-19.³ Subsequent studies and case reports have confirmed impaired consciousness as a possible symptom of COVID-19.⁴ The first case of encephalitis secondary to COVID-19 was reported by Chinese media on March 5, 2020 in Beijing, China.¹³ Subsequently, cases of encephalopathy secondary to COVID-19 have been reported in the United States. A 74-year-old man in Boca Raton, Florida who had recently returned from the Netherlands presented with altered mental status and was confirmed positive for COVID-19.¹⁴ A female airline worker in her late 50s who presented with altered mental status and tested positive for COVID-19 was found on imaging to have acute hemorrhagic necrotizing encephalopathy.¹⁵ There also have been cases of patients with confirmed COVID-19 who initially presented with complaints of seizures¹⁶ and Guillain-Barré syndrome.¹⁷ As such, neuro­psychiatric complications of COVID-19 are being increasingly recognized and are important to consider during psychiatric assessments.

Consider COVID-19 when assessing altered mental status

Psychiatrists are often consulted to assess patients with impaired consciousness, mental status changes, or confusion. Acute changes to mentation raise concern for delirium. In fact, delirium should always be ruled out when assessing new psychiatric symptoms. The astute psychiatrist is aware of the myriad of medical contributors to delirium. However, because knowledge of COVID-19 is in its infancy, it can be easy to overlook this virus as a potential contributor to delirium. Even patients whose confusion seems to be more in line with a major neurocognitive disorder should be evaluated for COVID-19, because the sudden onset of cognitive impairment may be due to hypoxia, inflammatory damage, or cerebrovascular changes secondary to infection with the virus or its respiratory complications, such as acute respiratory distress syndrome (ARDS).¹⁸

The most obvious clues to the possible presence of COVID-19 in a patient who is confused would be fever, dry cough, and shortness of breath. Because ACE2 receptors are also located in the GI tract, nausea, vomiting, and diarrhea also are possible. However, patients who are confused may be poor historians, demonstrating behavioral symptoms that might make physical assessments challenging, or simply may be pre- or asymptomatic carriers of the virus. Hence, a thorough review of the patient’s history and collateral information is invaluable. A recent history of travel or contact with COVID-19–positive individuals should raise suspicion for viral infection. A patient who mentions a loss of taste or smell would also alert the psychiatrist to the possibility of COVID-19. A patient might not directly state this information, but may mention that he/she has been eating less or has not been disturbed by odors. Neuroimaging can be useful because patients with severe cases are at increased risk for acute cerebrovascular diseases.⁴ Also, ordering a chest CT may prove helpful because this testing is highly sensitive for COVID-19.¹⁹ If there is sufficient clinical evidence to suspect viral infection, testing for COVID-19 should be performed immediately.

It is important to be vigilant for the possibility of COVID-19 infection in patients who present with confusion. Because the virus is highly contagious, the threshold for COVID-19 testing should be low. Viral infection in patients can manifest in ways other than classic respiratory symptoms. Psychiatrists should be aware of COVID-19’s potential to invade the CNS and cause neuropsychiatric symptoms. When assessing confusion in any setting, the clinical and historical clues for COVID-19 should be kept in mind. This will allow patients with COVID-19 to be quickly diagnosed to initiate appropriate management and minimize progression of the illness. Additionally, this will allow for efficient quarantine of the patient to prevent the spread of the virus to others. As such, psychiatrists can play an important role in containing this virus and resolving the COVID-19 pandemic.

Continue to: Bottom Line

 

 

Bottom Line

Although primarily considered a respiratory illness, coronavirus disease 2019 (COVID-19) also may have the potential to invade the CNS and cause neuropsychiatric symptoms, such as impaired consciousness, encephalitis, or a loss of taste or smell. When assessing a patient who presents with confusion, be vigilant for the possibility of COVID-19.

Related Resources

• American Psychiatry Association. APA coronavirus resources. https://www.psychiatry.org/psychiatrists/covid-19-coronavirus#psych.
• Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;S0889-1591(20)30489-X. doi: 10.1016/j.bbi.2020.04.027.

The direct oral anticoagulant (DOAC) drugs apixaban, dabigatran, and rivaroxaban are associated with a lower risk of osteoporotic fracture than is warfarin in patients with atrial fibrillation (AFib), according to a new retrospective analysis.

There was no difference in risk between individual DOAC medications.

The study drew from an EHR database of the Hong Kong Hospital Authority. It was led by Wallis C.Y. Lau, PhD, of the University of Hong Kong and appeared online May 19 in Annals of Internal Medicine.

Warfarin is suspected to contribute to osteoporotic fracturing in AFib patients, but previous studies returned mixed results. The more recently introduced DOACs were not tested for fracture risks, and it hasn’t been determined if individual DOACs have different risks. The question is even more important in AFib, in which patients are older and often have comorbidities that could predispose them to fractures.

The study included 23,515 patients with AFib who used anticoagulants. 3,241 used apixaban, 6,867 dabigatran, 3,866 rivaroxaban, and 9,541 used warfarin. The median follow-up was 423 days.

According to Cox proportional hazards model analyses, DOAC use was associated with fewer fractures than was warfarin (hazard ratio for apixaban vs. warfarin, 0.62; 95% confidence interval, 0.41-0.94; HR for dabigatran, 0.65; 95% CI, 0.49-0.86; HR for rivaroxaban, 0.52; 95% CI, 0.37-0.73). Subanalyses in men and women showed similar results (P for interaction >.05).

