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FDA moves to stop the spread of illicit ‘tranq’ in the U.S.
The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.
It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.
The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”
FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”
In November, the agency warned health care providers that because xylazine is not an opioid, the overdose reversal agent naloxone would not be effective. Xylazine acts as a central alpha-2-adrenergic receptor agonist in the brainstem, causing a rapid decrease in the release of norepinephrine and dopamine in the central nervous system. Its use can lead to central nervous system and respiratory depression, said the FDA.
Clinicians have scrambled to treat severe necrotic skin ulcerations that develop at injection sites.
Xylazine is relatively cheap and easy to access, said the Drug Enforcement Administration and Department of Justice in a November joint report. The drug is “readily available for purchase on other Internet sites in liquid and powder form, often with no association to the veterinary profession nor requirements to prove legitimate need,” said the Justice Department. A buyer can purchase xylazine powder online from Chinese suppliers for $6-$20 per kilogram, according to the report.
In 2021, xylazine-positive overdoses were highest in the South, which experienced a 1,127% increase from 2020, the Justice Department reported. The same year, there were 1,281 overdoses involving the substance in the Northeast and 351 in the Midwest.
There were just 34 overdoses involving xylazine in the West in 2021, but its use appears to be growing. The San Francisco Department of Public Health said it had detected low levels of xylazine in four people who died of overdoses in December and January.
“Identifying xylazine in San Francisco is concerning,” said the department in a statement, adding that it had not yet seen evidence of skin wounds in injection drug users in the city.
In late February, the Los Angeles County Department of Public Health issued a warning to first responders and health care professionals that xylazine had been detected in the area’s illicit drug supply.
The department said it will “work closely with other partners to understand the extent of the possible xylazine contamination in the illicit drug supply to increase awareness and education to the public.”
The FDA commissioner said the agency will coordinate with public health officials to more closely track xylazine.
“We will continue to use all tools at our disposal and partner with the Drug Enforcement Administration and other federal, state, local agencies, and stakeholders as appropriate to stem these illicit activities and protect public health,” said Dr. Califf.
A version of this article first appeared on Medscape.com.
The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.
It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.
The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”
FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”
In November, the agency warned health care providers that because xylazine is not an opioid, the overdose reversal agent naloxone would not be effective. Xylazine acts as a central alpha-2-adrenergic receptor agonist in the brainstem, causing a rapid decrease in the release of norepinephrine and dopamine in the central nervous system. Its use can lead to central nervous system and respiratory depression, said the FDA.
Clinicians have scrambled to treat severe necrotic skin ulcerations that develop at injection sites.
Xylazine is relatively cheap and easy to access, said the Drug Enforcement Administration and Department of Justice in a November joint report. The drug is “readily available for purchase on other Internet sites in liquid and powder form, often with no association to the veterinary profession nor requirements to prove legitimate need,” said the Justice Department. A buyer can purchase xylazine powder online from Chinese suppliers for $6-$20 per kilogram, according to the report.
In 2021, xylazine-positive overdoses were highest in the South, which experienced a 1,127% increase from 2020, the Justice Department reported. The same year, there were 1,281 overdoses involving the substance in the Northeast and 351 in the Midwest.
There were just 34 overdoses involving xylazine in the West in 2021, but its use appears to be growing. The San Francisco Department of Public Health said it had detected low levels of xylazine in four people who died of overdoses in December and January.
“Identifying xylazine in San Francisco is concerning,” said the department in a statement, adding that it had not yet seen evidence of skin wounds in injection drug users in the city.
In late February, the Los Angeles County Department of Public Health issued a warning to first responders and health care professionals that xylazine had been detected in the area’s illicit drug supply.
The department said it will “work closely with other partners to understand the extent of the possible xylazine contamination in the illicit drug supply to increase awareness and education to the public.”
The FDA commissioner said the agency will coordinate with public health officials to more closely track xylazine.
“We will continue to use all tools at our disposal and partner with the Drug Enforcement Administration and other federal, state, local agencies, and stakeholders as appropriate to stem these illicit activities and protect public health,” said Dr. Califf.
A version of this article first appeared on Medscape.com.
The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.
It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.
The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”
FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”
In November, the agency warned health care providers that because xylazine is not an opioid, the overdose reversal agent naloxone would not be effective. Xylazine acts as a central alpha-2-adrenergic receptor agonist in the brainstem, causing a rapid decrease in the release of norepinephrine and dopamine in the central nervous system. Its use can lead to central nervous system and respiratory depression, said the FDA.
Clinicians have scrambled to treat severe necrotic skin ulcerations that develop at injection sites.
Xylazine is relatively cheap and easy to access, said the Drug Enforcement Administration and Department of Justice in a November joint report. The drug is “readily available for purchase on other Internet sites in liquid and powder form, often with no association to the veterinary profession nor requirements to prove legitimate need,” said the Justice Department. A buyer can purchase xylazine powder online from Chinese suppliers for $6-$20 per kilogram, according to the report.
In 2021, xylazine-positive overdoses were highest in the South, which experienced a 1,127% increase from 2020, the Justice Department reported. The same year, there were 1,281 overdoses involving the substance in the Northeast and 351 in the Midwest.
There were just 34 overdoses involving xylazine in the West in 2021, but its use appears to be growing. The San Francisco Department of Public Health said it had detected low levels of xylazine in four people who died of overdoses in December and January.
“Identifying xylazine in San Francisco is concerning,” said the department in a statement, adding that it had not yet seen evidence of skin wounds in injection drug users in the city.
In late February, the Los Angeles County Department of Public Health issued a warning to first responders and health care professionals that xylazine had been detected in the area’s illicit drug supply.
The department said it will “work closely with other partners to understand the extent of the possible xylazine contamination in the illicit drug supply to increase awareness and education to the public.”
The FDA commissioner said the agency will coordinate with public health officials to more closely track xylazine.
“We will continue to use all tools at our disposal and partner with the Drug Enforcement Administration and other federal, state, local agencies, and stakeholders as appropriate to stem these illicit activities and protect public health,” said Dr. Califf.
A version of this article first appeared on Medscape.com.
DEA proposals on telehealth for controlled substances draw fire
The proposed rules – one for Schedule III-V substances, and the other for buprenorphine – are due to go into effect on May 11, when the COVID-19 public health emergency (PHE), and temporary flexibilities, end.
Essentially, both proposals would allow providers to prescribe a 30-day supply of a controlled substance or buprenorphine, but then require a face-to-face meeting for patients to receive additional prescriptions.
The DEA says that the rules are aimed at preventing abuse and diversion of the substances, but clinicians claim they are creating unnecessary hurdles that will probably lead to some patients dropping out of treatment.
“We were happy to see that there is ongoing flexibility to be able to initiate buprenorphine through telehealth, but we were disappointed to see that the DEA set an arbitrary time frame, in this case, a 30-day time frame after which the patient would have to be seen in person before ongoing care with buprenorphine for opioid use disorder could be provided,” Brian Hurley, MD, MBA, the president-elect of the American Society of Addiction Medicine told this news organization.
Dr. Hurley agreed that it is best practice to see patients in person for ongoing care, but he noted they have many reasons why they might not be able to make it into an office every month.
“What this rule would do if instituted as written is prevent me from continuing care for patients unless I can get them in in person,” he said. “And while I’d make every effort as a clinician, it’s not always feasible to do so.”
The addiction specialist noted that only about 20% of Americans with opioid use disorder have access to medications for the disorder. “I would posit that untreated opioid use disorder is a bigger threat to public safety currently than the risk of diversion,” he said.
The DEA is also proposing to allow state laws to supersede its regulations, which concerns Dr. Hurley and other clinicians because some states are more restrictive. “Our position is that state laws that restrict access to medications for opioid use disorder through telehealth means are inconsistent with our policy recommendation. I certainly hope that the DEA hears our concerns and amends the proposal,” said Dr. Hurley.
A potential ‘telehealth cliff’
Shabana Khan, MD, chair of the American Psychiatric Association’s telepsychiatry committee, said that “because of potential overlap with state rules that may be more stringent than these new regulations, APA is concerned that the proposed rules will create a telehealth cliff for those in most need of critical psychiatric and opioid use disorder treatment, particularly in communities where this specialty care is limited or nonexistent.”
Dr. Khan noted that “clarification is necessary on how patients who started treatment during the PHE can continue treatment with a prescribing provider, if at all, through an in-person evaluation with a DEA-registered provider referral.”
Telehealth companies were also disappointed in the DEA proposals.
“The continuity of care for countless Americans will be severed, potentially leaving these patients to fall through the cracks of our health care system without access to needed medications,” said Kyle Zebley, the American Telemedicine Association’s senior vice president of public policy, in a statement.
“Requiring every patient who has initiated treatment via telemedicine during the pandemic to now visit a provider in person clearly falls on the side of being overly restrictive,” Mr. Zebley added.
The DEA is proposing to allow patients who have been receiving telehealth over the past 3 years to continue to do so for 180 days after the PHE ends.
But the American Telemedicine Association and others said that they still want to see a change in the proposal as written. “Our hope is that the DEA works with us to avoid unnecessary and inappropriate restrictions on the prescription of essential medications for these vulnerable and underserved populations,” Mr. Zebley said in the statement.
DEA Administrator Anne Milgram said in a statement that the agency believes that “the telemedicine regulations would continue to expand access to buprenorphine for patients with opioid use disorder,” and that the DEA “is committed to the expansion of telemedicine with guardrails that prevent the online overprescribing of controlled medications that can cause harm.”
Rahul Gupta, MD, director of the White House Office of National Drug Control Policy, said in a statement that “This proposed rule builds on President Biden’s historic move to eliminate the X-waiver that prevented many prescribers from treating patients with buprenorphine.” He added, “Thanks to these changes, millions of Americans will be able to access the lifesaving care they need.”
The DEA estimated that there were 15.7 million prescriptions for buprenorphine in 2021 and that about 67,000 were for initial prescriptions.
Ketamine confusion
The rule on controlled substances has also caused some consternation, especially given that it does not differentiate between racemic ketamine and esketamine, said Lisa Marie Harding, MD, vice president of the board of the American Society of Ketamine Physicians, Psychotherapists & Practitioners.
Esketamine (Spravato) is approved by the Food and Drug Administration and, under a Risk Evaluation and Mitigation Strategy, can only be administered in FDA-monitored treatment facilities. Racemic ketamine is being prescribed – often for home use – with almost no regulatory oversight.
Dr. Harding, who is an approved Spravato provider and also administers intravenous ketamine in her practice, does not believe that ketamine should be used at home without supervision.
“I had a patient who had a very powerful dissociative experience in my office earlier this week,” Dr. Harding said in an interview. One of her staff asked what would happen if the patient had experienced that at home. “We don’t know. Nor do we want this to happen,” said Dr. Harding.
However, the DEA proposal would continue to allow for home use, at least initially. “If it’s open to interpretation, those people that prescribe ketamine for home use can use that leeway to then continue to do it,” she said. “That is not safe.”
Dr. Harding approves of the proposed DEA requirement for face-to-face visits. “It’s good patient care,” she said. But she wants the administration to adjust the rules to make it harder to offer home ketamine therapy.
“Lots of people are using racemic ketamine off-label for treating depression with success but doing it in treatment settings that are appropriate,” said Dr. Harding.
Dr. Hurley and Dr. Harding report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The proposed rules – one for Schedule III-V substances, and the other for buprenorphine – are due to go into effect on May 11, when the COVID-19 public health emergency (PHE), and temporary flexibilities, end.
Essentially, both proposals would allow providers to prescribe a 30-day supply of a controlled substance or buprenorphine, but then require a face-to-face meeting for patients to receive additional prescriptions.
The DEA says that the rules are aimed at preventing abuse and diversion of the substances, but clinicians claim they are creating unnecessary hurdles that will probably lead to some patients dropping out of treatment.
“We were happy to see that there is ongoing flexibility to be able to initiate buprenorphine through telehealth, but we were disappointed to see that the DEA set an arbitrary time frame, in this case, a 30-day time frame after which the patient would have to be seen in person before ongoing care with buprenorphine for opioid use disorder could be provided,” Brian Hurley, MD, MBA, the president-elect of the American Society of Addiction Medicine told this news organization.
Dr. Hurley agreed that it is best practice to see patients in person for ongoing care, but he noted they have many reasons why they might not be able to make it into an office every month.
“What this rule would do if instituted as written is prevent me from continuing care for patients unless I can get them in in person,” he said. “And while I’d make every effort as a clinician, it’s not always feasible to do so.”
The addiction specialist noted that only about 20% of Americans with opioid use disorder have access to medications for the disorder. “I would posit that untreated opioid use disorder is a bigger threat to public safety currently than the risk of diversion,” he said.
The DEA is also proposing to allow state laws to supersede its regulations, which concerns Dr. Hurley and other clinicians because some states are more restrictive. “Our position is that state laws that restrict access to medications for opioid use disorder through telehealth means are inconsistent with our policy recommendation. I certainly hope that the DEA hears our concerns and amends the proposal,” said Dr. Hurley.
A potential ‘telehealth cliff’
Shabana Khan, MD, chair of the American Psychiatric Association’s telepsychiatry committee, said that “because of potential overlap with state rules that may be more stringent than these new regulations, APA is concerned that the proposed rules will create a telehealth cliff for those in most need of critical psychiatric and opioid use disorder treatment, particularly in communities where this specialty care is limited or nonexistent.”
Dr. Khan noted that “clarification is necessary on how patients who started treatment during the PHE can continue treatment with a prescribing provider, if at all, through an in-person evaluation with a DEA-registered provider referral.”
Telehealth companies were also disappointed in the DEA proposals.
“The continuity of care for countless Americans will be severed, potentially leaving these patients to fall through the cracks of our health care system without access to needed medications,” said Kyle Zebley, the American Telemedicine Association’s senior vice president of public policy, in a statement.
“Requiring every patient who has initiated treatment via telemedicine during the pandemic to now visit a provider in person clearly falls on the side of being overly restrictive,” Mr. Zebley added.
The DEA is proposing to allow patients who have been receiving telehealth over the past 3 years to continue to do so for 180 days after the PHE ends.
But the American Telemedicine Association and others said that they still want to see a change in the proposal as written. “Our hope is that the DEA works with us to avoid unnecessary and inappropriate restrictions on the prescription of essential medications for these vulnerable and underserved populations,” Mr. Zebley said in the statement.
DEA Administrator Anne Milgram said in a statement that the agency believes that “the telemedicine regulations would continue to expand access to buprenorphine for patients with opioid use disorder,” and that the DEA “is committed to the expansion of telemedicine with guardrails that prevent the online overprescribing of controlled medications that can cause harm.”
Rahul Gupta, MD, director of the White House Office of National Drug Control Policy, said in a statement that “This proposed rule builds on President Biden’s historic move to eliminate the X-waiver that prevented many prescribers from treating patients with buprenorphine.” He added, “Thanks to these changes, millions of Americans will be able to access the lifesaving care they need.”
The DEA estimated that there were 15.7 million prescriptions for buprenorphine in 2021 and that about 67,000 were for initial prescriptions.
Ketamine confusion
The rule on controlled substances has also caused some consternation, especially given that it does not differentiate between racemic ketamine and esketamine, said Lisa Marie Harding, MD, vice president of the board of the American Society of Ketamine Physicians, Psychotherapists & Practitioners.
Esketamine (Spravato) is approved by the Food and Drug Administration and, under a Risk Evaluation and Mitigation Strategy, can only be administered in FDA-monitored treatment facilities. Racemic ketamine is being prescribed – often for home use – with almost no regulatory oversight.
Dr. Harding, who is an approved Spravato provider and also administers intravenous ketamine in her practice, does not believe that ketamine should be used at home without supervision.
“I had a patient who had a very powerful dissociative experience in my office earlier this week,” Dr. Harding said in an interview. One of her staff asked what would happen if the patient had experienced that at home. “We don’t know. Nor do we want this to happen,” said Dr. Harding.
However, the DEA proposal would continue to allow for home use, at least initially. “If it’s open to interpretation, those people that prescribe ketamine for home use can use that leeway to then continue to do it,” she said. “That is not safe.”
Dr. Harding approves of the proposed DEA requirement for face-to-face visits. “It’s good patient care,” she said. But she wants the administration to adjust the rules to make it harder to offer home ketamine therapy.
“Lots of people are using racemic ketamine off-label for treating depression with success but doing it in treatment settings that are appropriate,” said Dr. Harding.
Dr. Hurley and Dr. Harding report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The proposed rules – one for Schedule III-V substances, and the other for buprenorphine – are due to go into effect on May 11, when the COVID-19 public health emergency (PHE), and temporary flexibilities, end.
Essentially, both proposals would allow providers to prescribe a 30-day supply of a controlled substance or buprenorphine, but then require a face-to-face meeting for patients to receive additional prescriptions.
The DEA says that the rules are aimed at preventing abuse and diversion of the substances, but clinicians claim they are creating unnecessary hurdles that will probably lead to some patients dropping out of treatment.
“We were happy to see that there is ongoing flexibility to be able to initiate buprenorphine through telehealth, but we were disappointed to see that the DEA set an arbitrary time frame, in this case, a 30-day time frame after which the patient would have to be seen in person before ongoing care with buprenorphine for opioid use disorder could be provided,” Brian Hurley, MD, MBA, the president-elect of the American Society of Addiction Medicine told this news organization.
Dr. Hurley agreed that it is best practice to see patients in person for ongoing care, but he noted they have many reasons why they might not be able to make it into an office every month.
“What this rule would do if instituted as written is prevent me from continuing care for patients unless I can get them in in person,” he said. “And while I’d make every effort as a clinician, it’s not always feasible to do so.”
The addiction specialist noted that only about 20% of Americans with opioid use disorder have access to medications for the disorder. “I would posit that untreated opioid use disorder is a bigger threat to public safety currently than the risk of diversion,” he said.
The DEA is also proposing to allow state laws to supersede its regulations, which concerns Dr. Hurley and other clinicians because some states are more restrictive. “Our position is that state laws that restrict access to medications for opioid use disorder through telehealth means are inconsistent with our policy recommendation. I certainly hope that the DEA hears our concerns and amends the proposal,” said Dr. Hurley.
A potential ‘telehealth cliff’
Shabana Khan, MD, chair of the American Psychiatric Association’s telepsychiatry committee, said that “because of potential overlap with state rules that may be more stringent than these new regulations, APA is concerned that the proposed rules will create a telehealth cliff for those in most need of critical psychiatric and opioid use disorder treatment, particularly in communities where this specialty care is limited or nonexistent.”
Dr. Khan noted that “clarification is necessary on how patients who started treatment during the PHE can continue treatment with a prescribing provider, if at all, through an in-person evaluation with a DEA-registered provider referral.”
Telehealth companies were also disappointed in the DEA proposals.
“The continuity of care for countless Americans will be severed, potentially leaving these patients to fall through the cracks of our health care system without access to needed medications,” said Kyle Zebley, the American Telemedicine Association’s senior vice president of public policy, in a statement.
“Requiring every patient who has initiated treatment via telemedicine during the pandemic to now visit a provider in person clearly falls on the side of being overly restrictive,” Mr. Zebley added.
The DEA is proposing to allow patients who have been receiving telehealth over the past 3 years to continue to do so for 180 days after the PHE ends.
But the American Telemedicine Association and others said that they still want to see a change in the proposal as written. “Our hope is that the DEA works with us to avoid unnecessary and inappropriate restrictions on the prescription of essential medications for these vulnerable and underserved populations,” Mr. Zebley said in the statement.
DEA Administrator Anne Milgram said in a statement that the agency believes that “the telemedicine regulations would continue to expand access to buprenorphine for patients with opioid use disorder,” and that the DEA “is committed to the expansion of telemedicine with guardrails that prevent the online overprescribing of controlled medications that can cause harm.”
Rahul Gupta, MD, director of the White House Office of National Drug Control Policy, said in a statement that “This proposed rule builds on President Biden’s historic move to eliminate the X-waiver that prevented many prescribers from treating patients with buprenorphine.” He added, “Thanks to these changes, millions of Americans will be able to access the lifesaving care they need.”
The DEA estimated that there were 15.7 million prescriptions for buprenorphine in 2021 and that about 67,000 were for initial prescriptions.
Ketamine confusion
The rule on controlled substances has also caused some consternation, especially given that it does not differentiate between racemic ketamine and esketamine, said Lisa Marie Harding, MD, vice president of the board of the American Society of Ketamine Physicians, Psychotherapists & Practitioners.
Esketamine (Spravato) is approved by the Food and Drug Administration and, under a Risk Evaluation and Mitigation Strategy, can only be administered in FDA-monitored treatment facilities. Racemic ketamine is being prescribed – often for home use – with almost no regulatory oversight.
Dr. Harding, who is an approved Spravato provider and also administers intravenous ketamine in her practice, does not believe that ketamine should be used at home without supervision.
“I had a patient who had a very powerful dissociative experience in my office earlier this week,” Dr. Harding said in an interview. One of her staff asked what would happen if the patient had experienced that at home. “We don’t know. Nor do we want this to happen,” said Dr. Harding.
However, the DEA proposal would continue to allow for home use, at least initially. “If it’s open to interpretation, those people that prescribe ketamine for home use can use that leeway to then continue to do it,” she said. “That is not safe.”
Dr. Harding approves of the proposed DEA requirement for face-to-face visits. “It’s good patient care,” she said. But she wants the administration to adjust the rules to make it harder to offer home ketamine therapy.
“Lots of people are using racemic ketamine off-label for treating depression with success but doing it in treatment settings that are appropriate,” said Dr. Harding.
Dr. Hurley and Dr. Harding report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Clinician violence: Virtual reality to the rescue?
This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.
Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.
Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.
First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?
Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.
We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.
Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?
Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.
We are immersing learners into an actual hospital room to our specifications, very similar to exactly where we practice each and every day, and taking the learners through different situations that we designed with various levels of escalation and aggression, and asking the learner to manage that situation as best as they possibly can using the competencies and proficiencies that we taught them.
Dr. Glatter: Haptic feedback is an important part of the program and also the approach and technique that you’re using. Can you describe what haptic feedback means and what people actually feel?
Dr. Salazar: Absolutely. One of the most unfortunate things in my professional career is physical abuse suffered by people like me and you and our colleagues, nursing personnel, technicians, and others, resulting in injury.
We wanted to provide the most realistic experience that we could design. Haptics engage digital senses other than your auditory and your visuals. They really engage your tactile senses. These haptic vests and gloves and technology allow us to provide a third set of sensory stimuli for the learner.
At one of the modules, we have an actual physical assault that takes place, and the learner is actually able to feel in their body the strikes – of course, not painful – but just bringing in those senses and that stimulus, really leaving the learner with an experience that’s going to be long-lasting.
Dr. Glatter: Feeling that stimulus certainly affects your vital signs. Do you monitor a provider’s vital signs, such as their blood pressure and heart rate, as the situation and the threat escalate? That could potentially trigger some issues in people with prior PTSD or people with other mental health issues. Has that ever been considered in the design of your program?
Dr. Salazar: Yes, 100%. The beautiful thing about haptics is that they can be tailored to our specific parameters. The sensory stimulus that’s provided is actually very mild. It feels more like a tap than an actual strike. It just reminds us that when we’re having or experiencing an actual physical attack, we’re really engaging the senses.
We have an emergency physician or an EMT-paramedic on site at all times during the training so that we can monitor our subjects and make sure that they’re comfortable and healthy.
Dr. Glatter: Do they have actual sensors attached to their bodies that are part of your program or distinct in terms of monitoring their vital signs?
