Mixed Topics

The Ohio House of Representatives recently passed a bill that would enable patients to use drug manufacturer coupons and other co-pay assistance as payment toward their annual deductible.

According to the Kaiser Family Foundation, approximately 1 in 4 Americans have difficulty paying for their prescription drugs, while almost half of U.S. adults report difficulty paying out-of-pocket costs not covered by their health insurance.

Supporting the bill that restricts co-pay accumulators are groups such as the Ohio State Medical Association, the Crohn’s and Colitis Foundation, Susan C. Komen, the National Multiple Sclerosis Society, and the American Diabetes Association. The bill faced opposition from health insurers and pharmacy benefit managers, reported The Columbus Dispatch.

“The debate on the management of rising drug costs between manufacturers and insurers unfortunately leaves patients caught in the middle, and practices like co-pay accumulators can have a devastating impact,” Monica Hueckel, senior director of government relations for the Ohio State Medical Association, told this news organization.

“Patients often do not even know about these policies until the coupons are no longer usable. As you can imagine, for patients with expensive medications and/or high deductible health plans, the impact is disastrous,” she said.

Ohio State Representative Susan Manchester, who co-sponsored the bill, told The Columbus Dispatch that the legislation “is needed to assist our constituents who find themselves increasingly subjected to more out-of-pocket costs as part of their insurance coverage.”

Other states blocking health insurers’ co-pay policies

With the passage of the bill, Ohio joins 12 states and Puerto Rico in preventing the use of health insurers’ co-pays to increase patients’ out-of-pocket costs, reported The Columbus Dispatch; 15 states are also considering this type of legislation.

Eighty-three percent of patients are in plans that include a co-pay accumulator, according to consulting firm Avalere, which wrote that, beginning in 2023, the Center for Medicare & Medicaid Services requires patients with Medicaid to receive “the full value of co-pay assistance” on drugs.

According to the National Conference of State Legislatures, co-pay adjustment programs present challenges for patients, with plans that include high cost sharing or co-insurance whereby a patient pays a percentage of the cost instead of a flat amount.

For example, with a co-pay adjustment policy, a patient with a $2,000 deductible plan couldn’t use a $500 coupon toward meeting the deductible, writes the National Conference of State Legislatures. Conversely, a patient in a plan without a co-pay adjustment policy could use the coupon to satisfy their annual deductible.

Patients with complex conditions, such as cancer, rheumatoid arthritis, and diabetes, which often require expensive medications, may have little choice but to fork over the unexpected co-pays, according to the organization that represents state legislatures in the United States.

The bill now moves to the Ohio Senate, reported The Columbus Dispatch.

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

The Ohio House of Representatives recently passed a bill that would enable patients to use drug manufacturer coupons and other co-pay assistance as payment toward their annual deductible.

According to the Kaiser Family Foundation, approximately 1 in 4 Americans have difficulty paying for their prescription drugs, while almost half of U.S. adults report difficulty paying out-of-pocket costs not covered by their health insurance.

Supporting the bill that restricts co-pay accumulators are groups such as the Ohio State Medical Association, the Crohn’s and Colitis Foundation, Susan C. Komen, the National Multiple Sclerosis Society, and the American Diabetes Association. The bill faced opposition from health insurers and pharmacy benefit managers, reported The Columbus Dispatch.

“The debate on the management of rising drug costs between manufacturers and insurers unfortunately leaves patients caught in the middle, and practices like co-pay accumulators can have a devastating impact,” Monica Hueckel, senior director of government relations for the Ohio State Medical Association, told this news organization.

“Patients often do not even know about these policies until the coupons are no longer usable. As you can imagine, for patients with expensive medications and/or high deductible health plans, the impact is disastrous,” she said.

Ohio State Representative Susan Manchester, who co-sponsored the bill, told The Columbus Dispatch that the legislation “is needed to assist our constituents who find themselves increasingly subjected to more out-of-pocket costs as part of their insurance coverage.”

Other states blocking health insurers’ co-pay policies

With the passage of the bill, Ohio joins 12 states and Puerto Rico in preventing the use of health insurers’ co-pays to increase patients’ out-of-pocket costs, reported The Columbus Dispatch; 15 states are also considering this type of legislation.

Eighty-three percent of patients are in plans that include a co-pay accumulator, according to consulting firm Avalere, which wrote that, beginning in 2023, the Center for Medicare & Medicaid Services requires patients with Medicaid to receive “the full value of co-pay assistance” on drugs.

According to the National Conference of State Legislatures, co-pay adjustment programs present challenges for patients, with plans that include high cost sharing or co-insurance whereby a patient pays a percentage of the cost instead of a flat amount.

For example, with a co-pay adjustment policy, a patient with a $2,000 deductible plan couldn’t use a $500 coupon toward meeting the deductible, writes the National Conference of State Legislatures. Conversely, a patient in a plan without a co-pay adjustment policy could use the coupon to satisfy their annual deductible.