Head-to-head comparisons between individual DOACs yielded no statistically significant differences in osteoporotic fracture risk.

Although the findings couldn’t absolutely rule out a difference in osteoporotic fracture risk between different DOACs, the authors argue that any clinical significance would likely be small.

“Given the supportive evidence from experimental settings, findings from our study using clinical data, and the indirect evidence provided by the previous meta-analysis of randomized, controlled trials, there exists a compelling case for evaluating whether the risk for osteoporotic fractures should be considered at the point of prescribing an oral anticoagulant to minimize fracture risk,” the authors wrote.

The study is limited by the potential for residual confounding, the investigators noted.

The study was funded by the University of Hong Kong and University College London Strategic Partnership Fund.

SOURCE: Lau WCY et al. Ann Intern Med. 2020 May 19. doi: 10.7326/M19-3671.

The direct oral anticoagulant (DOAC) drugs apixaban, dabigatran, and rivaroxaban are associated with a lower risk of osteoporotic fracture than is warfarin in patients with atrial fibrillation (AFib), according to a new retrospective analysis.

There was no difference in risk between individual DOAC medications.

The study drew from an EHR database of the Hong Kong Hospital Authority. It was led by Wallis C.Y. Lau, PhD, of the University of Hong Kong and appeared online May 19 in Annals of Internal Medicine.

Warfarin is suspected to contribute to osteoporotic fracturing in AFib patients, but previous studies returned mixed results. The more recently introduced DOACs were not tested for fracture risks, and it hasn’t been determined if individual DOACs have different risks. The question is even more important in AFib, in which patients are older and often have comorbidities that could predispose them to fractures.

The study included 23,515 patients with AFib who used anticoagulants. 3,241 used apixaban, 6,867 dabigatran, 3,866 rivaroxaban, and 9,541 used warfarin. The median follow-up was 423 days.

According to Cox proportional hazards model analyses, DOAC use was associated with fewer fractures than was warfarin (hazard ratio for apixaban vs. warfarin, 0.62; 95% confidence interval, 0.41-0.94; HR for dabigatran, 0.65; 95% CI, 0.49-0.86; HR for rivaroxaban, 0.52; 95% CI, 0.37-0.73). Subanalyses in men and women showed similar results (P for interaction >.05).

Head-to-head comparisons between individual DOACs yielded no statistically significant differences in osteoporotic fracture risk.

Although the findings couldn’t absolutely rule out a difference in osteoporotic fracture risk between different DOACs, the authors argue that any clinical significance would likely be small.

“Given the supportive evidence from experimental settings, findings from our study using clinical data, and the indirect evidence provided by the previous meta-analysis of randomized, controlled trials, there exists a compelling case for evaluating whether the risk for osteoporotic fractures should be considered at the point of prescribing an oral anticoagulant to minimize fracture risk,” the authors wrote.

The study is limited by the potential for residual confounding, the investigators noted.

The study was funded by the University of Hong Kong and University College London Strategic Partnership Fund.

SOURCE: Lau WCY et al. Ann Intern Med. 2020 May 19. doi: 10.7326/M19-3671.

The direct oral anticoagulant (DOAC) drugs apixaban, dabigatran, and rivaroxaban are associated with a lower risk of osteoporotic fracture than is warfarin in patients with atrial fibrillation (AFib), according to a new retrospective analysis.

There was no difference in risk between individual DOAC medications.

The study drew from an EHR database of the Hong Kong Hospital Authority. It was led by Wallis C.Y. Lau, PhD, of the University of Hong Kong and appeared online May 19 in Annals of Internal Medicine.

Warfarin is suspected to contribute to osteoporotic fracturing in AFib patients, but previous studies returned mixed results. The more recently introduced DOACs were not tested for fracture risks, and it hasn’t been determined if individual DOACs have different risks. The question is even more important in AFib, in which patients are older and often have comorbidities that could predispose them to fractures.

The study included 23,515 patients with AFib who used anticoagulants. 3,241 used apixaban, 6,867 dabigatran, 3,866 rivaroxaban, and 9,541 used warfarin. The median follow-up was 423 days.

According to Cox proportional hazards model analyses, DOAC use was associated with fewer fractures than was warfarin (hazard ratio for apixaban vs. warfarin, 0.62; 95% confidence interval, 0.41-0.94; HR for dabigatran, 0.65; 95% CI, 0.49-0.86; HR for rivaroxaban, 0.52; 95% CI, 0.37-0.73). Subanalyses in men and women showed similar results (P for interaction >.05).

Head-to-head comparisons between individual DOACs yielded no statistically significant differences in osteoporotic fracture risk.

Although the findings couldn’t absolutely rule out a difference in osteoporotic fracture risk between different DOACs, the authors argue that any clinical significance would likely be small.

“Given the supportive evidence from experimental settings, findings from our study using clinical data, and the indirect evidence provided by the previous meta-analysis of randomized, controlled trials, there exists a compelling case for evaluating whether the risk for osteoporotic fractures should be considered at the point of prescribing an oral anticoagulant to minimize fracture risk,” the authors wrote.

The study is limited by the potential for residual confounding, the investigators noted.

The study was funded by the University of Hong Kong and University College London Strategic Partnership Fund.

SOURCE: Lau WCY et al. Ann Intern Med. 2020 May 19. doi: 10.7326/M19-3671.