Dr. Salazar: It’s completely different. We have two different systems that we are planning on utilizing. Frankly, in the final version of this virtual reality module, we may not even involve the haptics. We’re going to study it and see how our learners behave and how much information they’re able to acquire and retain.
It may be very possible that just the visuals – the auditory and the immersion taking place within the hospital room – may be enough. It’s very possible that, in the next final version of this, we may find that haptics bring in quite a bit of value, and we may incorporate that. If that is the case, then we will, of course, acquire different technology to monitor the patient’s vital signs.
Dr. Glatter: Clearly, when situations escalate in the department, everyone gets more concerned about the patient, but providers are part of this equation, as you allude to.
In 2022, there was a poll by the American College of Emergency Physicians that stated that 85% of emergency physicians reported an increase in violent activity in their ERs in the past 5 years. Nearly two-thirds of nearly 3,000 emergency physicians surveyed reported being assaulted in the past year. This is an important module that we integrate into training providers in terms of these types of tense situations that can result not only in mental anguish but also in physical injury.
Dr. Salazar: One hundred percent. I frankly got tired of seeing my friends and my colleagues suffer both the physical and mental effects of verbal and physical abuse, and I wanted to design a project that was very patient centric while allowing our personnel to really manage these situations a little bit better.
Frankly, we don’t receive great training in this space, and I wanted to rewrite that narrative and make things better for our clinicians out there while remaining patient centric. I wanted to do something about it, and hopefully this dream will become a reality.
Dr. Glatter: Absolutely. There are other data from the Bureau of Labor Statistics stating that health care workers are five times more likely than employees in any other area of work to experience workplace violence. This could, again, range from verbal to physical violence. This is a very important module that you’re developing.
Are there any thoughts to extend this to active-shooter scenarios or any other high-stakes scenarios that you can imagine in the department?
Dr. Salazar: We’re actually working with the same developer that’s helping us with this VR module in developing a mass-casualty incident module so that we can get better training in responding to these very unfortunate high-stakes situations.
Dr. Glatter: In terms of using the module remotely, certainly not requiring resources or having to be in a physical place, can providers in your plan be able to take such a headset home and practice on their own in the sense of being able to deal with a situation? Would this be more reserved for in-department use?
Dr. Salazar: That’s a phenomenal question. I wanted to create the most flexible module that I possibly could. Ideally, a dream scenario is leveraging a simulation center at an academic center and not just do the VR module but also have a brief didactics incorporating a small slide set, some feedback, and some standardized patients. I wanted it to be flexible enough so that folks here in my state, a different state, or even internationally could take advantage of this technology and do it from the comfort of their home.
As you mentioned, this is going to strike some people. It’s going to hit them heavier than others in terms of prior experience as PTSD. For some people, it may be more comfortable to do it in the comfort of their homes. I wanted to create something very flexible and dynamic.
Dr. Glatter: I think that’s ideal. Just one other point. Can you discuss the different levels of competencies involved in this module and how that would be attained?
Dr. Salazar: It’s all evidence based, so we borrowed from literature and the specialties of emergency medicine. We collaborated with psychiatrists within our medical center. We looked at all available literature and methods, proficiencies, competencies, and best practices, and we took all of them together to form something that we think is organized and concise.
We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.
This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.
Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.
Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.
Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.
Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.
Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.
Dr. Glatter: Are the data shared or confidential at present?
Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.
Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.
Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?
Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.
Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.
Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.
Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.
Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.
Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.
Dr. Salazar: It was my pleasure. Thank you so much for having me.
Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.
This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.
Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.
Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.
First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?
Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.
We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.
Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?
Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.
We are immersing learners into an actual hospital room to our specifications, very similar to exactly where we practice each and every day, and taking the learners through different situations that we designed with various levels of escalation and aggression, and asking the learner to manage that situation as best as they possibly can using the competencies and proficiencies that we taught them.
Dr. Glatter: Haptic feedback is an important part of the program and also the approach and technique that you’re using. Can you describe what haptic feedback means and what people actually feel?
Dr. Salazar: Absolutely. One of the most unfortunate things in my professional career is physical abuse suffered by people like me and you and our colleagues, nursing personnel, technicians, and others, resulting in injury.
We wanted to provide the most realistic experience that we could design. Haptics engage digital senses other than your auditory and your visuals. They really engage your tactile senses. These haptic vests and gloves and technology allow us to provide a third set of sensory stimuli for the learner.
At one of the modules, we have an actual physical assault that takes place, and the learner is actually able to feel in their body the strikes – of course, not painful – but just bringing in those senses and that stimulus, really leaving the learner with an experience that’s going to be long-lasting.
Dr. Glatter: Feeling that stimulus certainly affects your vital signs. Do you monitor a provider’s vital signs, such as their blood pressure and heart rate, as the situation and the threat escalate? That could potentially trigger some issues in people with prior PTSD or people with other mental health issues. Has that ever been considered in the design of your program?
Dr. Salazar: Yes, 100%. The beautiful thing about haptics is that they can be tailored to our specific parameters. The sensory stimulus that’s provided is actually very mild. It feels more like a tap than an actual strike. It just reminds us that when we’re having or experiencing an actual physical attack, we’re really engaging the senses.
We have an emergency physician or an EMT-paramedic on site at all times during the training so that we can monitor our subjects and make sure that they’re comfortable and healthy.
Dr. Glatter: Do they have actual sensors attached to their bodies that are part of your program or distinct in terms of monitoring their vital signs?
Dr. Salazar: It’s completely different. We have two different systems that we are planning on utilizing. Frankly, in the final version of this virtual reality module, we may not even involve the haptics. We’re going to study it and see how our learners behave and how much information they’re able to acquire and retain.
It may be very possible that just the visuals – the auditory and the immersion taking place within the hospital room – may be enough. It’s very possible that, in the next final version of this, we may find that haptics bring in quite a bit of value, and we may incorporate that. If that is the case, then we will, of course, acquire different technology to monitor the patient’s vital signs.
Dr. Glatter: Clearly, when situations escalate in the department, everyone gets more concerned about the patient, but providers are part of this equation, as you allude to.
In 2022, there was a poll by the American College of Emergency Physicians that stated that 85% of emergency physicians reported an increase in violent activity in their ERs in the past 5 years. Nearly two-thirds of nearly 3,000 emergency physicians surveyed reported being assaulted in the past year. This is an important module that we integrate into training providers in terms of these types of tense situations that can result not only in mental anguish but also in physical injury.
Dr. Salazar: One hundred percent. I frankly got tired of seeing my friends and my colleagues suffer both the physical and mental effects of verbal and physical abuse, and I wanted to design a project that was very patient centric while allowing our personnel to really manage these situations a little bit better.
Frankly, we don’t receive great training in this space, and I wanted to rewrite that narrative and make things better for our clinicians out there while remaining patient centric. I wanted to do something about it, and hopefully this dream will become a reality.
Dr. Glatter: Absolutely. There are other data from the Bureau of Labor Statistics stating that health care workers are five times more likely than employees in any other area of work to experience workplace violence. This could, again, range from verbal to physical violence. This is a very important module that you’re developing.
Are there any thoughts to extend this to active-shooter scenarios or any other high-stakes scenarios that you can imagine in the department?
Dr. Salazar: We’re actually working with the same developer that’s helping us with this VR module in developing a mass-casualty incident module so that we can get better training in responding to these very unfortunate high-stakes situations.
Dr. Glatter: In terms of using the module remotely, certainly not requiring resources or having to be in a physical place, can providers in your plan be able to take such a headset home and practice on their own in the sense of being able to deal with a situation? Would this be more reserved for in-department use?
Dr. Salazar: That’s a phenomenal question. I wanted to create the most flexible module that I possibly could. Ideally, a dream scenario is leveraging a simulation center at an academic center and not just do the VR module but also have a brief didactics incorporating a small slide set, some feedback, and some standardized patients. I wanted it to be flexible enough so that folks here in my state, a different state, or even internationally could take advantage of this technology and do it from the comfort of their home.
As you mentioned, this is going to strike some people. It’s going to hit them heavier than others in terms of prior experience as PTSD. For some people, it may be more comfortable to do it in the comfort of their homes. I wanted to create something very flexible and dynamic.
Dr. Glatter: I think that’s ideal. Just one other point. Can you discuss the different levels of competencies involved in this module and how that would be attained?
Dr. Salazar: It’s all evidence based, so we borrowed from literature and the specialties of emergency medicine. We collaborated with psychiatrists within our medical center. We looked at all available literature and methods, proficiencies, competencies, and best practices, and we took all of them together to form something that we think is organized and concise.
We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.
This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.
Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.
Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.
Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.
Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.
Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.
Dr. Glatter: Are the data shared or confidential at present?
Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.
Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.
Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?
Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.
Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.
Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.
Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.
Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.
Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.
Dr. Salazar: It was my pleasure. Thank you so much for having me.
Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.
This discussion was recorded on Feb. 21, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Welcome, Dr. Salazar. It’s a pleasure to have you join us today.
Gilberto A. Salazar, MD: The pleasure is all mine, Dr. Glatter. Thank you so much for having me.
Dr. Glatter: This is such an important topic, as you can imagine. Workplace violence is affecting so many providers in hospital emergency departments but also throughout other parts of the hospital.
First, can you describe how the virtual reality (VR) program was designed that you developed and what type of situations it simulates?
Dr. Salazar: We worked in conjunction with the University of Texas at Dallas. They help people like me, subject matter experts in health care, to bring ideas to reality. I worked very closely with a group of engineers from their department in designing a module specifically designed to tackle, as you mentioned, one of our biggest threats in workplace violence.
We decided to bring in a series of competencies and proficiencies that we wanted to bring into the virtual reality space. In leveraging the technology and the expertise from UT Dallas, we were able to make that happen.
Dr. Glatter: I think it’s important to understand, in terms of virtual reality, what type of environment the program creates. Can you describe what a provider who puts the goggles on is experiencing? Do they feel anything? Is there technology that enables this?
Dr. Salazar: Yes, absolutely. We were able to bring to reality a series of scenarios very common from what you and I see in the emergency department on a daily basis. We wanted to immerse a learner into that specific environment. We didn’t feel that a module or something on a computer or a slide set could really bring the reality of what it’s like to interact with a patient who may be escalating or may be aggressive.
We are immersing learners into an actual hospital room to our specifications, very similar to exactly where we practice each and every day, and taking the learners through different situations that we designed with various levels of escalation and aggression, and asking the learner to manage that situation as best as they possibly can using the competencies and proficiencies that we taught them.
Dr. Glatter: Haptic feedback is an important part of the program and also the approach and technique that you’re using. Can you describe what haptic feedback means and what people actually feel?
Dr. Salazar: Absolutely. One of the most unfortunate things in my professional career is physical abuse suffered by people like me and you and our colleagues, nursing personnel, technicians, and others, resulting in injury.
We wanted to provide the most realistic experience that we could design. Haptics engage digital senses other than your auditory and your visuals. They really engage your tactile senses. These haptic vests and gloves and technology allow us to provide a third set of sensory stimuli for the learner.
At one of the modules, we have an actual physical assault that takes place, and the learner is actually able to feel in their body the strikes – of course, not painful – but just bringing in those senses and that stimulus, really leaving the learner with an experience that’s going to be long-lasting.
Dr. Glatter: Feeling that stimulus certainly affects your vital signs. Do you monitor a provider’s vital signs, such as their blood pressure and heart rate, as the situation and the threat escalate? That could potentially trigger some issues in people with prior PTSD or people with other mental health issues. Has that ever been considered in the design of your program?
Dr. Salazar: Yes, 100%. The beautiful thing about haptics is that they can be tailored to our specific parameters. The sensory stimulus that’s provided is actually very mild. It feels more like a tap than an actual strike. It just reminds us that when we’re having or experiencing an actual physical attack, we’re really engaging the senses.
We have an emergency physician or an EMT-paramedic on site at all times during the training so that we can monitor our subjects and make sure that they’re comfortable and healthy.
Dr. Glatter: Do they have actual sensors attached to their bodies that are part of your program or distinct in terms of monitoring their vital signs?
Dr. Salazar: It’s completely different. We have two different systems that we are planning on utilizing. Frankly, in the final version of this virtual reality module, we may not even involve the haptics. We’re going to study it and see how our learners behave and how much information they’re able to acquire and retain.
It may be very possible that just the visuals – the auditory and the immersion taking place within the hospital room – may be enough. It’s very possible that, in the next final version of this, we may find that haptics bring in quite a bit of value, and we may incorporate that. If that is the case, then we will, of course, acquire different technology to monitor the patient’s vital signs.
Dr. Glatter: Clearly, when situations escalate in the department, everyone gets more concerned about the patient, but providers are part of this equation, as you allude to.
In 2022, there was a poll by the American College of Emergency Physicians that stated that 85% of emergency physicians reported an increase in violent activity in their ERs in the past 5 years. Nearly two-thirds of nearly 3,000 emergency physicians surveyed reported being assaulted in the past year. This is an important module that we integrate into training providers in terms of these types of tense situations that can result not only in mental anguish but also in physical injury.
Dr. Salazar: One hundred percent. I frankly got tired of seeing my friends and my colleagues suffer both the physical and mental effects of verbal and physical abuse, and I wanted to design a project that was very patient centric while allowing our personnel to really manage these situations a little bit better.
Frankly, we don’t receive great training in this space, and I wanted to rewrite that narrative and make things better for our clinicians out there while remaining patient centric. I wanted to do something about it, and hopefully this dream will become a reality.
Dr. Glatter: Absolutely. There are other data from the Bureau of Labor Statistics stating that health care workers are five times more likely than employees in any other area of work to experience workplace violence. This could, again, range from verbal to physical violence. This is a very important module that you’re developing.
Are there any thoughts to extend this to active-shooter scenarios or any other high-stakes scenarios that you can imagine in the department?
Dr. Salazar: We’re actually working with the same developer that’s helping us with this VR module in developing a mass-casualty incident module so that we can get better training in responding to these very unfortunate high-stakes situations.
Dr. Glatter: In terms of using the module remotely, certainly not requiring resources or having to be in a physical place, can providers in your plan be able to take such a headset home and practice on their own in the sense of being able to deal with a situation? Would this be more reserved for in-department use?
Dr. Salazar: That’s a phenomenal question. I wanted to create the most flexible module that I possibly could. Ideally, a dream scenario is leveraging a simulation center at an academic center and not just do the VR module but also have a brief didactics incorporating a small slide set, some feedback, and some standardized patients. I wanted it to be flexible enough so that folks here in my state, a different state, or even internationally could take advantage of this technology and do it from the comfort of their home.
As you mentioned, this is going to strike some people. It’s going to hit them heavier than others in terms of prior experience as PTSD. For some people, it may be more comfortable to do it in the comfort of their homes. I wanted to create something very flexible and dynamic.
Dr. Glatter: I think that’s ideal. Just one other point. Can you discuss the different levels of competencies involved in this module and how that would be attained?
Dr. Salazar: It’s all evidence based, so we borrowed from literature and the specialties of emergency medicine. We collaborated with psychiatrists within our medical center. We looked at all available literature and methods, proficiencies, competencies, and best practices, and we took all of them together to form something that we think is organized and concise.
We were able to create our own algorithm, but it’s not brand new. We’re just borrowing what we think is the best to create something that the majority of health care personnel are going to be able to relate to and be able to really be proficient at.
This includes things like active listening, bargaining, how to respond, where to put yourself in a situation, and the best possible situation to respond to a scenario, how to prevent things – how to get out of a chokehold, for example. We’re borrowing from several different disciplines and creating something that can be very concise and organized.
Dr. Glatter: Does this program that you’ve developed allow the provider to get feedback in the sense that when they’re in such a danger, their life could be at risk? For example, if they don’t remove themselves in a certain amount of time, this could be lethal.
Dr. Salazar: Yes, 100%. Probably the one thing that differentiates our project from any others is the ability to customize the experience so that a learner who is doing the things that we ask them to do in terms of safety and response is able to get out of a situation successfully within the environment. If they don’t, they get some kind of feedback.
Not to spoil the surprise here, but we’re going to be doing things like looking at decibel meters to see what the volume in the room is doing and how you’re managing the volume and the stimulation within the room. If you are able to maintain the decibel readings at a specific level, you’re going to succeed through the module. If you don’t, we keep the patient escalation going.
Dr. Glatter: There is a debrief built into this type of approach where, in other words, learning points are emphasized – where you could have done better and such.
Dr. Salazar: Yes, absolutely. We are going to be able to get individualized data for each learner so that we can tailor the debrief to their own performance and be able to give them actionable items to work on. It’s a debrief that’s productive and individualized, and folks can walk away with something useful in the end.
Dr. Glatter: Are the data shared or confidential at present?
Dr. Salazar: At this very moment, the data are confidential. We are going to look at how to best use this. We’re hoping to eventually write this up and see how this information can be best used to train personnel.
Eventually, we may see that some of the advice that we’re giving is very common to most folks. Others may require some individualized type of feedback. That said, it remains to be seen, but right now, it’s confidential.
Dr. Glatter: Is this currently being implemented as part of your curriculum for emergency medicine residents?
Dr. Salazar: We’re going to study it first. We’re very excited to include our emergency medicine residents as one of our cohorts that’s going to be undergoing the module, and we’re going to be studying other forms of workplace violence mitigation strategies. We’re really excited about the possibility of this eventually becoming the standard of education for not only our emergency medicine residents, but also health care personnel all over the world.
Dr. Glatter: I’m glad you mentioned that, because obviously nurses, clerks in the department, and anyone who’s working in the department, for that matter, and who interfaces with patients really should undergo such training.
Dr. Salazar: Absolutely. The folks at intake, at check-in, and at kiosks. Do they go through a separate area for screening? You’re absolutely right. There are many folks who interface with patients and all of us are potential victims of workplace violence. We want to give our health care family the best opportunity to succeed in these situations.
Dr. Glatter:: Absolutely. Even EMS providers, being on the front lines and encountering patients in such situations, would benefit, in my opinion.
Dr. Salazar: Yes, absolutely. Behavioral health emergencies and organically induced altered mental status results in injury, both physical and mental, to EMS professionals as well, and there’s good evidence of that. I’ll be very glad to see this type of education make it out to our initial and continuing education efforts for EMS as well.
Dr. Glatter: I want to thank you. This has been very helpful. It’s such an important task that you’ve started to explore, and I look forward to follow-up on this. Again, thank you for your time.
Dr. Salazar: It was my pleasure. Thank you so much for having me.
Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, N.Y. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes. Dr. Salazar is a board-certified emergency physician and associate professor at UT Southwestern Medicine Center in Dallas. He is involved with the UTSW Emergency Medicine Education Program and serves as the medical director to teach both initial and continuing the emergency medicine education for emergency medical technicians and paramedics, which trains most of the Dallas Fire Rescue personnel and the vast majority for EMS providers in the Dallas County. In addition, he serves as an associate chief of service at Parkland’s emergency department, and liaison to surgical services. A version of this article originally appeared on Medscape.com.
Antipsychotic cuts Alzheimer’s-related agitation
results of a phase 3 study suggest.
“In this phase 3 trial of patients with agitation in Alzheimer’s dementia, treatment with brexpiprazole 2 or 3 mg/day resulted in statistically significantly greater improvements in agitation versus placebo on the primary and key secondary endpoints,” said study investigator George Grossberg, MD, professor and director of the division of geriatric psychiatry, department of psychiatry & behavioral neuroscience, Saint Louis University.
Dr. Grossberg presented the findings as part of the annual meeting of the American Association for Geriatric Psychiatry.
Agitation common, distressing
With two previous studies also showing efficacy of brexpiprazole in AD-related agitation, Dr. Grossberg speculated that brexpiprazole will become the first drug to be approved for agitation in AD.
Agitation is one of the most common AD symptoms and is arguably the most distressing for patients and caregivers alike, Dr. Grossberg noted.
The drug was approved by the Food and Drug Administration in 2015 as an adjunctive therapy to antidepressants for adults with major depressive disorder and for adults with schizophrenia.
To investigate the drug at effective doses for AD-related agitation, the researchers conducted a phase 3 multicenter trial that included 345 patients with AD who met criteria for agitation and aggression.
Study participants had a mean Mini-Mental State Examination (MMSE) score between 5 and 22 at screening and baseline and a mean Cohen-Mansfield Agitation Inventory (CMAI) total score of about 79. A score above 45 is considered clinically significant agitation. Use of AD medications were permitted.
Patients had a mean age of 74 years and were randomly assigned in a 2:1 ratio to receive treatment with brexpiprazole 2 mg (n = 75) or 3 mg (n = 153) per day, or placebo (n = 117).
The study’s primary endpoint was improvement as assessed by the CMAI. Over 12 weeks, participants in the brexpiprazole group experienced greater improvement in agitation, with a mean change of –22.6 with brexpiprazole vs. –17.3 with placebo (P = .0026).
Brexpiprazole was also associated with significantly greater improvement in the secondary outcome of change from baseline to week 12 in agitation severity, as assessed using the Clinical Global Impression-Severity of Illness (CGI-S) score (mean change, –1.20 with brexpiprazole vs. –0.93 with placebo; P = .0078).
Specifically, treatment with the drug resulted in improvements in three key subscales of agitation, including aggressive behavior, such as physically striking out (P < .01 vs. placebo); physically nonaggressive; and verbally agitated, such as screaming or cursing (both P < .05).
Treatment-emergent adverse events (TEAEs) associated with brexpiprazole vs. placebo included somnolence (3.5% vs. 0.9%), nasopharyngitis (3.1% vs. 1.7%), dizziness (2.7% vs. 1.7%), diarrhea (2.2% vs. 0.9%), urinary tract infection (2.2% vs. 0.9%), and asthenia (2.2% vs. 0.0%).
“Aside from headache, no other TEAEs had an incidence of more than 5% in the brexpiprazole (2 or 3 mg) group, or in either dose group,” Dr. Grossberg said. “Cognition also remained stable,” he added.
Boxed warnings
Adverse events commonly associated with brexpiprazole include weight change, extrapyramidal events, falls, cardiovascular events, and sedation. In the study, all occurred at an incidence of less than 2% in both study groups, he noted.
Compared with the antipsychotic aripiprazole, brexpiprazole is associated with lower weight gain and akathisia, or motor restlessness.
One death occurred in the brexpiprazole 3 mg group in a patient who had heart failure, pneumonia, and cachexia. At autopsy, it was found the patient had cerebral and coronary atherosclerosis. The death was considered to be unrelated to brexpiprazole, said Dr. Grossberg.
This finding is notable because a caveat is that brexpiprazole, like aripiprazole and other typical and atypical antipsychotics, carries an FDA boxed warning related to an increased risk for death in older patients when used for dementia-related psychosis.
Noting that a black box warning about mortality risk is not a minor issue, Dr. Grossberg added that the risks are relatively low, whereas the risks associated with agitation in dementia can be high.
“If it’s an emergency situation, you have to treat the patient because otherwise they may harm someone else, or harm the staff, or harm their loved ones or themselves, and in those cases, we want to treat the patient first, get them under control, and then we worry about the black box,” he said.
In addition, “the No. 1 reason for getting kicked out of a nursing home is agitation or severe behaviors in the context of a dementia or a major neurocognitive disorder that the facility cannot control,” Dr. Grossberg added.
In such cases, patients may wind up in an emergency department and may not be welcome back at the nursing home.
“There’s always a risk/benefit ratio, and I have that discussion with patients and their families, but I can tell you that I’ve never had a family ask me not to use a medication because of the black box warning, because they see how miserable and how out of control their loved one is and they’re miserable because they see the suffering and will ask that we do anything that we can to get this behavior under control,” Dr. Grossberg said.