Patients with complex conditions, such as cancer, rheumatoid arthritis, and diabetes, which often require expensive medications, may have little choice but to fork over the unexpected co-pays, according to the organization that represents state legislatures in the United States.

The bill now moves to the Ohio Senate, reported The Columbus Dispatch.

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

The Ohio House of Representatives recently passed a bill that would enable patients to use drug manufacturer coupons and other co-pay assistance as payment toward their annual deductible.

According to the Kaiser Family Foundation, approximately 1 in 4 Americans have difficulty paying for their prescription drugs, while almost half of U.S. adults report difficulty paying out-of-pocket costs not covered by their health insurance.

Supporting the bill that restricts co-pay accumulators are groups such as the Ohio State Medical Association, the Crohn’s and Colitis Foundation, Susan C. Komen, the National Multiple Sclerosis Society, and the American Diabetes Association. The bill faced opposition from health insurers and pharmacy benefit managers, reported The Columbus Dispatch.

“The debate on the management of rising drug costs between manufacturers and insurers unfortunately leaves patients caught in the middle, and practices like co-pay accumulators can have a devastating impact,” Monica Hueckel, senior director of government relations for the Ohio State Medical Association, told this news organization.

“Patients often do not even know about these policies until the coupons are no longer usable. As you can imagine, for patients with expensive medications and/or high deductible health plans, the impact is disastrous,” she said.

Ohio State Representative Susan Manchester, who co-sponsored the bill, told The Columbus Dispatch that the legislation “is needed to assist our constituents who find themselves increasingly subjected to more out-of-pocket costs as part of their insurance coverage.”

Other states blocking health insurers’ co-pay policies

With the passage of the bill, Ohio joins 12 states and Puerto Rico in preventing the use of health insurers’ co-pays to increase patients’ out-of-pocket costs, reported The Columbus Dispatch; 15 states are also considering this type of legislation.

Eighty-three percent of patients are in plans that include a co-pay accumulator, according to consulting firm Avalere, which wrote that, beginning in 2023, the Center for Medicare & Medicaid Services requires patients with Medicaid to receive “the full value of co-pay assistance” on drugs.

According to the National Conference of State Legislatures, co-pay adjustment programs present challenges for patients, with plans that include high cost sharing or co-insurance whereby a patient pays a percentage of the cost instead of a flat amount.

For example, with a co-pay adjustment policy, a patient with a $2,000 deductible plan couldn’t use a $500 coupon toward meeting the deductible, writes the National Conference of State Legislatures. Conversely, a patient in a plan without a co-pay adjustment policy could use the coupon to satisfy their annual deductible.

Patients with complex conditions, such as cancer, rheumatoid arthritis, and diabetes, which often require expensive medications, may have little choice but to fork over the unexpected co-pays, according to the organization that represents state legislatures in the United States.

The bill now moves to the Ohio Senate, reported The Columbus Dispatch.

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

Most surgeons report being affected by performance anxiety in relation to their work, with the anxiety frequently having a negative effect on well-being, a new study of surgeons in the United Kingdom shows.

“Performance anxiety or stage fright is a widely recognized problem in music and sports, and there are many similarities between these arenas and the operating theater,” first author Robert Miller, MRCS, of the Surgical Psychology and Performance Group and the department of plastic and reconstructive surgery at St. George’s Hospital NHS Trust, London, said in an interview. “We were aware of it anecdotally in a surgical context, but for one reason or another, perhaps professional pride and fear of negative perception, this is rarely openly discussed amongst surgeons.”

In the cross-sectional study, published in Annals of Surgery, Dr. Miller and colleagues surveyed surgeons in all specialties working in the United Kingdom who had at least 1 year of postgraduate surgical training.

Of a total of 631 responses received, 523 (83%) were included in the analysis. The median age of those who responded was 41.2 years, and the mean duration of surgical experience was 15.3 years (range, 1-52 years). Among them, 62% were men, and 52% were of consultant/attending grade.

All of the respondents – 100% – said they believed that performance anxiety affected surgeons, 87% reported having experienced it themselves, and 65% said they felt that performance anxiety had an effect on their surgical performance.

Both male and female surgeons who reported experiencing performance anxiety had significantly worse mental well-being, as assessed using the Short Warwick Edinburgh Mental Wellbeing Scale, compared with those who did not have performance anxiety (P < .0001 for men and P < .001 for women).

Overall, however, male surgeons had significantly better mental well-being, compared with female surgeons (P = .003), yet both genders had significantly lower mental well-being scores compared with U.K. population norms (P = .0019 for men and P = .0001 for women).

The gender differences are “clearly an important topic, which is likely multifactorial,” Dr. Miller told this news organization. “The gender well-being gap requires more in-depth research, and qualitative work involving female surgeons is critical.”

Surgical perfectionism was significantly more common among respondents who did have performance anxiety in comparison with those who did not (P < .0001).