Caution still warranted
Commenting on the study, Rajesh R. Tampi, MD, professor and chairman of the department of psychiatry and the Bhatia Family Endowed Chair in Psychiatry at Creighton University, Omaha, Neb., underscored that, owing to the concerns behind the FDA warnings, “nonpharmacologic management is the cornerstone of treating agitation in Alzheimer’s dementia.”
He noted that the lack of an FDA-approved drug for agitation with AD is the result of “the overall benefits of any of the drug classes or drugs trialed to treat agitation in Alzheimer’s dementia vs. their adverse effect profile,” he said.
Therefore, he continued, “any medication or medication class should be used with caution among these individuals who often have polymorbidity.”
Dr. Tampi agreed that “the use of each drug for agitation in AD should be on a case-by-case basis with a clear and documented risk/benefit discussion with the patient and their families.”
“These medications should only be used for refractory symptoms or emergency situations where the agitation is not managed adequately with nonpharmacologic techniques and with a clear and documented risk/benefit discussion with patients and their families,” Dr. Tampi said.
The study was supported by Otsuka Pharmaceutical Development & Commercialization and H. Lundbeck. Dr. Grossberg has received consulting fees from Acadia, Avanir, Biogen, BioXcel, Genentech, Karuna, Lundbeck, Otsuka, Roche, and Takeda. Dr. Tampi had no disclosures to report.
A version of this article first appeared on Medscape.com.
This article was updated 3/14/23.
results of a phase 3 study suggest.
“In this phase 3 trial of patients with agitation in Alzheimer’s dementia, treatment with brexpiprazole 2 or 3 mg/day resulted in statistically significantly greater improvements in agitation versus placebo on the primary and key secondary endpoints,” said study investigator George Grossberg, MD, professor and director of the division of geriatric psychiatry, department of psychiatry & behavioral neuroscience, Saint Louis University.
Dr. Grossberg presented the findings as part of the annual meeting of the American Association for Geriatric Psychiatry.
Agitation common, distressing
With two previous studies also showing efficacy of brexpiprazole in AD-related agitation, Dr. Grossberg speculated that brexpiprazole will become the first drug to be approved for agitation in AD.
Agitation is one of the most common AD symptoms and is arguably the most distressing for patients and caregivers alike, Dr. Grossberg noted.
The drug was approved by the Food and Drug Administration in 2015 as an adjunctive therapy to antidepressants for adults with major depressive disorder and for adults with schizophrenia.
To investigate the drug at effective doses for AD-related agitation, the researchers conducted a phase 3 multicenter trial that included 345 patients with AD who met criteria for agitation and aggression.
Study participants had a mean Mini-Mental State Examination (MMSE) score between 5 and 22 at screening and baseline and a mean Cohen-Mansfield Agitation Inventory (CMAI) total score of about 79. A score above 45 is considered clinically significant agitation. Use of AD medications were permitted.
Patients had a mean age of 74 years and were randomly assigned in a 2:1 ratio to receive treatment with brexpiprazole 2 mg (n = 75) or 3 mg (n = 153) per day, or placebo (n = 117).
The study’s primary endpoint was improvement as assessed by the CMAI. Over 12 weeks, participants in the brexpiprazole group experienced greater improvement in agitation, with a mean change of –22.6 with brexpiprazole vs. –17.3 with placebo (P = .0026).
Brexpiprazole was also associated with significantly greater improvement in the secondary outcome of change from baseline to week 12 in agitation severity, as assessed using the Clinical Global Impression-Severity of Illness (CGI-S) score (mean change, –1.20 with brexpiprazole vs. –0.93 with placebo; P = .0078).
Specifically, treatment with the drug resulted in improvements in three key subscales of agitation, including aggressive behavior, such as physically striking out (P < .01 vs. placebo); physically nonaggressive; and verbally agitated, such as screaming or cursing (both P < .05).
Treatment-emergent adverse events (TEAEs) associated with brexpiprazole vs. placebo included somnolence (3.5% vs. 0.9%), nasopharyngitis (3.1% vs. 1.7%), dizziness (2.7% vs. 1.7%), diarrhea (2.2% vs. 0.9%), urinary tract infection (2.2% vs. 0.9%), and asthenia (2.2% vs. 0.0%).
“Aside from headache, no other TEAEs had an incidence of more than 5% in the brexpiprazole (2 or 3 mg) group, or in either dose group,” Dr. Grossberg said. “Cognition also remained stable,” he added.
Boxed warnings
Adverse events commonly associated with brexpiprazole include weight change, extrapyramidal events, falls, cardiovascular events, and sedation. In the study, all occurred at an incidence of less than 2% in both study groups, he noted.
Compared with the antipsychotic aripiprazole, brexpiprazole is associated with lower weight gain and akathisia, or motor restlessness.
One death occurred in the brexpiprazole 3 mg group in a patient who had heart failure, pneumonia, and cachexia. At autopsy, it was found the patient had cerebral and coronary atherosclerosis. The death was considered to be unrelated to brexpiprazole, said Dr. Grossberg.
This finding is notable because a caveat is that brexpiprazole, like aripiprazole and other typical and atypical antipsychotics, carries an FDA boxed warning related to an increased risk for death in older patients when used for dementia-related psychosis.
Noting that a black box warning about mortality risk is not a minor issue, Dr. Grossberg added that the risks are relatively low, whereas the risks associated with agitation in dementia can be high.
“If it’s an emergency situation, you have to treat the patient because otherwise they may harm someone else, or harm the staff, or harm their loved ones or themselves, and in those cases, we want to treat the patient first, get them under control, and then we worry about the black box,” he said.
In addition, “the No. 1 reason for getting kicked out of a nursing home is agitation or severe behaviors in the context of a dementia or a major neurocognitive disorder that the facility cannot control,” Dr. Grossberg added.
In such cases, patients may wind up in an emergency department and may not be welcome back at the nursing home.
“There’s always a risk/benefit ratio, and I have that discussion with patients and their families, but I can tell you that I’ve never had a family ask me not to use a medication because of the black box warning, because they see how miserable and how out of control their loved one is and they’re miserable because they see the suffering and will ask that we do anything that we can to get this behavior under control,” Dr. Grossberg said.
Caution still warranted
Commenting on the study, Rajesh R. Tampi, MD, professor and chairman of the department of psychiatry and the Bhatia Family Endowed Chair in Psychiatry at Creighton University, Omaha, Neb., underscored that, owing to the concerns behind the FDA warnings, “nonpharmacologic management is the cornerstone of treating agitation in Alzheimer’s dementia.”
He noted that the lack of an FDA-approved drug for agitation with AD is the result of “the overall benefits of any of the drug classes or drugs trialed to treat agitation in Alzheimer’s dementia vs. their adverse effect profile,” he said.
Therefore, he continued, “any medication or medication class should be used with caution among these individuals who often have polymorbidity.”
Dr. Tampi agreed that “the use of each drug for agitation in AD should be on a case-by-case basis with a clear and documented risk/benefit discussion with the patient and their families.”
“These medications should only be used for refractory symptoms or emergency situations where the agitation is not managed adequately with nonpharmacologic techniques and with a clear and documented risk/benefit discussion with patients and their families,” Dr. Tampi said.
The study was supported by Otsuka Pharmaceutical Development & Commercialization and H. Lundbeck. Dr. Grossberg has received consulting fees from Acadia, Avanir, Biogen, BioXcel, Genentech, Karuna, Lundbeck, Otsuka, Roche, and Takeda. Dr. Tampi had no disclosures to report.
A version of this article first appeared on Medscape.com.
This article was updated 3/14/23.
results of a phase 3 study suggest.
“In this phase 3 trial of patients with agitation in Alzheimer’s dementia, treatment with brexpiprazole 2 or 3 mg/day resulted in statistically significantly greater improvements in agitation versus placebo on the primary and key secondary endpoints,” said study investigator George Grossberg, MD, professor and director of the division of geriatric psychiatry, department of psychiatry & behavioral neuroscience, Saint Louis University.
Dr. Grossberg presented the findings as part of the annual meeting of the American Association for Geriatric Psychiatry.
Agitation common, distressing
With two previous studies also showing efficacy of brexpiprazole in AD-related agitation, Dr. Grossberg speculated that brexpiprazole will become the first drug to be approved for agitation in AD.
Agitation is one of the most common AD symptoms and is arguably the most distressing for patients and caregivers alike, Dr. Grossberg noted.
The drug was approved by the Food and Drug Administration in 2015 as an adjunctive therapy to antidepressants for adults with major depressive disorder and for adults with schizophrenia.
To investigate the drug at effective doses for AD-related agitation, the researchers conducted a phase 3 multicenter trial that included 345 patients with AD who met criteria for agitation and aggression.
Study participants had a mean Mini-Mental State Examination (MMSE) score between 5 and 22 at screening and baseline and a mean Cohen-Mansfield Agitation Inventory (CMAI) total score of about 79. A score above 45 is considered clinically significant agitation. Use of AD medications were permitted.
Patients had a mean age of 74 years and were randomly assigned in a 2:1 ratio to receive treatment with brexpiprazole 2 mg (n = 75) or 3 mg (n = 153) per day, or placebo (n = 117).
The study’s primary endpoint was improvement as assessed by the CMAI. Over 12 weeks, participants in the brexpiprazole group experienced greater improvement in agitation, with a mean change of –22.6 with brexpiprazole vs. –17.3 with placebo (P = .0026).
Brexpiprazole was also associated with significantly greater improvement in the secondary outcome of change from baseline to week 12 in agitation severity, as assessed using the Clinical Global Impression-Severity of Illness (CGI-S) score (mean change, –1.20 with brexpiprazole vs. –0.93 with placebo; P = .0078).
Specifically, treatment with the drug resulted in improvements in three key subscales of agitation, including aggressive behavior, such as physically striking out (P < .01 vs. placebo); physically nonaggressive; and verbally agitated, such as screaming or cursing (both P < .05).
Treatment-emergent adverse events (TEAEs) associated with brexpiprazole vs. placebo included somnolence (3.5% vs. 0.9%), nasopharyngitis (3.1% vs. 1.7%), dizziness (2.7% vs. 1.7%), diarrhea (2.2% vs. 0.9%), urinary tract infection (2.2% vs. 0.9%), and asthenia (2.2% vs. 0.0%).
“Aside from headache, no other TEAEs had an incidence of more than 5% in the brexpiprazole (2 or 3 mg) group, or in either dose group,” Dr. Grossberg said. “Cognition also remained stable,” he added.
Boxed warnings
Adverse events commonly associated with brexpiprazole include weight change, extrapyramidal events, falls, cardiovascular events, and sedation. In the study, all occurred at an incidence of less than 2% in both study groups, he noted.
Compared with the antipsychotic aripiprazole, brexpiprazole is associated with lower weight gain and akathisia, or motor restlessness.
One death occurred in the brexpiprazole 3 mg group in a patient who had heart failure, pneumonia, and cachexia. At autopsy, it was found the patient had cerebral and coronary atherosclerosis. The death was considered to be unrelated to brexpiprazole, said Dr. Grossberg.
This finding is notable because a caveat is that brexpiprazole, like aripiprazole and other typical and atypical antipsychotics, carries an FDA boxed warning related to an increased risk for death in older patients when used for dementia-related psychosis.
Noting that a black box warning about mortality risk is not a minor issue, Dr. Grossberg added that the risks are relatively low, whereas the risks associated with agitation in dementia can be high.
“If it’s an emergency situation, you have to treat the patient because otherwise they may harm someone else, or harm the staff, or harm their loved ones or themselves, and in those cases, we want to treat the patient first, get them under control, and then we worry about the black box,” he said.
In addition, “the No. 1 reason for getting kicked out of a nursing home is agitation or severe behaviors in the context of a dementia or a major neurocognitive disorder that the facility cannot control,” Dr. Grossberg added.
In such cases, patients may wind up in an emergency department and may not be welcome back at the nursing home.
“There’s always a risk/benefit ratio, and I have that discussion with patients and their families, but I can tell you that I’ve never had a family ask me not to use a medication because of the black box warning, because they see how miserable and how out of control their loved one is and they’re miserable because they see the suffering and will ask that we do anything that we can to get this behavior under control,” Dr. Grossberg said.
Caution still warranted
Commenting on the study, Rajesh R. Tampi, MD, professor and chairman of the department of psychiatry and the Bhatia Family Endowed Chair in Psychiatry at Creighton University, Omaha, Neb., underscored that, owing to the concerns behind the FDA warnings, “nonpharmacologic management is the cornerstone of treating agitation in Alzheimer’s dementia.”
He noted that the lack of an FDA-approved drug for agitation with AD is the result of “the overall benefits of any of the drug classes or drugs trialed to treat agitation in Alzheimer’s dementia vs. their adverse effect profile,” he said.
Therefore, he continued, “any medication or medication class should be used with caution among these individuals who often have polymorbidity.”
Dr. Tampi agreed that “the use of each drug for agitation in AD should be on a case-by-case basis with a clear and documented risk/benefit discussion with the patient and their families.”
“These medications should only be used for refractory symptoms or emergency situations where the agitation is not managed adequately with nonpharmacologic techniques and with a clear and documented risk/benefit discussion with patients and their families,” Dr. Tampi said.
The study was supported by Otsuka Pharmaceutical Development & Commercialization and H. Lundbeck. Dr. Grossberg has received consulting fees from Acadia, Avanir, Biogen, BioXcel, Genentech, Karuna, Lundbeck, Otsuka, Roche, and Takeda. Dr. Tampi had no disclosures to report.
A version of this article first appeared on Medscape.com.
This article was updated 3/14/23.
AT AAGP 2023
Buprenorphine proves effective for fentanyl users in the ED
based on data from nearly 900 individuals.
California EDs include a facilitation program known as CA Bridge for the treatment of opioid use disorder. Guidelines for CA Bridge call for high-dose buprenorphine to treat patients in drug withdrawal, with doses starting at 8-16 mg, Hannah Snyder, MD, of the University of California, San Francisco, and colleagues wrote.
“Buprenorphine has been repeatedly shown to save lives and prevent overdoses,” Dr. Snyder said in an interview. “We know that emergency department–initiated buprenorphine is an essential tool for increasing access. In the era of fentanyl, both patients and providers have expressed concerns that buprenorphine may not work as well as it did when patients were more likely to be using heroin or opioid pills.
“This retrospective cohort study provides additional information about emergency department buprenorphine as fentanyl becomes increasingly prevalent.”
In a research letter published in JAMA Network Open, the investigators reviewed data from the electronic health records of 896 patients who presented with opioid use disorder (OUD) at 16 CA Bridge EDs between Jan. 1, 2020, and April 30, 2020. All patients with OUD were included regardless of chief concern, current treatment, treatment desires, or withdrawal. A total of 87 individuals reported fentanyl use; if no fentanyl use was reported, the patient was classified as not using fentanyl. The median age of the patients was 35 years, two thirds were male, approximately 46% were White and non-Hispanic, and 30% had unstable housing.
The primary outcome was follow-up engagement at 7-14 days and 25-37 days.
A total of 492 patients received buprenorphine, including 44 fentanyl users, and 439 initiated high doses of 8-32 mg. At a 30-day follow-up, eight patients had precipitated withdrawal, including two cases in fentanyl users; none of these cases required hospital admission.
The follow-up engagement was similar for both groups, with adjusted odds ratios of 0.60 for administered buprenorphine at the initial ED encounter, 1.09 for 7-day follow-up, and 1.33 for 30-day follow-up.
The findings were limited by the retrospective design and use of clinical documentation, which likely resulted in underreporting of fentanyl use and follow-up, the researchers noted. However, the results supported the effectiveness of buprenorphine for ED patients in withdrawal with a history of fentanyl exposure.
“We were pleased to see that precipitated withdrawal was relatively uncommon in this study, and that patients who did and did not use fentanyl followed up at similar rates,” said Dr. Snyder. “This aligns with our clinical experience and prior research showing that emergency department buprenorphine starts continue to be an essential tool.”
The message for clinicians: “If a patient presents to the emergency department in objective opioid withdrawal and desires buprenorphine, they should be offered treatment in that moment,” Dr. Snyder said. “Treatment protocols used by hospitals in this study are available online. Emergency departments can offer compassionate and evidence-based treatment initiation 24 hours a day, 7 days a week, 365 days a year.”
More data needed on dosing strategies
“We need additional research to determine best practices for patients who use fentanyl and want to start buprenorphine, but are not yet in withdrawal,” Dr. Snyder said. “Doses of buprenorphine like those in this study are only appropriate for patients who are in withdrawal with objective signs, so some patients may struggle to wait long enough after their last use to go into sufficient withdrawal.”
Precipitated withdrawal does occur in some cases, said Dr. Snyder. “If it does, the emergency department is a very good place to manage it. We need additional research to determine best practices in management to make patients as comfortable as possible, including additional high-dose buprenorphine as well as additional adjunctive agents.”
Findings support buprenorphine
“The classic approach to buprenorphine initiation, which emerged from psychiatry outpatient office visits, is to start with very small doses of buprenorphine [2-4 mg] and titrate up slowly,” Reuben J. Strayer, MD, said in an interview.
“This dose range turns out to be the ‘sour spot’ most likely to cause the most important complication around buprenorphine initiation–precipitated withdrawal,” said Dr. Strayer, the director of addiction medicine in the emergency medicine department at Maimonides Medical Center, New York.
“One of the current focus areas of OUD treatment research is determining how to initiate buprenorphine without entailing a period of spontaneous withdrawal and without causing precipitated withdrawal,” Strayer explained. “The two primary strategies are low-dose buprenorphine initiation [LDBI, less than 2 mg, sometimes called microdosing] and high-dose [HDBI, ≥ 16 mg] buprenorphine initiation. HDBI is attractive because the primary treatment of buprenorphine-precipitated withdrawal is more buprenorphine.
“Additionally, using a high dose up front immediately transitions the patient to therapeutic blood levels, which protects the patient from withdrawal, cravings, and overdose from dangerous opioids (heroin, fentanyl, oxycodone).”
However, “the contamination and now replacement of heroin with fentanyl in the street drug supply has challenged buprenorphine initiation, because fentanyl, when used chronically, accumulates in the body and leaks into the bloodstream slowly over time, preventing the opioid washout that is required to eliminate the risk of precipitated withdrawal when buprenorphine is administered,” said Dr. Strayer.
The current study demonstrates that patients who are initiated with a first dose of 8-16 mg buprenorphine are unlikely to experience precipitated withdrawal and are successfully transitioned to buprenorphine maintenance and clinic follow-up, Dr. Snyder said, but he was surprised by the low rate of precipitated withdrawal in the current study, “which is discordant with what is being anecdotally reported across the country.”
However, the take-home message for clinicians is the support for the initiation of buprenorphine in emergency department settings at a starting dose of 8-16 mg, regardless of reported fentanyl use, he said. “Given the huge impact buprenorphine therapy has on OUD-related mortality, clinicians should make every effort to initiate buprenorphine for OUD patients at every opportunity, and precipitated withdrawal is very unlikely in appropriately selected patients.
“Many clinicians remain reluctant to initiate buprenorphine in ED settings for unfamiliarity with the drug, fear of precipitated withdrawal, or concerns around the certainty of outpatient follow-up,” Dr. Snyder said. “Education, encouragement, systems programming, such as including decision support within the electronic health record, and role-modeling from local champions will promote wider adoption of this lifesaving practice.”
Looking ahead, “more research, including prospective research, is needed to refine best practices around buprenorphine administration,” said Dr. Snyder. Questions to address include which patients are most at risk for precipitated withdrawal and whether there are alternatives to standard initiation dosing that are sufficiently unlikely to cause precipitated withdrawal. “Possibly effective alternatives include buprenorphine initiation by administration of long-acting injectable depot buprenorphine, which accumulates slowly, potentially avoiding precipitated withdrawal, as well as a slow intravenous buprenorphine infusion such as 9 mg given over 12 hours.”
The study received no outside funding. Dr. Snyder disclosed grants from the Substance Abuse and Mental Health Services Administration and the California Department of Health Care Services during the study. Dr. Strayer reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
based on data from nearly 900 individuals.
California EDs include a facilitation program known as CA Bridge for the treatment of opioid use disorder. Guidelines for CA Bridge call for high-dose buprenorphine to treat patients in drug withdrawal, with doses starting at 8-16 mg, Hannah Snyder, MD, of the University of California, San Francisco, and colleagues wrote.
“Buprenorphine has been repeatedly shown to save lives and prevent overdoses,” Dr. Snyder said in an interview. “We know that emergency department–initiated buprenorphine is an essential tool for increasing access. In the era of fentanyl, both patients and providers have expressed concerns that buprenorphine may not work as well as it did when patients were more likely to be using heroin or opioid pills.
“This retrospective cohort study provides additional information about emergency department buprenorphine as fentanyl becomes increasingly prevalent.”
In a research letter published in JAMA Network Open, the investigators reviewed data from the electronic health records of 896 patients who presented with opioid use disorder (OUD) at 16 CA Bridge EDs between Jan. 1, 2020, and April 30, 2020. All patients with OUD were included regardless of chief concern, current treatment, treatment desires, or withdrawal. A total of 87 individuals reported fentanyl use; if no fentanyl use was reported, the patient was classified as not using fentanyl. The median age of the patients was 35 years, two thirds were male, approximately 46% were White and non-Hispanic, and 30% had unstable housing.
The primary outcome was follow-up engagement at 7-14 days and 25-37 days.
A total of 492 patients received buprenorphine, including 44 fentanyl users, and 439 initiated high doses of 8-32 mg. At a 30-day follow-up, eight patients had precipitated withdrawal, including two cases in fentanyl users; none of these cases required hospital admission.
The follow-up engagement was similar for both groups, with adjusted odds ratios of 0.60 for administered buprenorphine at the initial ED encounter, 1.09 for 7-day follow-up, and 1.33 for 30-day follow-up.
The findings were limited by the retrospective design and use of clinical documentation, which likely resulted in underreporting of fentanyl use and follow-up, the researchers noted. However, the results supported the effectiveness of buprenorphine for ED patients in withdrawal with a history of fentanyl exposure.
“We were pleased to see that precipitated withdrawal was relatively uncommon in this study, and that patients who did and did not use fentanyl followed up at similar rates,” said Dr. Snyder. “This aligns with our clinical experience and prior research showing that emergency department buprenorphine starts continue to be an essential tool.”
The message for clinicians: “If a patient presents to the emergency department in objective opioid withdrawal and desires buprenorphine, they should be offered treatment in that moment,” Dr. Snyder said. “Treatment protocols used by hospitals in this study are available online. Emergency departments can offer compassionate and evidence-based treatment initiation 24 hours a day, 7 days a week, 365 days a year.”
More data needed on dosing strategies
“We need additional research to determine best practices for patients who use fentanyl and want to start buprenorphine, but are not yet in withdrawal,” Dr. Snyder said. “Doses of buprenorphine like those in this study are only appropriate for patients who are in withdrawal with objective signs, so some patients may struggle to wait long enough after their last use to go into sufficient withdrawal.”
Precipitated withdrawal does occur in some cases, said Dr. Snyder. “If it does, the emergency department is a very good place to manage it. We need additional research to determine best practices in management to make patients as comfortable as possible, including additional high-dose buprenorphine as well as additional adjunctive agents.”
Findings support buprenorphine
“The classic approach to buprenorphine initiation, which emerged from psychiatry outpatient office visits, is to start with very small doses of buprenorphine [2-4 mg] and titrate up slowly,” Reuben J. Strayer, MD, said in an interview.
“This dose range turns out to be the ‘sour spot’ most likely to cause the most important complication around buprenorphine initiation–precipitated withdrawal,” said Dr. Strayer, the director of addiction medicine in the emergency medicine department at Maimonides Medical Center, New York.
“One of the current focus areas of OUD treatment research is determining how to initiate buprenorphine without entailing a period of spontaneous withdrawal and without causing precipitated withdrawal,” Strayer explained. “The two primary strategies are low-dose buprenorphine initiation [LDBI, less than 2 mg, sometimes called microdosing] and high-dose [HDBI, ≥ 16 mg] buprenorphine initiation. HDBI is attractive because the primary treatment of buprenorphine-precipitated withdrawal is more buprenorphine.
“Additionally, using a high dose up front immediately transitions the patient to therapeutic blood levels, which protects the patient from withdrawal, cravings, and overdose from dangerous opioids (heroin, fentanyl, oxycodone).”
However, “the contamination and now replacement of heroin with fentanyl in the street drug supply has challenged buprenorphine initiation, because fentanyl, when used chronically, accumulates in the body and leaks into the bloodstream slowly over time, preventing the opioid washout that is required to eliminate the risk of precipitated withdrawal when buprenorphine is administered,” said Dr. Strayer.
The current study demonstrates that patients who are initiated with a first dose of 8-16 mg buprenorphine are unlikely to experience precipitated withdrawal and are successfully transitioned to buprenorphine maintenance and clinic follow-up, Dr. Snyder said, but he was surprised by the low rate of precipitated withdrawal in the current study, “which is discordant with what is being anecdotally reported across the country.”
However, the take-home message for clinicians is the support for the initiation of buprenorphine in emergency department settings at a starting dose of 8-16 mg, regardless of reported fentanyl use, he said. “Given the huge impact buprenorphine therapy has on OUD-related mortality, clinicians should make every effort to initiate buprenorphine for OUD patients at every opportunity, and precipitated withdrawal is very unlikely in appropriately selected patients.
“Many clinicians remain reluctant to initiate buprenorphine in ED settings for unfamiliarity with the drug, fear of precipitated withdrawal, or concerns around the certainty of outpatient follow-up,” Dr. Snyder said. “Education, encouragement, systems programming, such as including decision support within the electronic health record, and role-modeling from local champions will promote wider adoption of this lifesaving practice.”
Looking ahead, “more research, including prospective research, is needed to refine best practices around buprenorphine administration,” said Dr. Snyder. Questions to address include which patients are most at risk for precipitated withdrawal and whether there are alternatives to standard initiation dosing that are sufficiently unlikely to cause precipitated withdrawal. “Possibly effective alternatives include buprenorphine initiation by administration of long-acting injectable depot buprenorphine, which accumulates slowly, potentially avoiding precipitated withdrawal, as well as a slow intravenous buprenorphine infusion such as 9 mg given over 12 hours.”
The study received no outside funding. Dr. Snyder disclosed grants from the Substance Abuse and Mental Health Services Administration and the California Department of Health Care Services during the study. Dr. Strayer reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
based on data from nearly 900 individuals.
California EDs include a facilitation program known as CA Bridge for the treatment of opioid use disorder. Guidelines for CA Bridge call for high-dose buprenorphine to treat patients in drug withdrawal, with doses starting at 8-16 mg, Hannah Snyder, MD, of the University of California, San Francisco, and colleagues wrote.
“Buprenorphine has been repeatedly shown to save lives and prevent overdoses,” Dr. Snyder said in an interview. “We know that emergency department–initiated buprenorphine is an essential tool for increasing access. In the era of fentanyl, both patients and providers have expressed concerns that buprenorphine may not work as well as it did when patients were more likely to be using heroin or opioid pills.
“This retrospective cohort study provides additional information about emergency department buprenorphine as fentanyl becomes increasingly prevalent.”
In a research letter published in JAMA Network Open, the investigators reviewed data from the electronic health records of 896 patients who presented with opioid use disorder (OUD) at 16 CA Bridge EDs between Jan. 1, 2020, and April 30, 2020. All patients with OUD were included regardless of chief concern, current treatment, treatment desires, or withdrawal. A total of 87 individuals reported fentanyl use; if no fentanyl use was reported, the patient was classified as not using fentanyl. The median age of the patients was 35 years, two thirds were male, approximately 46% were White and non-Hispanic, and 30% had unstable housing.
The primary outcome was follow-up engagement at 7-14 days and 25-37 days.
A total of 492 patients received buprenorphine, including 44 fentanyl users, and 439 initiated high doses of 8-32 mg. At a 30-day follow-up, eight patients had precipitated withdrawal, including two cases in fentanyl users; none of these cases required hospital admission.
The follow-up engagement was similar for both groups, with adjusted odds ratios of 0.60 for administered buprenorphine at the initial ED encounter, 1.09 for 7-day follow-up, and 1.33 for 30-day follow-up.
The findings were limited by the retrospective design and use of clinical documentation, which likely resulted in underreporting of fentanyl use and follow-up, the researchers noted. However, the results supported the effectiveness of buprenorphine for ED patients in withdrawal with a history of fentanyl exposure.
“We were pleased to see that precipitated withdrawal was relatively uncommon in this study, and that patients who did and did not use fentanyl followed up at similar rates,” said Dr. Snyder. “This aligns with our clinical experience and prior research showing that emergency department buprenorphine starts continue to be an essential tool.”
The message for clinicians: “If a patient presents to the emergency department in objective opioid withdrawal and desires buprenorphine, they should be offered treatment in that moment,” Dr. Snyder said. “Treatment protocols used by hospitals in this study are available online. Emergency departments can offer compassionate and evidence-based treatment initiation 24 hours a day, 7 days a week, 365 days a year.”
More data needed on dosing strategies
“We need additional research to determine best practices for patients who use fentanyl and want to start buprenorphine, but are not yet in withdrawal,” Dr. Snyder said. “Doses of buprenorphine like those in this study are only appropriate for patients who are in withdrawal with objective signs, so some patients may struggle to wait long enough after their last use to go into sufficient withdrawal.”
Precipitated withdrawal does occur in some cases, said Dr. Snyder. “If it does, the emergency department is a very good place to manage it. We need additional research to determine best practices in management to make patients as comfortable as possible, including additional high-dose buprenorphine as well as additional adjunctive agents.”
Findings support buprenorphine
“The classic approach to buprenorphine initiation, which emerged from psychiatry outpatient office visits, is to start with very small doses of buprenorphine [2-4 mg] and titrate up slowly,” Reuben J. Strayer, MD, said in an interview.
“This dose range turns out to be the ‘sour spot’ most likely to cause the most important complication around buprenorphine initiation–precipitated withdrawal,” said Dr. Strayer, the director of addiction medicine in the emergency medicine department at Maimonides Medical Center, New York.
“One of the current focus areas of OUD treatment research is determining how to initiate buprenorphine without entailing a period of spontaneous withdrawal and without causing precipitated withdrawal,” Strayer explained. “The two primary strategies are low-dose buprenorphine initiation [LDBI, less than 2 mg, sometimes called microdosing] and high-dose [HDBI, ≥ 16 mg] buprenorphine initiation. HDBI is attractive because the primary treatment of buprenorphine-precipitated withdrawal is more buprenorphine.
“Additionally, using a high dose up front immediately transitions the patient to therapeutic blood levels, which protects the patient from withdrawal, cravings, and overdose from dangerous opioids (heroin, fentanyl, oxycodone).”
However, “the contamination and now replacement of heroin with fentanyl in the street drug supply has challenged buprenorphine initiation, because fentanyl, when used chronically, accumulates in the body and leaks into the bloodstream slowly over time, preventing the opioid washout that is required to eliminate the risk of precipitated withdrawal when buprenorphine is administered,” said Dr. Strayer.
The current study demonstrates that patients who are initiated with a first dose of 8-16 mg buprenorphine are unlikely to experience precipitated withdrawal and are successfully transitioned to buprenorphine maintenance and clinic follow-up, Dr. Snyder said, but he was surprised by the low rate of precipitated withdrawal in the current study, “which is discordant with what is being anecdotally reported across the country.”
However, the take-home message for clinicians is the support for the initiation of buprenorphine in emergency department settings at a starting dose of 8-16 mg, regardless of reported fentanyl use, he said. “Given the huge impact buprenorphine therapy has on OUD-related mortality, clinicians should make every effort to initiate buprenorphine for OUD patients at every opportunity, and precipitated withdrawal is very unlikely in appropriately selected patients.
“Many clinicians remain reluctant to initiate buprenorphine in ED settings for unfamiliarity with the drug, fear of precipitated withdrawal, or concerns around the certainty of outpatient follow-up,” Dr. Snyder said. “Education, encouragement, systems programming, such as including decision support within the electronic health record, and role-modeling from local champions will promote wider adoption of this lifesaving practice.”
Looking ahead, “more research, including prospective research, is needed to refine best practices around buprenorphine administration,” said Dr. Snyder. Questions to address include which patients are most at risk for precipitated withdrawal and whether there are alternatives to standard initiation dosing that are sufficiently unlikely to cause precipitated withdrawal. “Possibly effective alternatives include buprenorphine initiation by administration of long-acting injectable depot buprenorphine, which accumulates slowly, potentially avoiding precipitated withdrawal, as well as a slow intravenous buprenorphine infusion such as 9 mg given over 12 hours.”
The study received no outside funding. Dr. Snyder disclosed grants from the Substance Abuse and Mental Health Services Administration and the California Department of Health Care Services during the study. Dr. Strayer reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Once-daily stimulant for ADHD safe, effective at 1 year
new research shows.
Results from a phase 3, multicenter, dose-optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.
“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.
The study was published online in the Journal of Child and Adolescent Psychopharmacology.
Safety at 1 year
The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate, coformulated with immediate-release d-MPH.
SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.
Azstarys was approved by the Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.
For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial.
After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.
After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study because of a TEAE during the treatment phase.
The investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.
There were no life-threatening TEAEs and no deaths reported during the study.
The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.
Efficacy at 1 year
ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.
At baseline, participants’ mean ADHD Rating Scale–5 score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).
The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.
Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).
CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.
These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.
“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”
‘Reassuring data’
Commenting on the findings, Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.
“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.
“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.
Overall, the safety data reported in the study are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.
However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.
“These comorbidities often require stimulants as a part of treatment, and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”
The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos.
A version of this article first appeared on Medscape.com.
new research shows.
Results from a phase 3, multicenter, dose-optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.
“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.
The study was published online in the Journal of Child and Adolescent Psychopharmacology.
Safety at 1 year
The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate, coformulated with immediate-release d-MPH.
SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.
Azstarys was approved by the Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.
For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial.
After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.
After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study because of a TEAE during the treatment phase.
The investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.
There were no life-threatening TEAEs and no deaths reported during the study.
The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.
Efficacy at 1 year
ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.
At baseline, participants’ mean ADHD Rating Scale–5 score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).
The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.
Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).
CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.
These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.
“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”
‘Reassuring data’
Commenting on the findings, Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.
“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.
“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.
Overall, the safety data reported in the study are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.
However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.
“These comorbidities often require stimulants as a part of treatment, and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”
The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos.
A version of this article first appeared on Medscape.com.
new research shows.
Results from a phase 3, multicenter, dose-optimization, open-label safety study of Azstarys (KemPharm) found that most treatment-emergent adverse events (TEAEs) were mild to moderate.
“This data show that Azstarys remains safe and effective for the treatment of ADHD when given for up to a year,” lead investigator Ann Childress, MD, president of the Center for Psychiatry and Behavioral Medicine, Las Vegas, said in an interview.
The study was published online in the Journal of Child and Adolescent Psychopharmacology.
Safety at 1 year
The drug is a combination of extended-release serdexmethylphenidate (SDX), KemPharm’s prodrug of dexmethylphenidate, coformulated with immediate-release d-MPH.
SDX is converted to d-MPH after it is absorbed in the gastrointestinal tract. The d-MPH is released gradually throughout the day, providing quick symptom control with the d-MPH and extended control with SDX.
Azstarys was approved by the Food and Drug Administration in 2021 on the basis of results from a laboratory classroom phase 3 trial, which showed significant improvement in ADHD symptoms, compared with placebo.
For this study, the second phase 3 trial of Azstarys, investigators analyzed data from 282 children aged 6-12 years in the United States, including 70 who participated in an earlier 1-month efficacy trial.
After screening and a 3-week dose-optimization phase for new participants, patients received once-daily treatment with doses of 26.1 mg/5.2 mg, 39.2 mg/7.8 mg, or 52.3 mg/10.4 mg of SDX/d-MPH.
After 1 year of treatment, 60.1% of participants reported at least one TEAE, the majority of which were moderate. Twelve patients reported severe TEAEs. Six children (2.5%) discontinued the study because of a TEAE during the treatment phase.
The investigators also measured growth and changes in sleep with the Children’s Sleep Habits Questionnaire during the 12-month study. Sleep improved on most measures and the impact on growth was mild.
There were no life-threatening TEAEs and no deaths reported during the study.
The most common TEAEs during the treatment phase were decreased appetite, upper respiratory tract infection, nasopharyngitis, decreased weight, irritability, and increased weight.
Efficacy at 1 year
ADHD symptoms improved considerably after 1 month of treatment, with responses continuing at 1 year.
At baseline, participants’ mean ADHD Rating Scale–5 score was 41.5. After 1 month of treatment, scores averaged 16.1, a decline of –25.3 (P < .001).
The mean score stabilized in the 12-15 range for the remainder of the study. After 1 year of treatment, ADHD symptoms had decreased approximately 70% from baseline.
Investigators found similar results in clinical severity. After 1 month of treatment, the average Clinical Global Impressions–Severity (CGI-S) scale score was 2.5, a decline of –2.2 (P < .0001).
CGI-S scale scores remained in the 2.2-2.4 range for the remainder of the study.
These results, combined with the results of the original classroom trial, suggest Azstarys may offer advantages over other ADHD drugs, Dr. Childress said.
“In the laboratory classroom trial, subjects taking Azstarys completed significantly more math problems than subjects taking placebo beginning at 30 minutes and up to 13 hours after dosing,” Dr. Childress said. “No other methylphenidate extended-release product currently marketed in the United States has a 13-hour duration of effect.”
‘Reassuring data’
Commenting on the findings, Aditya Pawar, MD, a child and adolescent psychiatrist with the Kennedy Krieger Institute and an assistant professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, said that the study suggests the drug may be a valuable addition to ADHD treatment options for pediatric patients.
“The study provides reassuring data on the safety of stimulants in patients without significant history of cardiac events or blood pressure changes, which are usual concerns among patients and clinicians despite the evidence supporting safety, said Dr. Pawar, who was not part of the study.
“Additionally, the 1-year data on efficacy and safety of a new stimulant medication is valuable for clinicians looking for sustained relief for their patients, despite the limitations of an open-label trial,” she added.
Overall, the safety data reported in the study are fairly consistent with the safety profile of other methylphenidates used for treating ADHD, Dr. Pawar said.
However, she noted, the study does have some limitations, including its open-label design and lack of blinding. The research also excluded children with autism, disruptive mood dysregulation disorders, and other common comorbidities of ADHD, which may limit the generalizability of the results.
“These comorbidities often require stimulants as a part of treatment, and yet have a higher risk of side effects,” Dr. Pawar said. “Future studies with a broader population may be needed to better understand treatment effectiveness and potential risks.”
The study was funded by KemPharm. Dr. Childress serves as consultant for Aardvark, Arbor, Attentive, Cingulate, Ironshore, Neos Therapeutics, Neurocentria, Otsuka, Purdue, Rhodes, Sunovion, Tris Pharma, KemPharm, Supernus, Jazz, Corium, Tulex, and Lumos.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
Who can sue docs for wrongful death? Some states are trying to expand that group
In addition, the types of emotional damage that physicians can be sued for is expanding in pockets across the nation. The latest effort to expand the capacity to sue, a bill in New York state, failed when it was not signed by the governor – but a toned-down bill is in the works.
The impact of New York’s proposed expansion of wrongful death lawsuits would have been widespread. The New York legislation would have expanded the definition of “close family members” to include spouses, domestic partners, children, parents, stepparents, siblings, grandparents, and perhaps more. Additionally, lawsuits could have allowed juries to determine “close family members” of the deceased patient on the basis of specific circumstances of the person’s relationship with the decedent.
Currently, every state allows a wrongful death claim to be filed by immediate family members. If the patient who died was married, a surviving spouse could bring the lawsuit. If the patient had been unmarried, an adult child could bring the lawsuit in some states. A parent typically brings a lawsuit if their minor child has died from alleged wrongful death. In some states, one member of a civil union or domestic partnership may bring a wrongful death lawsuit. And if a single adult has no children or spouse/partner, more distant family members, including aunts, uncles, siblings, or grandparents, may file the suit.
The New York bill would also have expanded compensable damages to include loss of affection and companionship, and it would have expanded emotional damages, which are not currently included in New York. It would also have extended the statute of limitations of a wrongful death claim from 2 years to 3.5 years.
In general, in states that allow emotional distress to be included in wrongful death lawsuits, attorneys must demonstrate that survivors have suffered mental harm, such as depression, loss of sleep, fear, and anger, says Russ Haven, JD, general counsel for the New York Public Interest Research Group. While mental harm is not particularly easy to prove, attorneys must show that survivors have ongoing distress that is the direct result of the loss of the loved one and that the distress is significant enough to severely affect their quality of life.
Mr. Haven gives an example of emotional distress: “We worked with a woman who lost her fiancé in a motor vehicle accident,” he says. “The funeral ended up on the day she had scheduled her wedding dress fitting. A situation like that causes a good deal of lasting emotional distress.”
Expanding family members who can bring the lawsuit
The fact that a fiancé could be included in a wrongful death settlement is another aspect of the New York bill that was central to arguments both for and against the expansion of family members who can make claims. “We think a modern society includes unmarried partners, grandparents, siblings, and others,” says Mr. Haven.
“The language of who is a close family member might seem clear, but to a defense attorney, it isn’t,” says Tom Stebbins, executive director of the Lawsuit Reform Alliance of New York. “This could end up being a situation where someone has 40 grandchildren, and all could be considered close family members.”
Many states currently allow damages for claims of grief and mental anguish resulting from a wrongful death.
In her recent veto of the Grieving Families Act, New York Gov. Kathy Hochul took fire for her choices. The bill represented years of effort by the state legislature to expand the qualifiers for wrongful death lawsuits. Those supporting what ultimately became Senate Bill S74A believed they finally had the law over the finish line. Those opposed breathed a sigh of relief when the bill was vetoed.
Had Gov. Hochul signed Bill 274A, the effect on costs would have been enormous for physicians. New York already has the highest cumulative medical liability payouts in the nation, according to the Medical Society of the State of New York.
The MSSNY was among many parties that fought against the law. The Greater New York Hospital Association, insurance companies, the Defense Association of New York, and the New York Conference of Mayors all joined in lobbying against the bill.
“Gov. Hochul, in her veto message, correctly noted that the proposed New York legislation represented an extraordinary departure from New York’s wrongful death jurisprudence,” says Remi Stone, director of government relations at The Doctors Company, part of the TDC Group. “I would add that while there are some other states that allow grief damages, none are as wide-ranging as the proposed legislation.”
The NYPIRG, the AARP, and the New York Immigration Coalition supported the bill. In a statement following the veto, the New York State Trial Lawyers Association said: “By vetoing the Grieving Families Act, Gov. Hochul has sided with insurance companies, the health care industry, big corporations, and anyone else who doesn’t want to be held accountable for the negligent killing of a person. This bill passed with overwhelming bipartisan support and would rectify over a century of injustice.”
Following Gov. Hochul’s veto, the bill’s proponents and the state legislature vowed to return to the drawing board and construct a bill that the governor would eventually approve. For now, however, the controversial legislation has been put to rest.
Mr. Haven and the NYPIRG argue that New York lags behind many other states in allowing survivors to claim loss for their emotional distress. “When there is relationship loss, it has a great impact on your life,” Mr. Haven says, “and this goes beyond simply the financial impact.”
“The bill was well intended but completely vague on who could bring lawsuits and would have increased medical malpractice insurance by far too much,” says MSSNY President Parag Mehta, MD. “For safety net hospitals, one lawsuit would halt their ability to provide many programs aimed at underserved populations.”
Peter Kolbert, JD, senior vice president of claim and litigation services at Healthcare Risk Advisors (part of the TDC Group), had this to say: “The current ‘recoverable’ damages in New York in a wrongful death case include loss of guidance and support for minor children of a decedent. Those damages have been sustained at $2 million per child. It is rationally very challenging, if not impossible, to distinguish between those damages and the proposed damages that the very same people would have been entitled to under the proposed statute.”
What will happen in the future?
While the veto has stalled New York’s wrongful death expansion for now, supporters in and out of the legislature remain determined to continue their fight. “Advocates argue that the bill would have brought the state in line with wrongful death law in others,” says Brian Whitelaw, JD, a partner at Michigan’s Foley, Baron, Metzger & Juip. “But if the bill had become law as written, the economic impact would have been substantial.”
Mr. Whitelaw says that such wide-ranging lawsuits can have consequences that extend far beyond physicians’ insurance premiums. “This could impact the average person on the street’s ability to obtain the medical care they need, because doctors will go elsewhere to practice,” he says. “Beyond impacting the health care system, it can hurt small businesses as well.”
Mr. Haven says supporters of the expansion are far from finished with their efforts. “New York’s current law dates back to 1847, and it was cutting edge then,” he says. “It was designed for an agrarian society where if the husband died, his widow and children wouldn’t become destitute. Now, 175 years later, we realize that the law has biases, and tort law has evolved. The state needs to evolve as well.”
For his part, Dr. Mehta is open to a dialogue with lawmakers to revise the law in a manner agreeable to all parties. “We want to work together to make the system right,” he says. “The liability system in New York needs an overall holistic change, and we are available at any time to have discussions. The vetoed bill was a Band-Aid and didn’t address the main, underlying issues in the state.”
Mr. Stebbins, too, says he would like to continue the debate over how an expansion should look. “We hope to go through a discussion on caps to these suits,” he explains. “We have already seen the cap of $10 million broken four times in the past few years through nuclear verdicts. That’s something we need to address.”
Given the legislature’s overwhelming support for the bill, some version of it will likely make another appearance in the coming session. Whether or not it can strike the middle ground that will make all parties happy – including the governor – is yet to be seen. “Is it wrong to seek compensation for pain and suffering from a wrongful death?” asks Mr. Whitelaw. “No. But there must be limits to such laws, or where does it end?”
A version of this article first appeared on Medscape.com.
In addition, the types of emotional damage that physicians can be sued for is expanding in pockets across the nation. The latest effort to expand the capacity to sue, a bill in New York state, failed when it was not signed by the governor – but a toned-down bill is in the works.
The impact of New York’s proposed expansion of wrongful death lawsuits would have been widespread. The New York legislation would have expanded the definition of “close family members” to include spouses, domestic partners, children, parents, stepparents, siblings, grandparents, and perhaps more. Additionally, lawsuits could have allowed juries to determine “close family members” of the deceased patient on the basis of specific circumstances of the person’s relationship with the decedent.
Currently, every state allows a wrongful death claim to be filed by immediate family members. If the patient who died was married, a surviving spouse could bring the lawsuit. If the patient had been unmarried, an adult child could bring the lawsuit in some states. A parent typically brings a lawsuit if their minor child has died from alleged wrongful death. In some states, one member of a civil union or domestic partnership may bring a wrongful death lawsuit. And if a single adult has no children or spouse/partner, more distant family members, including aunts, uncles, siblings, or grandparents, may file the suit.
The New York bill would also have expanded compensable damages to include loss of affection and companionship, and it would have expanded emotional damages, which are not currently included in New York. It would also have extended the statute of limitations of a wrongful death claim from 2 years to 3.5 years.
In general, in states that allow emotional distress to be included in wrongful death lawsuits, attorneys must demonstrate that survivors have suffered mental harm, such as depression, loss of sleep, fear, and anger, says Russ Haven, JD, general counsel for the New York Public Interest Research Group. While mental harm is not particularly easy to prove, attorneys must show that survivors have ongoing distress that is the direct result of the loss of the loved one and that the distress is significant enough to severely affect their quality of life.
Mr. Haven gives an example of emotional distress: “We worked with a woman who lost her fiancé in a motor vehicle accident,” he says. “The funeral ended up on the day she had scheduled her wedding dress fitting. A situation like that causes a good deal of lasting emotional distress.”
Expanding family members who can bring the lawsuit
The fact that a fiancé could be included in a wrongful death settlement is another aspect of the New York bill that was central to arguments both for and against the expansion of family members who can make claims. “We think a modern society includes unmarried partners, grandparents, siblings, and others,” says Mr. Haven.
“The language of who is a close family member might seem clear, but to a defense attorney, it isn’t,” says Tom Stebbins, executive director of the Lawsuit Reform Alliance of New York. “This could end up being a situation where someone has 40 grandchildren, and all could be considered close family members.”
Many states currently allow damages for claims of grief and mental anguish resulting from a wrongful death.
In her recent veto of the Grieving Families Act, New York Gov. Kathy Hochul took fire for her choices. The bill represented years of effort by the state legislature to expand the qualifiers for wrongful death lawsuits. Those supporting what ultimately became Senate Bill S74A believed they finally had the law over the finish line. Those opposed breathed a sigh of relief when the bill was vetoed.
Had Gov. Hochul signed Bill 274A, the effect on costs would have been enormous for physicians. New York already has the highest cumulative medical liability payouts in the nation, according to the Medical Society of the State of New York.
The MSSNY was among many parties that fought against the law. The Greater New York Hospital Association, insurance companies, the Defense Association of New York, and the New York Conference of Mayors all joined in lobbying against the bill.
“Gov. Hochul, in her veto message, correctly noted that the proposed New York legislation represented an extraordinary departure from New York’s wrongful death jurisprudence,” says Remi Stone, director of government relations at The Doctors Company, part of the TDC Group. “I would add that while there are some other states that allow grief damages, none are as wide-ranging as the proposed legislation.”
The NYPIRG, the AARP, and the New York Immigration Coalition supported the bill. In a statement following the veto, the New York State Trial Lawyers Association said: “By vetoing the Grieving Families Act, Gov. Hochul has sided with insurance companies, the health care industry, big corporations, and anyone else who doesn’t want to be held accountable for the negligent killing of a person. This bill passed with overwhelming bipartisan support and would rectify over a century of injustice.”
Following Gov. Hochul’s veto, the bill’s proponents and the state legislature vowed to return to the drawing board and construct a bill that the governor would eventually approve. For now, however, the controversial legislation has been put to rest.
Mr. Haven and the NYPIRG argue that New York lags behind many other states in allowing survivors to claim loss for their emotional distress. “When there is relationship loss, it has a great impact on your life,” Mr. Haven says, “and this goes beyond simply the financial impact.”
“The bill was well intended but completely vague on who could bring lawsuits and would have increased medical malpractice insurance by far too much,” says MSSNY President Parag Mehta, MD. “For safety net hospitals, one lawsuit would halt their ability to provide many programs aimed at underserved populations.”
Peter Kolbert, JD, senior vice president of claim and litigation services at Healthcare Risk Advisors (part of the TDC Group), had this to say: “The current ‘recoverable’ damages in New York in a wrongful death case include loss of guidance and support for minor children of a decedent. Those damages have been sustained at $2 million per child. It is rationally very challenging, if not impossible, to distinguish between those damages and the proposed damages that the very same people would have been entitled to under the proposed statute.”
What will happen in the future?
While the veto has stalled New York’s wrongful death expansion for now, supporters in and out of the legislature remain determined to continue their fight. “Advocates argue that the bill would have brought the state in line with wrongful death law in others,” says Brian Whitelaw, JD, a partner at Michigan’s Foley, Baron, Metzger & Juip. “But if the bill had become law as written, the economic impact would have been substantial.”
Mr. Whitelaw says that such wide-ranging lawsuits can have consequences that extend far beyond physicians’ insurance premiums. “This could impact the average person on the street’s ability to obtain the medical care they need, because doctors will go elsewhere to practice,” he says. “Beyond impacting the health care system, it can hurt small businesses as well.”
Mr. Haven says supporters of the expansion are far from finished with their efforts. “New York’s current law dates back to 1847, and it was cutting edge then,” he says. “It was designed for an agrarian society where if the husband died, his widow and children wouldn’t become destitute. Now, 175 years later, we realize that the law has biases, and tort law has evolved. The state needs to evolve as well.”
For his part, Dr. Mehta is open to a dialogue with lawmakers to revise the law in a manner agreeable to all parties. “We want to work together to make the system right,” he says. “The liability system in New York needs an overall holistic change, and we are available at any time to have discussions. The vetoed bill was a Band-Aid and didn’t address the main, underlying issues in the state.”
Mr. Stebbins, too, says he would like to continue the debate over how an expansion should look. “We hope to go through a discussion on caps to these suits,” he explains. “We have already seen the cap of $10 million broken four times in the past few years through nuclear verdicts. That’s something we need to address.”
Given the legislature’s overwhelming support for the bill, some version of it will likely make another appearance in the coming session. Whether or not it can strike the middle ground that will make all parties happy – including the governor – is yet to be seen. “Is it wrong to seek compensation for pain and suffering from a wrongful death?” asks Mr. Whitelaw. “No. But there must be limits to such laws, or where does it end?”
A version of this article first appeared on Medscape.com.
In addition, the types of emotional damage that physicians can be sued for is expanding in pockets across the nation. The latest effort to expand the capacity to sue, a bill in New York state, failed when it was not signed by the governor – but a toned-down bill is in the works.
The impact of New York’s proposed expansion of wrongful death lawsuits would have been widespread. The New York legislation would have expanded the definition of “close family members” to include spouses, domestic partners, children, parents, stepparents, siblings, grandparents, and perhaps more. Additionally, lawsuits could have allowed juries to determine “close family members” of the deceased patient on the basis of specific circumstances of the person’s relationship with the decedent.
Currently, every state allows a wrongful death claim to be filed by immediate family members. If the patient who died was married, a surviving spouse could bring the lawsuit. If the patient had been unmarried, an adult child could bring the lawsuit in some states. A parent typically brings a lawsuit if their minor child has died from alleged wrongful death. In some states, one member of a civil union or domestic partnership may bring a wrongful death lawsuit. And if a single adult has no children or spouse/partner, more distant family members, including aunts, uncles, siblings, or grandparents, may file the suit.
The New York bill would also have expanded compensable damages to include loss of affection and companionship, and it would have expanded emotional damages, which are not currently included in New York. It would also have extended the statute of limitations of a wrongful death claim from 2 years to 3.5 years.
In general, in states that allow emotional distress to be included in wrongful death lawsuits, attorneys must demonstrate that survivors have suffered mental harm, such as depression, loss of sleep, fear, and anger, says Russ Haven, JD, general counsel for the New York Public Interest Research Group. While mental harm is not particularly easy to prove, attorneys must show that survivors have ongoing distress that is the direct result of the loss of the loved one and that the distress is significant enough to severely affect their quality of life.
Mr. Haven gives an example of emotional distress: “We worked with a woman who lost her fiancé in a motor vehicle accident,” he says. “The funeral ended up on the day she had scheduled her wedding dress fitting. A situation like that causes a good deal of lasting emotional distress.”
Expanding family members who can bring the lawsuit
The fact that a fiancé could be included in a wrongful death settlement is another aspect of the New York bill that was central to arguments both for and against the expansion of family members who can make claims. “We think a modern society includes unmarried partners, grandparents, siblings, and others,” says Mr. Haven.
“The language of who is a close family member might seem clear, but to a defense attorney, it isn’t,” says Tom Stebbins, executive director of the Lawsuit Reform Alliance of New York. “This could end up being a situation where someone has 40 grandchildren, and all could be considered close family members.”
Many states currently allow damages for claims of grief and mental anguish resulting from a wrongful death.
In her recent veto of the Grieving Families Act, New York Gov. Kathy Hochul took fire for her choices. The bill represented years of effort by the state legislature to expand the qualifiers for wrongful death lawsuits. Those supporting what ultimately became Senate Bill S74A believed they finally had the law over the finish line. Those opposed breathed a sigh of relief when the bill was vetoed.
Had Gov. Hochul signed Bill 274A, the effect on costs would have been enormous for physicians. New York already has the highest cumulative medical liability payouts in the nation, according to the Medical Society of the State of New York.
The MSSNY was among many parties that fought against the law. The Greater New York Hospital Association, insurance companies, the Defense Association of New York, and the New York Conference of Mayors all joined in lobbying against the bill.
“Gov. Hochul, in her veto message, correctly noted that the proposed New York legislation represented an extraordinary departure from New York’s wrongful death jurisprudence,” says Remi Stone, director of government relations at The Doctors Company, part of the TDC Group. “I would add that while there are some other states that allow grief damages, none are as wide-ranging as the proposed legislation.”
The NYPIRG, the AARP, and the New York Immigration Coalition supported the bill. In a statement following the veto, the New York State Trial Lawyers Association said: “By vetoing the Grieving Families Act, Gov. Hochul has sided with insurance companies, the health care industry, big corporations, and anyone else who doesn’t want to be held accountable for the negligent killing of a person. This bill passed with overwhelming bipartisan support and would rectify over a century of injustice.”
Following Gov. Hochul’s veto, the bill’s proponents and the state legislature vowed to return to the drawing board and construct a bill that the governor would eventually approve. For now, however, the controversial legislation has been put to rest.
Mr. Haven and the NYPIRG argue that New York lags behind many other states in allowing survivors to claim loss for their emotional distress. “When there is relationship loss, it has a great impact on your life,” Mr. Haven says, “and this goes beyond simply the financial impact.”
“The bill was well intended but completely vague on who could bring lawsuits and would have increased medical malpractice insurance by far too much,” says MSSNY President Parag Mehta, MD. “For safety net hospitals, one lawsuit would halt their ability to provide many programs aimed at underserved populations.”
Peter Kolbert, JD, senior vice president of claim and litigation services at Healthcare Risk Advisors (part of the TDC Group), had this to say: “The current ‘recoverable’ damages in New York in a wrongful death case include loss of guidance and support for minor children of a decedent. Those damages have been sustained at $2 million per child. It is rationally very challenging, if not impossible, to distinguish between those damages and the proposed damages that the very same people would have been entitled to under the proposed statute.”
What will happen in the future?
While the veto has stalled New York’s wrongful death expansion for now, supporters in and out of the legislature remain determined to continue their fight. “Advocates argue that the bill would have brought the state in line with wrongful death law in others,” says Brian Whitelaw, JD, a partner at Michigan’s Foley, Baron, Metzger & Juip. “But if the bill had become law as written, the economic impact would have been substantial.”
Mr. Whitelaw says that such wide-ranging lawsuits can have consequences that extend far beyond physicians’ insurance premiums. “This could impact the average person on the street’s ability to obtain the medical care they need, because doctors will go elsewhere to practice,” he says. “Beyond impacting the health care system, it can hurt small businesses as well.”
Mr. Haven says supporters of the expansion are far from finished with their efforts. “New York’s current law dates back to 1847, and it was cutting edge then,” he says. “It was designed for an agrarian society where if the husband died, his widow and children wouldn’t become destitute. Now, 175 years later, we realize that the law has biases, and tort law has evolved. The state needs to evolve as well.”
For his part, Dr. Mehta is open to a dialogue with lawmakers to revise the law in a manner agreeable to all parties. “We want to work together to make the system right,” he says. “The liability system in New York needs an overall holistic change, and we are available at any time to have discussions. The vetoed bill was a Band-Aid and didn’t address the main, underlying issues in the state.”
Mr. Stebbins, too, says he would like to continue the debate over how an expansion should look. “We hope to go through a discussion on caps to these suits,” he explains. “We have already seen the cap of $10 million broken four times in the past few years through nuclear verdicts. That’s something we need to address.”
Given the legislature’s overwhelming support for the bill, some version of it will likely make another appearance in the coming session. Whether or not it can strike the middle ground that will make all parties happy – including the governor – is yet to be seen. “Is it wrong to seek compensation for pain and suffering from a wrongful death?” asks Mr. Whitelaw. “No. But there must be limits to such laws, or where does it end?”
A version of this article first appeared on Medscape.com.
Tips for treating patients with late-life depression
Late-life depression is the onset of a major depressive disorder in an individual ≥ 60 years of age. Depressive illness compromises quality of life and is especially troublesome for older people. The prevalence of depression among individuals > 65 years of age is about 4% in women and 3% in men.1 The estimated lifetime prevalence is approximately 24% for women and 10% for men.2 Three factors account for this disparity: women exhibit greater susceptibility to depression; the illness persists longer in women than it does in men; and the probability of death related to depression is lower in women.2
Beyond its direct mental and emotional impacts, depression takes a financial toll; health care costs are higher for those with depression than for those without depression.3 Unpaid caregiver expense is the largest indirect financial burden with late-life depression.4 Additional indirect costs include less work productivity, early retirement, and diminished financial security.4
Many individuals with depression never receive treatment. Fortunately, there are many interventions in the primary care arsenal that can be used to treat older patients with depression and dramatically improve mood, comfort, and function.
The interactions of emotional and physical health
The pathophysiology of depression remains unclear. However, numerous factors are known to contribute to, exacerbate, or prolong depression among elderly populations. Insufficient social engagement and support is strongly associated with depressive mood.5 The loss of independence in giving up automobile driving can compromise self-confidence.6 Sleep difficulties predispose to, and predict, the emergence of a mood disorder, independent of other symptoms.7 Age-related hearing deficits also are associated with depression.8
There is a close relationship between emotional and physical health.9 Depression adds to the likelihood of medical illness, and somatic pathology increases the risk for mood disorders.9 Depression has been linked with obesity, frailty, diabetes, cognitive impairment, and terminal illness.9
Inflammatory markers and depression may also be related. Plasma levels of interleukin-6 and C-reactive protein were measured in a longitudinal aging study.14 A high level of interleukin-6, but not C-reactive protein, correlated with an increased prevalence of depression in older people.
Chronic cerebral ischemia can result in a “vascular depression”13 in which disruption of prefrontal systems by ischemic lesions is hypothesized to be an important factor in developing despair. Psychomotor retardation, executive dysfunction, severe disability, and a heightened risk for relapse are common features of vascular depression.15 Poststroke depression often follows a cerebrovascular episode16; the exact pathogenic mechanism is unknown.17
Continue to: A summation of common risk factors
A summation of common risk factors. A personal or family history of depression increases the risk for late-life depression. Other risk factors are female gender, bereavement, sleep disturbance, and disability.18 Poor general health, chronic pain, cognitive impairment, poor social support, and medical comorbidities with impaired functioning increase the likelihood of resultant mood disorders.18
Somatic complaints may overshadow diagnostic symptoms
Manifestations of depression include disturbed sleep and reductions in appetite, concentration, activity, and energy for daily function.19 These features, of course, may accompany medical disorders and some normal physiologic changes among elderly people. We find that while older individuals may report a sad mood, disturbed sleep, or other dysfunctions, they frequently emphasize their somatic complaints much more prominently than their emotions. This can make it difficult to recognize clinical depression.
For a diagnosis of major depression, 5 of the following 9 symptoms must be present for most of the day or nearly every day over a period of at least 2 weeks19: depressed mood; diminished interest in most activities; significant weight loss or decreased appetite; insomnia or hypersomnia; agitation or retardation; fatigue or loss of energy; feelings of worthlessness or guilt; diminished concentration; and recurrent thoughts of death or suicide.19
Planning difficulties, apathy, disability, and anhedonia frequently occur. Executive dysfunction and inefficacy of antidepressant pharmacotherapy are related to compromised frontal-striatal-limbic pathways.20 Since difficulties with planning and organization are associated with suboptimal response to antidepressant medications, a psychotherapeutic focus on these executive functions can augment drug-induced benefit.
Rule out these alternative diagnoses
Dementias can manifest as depression. Other brain pathologies, particularly Parkinson disease or stroke, also should be ruled out. Overmedication can simulate depression, so be sure to review the prescription and over-the-counter agents a patient is taking. Some medications can occasionally precipitate a clinical depression; these include stimulants, steroids, methyldopa, triptans, chemotherapeutic agents, and immunologic drugs, to name a few.19
Continue to: Pharmacotherapy, Yes, but first, consider these factors
Pharmacotherapy, Yes, but first, consider these factors
Maintaining a close patient–doctor relationship augments all therapeutic interventions. Good eye contact when listening to and counseling patients is key, as is providing close follow-up appointments.
Encourage social interactions with family and friends, which can be particularly productive. Encouraging spiritual endeavors, such as attendance at religious services, can be beneficial.21
Recommend exercise. Physical exercise yields positive outcomes22; it can enhance mood, improve sleep, and help to diminish anxiety. Encourage patients with depression to take a daily walk during the day; doing so can enhance emotional outlook, health, and even socialization.
What treatment will best serve your patient?
It’s important when caring for patients with depression to assess and address suicidal ideation. Depression with a previous suicide attempt is a strong risk factor for suicide. Inquire about suicidal intent or death wishes, access to guns, and other life-ending behaviors. Whenever suicide is an active issue, immediate crisis management is required. Psychiatric referral is an option, and hospitalization may be indicated. Advise family members to remove firearms or restrict access, be with the patient as much as possible, and assist at intervention planning and implementation.
It is worth mentioning, here, the connection between chronic pain and suicidal ideation. Pain management reduces suicidal ideation, regardless of depression severity.23
Continue to: Psychotherapy and pharmacotherapies...
Psychotherapy and pharmacotherapies offered for the treatment of depression in geriatric practices are both effective, without much difference seen in efficacy.24 Psychotherapy might include direct physician and family support to the patient or referral to a mental health professional. Base treatment choices on clinical access, patient preference, and medical contraindications and other illnesses.
Pros and cons of various pharmacotherapies
Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed first for elderly patients with depression.25 Escitalopram is often better tolerated than paroxetine, which exhibits muscarinic antagonism and enzyme inhibition of cytochrome P450-2D6.26 Escitalopram also has fewer pharmaceutical interactions compared with sertraline.26
Generally, when prescribing an antidepressant drug, stay with the initial choice, gradually increasing the dose as clinically needed to its maximum limit. Suicidal ideation may be worsened by too quickly switching from one antidepressant to another or by co-prescribing anxiolytic or hypnotic medicines. Benzodiazepines have addictive and disinhibiting properties and should be avoided, if possible.27 For patients withinsomnia, consider initially selecting a sedating antidepressant medication such as paroxetine or mirtazapine to augment sleep.
Alternatives to SSRIs. Nonselective serotonin reuptake inhibitors have similar efficacy as SSRIs. However, escitalopram is as effective as venlafaxine (a selective serotonin and norepinephrine reuptake inhibitor [SSNRI]) and is better tolerated.28 Duloxetine, another SSNRI, improves mood and often diminishes chronic pain.29 Mirtazapine, an alpha-2 antagonist, might cause fewer drug-drug interactions and is effective, well tolerated, and especially helpful for patients with anxiety or insomnia.30 Dry mouth, sedation, and weight gain are common adverse effects of mirtazapine. Obesity precautions are often necessary during mirtazapine therapy; this includes monitoring body weight and metabolic profiles, instituting dietary changes, and recommending an exercise regimen. In contrast to SSRIs, mirtazapine might induce less sexual dysfunction.31
Tricyclic antidepressant drugs can also be effective but may worsen cardiac conduction abnormalities, prostatic hypertrophy, or narrow angle glaucoma. Tricyclic antidepressants may be useful in patients without cardiac disease who have not responded to an SSRI or an SSNRI.
Continue to: The role of aripiprazole
The role of aripiprazole. Elderly patients not achieving remission from depression with antidepressant agents alone may benefit from co-prescribing aripiprazole.32 As an adjunct, aripiprazole is effective in achieving and sustaining remission
Minimize risks and maximize benefits of antidepressants by following these recommendations:
- Ascertain whether any antidepressant treatments have worked well in the past.
- Start with an SSRI if no other antidepressant treatment has worked in the past.
- Counsel patients about the need for treatment adherence. Antidepressants may take 2 weeks to 2 months to provide noticeable improvement.
- Prescribe up to the maximum drug dose if needed to enhance benefit.
- Use a mood measurement tool (eg, the Patient Health Questionnaire-9) to help evaluate treatment response.
Try a different class of drugs for patients who do not respond to treatment. For patients who have a partial response, augment with bupropion XL, mirtazapine, aripiprazole, or quetiapine.33 Sertraline and nortriptyline are similarly effective on a population-wide basis, with sertraline having less-problematic adverse effects.34 Trial-and-error treatments in practice may find one patient responding only to sertraline and another patient only to nortriptyline.
Combinations of different drug classes may provide benefit for patients not responding to a single antidepressant. In geriatric patients, combined treatment with methylphenidate and citalopram enhances mood and well-being.35 Compared with either drug alone, the combination yielded an augmented clinical response profile and a higher rate of remission. Cognitive functioning, energy, and mood improve even with methylphenidate alone, especially when fatigue is an issue. However, addictive properties limit its use to cases in which conventional antidepressant medications are not effective or indicated, and only when drug refills are closely monitored.
The challenges of advancing age. Antidepressant treatment needs increase with advanced age.36 As mentioned earlier, elderly people often have medical illnesses complicating their depression and frequently are dealing with pain from the medical illness. When dementia coexists with depression, the efficacy of pharmacotherapies is compromised.
Continue to: When drug-related interventions fail
When drug-related interventions fail, therapy ought to be more psychologically focused.37 Psychotherapy is usually helpful and is particularly indicated when recovery is suboptimal. Counseling might come from the treating physician or referral to a psychotherapist.
Nasal esketamine can be efficacious when supplementing antidepressant pharmacotherapy among older patients with treatment-resistant depression.38 Elderly individuals responding to antidepressants do not benefit from adjunctive donepezil to correct mild cognitive impairment.39 There is no advantage to off-label cholinesterase inhibitor prescribing for patients with both depression and dementia.
Other options. Electroconvulsive therapy (ECT) does not cause long-term cognitive problems and is reserved for treatment-resistant cases.40 Patients with depression who also have had previous cognitive impairment often improve in mental ability following ECT.41
A promising new option. Transcranial magnetic stimulation (TMS) is a promising, relatively new therapeutic option for treating refractory cases of depressive mood disorders. In TMS, an electromagnetic coil that creates a magnetic field is placed over the left dorsolateral prefrontal cortex (which is responsible for mood regulation). Referral for TMS administration may offer new hope for older patients with treatment-resistant depression.42
Keep comorbidities in mind as you address depression
Coexisting psychiatric illnesses worsen emotions. Geriatric patients are susceptible to psychiatric comorbidities that include substance abuse, obsessive-compulsive characteristics, dysfunctional eating, and panic disorder.19 Myocardial and cerebral infarctions are detrimental to mental health, especially soon after such events.43 Poststroke depression magnifies the risk for disability and mortality,16,17 yet antidepressant pharmacotherapy often enhances prognoses. Along with early intervention algorithm-based plans and inclusion of a depression care manager, antidepressants often diminish poststroke depression severity.44 Even when cancer is present, depression care reduces mortality.44 So with this in mind, persist with antidepressant treatment, which will often benefit an elderly individual with depression.
Continue to: When possible, get ahead of depression before it sets in
When possible, get ahead of depression before it sets in
Social participation and employment help to sustain an optimistic, euthymic mood.45 Maintaining good physical health, in part through consistent activity levels (including exercise), can help prevent depression. Since persistent sleep disturbance predicts depression among those with a depression history, optimizing sleep among geriatric adults can avoid or alleviate depression.46
Sleep hygiene education for patients is also helpful. A regular waking time often promotes a better sleeping schedule. Restful sleep also is more likely when an individual avoids excess caffeine, exercises during the day, and uses the bed only for sleeping (not for listening to music or watching television).
Because inflammation may precede depression, anti-inflammatory medications have been proposed as potential treatment, but such pharmacotherapies are often ineffective. Older adults generally do not benefit from low-dose aspirin administration to prevent depression.47 Low vitamin D levels can contribute to depression, yet vitamin D supplementation may not improve mood.48
Offering hope. Tell your patients that if they are feeling depressed, they should make an appointment with you, their primary care physician, because there are medications they can take and counseling they can avail themselves of that could help.
CORRESPONDENCE
Steven Lippmann, MD, University of Louisville-Psychiatry, 401 East Chestnut Street, Suite 610, Louisville, KY 40202; [email protected].
1. Steffens DC, Skoog I, Norton MC, et al. Prevalence of depression and its treatment in an elderly population: the Cache County study. Arch Gen Psych. 2000;57:601-607. doi: 10.1001/ archpsyc.57.6.601
2. Barry LC, Allore HG, Guo Z, et al. Higher burden of depression among older women: the effect of onset, persistence, and mortality over time. Arch Gen Psych. 2008;65:172-178. doi: 10.1001/archgenpsychiatry.2007.17
3. Katon WJ, Lin E, Russo J, et al. Increased medical costs of a population-based sample of depressed elderly patients. Arch Gen Psych. 2003;60:897-903. doi: 10.1001/archpsyc.60.9.897
4. Snow CE, Abrams RC. The indirect costs of late-life depression in the United States: a literature review and perspective. Geriatrics. 2016;1,30. doi.org/10.3390/geriatrics/1040030
5. George LK, Blazer DG, Hughes D, et al. Social support and the outcome of major depression. Br J Psych. 1989;154:478-485. doi: 10.1192/bjp.154.4.478
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10. Starkstein SE, Preziosi TJ, Bolduc PL, et al. Depression in Parkinson’s disease. J Nerv Ment Disord. 1990;178:27-31. doi: 10.1097/00005053-199001000-00005
11. Gilman SE, Abraham HE. A longitudinal study of the order of onset of alcohol dependence and major depression. Drug Alco Depend. 2001;63:277-286. doi: 10.1016/s0376-8716(00)00216-7
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17. Cai W, Mueller C, Li YJ, et al. Post stroke depression and risk of stroke recurrence and mortality: a systematic review and meta-analysis. Ageing Res Rev. 2019;50:102-109. doi: 10.1016/ j.arr.2019.01.013
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19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). 2013:160-168.
20. Pimontel MA, Rindskopf D, Rutherford BR, et al. A meta-analysis of executive dysfunction and antidepressant treatment response in late-life depression. Am J Geriatr Psych. 2016;24:31-34. doi: 10.1016/j.jagp.2015.05.010
21. Koenig HG, Cohen HJ, Blazer DG, et al. Religious coping and depression in elderly hospitalized medically ill men. Am J Psychiatry. 1992;149:1693-1700. doi: 10.1176/ajp.149.12.1693
22. Blake H, Mo P, Malik S, et al. How effective are physical activity interventions for alleviating depressive symptoms in older people? A systematic review. Clin Rehabil. 2009;10:873-887. doi: 10.1177/0269215509337449
23. Bruce ML, Ten Have TR, Reynolds CF, et al. Reducing suicidal and depressive symptoms in depressed older primary care patients: a randomized controlled trial. JAMA. 2004;291:1081-1091. doi: 10.1001/jama.291.9.1081
24. Pinquart M, Duberstein PR, Lyness JM. Treatments for later-life depressive conditions: a meta-analytic comparison of pharmacotherapy and psychotherapy. Am J Psychiatry. 2006;163:1493-1501. doi: 10.1176/ajp.2006.163.9.1493
25. Solai LK, Mulsant BH, Pollack BG. Selective serotonin reuptake inhibitors for late-life depression: a comparative review. Drugs Aging. 2001;18:355-368. doi: 10.2165/00002512-200118050-00006
26. Sanchez C, Reines EH, Montgomery SA. A comparative review of escitalopram, paroxetine, and sertraline. Are they all alike? Int Clin Psychopharmacol. 2014;29:185-196. doi: 10.1097/YIC.0000000000000023
27. Hedna K, Sundell KA, Hamidi A, et al. Antidepressants and suicidal behaviour in late life: a prospective population-based study of use patterns in new users aged 75 and above. Eur J Clin Pharmacol. 2018;74:201-208. doi: 10.1007/s00228-017-2360-x
28. Bielski RJ, Ventura D, Chang CC. A double-blind comparison of escitalopram and venlafaxine extended release in the treatment of major depressive disorder. J Clin Psychiatry. 2004;65:1190-1196. doi: 10.4088/jcp.v65n0906
29. Robinson M, Oakes TM, Raskin J, et al. Acute and long-term treatment of late-life major depressive disorder: duloxetine versus placebo. Am J Geriatr Psychiatry. 2014;22:34-45. doi: 10.1016/ j.jagp.2013.01.019
30. Holm KJ, Markham A. Mirtazapine: a review of its use in major depression. Drugs. 1999;57:607-631. doi: 10.2165/00003495-199957040-00010
31. Anttila SA, Leinonen EV. A review of the pharmacological and clinical profile of mirtazapine. CNS Drug Rev. 2001;7:249-264. doi: 10.1111/j.1527-3458.2001.tb00198.x
32. Lenze EJ, Mulsant BH, Blumberger DM, et al. Efficacy, safety and tolerability of augmentation pharmacotherapy with aripiprazole for treatment-resistant depression in late life: a randomised double-blind, placebo-controlled trial. Lancet. 2015;386:2404-2412. doi: 10.1016/S0140-6736(15)00308-6
33. Lenze EJ, Oughli HA. Antidepressant treatment for late-life depression: considering risks and benefits. J Am Geriatr Soc. 2019;67:1555-1556. doi: 10.1111/jgs.15964
34. Bondareff W, Alpert M, Friedhoff AJ, et al: Comparison of sertraline and nortriptyline in the treatment of major depressive disorder in late life. Am J Psychiatry. 2000;157:729-736. doi: 10.1176/appi.ajp.157.5.729
35. Lavretsky H, Reinlieb M, St Cyr N. Citalopram, methylphenidate, or their combination in geriatric depression: a randomized, double-blind, placebo controlled trial. Am J Psych. 2015;72:561-569. doi: 10.1176/appi.ajp.2014.14070889
36. Arthur A, Savva GM, Barnes LE, et al. Changing prevalence and treatment of depression among older people over two decades. Br J Psychiatry. 2020;21:49-54. doi: 10.1192/bjp.2019.193
37. Zuidersma M, Chua K-C, Hellier J, et al. Sertraline and mirtazapine versus placebo in subgroups of depression in dementia: findings from the HTA-SADD randomized controlled trial. Am J Geriatr Psychiatry. 2019;27:920-931. doi: 10.1016/ j.jagp.2019.03.021
38. Ochs-Ross R, Wajs E, Daly EJ, et al. Comparison of long-term efficacy and safety of esketamine nasal spray plus oral antidepressant in younger versus older patients with treatment-resistant depression: post-hoc analysis of SUSTAIN-2, a long-term open-label phase 3 safety and efficacy study. Am J Geriatr Psychiatry. 2022;30:541-556. doi: 10.1016/j.jagp.2021.09.014
39. Devanand DP, Pelton GH, D’Antonio K, et al. Donepezil treatment in patients with depression and cognitive impairment on stable antidepressant treatment: a randomized controlled trial. Am J Geriatr Psychiatry. 2018;26:1050-1060. doi: 10.1016/ j.jagp.2018.05.008
40. Obbels J, Vansteelandt K, Verwijk E, et al. MMSE changes during and after ECT in late life depression: a prospective study. Am J Geriatr Psychiatry. 2019;27:934-944. doi: 10.1016/ j.jagp.2019.04.006
41. Wagenmakers MJ, Vansteelandt K, van Exel E, et al. Transient cognitive impairment and white matter hyperintensities in severely depressed older patients treated with electroconvulsive therapy. Am J Geriatr Psychiatry. 2021:29:1117-1128. doi: 10.1016/j.jagp.2020.12.028
42. Trevizol AP, Goldberger KW, Mulsant BH, et al. Unilateral and bilateral repetitive transcranial magnetic stimulation for treatment-resistant late-life depression. Int J Ger Psychiatry. 2019;34:822-827. doi: 10.1002/gps.5091
43. Aben I, Verhey F, Stik J, et al. A comparative study into the one year cumulative incidence of depression after stroke and myocardial infarction. J Neurol Neurosurg Psychiatry. 2003;74:581-585. doi: 10.1136/jnnp.74.5.581
44. Gallo JJ, Bogner HR, Morales KH, et al. The effect of a primary care practice-based depression intervention on mortality in older adults: a randomized trial. Ann Intern Med. 2007;146:689-698. doi: 10.7326/0003-4819-146-10-200705150-00002
45. Lee J, Jang SN, Cho SL. Gender differences in the trajectories and the risk factors of depressive symptoms in later life. Int Psychogeriatr. 2017;29:1495-1505. doi: 10.1017/S1041610217000709
46. Lee E, Cho HJ, Olmstead R, et al. Persistent sleep disturbance: a risk factor for recurrent depression in community-dwelling older adults. Sleep. 2013;36:1685-1691. doi: 10.5665/sleep.3128
47. Berk M, Woods RL, Nelson MR, et al. Effect of aspirin vs placebo on the prevention of depression in older people: a randomized clinical trial. J Am Med A Psych. 2020;77:1012-1020. doi: 10.1001/jamapsychiatry.2020.1214
48. Okereke OI, Reynolds CF, Mischoulon D, et al. Effect of long-term vitamin D3 supplementation vs placebo on risk of depression or clinically relevant depressive symptoms and on change in mood scores: a randomized clinical trial. JAMA. 2020;324:471-480. doi: 10.1001/jama.2020.10224
Late-life depression is the onset of a major depressive disorder in an individual ≥ 60 years of age. Depressive illness compromises quality of life and is especially troublesome for older people. The prevalence of depression among individuals > 65 years of age is about 4% in women and 3% in men.1 The estimated lifetime prevalence is approximately 24% for women and 10% for men.2 Three factors account for this disparity: women exhibit greater susceptibility to depression; the illness persists longer in women than it does in men; and the probability of death related to depression is lower in women.2
Beyond its direct mental and emotional impacts, depression takes a financial toll; health care costs are higher for those with depression than for those without depression.3 Unpaid caregiver expense is the largest indirect financial burden with late-life depression.4 Additional indirect costs include less work productivity, early retirement, and diminished financial security.4
Many individuals with depression never receive treatment. Fortunately, there are many interventions in the primary care arsenal that can be used to treat older patients with depression and dramatically improve mood, comfort, and function.
The interactions of emotional and physical health
The pathophysiology of depression remains unclear. However, numerous factors are known to contribute to, exacerbate, or prolong depression among elderly populations. Insufficient social engagement and support is strongly associated with depressive mood.5 The loss of independence in giving up automobile driving can compromise self-confidence.6 Sleep difficulties predispose to, and predict, the emergence of a mood disorder, independent of other symptoms.7 Age-related hearing deficits also are associated with depression.8
There is a close relationship between emotional and physical health.9 Depression adds to the likelihood of medical illness, and somatic pathology increases the risk for mood disorders.9 Depression has been linked with obesity, frailty, diabetes, cognitive impairment, and terminal illness.9
Inflammatory markers and depression may also be related. Plasma levels of interleukin-6 and C-reactive protein were measured in a longitudinal aging study.14 A high level of interleukin-6, but not C-reactive protein, correlated with an increased prevalence of depression in older people.
Chronic cerebral ischemia can result in a “vascular depression”13 in which disruption of prefrontal systems by ischemic lesions is hypothesized to be an important factor in developing despair. Psychomotor retardation, executive dysfunction, severe disability, and a heightened risk for relapse are common features of vascular depression.15 Poststroke depression often follows a cerebrovascular episode16; the exact pathogenic mechanism is unknown.17
Continue to: A summation of common risk factors
A summation of common risk factors. A personal or family history of depression increases the risk for late-life depression. Other risk factors are female gender, bereavement, sleep disturbance, and disability.18 Poor general health, chronic pain, cognitive impairment, poor social support, and medical comorbidities with impaired functioning increase the likelihood of resultant mood disorders.18
Somatic complaints may overshadow diagnostic symptoms
Manifestations of depression include disturbed sleep and reductions in appetite, concentration, activity, and energy for daily function.19 These features, of course, may accompany medical disorders and some normal physiologic changes among elderly people. We find that while older individuals may report a sad mood, disturbed sleep, or other dysfunctions, they frequently emphasize their somatic complaints much more prominently than their emotions. This can make it difficult to recognize clinical depression.
For a diagnosis of major depression, 5 of the following 9 symptoms must be present for most of the day or nearly every day over a period of at least 2 weeks19: depressed mood; diminished interest in most activities; significant weight loss or decreased appetite; insomnia or hypersomnia; agitation or retardation; fatigue or loss of energy; feelings of worthlessness or guilt; diminished concentration; and recurrent thoughts of death or suicide.19
Planning difficulties, apathy, disability, and anhedonia frequently occur. Executive dysfunction and inefficacy of antidepressant pharmacotherapy are related to compromised frontal-striatal-limbic pathways.20 Since difficulties with planning and organization are associated with suboptimal response to antidepressant medications, a psychotherapeutic focus on these executive functions can augment drug-induced benefit.
Rule out these alternative diagnoses
Dementias can manifest as depression. Other brain pathologies, particularly Parkinson disease or stroke, also should be ruled out. Overmedication can simulate depression, so be sure to review the prescription and over-the-counter agents a patient is taking. Some medications can occasionally precipitate a clinical depression; these include stimulants, steroids, methyldopa, triptans, chemotherapeutic agents, and immunologic drugs, to name a few.19
Continue to: Pharmacotherapy, Yes, but first, consider these factors
Pharmacotherapy, Yes, but first, consider these factors
Maintaining a close patient–doctor relationship augments all therapeutic interventions. Good eye contact when listening to and counseling patients is key, as is providing close follow-up appointments.
Encourage social interactions with family and friends, which can be particularly productive. Encouraging spiritual endeavors, such as attendance at religious services, can be beneficial.21
Recommend exercise. Physical exercise yields positive outcomes22; it can enhance mood, improve sleep, and help to diminish anxiety. Encourage patients with depression to take a daily walk during the day; doing so can enhance emotional outlook, health, and even socialization.
What treatment will best serve your patient?
It’s important when caring for patients with depression to assess and address suicidal ideation. Depression with a previous suicide attempt is a strong risk factor for suicide. Inquire about suicidal intent or death wishes, access to guns, and other life-ending behaviors. Whenever suicide is an active issue, immediate crisis management is required. Psychiatric referral is an option, and hospitalization may be indicated. Advise family members to remove firearms or restrict access, be with the patient as much as possible, and assist at intervention planning and implementation.
It is worth mentioning, here, the connection between chronic pain and suicidal ideation. Pain management reduces suicidal ideation, regardless of depression severity.23
Continue to: Psychotherapy and pharmacotherapies...
Psychotherapy and pharmacotherapies offered for the treatment of depression in geriatric practices are both effective, without much difference seen in efficacy.24 Psychotherapy might include direct physician and family support to the patient or referral to a mental health professional. Base treatment choices on clinical access, patient preference, and medical contraindications and other illnesses.
Pros and cons of various pharmacotherapies
Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed first for elderly patients with depression.25 Escitalopram is often better tolerated than paroxetine, which exhibits muscarinic antagonism and enzyme inhibition of cytochrome P450-2D6.26 Escitalopram also has fewer pharmaceutical interactions compared with sertraline.26
Generally, when prescribing an antidepressant drug, stay with the initial choice, gradually increasing the dose as clinically needed to its maximum limit. Suicidal ideation may be worsened by too quickly switching from one antidepressant to another or by co-prescribing anxiolytic or hypnotic medicines. Benzodiazepines have addictive and disinhibiting properties and should be avoided, if possible.27 For patients withinsomnia, consider initially selecting a sedating antidepressant medication such as paroxetine or mirtazapine to augment sleep.
Alternatives to SSRIs. Nonselective serotonin reuptake inhibitors have similar efficacy as SSRIs. However, escitalopram is as effective as venlafaxine (a selective serotonin and norepinephrine reuptake inhibitor [SSNRI]) and is better tolerated.28 Duloxetine, another SSNRI, improves mood and often diminishes chronic pain.29 Mirtazapine, an alpha-2 antagonist, might cause fewer drug-drug interactions and is effective, well tolerated, and especially helpful for patients with anxiety or insomnia.30 Dry mouth, sedation, and weight gain are common adverse effects of mirtazapine. Obesity precautions are often necessary during mirtazapine therapy; this includes monitoring body weight and metabolic profiles, instituting dietary changes, and recommending an exercise regimen. In contrast to SSRIs, mirtazapine might induce less sexual dysfunction.31
Tricyclic antidepressant drugs can also be effective but may worsen cardiac conduction abnormalities, prostatic hypertrophy, or narrow angle glaucoma. Tricyclic antidepressants may be useful in patients without cardiac disease who have not responded to an SSRI or an SSNRI.
Continue to: The role of aripiprazole
The role of aripiprazole. Elderly patients not achieving remission from depression with antidepressant agents alone may benefit from co-prescribing aripiprazole.32 As an adjunct, aripiprazole is effective in achieving and sustaining remission
Minimize risks and maximize benefits of antidepressants by following these recommendations:
- Ascertain whether any antidepressant treatments have worked well in the past.
- Start with an SSRI if no other antidepressant treatment has worked in the past.
- Counsel patients about the need for treatment adherence. Antidepressants may take 2 weeks to 2 months to provide noticeable improvement.
- Prescribe up to the maximum drug dose if needed to enhance benefit.
- Use a mood measurement tool (eg, the Patient Health Questionnaire-9) to help evaluate treatment response.
Try a different class of drugs for patients who do not respond to treatment. For patients who have a partial response, augment with bupropion XL, mirtazapine, aripiprazole, or quetiapine.33 Sertraline and nortriptyline are similarly effective on a population-wide basis, with sertraline having less-problematic adverse effects.34 Trial-and-error treatments in practice may find one patient responding only to sertraline and another patient only to nortriptyline.
Combinations of different drug classes may provide benefit for patients not responding to a single antidepressant. In geriatric patients, combined treatment with methylphenidate and citalopram enhances mood and well-being.35 Compared with either drug alone, the combination yielded an augmented clinical response profile and a higher rate of remission. Cognitive functioning, energy, and mood improve even with methylphenidate alone, especially when fatigue is an issue. However, addictive properties limit its use to cases in which conventional antidepressant medications are not effective or indicated, and only when drug refills are closely monitored.
The challenges of advancing age. Antidepressant treatment needs increase with advanced age.36 As mentioned earlier, elderly people often have medical illnesses complicating their depression and frequently are dealing with pain from the medical illness. When dementia coexists with depression, the efficacy of pharmacotherapies is compromised.
Continue to: When drug-related interventions fail
When drug-related interventions fail, therapy ought to be more psychologically focused.37 Psychotherapy is usually helpful and is particularly indicated when recovery is suboptimal. Counseling might come from the treating physician or referral to a psychotherapist.
Nasal esketamine can be efficacious when supplementing antidepressant pharmacotherapy among older patients with treatment-resistant depression.38 Elderly individuals responding to antidepressants do not benefit from adjunctive donepezil to correct mild cognitive impairment.39 There is no advantage to off-label cholinesterase inhibitor prescribing for patients with both depression and dementia.
Other options. Electroconvulsive therapy (ECT) does not cause long-term cognitive problems and is reserved for treatment-resistant cases.40 Patients with depression who also have had previous cognitive impairment often improve in mental ability following ECT.41
A promising new option. Transcranial magnetic stimulation (TMS) is a promising, relatively new therapeutic option for treating refractory cases of depressive mood disorders. In TMS, an electromagnetic coil that creates a magnetic field is placed over the left dorsolateral prefrontal cortex (which is responsible for mood regulation). Referral for TMS administration may offer new hope for older patients with treatment-resistant depression.42
Keep comorbidities in mind as you address depression
Coexisting psychiatric illnesses worsen emotions. Geriatric patients are susceptible to psychiatric comorbidities that include substance abuse, obsessive-compulsive characteristics, dysfunctional eating, and panic disorder.19 Myocardial and cerebral infarctions are detrimental to mental health, especially soon after such events.43 Poststroke depression magnifies the risk for disability and mortality,16,17 yet antidepressant pharmacotherapy often enhances prognoses. Along with early intervention algorithm-based plans and inclusion of a depression care manager, antidepressants often diminish poststroke depression severity.44 Even when cancer is present, depression care reduces mortality.44 So with this in mind, persist with antidepressant treatment, which will often benefit an elderly individual with depression.
Continue to: When possible, get ahead of depression before it sets in
When possible, get ahead of depression before it sets in
Social participation and employment help to sustain an optimistic, euthymic mood.45 Maintaining good physical health, in part through consistent activity levels (including exercise), can help prevent depression. Since persistent sleep disturbance predicts depression among those with a depression history, optimizing sleep among geriatric adults can avoid or alleviate depression.46
Sleep hygiene education for patients is also helpful. A regular waking time often promotes a better sleeping schedule. Restful sleep also is more likely when an individual avoids excess caffeine, exercises during the day, and uses the bed only for sleeping (not for listening to music or watching television).
Because inflammation may precede depression, anti-inflammatory medications have been proposed as potential treatment, but such pharmacotherapies are often ineffective. Older adults generally do not benefit from low-dose aspirin administration to prevent depression.47 Low vitamin D levels can contribute to depression, yet vitamin D supplementation may not improve mood.48
Offering hope. Tell your patients that if they are feeling depressed, they should make an appointment with you, their primary care physician, because there are medications they can take and counseling they can avail themselves of that could help.
CORRESPONDENCE
Steven Lippmann, MD, University of Louisville-Psychiatry, 401 East Chestnut Street, Suite 610, Louisville, KY 40202; [email protected].
Late-life depression is the onset of a major depressive disorder in an individual ≥ 60 years of age. Depressive illness compromises quality of life and is especially troublesome for older people. The prevalence of depression among individuals > 65 years of age is about 4% in women and 3% in men.1 The estimated lifetime prevalence is approximately 24% for women and 10% for men.2 Three factors account for this disparity: women exhibit greater susceptibility to depression; the illness persists longer in women than it does in men; and the probability of death related to depression is lower in women.2
Beyond its direct mental and emotional impacts, depression takes a financial toll; health care costs are higher for those with depression than for those without depression.3 Unpaid caregiver expense is the largest indirect financial burden with late-life depression.4 Additional indirect costs include less work productivity, early retirement, and diminished financial security.4
Many individuals with depression never receive treatment. Fortunately, there are many interventions in the primary care arsenal that can be used to treat older patients with depression and dramatically improve mood, comfort, and function.
The interactions of emotional and physical health
The pathophysiology of depression remains unclear. However, numerous factors are known to contribute to, exacerbate, or prolong depression among elderly populations. Insufficient social engagement and support is strongly associated with depressive mood.5 The loss of independence in giving up automobile driving can compromise self-confidence.6 Sleep difficulties predispose to, and predict, the emergence of a mood disorder, independent of other symptoms.7 Age-related hearing deficits also are associated with depression.8
There is a close relationship between emotional and physical health.9 Depression adds to the likelihood of medical illness, and somatic pathology increases the risk for mood disorders.9 Depression has been linked with obesity, frailty, diabetes, cognitive impairment, and terminal illness.9
Inflammatory markers and depression may also be related. Plasma levels of interleukin-6 and C-reactive protein were measured in a longitudinal aging study.14 A high level of interleukin-6, but not C-reactive protein, correlated with an increased prevalence of depression in older people.
Chronic cerebral ischemia can result in a “vascular depression”13 in which disruption of prefrontal systems by ischemic lesions is hypothesized to be an important factor in developing despair. Psychomotor retardation, executive dysfunction, severe disability, and a heightened risk for relapse are common features of vascular depression.15 Poststroke depression often follows a cerebrovascular episode16; the exact pathogenic mechanism is unknown.17
Continue to: A summation of common risk factors
A summation of common risk factors. A personal or family history of depression increases the risk for late-life depression. Other risk factors are female gender, bereavement, sleep disturbance, and disability.18 Poor general health, chronic pain, cognitive impairment, poor social support, and medical comorbidities with impaired functioning increase the likelihood of resultant mood disorders.18
Somatic complaints may overshadow diagnostic symptoms
Manifestations of depression include disturbed sleep and reductions in appetite, concentration, activity, and energy for daily function.19 These features, of course, may accompany medical disorders and some normal physiologic changes among elderly people. We find that while older individuals may report a sad mood, disturbed sleep, or other dysfunctions, they frequently emphasize their somatic complaints much more prominently than their emotions. This can make it difficult to recognize clinical depression.
For a diagnosis of major depression, 5 of the following 9 symptoms must be present for most of the day or nearly every day over a period of at least 2 weeks19: depressed mood; diminished interest in most activities; significant weight loss or decreased appetite; insomnia or hypersomnia; agitation or retardation; fatigue or loss of energy; feelings of worthlessness or guilt; diminished concentration; and recurrent thoughts of death or suicide.19
Planning difficulties, apathy, disability, and anhedonia frequently occur. Executive dysfunction and inefficacy of antidepressant pharmacotherapy are related to compromised frontal-striatal-limbic pathways.20 Since difficulties with planning and organization are associated with suboptimal response to antidepressant medications, a psychotherapeutic focus on these executive functions can augment drug-induced benefit.
Rule out these alternative diagnoses
Dementias can manifest as depression. Other brain pathologies, particularly Parkinson disease or stroke, also should be ruled out. Overmedication can simulate depression, so be sure to review the prescription and over-the-counter agents a patient is taking. Some medications can occasionally precipitate a clinical depression; these include stimulants, steroids, methyldopa, triptans, chemotherapeutic agents, and immunologic drugs, to name a few.19
Continue to: Pharmacotherapy, Yes, but first, consider these factors
Pharmacotherapy, Yes, but first, consider these factors
Maintaining a close patient–doctor relationship augments all therapeutic interventions. Good eye contact when listening to and counseling patients is key, as is providing close follow-up appointments.
Encourage social interactions with family and friends, which can be particularly productive. Encouraging spiritual endeavors, such as attendance at religious services, can be beneficial.21
Recommend exercise. Physical exercise yields positive outcomes22; it can enhance mood, improve sleep, and help to diminish anxiety. Encourage patients with depression to take a daily walk during the day; doing so can enhance emotional outlook, health, and even socialization.
What treatment will best serve your patient?
It’s important when caring for patients with depression to assess and address suicidal ideation. Depression with a previous suicide attempt is a strong risk factor for suicide. Inquire about suicidal intent or death wishes, access to guns, and other life-ending behaviors. Whenever suicide is an active issue, immediate crisis management is required. Psychiatric referral is an option, and hospitalization may be indicated. Advise family members to remove firearms or restrict access, be with the patient as much as possible, and assist at intervention planning and implementation.
It is worth mentioning, here, the connection between chronic pain and suicidal ideation. Pain management reduces suicidal ideation, regardless of depression severity.23
Continue to: Psychotherapy and pharmacotherapies...
Psychotherapy and pharmacotherapies offered for the treatment of depression in geriatric practices are both effective, without much difference seen in efficacy.24 Psychotherapy might include direct physician and family support to the patient or referral to a mental health professional. Base treatment choices on clinical access, patient preference, and medical contraindications and other illnesses.
Pros and cons of various pharmacotherapies
Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed first for elderly patients with depression.25 Escitalopram is often better tolerated than paroxetine, which exhibits muscarinic antagonism and enzyme inhibition of cytochrome P450-2D6.26 Escitalopram also has fewer pharmaceutical interactions compared with sertraline.26
Generally, when prescribing an antidepressant drug, stay with the initial choice, gradually increasing the dose as clinically needed to its maximum limit. Suicidal ideation may be worsened by too quickly switching from one antidepressant to another or by co-prescribing anxiolytic or hypnotic medicines. Benzodiazepines have addictive and disinhibiting properties and should be avoided, if possible.27 For patients withinsomnia, consider initially selecting a sedating antidepressant medication such as paroxetine or mirtazapine to augment sleep.
Alternatives to SSRIs. Nonselective serotonin reuptake inhibitors have similar efficacy as SSRIs. However, escitalopram is as effective as venlafaxine (a selective serotonin and norepinephrine reuptake inhibitor [SSNRI]) and is better tolerated.28 Duloxetine, another SSNRI, improves mood and often diminishes chronic pain.29 Mirtazapine, an alpha-2 antagonist, might cause fewer drug-drug interactions and is effective, well tolerated, and especially helpful for patients with anxiety or insomnia.30 Dry mouth, sedation, and weight gain are common adverse effects of mirtazapine. Obesity precautions are often necessary during mirtazapine therapy; this includes monitoring body weight and metabolic profiles, instituting dietary changes, and recommending an exercise regimen. In contrast to SSRIs, mirtazapine might induce less sexual dysfunction.31
Tricyclic antidepressant drugs can also be effective but may worsen cardiac conduction abnormalities, prostatic hypertrophy, or narrow angle glaucoma. Tricyclic antidepressants may be useful in patients without cardiac disease who have not responded to an SSRI or an SSNRI.
Continue to: The role of aripiprazole
The role of aripiprazole. Elderly patients not achieving remission from depression with antidepressant agents alone may benefit from co-prescribing aripiprazole.32 As an adjunct, aripiprazole is effective in achieving and sustaining remission
Minimize risks and maximize benefits of antidepressants by following these recommendations:
- Ascertain whether any antidepressant treatments have worked well in the past.
- Start with an SSRI if no other antidepressant treatment has worked in the past.
- Counsel patients about the need for treatment adherence. Antidepressants may take 2 weeks to 2 months to provide noticeable improvement.
- Prescribe up to the maximum drug dose if needed to enhance benefit.
- Use a mood measurement tool (eg, the Patient Health Questionnaire-9) to help evaluate treatment response.
Try a different class of drugs for patients who do not respond to treatment. For patients who have a partial response, augment with bupropion XL, mirtazapine, aripiprazole, or quetiapine.33 Sertraline and nortriptyline are similarly effective on a population-wide basis, with sertraline having less-problematic adverse effects.34 Trial-and-error treatments in practice may find one patient responding only to sertraline and another patient only to nortriptyline.
Combinations of different drug classes may provide benefit for patients not responding to a single antidepressant. In geriatric patients, combined treatment with methylphenidate and citalopram enhances mood and well-being.35 Compared with either drug alone, the combination yielded an augmented clinical response profile and a higher rate of remission. Cognitive functioning, energy, and mood improve even with methylphenidate alone, especially when fatigue is an issue. However, addictive properties limit its use to cases in which conventional antidepressant medications are not effective or indicated, and only when drug refills are closely monitored.
The challenges of advancing age. Antidepressant treatment needs increase with advanced age.36 As mentioned earlier, elderly people often have medical illnesses complicating their depression and frequently are dealing with pain from the medical illness. When dementia coexists with depression, the efficacy of pharmacotherapies is compromised.
Continue to: When drug-related interventions fail
When drug-related interventions fail, therapy ought to be more psychologically focused.37 Psychotherapy is usually helpful and is particularly indicated when recovery is suboptimal. Counseling might come from the treating physician or referral to a psychotherapist.
Nasal esketamine can be efficacious when supplementing antidepressant pharmacotherapy among older patients with treatment-resistant depression.38 Elderly individuals responding to antidepressants do not benefit from adjunctive donepezil to correct mild cognitive impairment.39 There is no advantage to off-label cholinesterase inhibitor prescribing for patients with both depression and dementia.
Other options. Electroconvulsive therapy (ECT) does not cause long-term cognitive problems and is reserved for treatment-resistant cases.40 Patients with depression who also have had previous cognitive impairment often improve in mental ability following ECT.41
A promising new option. Transcranial magnetic stimulation (TMS) is a promising, relatively new therapeutic option for treating refractory cases of depressive mood disorders. In TMS, an electromagnetic coil that creates a magnetic field is placed over the left dorsolateral prefrontal cortex (which is responsible for mood regulation). Referral for TMS administration may offer new hope for older patients with treatment-resistant depression.42
Keep comorbidities in mind as you address depression
Coexisting psychiatric illnesses worsen emotions. Geriatric patients are susceptible to psychiatric comorbidities that include substance abuse, obsessive-compulsive characteristics, dysfunctional eating, and panic disorder.19 Myocardial and cerebral infarctions are detrimental to mental health, especially soon after such events.43 Poststroke depression magnifies the risk for disability and mortality,16,17 yet antidepressant pharmacotherapy often enhances prognoses. Along with early intervention algorithm-based plans and inclusion of a depression care manager, antidepressants often diminish poststroke depression severity.44 Even when cancer is present, depression care reduces mortality.44 So with this in mind, persist with antidepressant treatment, which will often benefit an elderly individual with depression.
Continue to: When possible, get ahead of depression before it sets in
When possible, get ahead of depression before it sets in
Social participation and employment help to sustain an optimistic, euthymic mood.45 Maintaining good physical health, in part through consistent activity levels (including exercise), can help prevent depression. Since persistent sleep disturbance predicts depression among those with a depression history, optimizing sleep among geriatric adults can avoid or alleviate depression.46
Sleep hygiene education for patients is also helpful. A regular waking time often promotes a better sleeping schedule. Restful sleep also is more likely when an individual avoids excess caffeine, exercises during the day, and uses the bed only for sleeping (not for listening to music or watching television).
Because inflammation may precede depression, anti-inflammatory medications have been proposed as potential treatment, but such pharmacotherapies are often ineffective. Older adults generally do not benefit from low-dose aspirin administration to prevent depression.47 Low vitamin D levels can contribute to depression, yet vitamin D supplementation may not improve mood.48
Offering hope. Tell your patients that if they are feeling depressed, they should make an appointment with you, their primary care physician, because there are medications they can take and counseling they can avail themselves of that could help.
CORRESPONDENCE
Steven Lippmann, MD, University of Louisville-Psychiatry, 401 East Chestnut Street, Suite 610, Louisville, KY 40202; [email protected].
1. Steffens DC, Skoog I, Norton MC, et al. Prevalence of depression and its treatment in an elderly population: the Cache County study. Arch Gen Psych. 2000;57:601-607. doi: 10.1001/ archpsyc.57.6.601
2. Barry LC, Allore HG, Guo Z, et al. Higher burden of depression among older women: the effect of onset, persistence, and mortality over time. Arch Gen Psych. 2008;65:172-178. doi: 10.1001/archgenpsychiatry.2007.17
3. Katon WJ, Lin E, Russo J, et al. Increased medical costs of a population-based sample of depressed elderly patients. Arch Gen Psych. 2003;60:897-903. doi: 10.1001/archpsyc.60.9.897
4. Snow CE, Abrams RC. The indirect costs of late-life depression in the United States: a literature review and perspective. Geriatrics. 2016;1,30. doi.org/10.3390/geriatrics/1040030
5. George LK, Blazer DG, Hughes D, et al. Social support and the outcome of major depression. Br J Psych. 1989;154:478-485. doi: 10.1192/bjp.154.4.478
6. Fonda SJ, Wallace RB, Herzog AR. Changes in driving patterns and worsening depressive symptoms among older adults. J Gerontol Psychol Soc Sci. 2001;56:S343-S351. doi: 10.1093/geronb/56.6.s343
7. Cho HJ, Lavretsky H, Olmstead R, et al. Sleep disturbance and depression recurrence in community dwelling older adults—a prospective study. Am J Psych. 2008;165:1543-1550. doi: 10.1176/appi.ajp.2008.07121882
8. Golub JS, Brewster KK, Brickman AM, et al. Subclinical hearing loss is associated with depressive symptoms. Am J Geriatr Psychiatry. 2020;28:545-556. doi: 10.1016/j.jagp.2019.12.008
9. Alexopoulos GS. Mechanisms and treatment of late-life depression. Focus (Am Psychiatr Publ). 2021;19:340-354. doi: 10.1176/appi.focus.19304
10. Starkstein SE, Preziosi TJ, Bolduc PL, et al. Depression in Parkinson’s disease. J Nerv Ment Disord. 1990;178:27-31. doi: 10.1097/00005053-199001000-00005
11. Gilman SE, Abraham HE. A longitudinal study of the order of onset of alcohol dependence and major depression. Drug Alco Depend. 2001;63:277-286. doi: 10.1016/s0376-8716(00)00216-7
12. Parmelee PA, Katz IR, Lawton MP. The relation of pain to depression among institutionalized aged. J Gerontol. 1991;46:P15-P21. doi: 10.1093/geronj/46.1.p15
13. Alexopoulos GS, Meyers BS, Young RC, et al. ‘Vascular depression’ hypothesis. Arch Gen Psych. 1997;54:915-922. doi: 10.1001/archpsyc.1997.01830220033006
14. Bremmer MA, Beekman AT, Deeg DJ, et al. Inflammatory markers in late-life depression: results from a population-based study. J Affect Disord. 2008;106:249-255. doi: 10.1016/j.jad.2007.07.002
15. Taylor WD, Aizenstein HJ, Alexopoulos GS. The vascular depression hypothesis: mechanisms linking vascular disease with depression. Mol Psych. 2013;18:963-974. doi: 10.1038/mp.2013.20
16. Robinson RG, Jorge RE. Post-stroke depression: a review. Am J Psych. 2016;173:221-231. doi: 10.1176/appi.ajp.2015.15030363
17. Cai W, Mueller C, Li YJ, et al. Post stroke depression and risk of stroke recurrence and mortality: a systematic review and meta-analysis. Ageing Res Rev. 2019;50:102-109. doi: 10.1016/ j.arr.2019.01.013
18. Cole MG, Dendukuri N. Risk factors for depression among elderly community subjects: a systematic review and meta-analysis. Am J Psych. 2003;160:1147-1156. doi: 10.1176/appi.ajp.160.6.1147
19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). 2013:160-168.
20. Pimontel MA, Rindskopf D, Rutherford BR, et al. A meta-analysis of executive dysfunction and antidepressant treatment response in late-life depression. Am J Geriatr Psych. 2016;24:31-34. doi: 10.1016/j.jagp.2015.05.010
21. Koenig HG, Cohen HJ, Blazer DG, et al. Religious coping and depression in elderly hospitalized medically ill men. Am J Psychiatry. 1992;149:1693-1700. doi: 10.1176/ajp.149.12.1693
22. Blake H, Mo P, Malik S, et al. How effective are physical activity interventions for alleviating depressive symptoms in older people? A systematic review. Clin Rehabil. 2009;10:873-887. doi: 10.1177/0269215509337449
23. Bruce ML, Ten Have TR, Reynolds CF, et al. Reducing suicidal and depressive symptoms in depressed older primary care patients: a randomized controlled trial. JAMA. 2004;291:1081-1091. doi: 10.1001/jama.291.9.1081
24. Pinquart M, Duberstein PR, Lyness JM. Treatments for later-life depressive conditions: a meta-analytic comparison of pharmacotherapy and psychotherapy. Am J Psychiatry. 2006;163:1493-1501. doi: 10.1176/ajp.2006.163.9.1493
25. Solai LK, Mulsant BH, Pollack BG. Selective serotonin reuptake inhibitors for late-life depression: a comparative review. Drugs Aging. 2001;18:355-368. doi: 10.2165/00002512-200118050-00006
26. Sanchez C, Reines EH, Montgomery SA. A comparative review of escitalopram, paroxetine, and sertraline. Are they all alike? Int Clin Psychopharmacol. 2014;29:185-196. doi: 10.1097/YIC.0000000000000023
27. Hedna K, Sundell KA, Hamidi A, et al. Antidepressants and suicidal behaviour in late life: a prospective population-based study of use patterns in new users aged 75 and above. Eur J Clin Pharmacol. 2018;74:201-208. doi: 10.1007/s00228-017-2360-x
28. Bielski RJ, Ventura D, Chang CC. A double-blind comparison of escitalopram and venlafaxine extended release in the treatment of major depressive disorder. J Clin Psychiatry. 2004;65:1190-1196. doi: 10.4088/jcp.v65n0906
29. Robinson M, Oakes TM, Raskin J, et al. Acute and long-term treatment of late-life major depressive disorder: duloxetine versus placebo. Am J Geriatr Psychiatry. 2014;22:34-45. doi: 10.1016/ j.jagp.2013.01.019
30. Holm KJ, Markham A. Mirtazapine: a review of its use in major depression. Drugs. 1999;57:607-631. doi: 10.2165/00003495-199957040-00010
31. Anttila SA, Leinonen EV. A review of the pharmacological and clinical profile of mirtazapine. CNS Drug Rev. 2001;7:249-264. doi: 10.1111/j.1527-3458.2001.tb00198.x
32. Lenze EJ, Mulsant BH, Blumberger DM, et al. Efficacy, safety and tolerability of augmentation pharmacotherapy with aripiprazole for treatment-resistant depression in late life: a randomised double-blind, placebo-controlled trial. Lancet. 2015;386:2404-2412. doi: 10.1016/S0140-6736(15)00308-6
33. Lenze EJ, Oughli HA. Antidepressant treatment for late-life depression: considering risks and benefits. J Am Geriatr Soc. 2019;67:1555-1556. doi: 10.1111/jgs.15964
34. Bondareff W, Alpert M, Friedhoff AJ, et al: Comparison of sertraline and nortriptyline in the treatment of major depressive disorder in late life. Am J Psychiatry. 2000;157:729-736. doi: 10.1176/appi.ajp.157.5.729
35. Lavretsky H, Reinlieb M, St Cyr N. Citalopram, methylphenidate, or their combination in geriatric depression: a randomized, double-blind, placebo controlled trial. Am J Psych. 2015;72:561-569. doi: 10.1176/appi.ajp.2014.14070889
36. Arthur A, Savva GM, Barnes LE, et al. Changing prevalence and treatment of depression among older people over two decades. Br J Psychiatry. 2020;21:49-54. doi: 10.1192/bjp.2019.193
37. Zuidersma M, Chua K-C, Hellier J, et al. Sertraline and mirtazapine versus placebo in subgroups of depression in dementia: findings from the HTA-SADD randomized controlled trial. Am J Geriatr Psychiatry. 2019;27:920-931. doi: 10.1016/ j.jagp.2019.03.021
38. Ochs-Ross R, Wajs E, Daly EJ, et al. Comparison of long-term efficacy and safety of esketamine nasal spray plus oral antidepressant in younger versus older patients with treatment-resistant depression: post-hoc analysis of SUSTAIN-2, a long-term open-label phase 3 safety and efficacy study. Am J Geriatr Psychiatry. 2022;30:541-556. doi: 10.1016/j.jagp.2021.09.014
39. Devanand DP, Pelton GH, D’Antonio K, et al. Donepezil treatment in patients with depression and cognitive impairment on stable antidepressant treatment: a randomized controlled trial. Am J Geriatr Psychiatry. 2018;26:1050-1060. doi: 10.1016/ j.jagp.2018.05.008
40. Obbels J, Vansteelandt K, Verwijk E, et al. MMSE changes during and after ECT in late life depression: a prospective study. Am J Geriatr Psychiatry. 2019;27:934-944. doi: 10.1016/ j.jagp.2019.04.006
41. Wagenmakers MJ, Vansteelandt K, van Exel E, et al. Transient cognitive impairment and white matter hyperintensities in severely depressed older patients treated with electroconvulsive therapy. Am J Geriatr Psychiatry. 2021:29:1117-1128. doi: 10.1016/j.jagp.2020.12.028
42. Trevizol AP, Goldberger KW, Mulsant BH, et al. Unilateral and bilateral repetitive transcranial magnetic stimulation for treatment-resistant late-life depression. Int J Ger Psychiatry. 2019;34:822-827. doi: 10.1002/gps.5091
43. Aben I, Verhey F, Stik J, et al. A comparative study into the one year cumulative incidence of depression after stroke and myocardial infarction. J Neurol Neurosurg Psychiatry. 2003;74:581-585. doi: 10.1136/jnnp.74.5.581
44. Gallo JJ, Bogner HR, Morales KH, et al. The effect of a primary care practice-based depression intervention on mortality in older adults: a randomized trial. Ann Intern Med. 2007;146:689-698. doi: 10.7326/0003-4819-146-10-200705150-00002
45. Lee J, Jang SN, Cho SL. Gender differences in the trajectories and the risk factors of depressive symptoms in later life. Int Psychogeriatr. 2017;29:1495-1505. doi: 10.1017/S1041610217000709
46. Lee E, Cho HJ, Olmstead R, et al. Persistent sleep disturbance: a risk factor for recurrent depression in community-dwelling older adults. Sleep. 2013;36:1685-1691. doi: 10.5665/sleep.3128
47. Berk M, Woods RL, Nelson MR, et al. Effect of aspirin vs placebo on the prevention of depression in older people: a randomized clinical trial. J Am Med A Psych. 2020;77:1012-1020. doi: 10.1001/jamapsychiatry.2020.1214
48. Okereke OI, Reynolds CF, Mischoulon D, et al. Effect of long-term vitamin D3 supplementation vs placebo on risk of depression or clinically relevant depressive symptoms and on change in mood scores: a randomized clinical trial. JAMA. 2020;324:471-480. doi: 10.1001/jama.2020.10224
1. Steffens DC, Skoog I, Norton MC, et al. Prevalence of depression and its treatment in an elderly population: the Cache County study. Arch Gen Psych. 2000;57:601-607. doi: 10.1001/ archpsyc.57.6.601
2. Barry LC, Allore HG, Guo Z, et al. Higher burden of depression among older women: the effect of onset, persistence, and mortality over time. Arch Gen Psych. 2008;65:172-178. doi: 10.1001/archgenpsychiatry.2007.17
3. Katon WJ, Lin E, Russo J, et al. Increased medical costs of a population-based sample of depressed elderly patients. Arch Gen Psych. 2003;60:897-903. doi: 10.1001/archpsyc.60.9.897
4. Snow CE, Abrams RC. The indirect costs of late-life depression in the United States: a literature review and perspective. Geriatrics. 2016;1,30. doi.org/10.3390/geriatrics/1040030
5. George LK, Blazer DG, Hughes D, et al. Social support and the outcome of major depression. Br J Psych. 1989;154:478-485. doi: 10.1192/bjp.154.4.478
6. Fonda SJ, Wallace RB, Herzog AR. Changes in driving patterns and worsening depressive symptoms among older adults. J Gerontol Psychol Soc Sci. 2001;56:S343-S351. doi: 10.1093/geronb/56.6.s343
7. Cho HJ, Lavretsky H, Olmstead R, et al. Sleep disturbance and depression recurrence in community dwelling older adults—a prospective study. Am J Psych. 2008;165:1543-1550. doi: 10.1176/appi.ajp.2008.07121882
8. Golub JS, Brewster KK, Brickman AM, et al. Subclinical hearing loss is associated with depressive symptoms. Am J Geriatr Psychiatry. 2020;28:545-556. doi: 10.1016/j.jagp.2019.12.008
9. Alexopoulos GS. Mechanisms and treatment of late-life depression. Focus (Am Psychiatr Publ). 2021;19:340-354. doi: 10.1176/appi.focus.19304
10. Starkstein SE, Preziosi TJ, Bolduc PL, et al. Depression in Parkinson’s disease. J Nerv Ment Disord. 1990;178:27-31. doi: 10.1097/00005053-199001000-00005
11. Gilman SE, Abraham HE. A longitudinal study of the order of onset of alcohol dependence and major depression. Drug Alco Depend. 2001;63:277-286. doi: 10.1016/s0376-8716(00)00216-7
12. Parmelee PA, Katz IR, Lawton MP. The relation of pain to depression among institutionalized aged. J Gerontol. 1991;46:P15-P21. doi: 10.1093/geronj/46.1.p15
13. Alexopoulos GS, Meyers BS, Young RC, et al. ‘Vascular depression’ hypothesis. Arch Gen Psych. 1997;54:915-922. doi: 10.1001/archpsyc.1997.01830220033006
14. Bremmer MA, Beekman AT, Deeg DJ, et al. Inflammatory markers in late-life depression: results from a population-based study. J Affect Disord. 2008;106:249-255. doi: 10.1016/j.jad.2007.07.002
15. Taylor WD, Aizenstein HJ, Alexopoulos GS. The vascular depression hypothesis: mechanisms linking vascular disease with depression. Mol Psych. 2013;18:963-974. doi: 10.1038/mp.2013.20
16. Robinson RG, Jorge RE. Post-stroke depression: a review. Am J Psych. 2016;173:221-231. doi: 10.1176/appi.ajp.2015.15030363
17. Cai W, Mueller C, Li YJ, et al. Post stroke depression and risk of stroke recurrence and mortality: a systematic review and meta-analysis. Ageing Res Rev. 2019;50:102-109. doi: 10.1016/ j.arr.2019.01.013
18. Cole MG, Dendukuri N. Risk factors for depression among elderly community subjects: a systematic review and meta-analysis. Am J Psych. 2003;160:1147-1156. doi: 10.1176/appi.ajp.160.6.1147
19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). 2013:160-168.
20. Pimontel MA, Rindskopf D, Rutherford BR, et al. A meta-analysis of executive dysfunction and antidepressant treatment response in late-life depression. Am J Geriatr Psych. 2016;24:31-34. doi: 10.1016/j.jagp.2015.05.010
21. Koenig HG, Cohen HJ, Blazer DG, et al. Religious coping and depression in elderly hospitalized medically ill men. Am J Psychiatry. 1992;149:1693-1700. doi: 10.1176/ajp.149.12.1693
22. Blake H, Mo P, Malik S, et al. How effective are physical activity interventions for alleviating depressive symptoms in older people? A systematic review. Clin Rehabil. 2009;10:873-887. doi: 10.1177/0269215509337449
23. Bruce ML, Ten Have TR, Reynolds CF, et al. Reducing suicidal and depressive symptoms in depressed older primary care patients: a randomized controlled trial. JAMA. 2004;291:1081-1091. doi: 10.1001/jama.291.9.1081
24. Pinquart M, Duberstein PR, Lyness JM. Treatments for later-life depressive conditions: a meta-analytic comparison of pharmacotherapy and psychotherapy. Am J Psychiatry. 2006;163:1493-1501. doi: 10.1176/ajp.2006.163.9.1493
25. Solai LK, Mulsant BH, Pollack BG. Selective serotonin reuptake inhibitors for late-life depression: a comparative review. Drugs Aging. 2001;18:355-368. doi: 10.2165/00002512-200118050-00006
26. Sanchez C, Reines EH, Montgomery SA. A comparative review of escitalopram, paroxetine, and sertraline. Are they all alike? Int Clin Psychopharmacol. 2014;29:185-196. doi: 10.1097/YIC.0000000000000023
27. Hedna K, Sundell KA, Hamidi A, et al. Antidepressants and suicidal behaviour in late life: a prospective population-based study of use patterns in new users aged 75 and above. Eur J Clin Pharmacol. 2018;74:201-208. doi: 10.1007/s00228-017-2360-x
28. Bielski RJ, Ventura D, Chang CC. A double-blind comparison of escitalopram and venlafaxine extended release in the treatment of major depressive disorder. J Clin Psychiatry. 2004;65:1190-1196. doi: 10.4088/jcp.v65n0906
29. Robinson M, Oakes TM, Raskin J, et al. Acute and long-term treatment of late-life major depressive disorder: duloxetine versus placebo. Am J Geriatr Psychiatry. 2014;22:34-45. doi: 10.1016/ j.jagp.2013.01.019
30. Holm KJ, Markham A. Mirtazapine: a review of its use in major depression. Drugs. 1999;57:607-631. doi: 10.2165/00003495-199957040-00010
31. Anttila SA, Leinonen EV. A review of the pharmacological and clinical profile of mirtazapine. CNS Drug Rev. 2001;7:249-264. doi: 10.1111/j.1527-3458.2001.tb00198.x
32. Lenze EJ, Mulsant BH, Blumberger DM, et al. Efficacy, safety and tolerability of augmentation pharmacotherapy with aripiprazole for treatment-resistant depression in late life: a randomised double-blind, placebo-controlled trial. Lancet. 2015;386:2404-2412. doi: 10.1016/S0140-6736(15)00308-6
33. Lenze EJ, Oughli HA. Antidepressant treatment for late-life depression: considering risks and benefits. J Am Geriatr Soc. 2019;67:1555-1556. doi: 10.1111/jgs.15964
34. Bondareff W, Alpert M, Friedhoff AJ, et al: Comparison of sertraline and nortriptyline in the treatment of major depressive disorder in late life. Am J Psychiatry. 2000;157:729-736. doi: 10.1176/appi.ajp.157.5.729
35. Lavretsky H, Reinlieb M, St Cyr N. Citalopram, methylphenidate, or their combination in geriatric depression: a randomized, double-blind, placebo controlled trial. Am J Psych. 2015;72:561-569. doi: 10.1176/appi.ajp.2014.14070889
36. Arthur A, Savva GM, Barnes LE, et al. Changing prevalence and treatment of depression among older people over two decades. Br J Psychiatry. 2020;21:49-54. doi: 10.1192/bjp.2019.193
37. Zuidersma M, Chua K-C, Hellier J, et al. Sertraline and mirtazapine versus placebo in subgroups of depression in dementia: findings from the HTA-SADD randomized controlled trial. Am J Geriatr Psychiatry. 2019;27:920-931. doi: 10.1016/ j.jagp.2019.03.021
38. Ochs-Ross R, Wajs E, Daly EJ, et al. Comparison of long-term efficacy and safety of esketamine nasal spray plus oral antidepressant in younger versus older patients with treatment-resistant depression: post-hoc analysis of SUSTAIN-2, a long-term open-label phase 3 safety and efficacy study. Am J Geriatr Psychiatry. 2022;30:541-556. doi: 10.1016/j.jagp.2021.09.014
39. Devanand DP, Pelton GH, D’Antonio K, et al. Donepezil treatment in patients with depression and cognitive impairment on stable antidepressant treatment: a randomized controlled trial. Am J Geriatr Psychiatry. 2018;26:1050-1060. doi: 10.1016/ j.jagp.2018.05.008
40. Obbels J, Vansteelandt K, Verwijk E, et al. MMSE changes during and after ECT in late life depression: a prospective study. Am J Geriatr Psychiatry. 2019;27:934-944. doi: 10.1016/ j.jagp.2019.04.006
41. Wagenmakers MJ, Vansteelandt K, van Exel E, et al. Transient cognitive impairment and white matter hyperintensities in severely depressed older patients treated with electroconvulsive therapy. Am J Geriatr Psychiatry. 2021:29:1117-1128. doi: 10.1016/j.jagp.2020.12.028
42. Trevizol AP, Goldberger KW, Mulsant BH, et al. Unilateral and bilateral repetitive transcranial magnetic stimulation for treatment-resistant late-life depression. Int J Ger Psychiatry. 2019;34:822-827. doi: 10.1002/gps.5091
43. Aben I, Verhey F, Stik J, et al. A comparative study into the one year cumulative incidence of depression after stroke and myocardial infarction. J Neurol Neurosurg Psychiatry. 2003;74:581-585. doi: 10.1136/jnnp.74.5.581
44. Gallo JJ, Bogner HR, Morales KH, et al. The effect of a primary care practice-based depression intervention on mortality in older adults: a randomized trial. Ann Intern Med. 2007;146:689-698. doi: 10.7326/0003-4819-146-10-200705150-00002
45. Lee J, Jang SN, Cho SL. Gender differences in the trajectories and the risk factors of depressive symptoms in later life. Int Psychogeriatr. 2017;29:1495-1505. doi: 10.1017/S1041610217000709
46. Lee E, Cho HJ, Olmstead R, et al. Persistent sleep disturbance: a risk factor for recurrent depression in community-dwelling older adults. Sleep. 2013;36:1685-1691. doi: 10.5665/sleep.3128
47. Berk M, Woods RL, Nelson MR, et al. Effect of aspirin vs placebo on the prevention of depression in older people: a randomized clinical trial. J Am Med A Psych. 2020;77:1012-1020. doi: 10.1001/jamapsychiatry.2020.1214
48. Okereke OI, Reynolds CF, Mischoulon D, et al. Effect of long-term vitamin D3 supplementation vs placebo on risk of depression or clinically relevant depressive symptoms and on change in mood scores: a randomized clinical trial. JAMA. 2020;324:471-480. doi: 10.1001/jama.2020.10224
PRACTICE RECOMMENDATIONS
› Begin treatment with a selective serotonin reuptake inhibitor (SSRI) unless another antidepressant has worked well in the past. A
› Consider augmenting therapy with bupropion XL, mirtazapine, aripiprazole, or quetiapine for any patient who responds only partially to an SSRI. C
› Add psychotherapy to antidepressant pharmacotherapy, particularly for patients who have difficulties with executive functions such as planning and organization. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Depressive symptoms tied to higher stroke risk, worse outcomes
new research suggests.
Data from the international INTERSTROKE study also showed that those with depressive symptoms before a stroke had worse outcomes, including a significantly higher mortality rate in the first month after a stroke.
These findings build on prior research on the link between depression and stroke, including one study that showed an increased risk for incident stroke among those with a high number of depressive symptoms and another that found that worsening depression can precede stroke in older adults.
“Depression is an important risk factor for acute stroke and is potentially a modifiable contributor to the global burden of stroke,” lead investigator Robert Murphy, MB, a consultant in stroke and geriatric medicine and a researcher with the clinical research facility at the University of Galway, Ireland, told this news organization. “Even mild depressive symptoms were found in this study to be associated with increased risk of stroke and this adds to the literature that across the full range of depressive symptoms there is an association with increased risk of stroke.”
The findings were published online March 8 in Neurology.
Significant stroke risk
For the analysis, investigators collected data on 26,877 cases and controls across 32 countries who participated in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. Participants were recruited between 2007 and 2015 and completed a series of questionnaires about stroke risk factors, including measures of depressive symptoms experienced in the past 12 months.
After adjustment for occupation, education, wealth index, diet, physical activity, alcohol consumption, and smoking history, having prestroke depressive symptoms was associated with greater odds for acute stroke (adjusted odds ratio [aOR], 1.46; 95% confidence interval [CI], 1.34-1.58), including both intracerebral hemorrhage (aOR, 1.56; 95% CI, 1.28-1.91) and ischemic stroke (aOR, 1.44; 95% CI, 1.31-1.58).
Stroke risk increased with increasing severity of depression, but even those with mild depression had a 35% increased risk (aOR, 1.35; 95% CI, 1.19-1.53).
The increased risk held even after the researchers adjusted further for diabetes, hypertension, atrial fibrillation, and body mass index, and work, home, and financial stress.
The association was consistent across geographical regions and age groups, but was stronger in men and in those without hypertension.
“This study looks at different constructs of depression and identifies that across the spectrum of mild, moderate, and severe depressive symptoms that there is an association present with acute stroke and that a biological gradient emerges with increasing burden of depressive symptoms associated with increasing risk,” Dr. Murphy said.
An antidepressant mediating effect?
While prestroke depressive symptoms were not associated with a greater odds of worse stroke severity, they were associated with worse outcomes (P < .001) and higher mortality (10% vs. 8.1%; P = .003) 1 month after a stroke.
In a subgroup analysis, researchers found no association between depressive symptoms and stroke risk in patients who were taking antidepressants.
While no assumptions of causality can be drawn from these findings, “this subgroup analysis does suggest that an increased risk of stroke in those with depression may be attenuated if a patient is on appropriate treatment,” Dr. Murphy said. “This is an area that warrants further exploration.”
The mechanisms that link depression to stroke are unclear, but these findings offer strong evidence that this link exists, Dr. Murphy said.
“We adjusted for potential confounders in sequential models and after adjusting for traditional cardiovascular risk factors there was a consistent association between depressive symptoms and stroke identifying that there is likely an independent association between depression and stroke,” Dr. Murphy said.
Questions remain
Commenting on the study, Daniel T. Lackland DrPH, professor, division of translational neurosciences and population studies, department of neurology, Medical University of South Carolina, Charleston, said it adds to a growing body of work on the association of stroke and depression.
“In this case, depression may be a risk factor for having a stroke,” said Dr. Lackland, who was not part of the study. In addition, the study suggests that “treating depression can have additional benefits beyond mental health, in this case, reduced stroke risks.”
However, it’s important, as with any observational study, that there may be confounding factors that may offer an alternative explanation for the findings.
“Further, it is often difficult to accurately assess depression in all individuals, and specifically in individuals who have had a stroke,” Dr. Lackland said. “While this particular study adds depression as a risk factor and suggests treatment of depression in reducing risks, it is important to emphasize that the traditional stroke risk factors including hypertension should [be] continually recognized and treat[ed] with high rigor.”
The INTERSTROKE study was funded by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada, the Canadian Stroke Network, the Swedish Research Council, the Swedish Heart Lung Foundation, AFA Insurance, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, and through unrestricted grants from several pharmaceutical companies with major contributions from AstraZeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), Merck Sharp & Dohme, the Swedish Heart Lung Foundation, Chest Heart & Stroke Scotland, and the Stroke Association (United Kingdom). Dr. Murphy and Dr. Lackland have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Data from the international INTERSTROKE study also showed that those with depressive symptoms before a stroke had worse outcomes, including a significantly higher mortality rate in the first month after a stroke.
These findings build on prior research on the link between depression and stroke, including one study that showed an increased risk for incident stroke among those with a high number of depressive symptoms and another that found that worsening depression can precede stroke in older adults.
“Depression is an important risk factor for acute stroke and is potentially a modifiable contributor to the global burden of stroke,” lead investigator Robert Murphy, MB, a consultant in stroke and geriatric medicine and a researcher with the clinical research facility at the University of Galway, Ireland, told this news organization. “Even mild depressive symptoms were found in this study to be associated with increased risk of stroke and this adds to the literature that across the full range of depressive symptoms there is an association with increased risk of stroke.”
The findings were published online March 8 in Neurology.
Significant stroke risk
For the analysis, investigators collected data on 26,877 cases and controls across 32 countries who participated in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. Participants were recruited between 2007 and 2015 and completed a series of questionnaires about stroke risk factors, including measures of depressive symptoms experienced in the past 12 months.
After adjustment for occupation, education, wealth index, diet, physical activity, alcohol consumption, and smoking history, having prestroke depressive symptoms was associated with greater odds for acute stroke (adjusted odds ratio [aOR], 1.46; 95% confidence interval [CI], 1.34-1.58), including both intracerebral hemorrhage (aOR, 1.56; 95% CI, 1.28-1.91) and ischemic stroke (aOR, 1.44; 95% CI, 1.31-1.58).
Stroke risk increased with increasing severity of depression, but even those with mild depression had a 35% increased risk (aOR, 1.35; 95% CI, 1.19-1.53).
The increased risk held even after the researchers adjusted further for diabetes, hypertension, atrial fibrillation, and body mass index, and work, home, and financial stress.
The association was consistent across geographical regions and age groups, but was stronger in men and in those without hypertension.
“This study looks at different constructs of depression and identifies that across the spectrum of mild, moderate, and severe depressive symptoms that there is an association present with acute stroke and that a biological gradient emerges with increasing burden of depressive symptoms associated with increasing risk,” Dr. Murphy said.
An antidepressant mediating effect?
While prestroke depressive symptoms were not associated with a greater odds of worse stroke severity, they were associated with worse outcomes (P < .001) and higher mortality (10% vs. 8.1%; P = .003) 1 month after a stroke.
In a subgroup analysis, researchers found no association between depressive symptoms and stroke risk in patients who were taking antidepressants.
While no assumptions of causality can be drawn from these findings, “this subgroup analysis does suggest that an increased risk of stroke in those with depression may be attenuated if a patient is on appropriate treatment,” Dr. Murphy said. “This is an area that warrants further exploration.”
The mechanisms that link depression to stroke are unclear, but these findings offer strong evidence that this link exists, Dr. Murphy said.
“We adjusted for potential confounders in sequential models and after adjusting for traditional cardiovascular risk factors there was a consistent association between depressive symptoms and stroke identifying that there is likely an independent association between depression and stroke,” Dr. Murphy said.
Questions remain
Commenting on the study, Daniel T. Lackland DrPH, professor, division of translational neurosciences and population studies, department of neurology, Medical University of South Carolina, Charleston, said it adds to a growing body of work on the association of stroke and depression.
“In this case, depression may be a risk factor for having a stroke,” said Dr. Lackland, who was not part of the study. In addition, the study suggests that “treating depression can have additional benefits beyond mental health, in this case, reduced stroke risks.”
However, it’s important, as with any observational study, that there may be confounding factors that may offer an alternative explanation for the findings.
“Further, it is often difficult to accurately assess depression in all individuals, and specifically in individuals who have had a stroke,” Dr. Lackland said. “While this particular study adds depression as a risk factor and suggests treatment of depression in reducing risks, it is important to emphasize that the traditional stroke risk factors including hypertension should [be] continually recognized and treat[ed] with high rigor.”
The INTERSTROKE study was funded by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada, the Canadian Stroke Network, the Swedish Research Council, the Swedish Heart Lung Foundation, AFA Insurance, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, and through unrestricted grants from several pharmaceutical companies with major contributions from AstraZeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), Merck Sharp & Dohme, the Swedish Heart Lung Foundation, Chest Heart & Stroke Scotland, and the Stroke Association (United Kingdom). Dr. Murphy and Dr. Lackland have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Data from the international INTERSTROKE study also showed that those with depressive symptoms before a stroke had worse outcomes, including a significantly higher mortality rate in the first month after a stroke.
These findings build on prior research on the link between depression and stroke, including one study that showed an increased risk for incident stroke among those with a high number of depressive symptoms and another that found that worsening depression can precede stroke in older adults.
“Depression is an important risk factor for acute stroke and is potentially a modifiable contributor to the global burden of stroke,” lead investigator Robert Murphy, MB, a consultant in stroke and geriatric medicine and a researcher with the clinical research facility at the University of Galway, Ireland, told this news organization. “Even mild depressive symptoms were found in this study to be associated with increased risk of stroke and this adds to the literature that across the full range of depressive symptoms there is an association with increased risk of stroke.”
The findings were published online March 8 in Neurology.
Significant stroke risk
For the analysis, investigators collected data on 26,877 cases and controls across 32 countries who participated in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. Participants were recruited between 2007 and 2015 and completed a series of questionnaires about stroke risk factors, including measures of depressive symptoms experienced in the past 12 months.
After adjustment for occupation, education, wealth index, diet, physical activity, alcohol consumption, and smoking history, having prestroke depressive symptoms was associated with greater odds for acute stroke (adjusted odds ratio [aOR], 1.46; 95% confidence interval [CI], 1.34-1.58), including both intracerebral hemorrhage (aOR, 1.56; 95% CI, 1.28-1.91) and ischemic stroke (aOR, 1.44; 95% CI, 1.31-1.58).
Stroke risk increased with increasing severity of depression, but even those with mild depression had a 35% increased risk (aOR, 1.35; 95% CI, 1.19-1.53).
The increased risk held even after the researchers adjusted further for diabetes, hypertension, atrial fibrillation, and body mass index, and work, home, and financial stress.
The association was consistent across geographical regions and age groups, but was stronger in men and in those without hypertension.
“This study looks at different constructs of depression and identifies that across the spectrum of mild, moderate, and severe depressive symptoms that there is an association present with acute stroke and that a biological gradient emerges with increasing burden of depressive symptoms associated with increasing risk,” Dr. Murphy said.
An antidepressant mediating effect?
While prestroke depressive symptoms were not associated with a greater odds of worse stroke severity, they were associated with worse outcomes (P < .001) and higher mortality (10% vs. 8.1%; P = .003) 1 month after a stroke.
In a subgroup analysis, researchers found no association between depressive symptoms and stroke risk in patients who were taking antidepressants.
While no assumptions of causality can be drawn from these findings, “this subgroup analysis does suggest that an increased risk of stroke in those with depression may be attenuated if a patient is on appropriate treatment,” Dr. Murphy said. “This is an area that warrants further exploration.”
The mechanisms that link depression to stroke are unclear, but these findings offer strong evidence that this link exists, Dr. Murphy said.
“We adjusted for potential confounders in sequential models and after adjusting for traditional cardiovascular risk factors there was a consistent association between depressive symptoms and stroke identifying that there is likely an independent association between depression and stroke,” Dr. Murphy said.
Questions remain
Commenting on the study, Daniel T. Lackland DrPH, professor, division of translational neurosciences and population studies, department of neurology, Medical University of South Carolina, Charleston, said it adds to a growing body of work on the association of stroke and depression.
“In this case, depression may be a risk factor for having a stroke,” said Dr. Lackland, who was not part of the study. In addition, the study suggests that “treating depression can have additional benefits beyond mental health, in this case, reduced stroke risks.”
However, it’s important, as with any observational study, that there may be confounding factors that may offer an alternative explanation for the findings.
“Further, it is often difficult to accurately assess depression in all individuals, and specifically in individuals who have had a stroke,” Dr. Lackland said. “While this particular study adds depression as a risk factor and suggests treatment of depression in reducing risks, it is important to emphasize that the traditional stroke risk factors including hypertension should [be] continually recognized and treat[ed] with high rigor.”
The INTERSTROKE study was funded by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Canada, the Canadian Stroke Network, the Swedish Research Council, the Swedish Heart Lung Foundation, AFA Insurance, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, and through unrestricted grants from several pharmaceutical companies with major contributions from AstraZeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), Merck Sharp & Dohme, the Swedish Heart Lung Foundation, Chest Heart & Stroke Scotland, and the Stroke Association (United Kingdom). Dr. Murphy and Dr. Lackland have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Telehealth doctor indicted on health care fraud, opioid distribution charges
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.