“Although perfectionism may be a beneficial trait in surgery, our findings from hierarchical multiple regression analysis also indicate that perfectionism, [as well as] sex and experience, may drive surgical performance anxiety and help predict those experiencing [the anxiety],” the authors noted.
 

Performing in presence of colleagues a key trigger

By far, the leading trigger that was identified as prompting surgeon performance anxiety was the presence – and scrutiny – of colleagues within the parent specialty. This was reported by 151 respondents. Other triggers were having to perform on highly complex or high-risk cases (66 responses) and a lack of experience (30 responses).

Next to planning and preparation, opening up and talking about the anxiety and shedding light on the issue was seen as a leading strategy to help with the problem, but very few respondents reported openly sharing their struggles. Only 9% reported that they had shared it openly; 27% said they had confided in someone, and 47% did not respond to the question.

“I wish we talked about it more and shared our insecurities,” one respondent lamented. “Most of my colleagues pretend they are living gods.”

Only about 45% of respondents reported a specific technique for overcoming their anxiety. In addition to being open about the problem, other techniques included self-care, such as exercise; and distraction outside of work to get perspective; relaxation techniques such as deep or controlled breathing; music; mindfulness; and positive self-statements.

About 9% said they had received psychological counseling for performance anxiety, and only 3% reported using medication for the problem.
 

Anxiety a positive factor?

Surprisingly, 70% of respondents reported feeling that surgical performance anxiety could have a positive impact on surgical performance, which the authors noted is consistent with some theories.

“This may be explained by the traditional bell-curve relationship between arousal and performance, which describes a dose-dependent relationship between performance and arousal until a ‘tipping point,’ after which performance declines,” the authors explained. “A heightened awareness secondary to anxiety may be beneficial, but at high doses, anxiety can negatively affect attentional control and cause somatic symptoms.”

They noted that “the challenge would be to reap the benefits of low-level stimulation without incurring possible adverse effects.”

Dr. Miller said that, in determining whether selection bias had a role in the results, a detailed analysis showed that “our respondents were not skewed to those with only high levels of trait anxiety.

“We also had a good spread of consultants versus trainees [about half and half], and different specialties, so we feel this is likely to be a representative sample,” he told this news organization.

That being said, the results underscore the need for increased awareness – and open discussion – of the issue of surgical performance anxiety.

“Within other professions, particularly the performing arts and sports, performance psychology is becoming an integral part of training and development,” Dr. Miller said. “We feel surgeons should be supported in a similar manner.

“Surgical performance anxiety is normal for surgeons at all levels and not something to be ashamed about,” Dr. Miller added. “Talk about it, acknowledge it, and be supportive to your colleagues.”
 

Many keep it to themselves in ‘prevailing culture of stoicism’

Commenting on the study, Carter C. Lebares, MD, an associate professor of surgery and director of the Center for Mindfulness in Surgery, department of surgery, University of California, San Francisco, said she was not surprised to see the high rates of performance anxiety among surgeons.

“As surgeons, no matter how hard we train or how thoroughly we prepare our intellectual understanding or the patient, the disease process, and the operation, there may be surprises, unforeseen challenges, or off days,” Dr. Lebares said.

“And whatever we encounter, we are managing these things directly under the scrutiny of others – people who can affect our reputation, operating privileges, and mental health. So, I am not surprised this is a prevalent and widely recognized issue.”

Dr. Lebares noted that the reluctance to share the anxiety is part of a “challenging and recognized conundrum in both medicine and surgery and is a matter of the prevailing culture of stoicism.

“We often are called to shoulder tremendous weight intraoperatively (having perseverance, self-confidence, or sustained focus), and in owning the weight of complications (which eventually we all will have),” she said.

“So, we do need to be strong and not complain, [but] we also need to be able to set that aside [when appropriate] and ask for help or allow others to shoulder the weight for a while, and this is not [yet] a common part of surgical culture.”

Dr. Lebares added that randomized, controlled trials have shown benefits of mindfulness interventions on burnout and anxiety.

“We have observed positive effects on mental noise, self-perception, conflict resolution, and resilience in surgical residents trained in mindfulness-based cognitive skills,” she said. “[Residents] report applying these skills in the OR, in their home lives, and in how they approach their training/education.”

The authors disclosed no relevant financial relationships. Dr. Lebares has developed mindfulness-based cognitive skills training for surgeons but receives no financial compensation for the activities.

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

Most surgeons report being affected by performance anxiety in relation to their work, with the anxiety frequently having a negative effect on well-being, a new study of surgeons in the United Kingdom shows.

“Performance anxiety or stage fright is a widely recognized problem in music and sports, and there are many similarities between these arenas and the operating theater,” first author Robert Miller, MRCS, of the Surgical Psychology and Performance Group and the department of plastic and reconstructive surgery at St. George’s Hospital NHS Trust, London, said in an interview. “We were aware of it anecdotally in a surgical context, but for one reason or another, perhaps professional pride and fear of negative perception, this is rarely openly discussed amongst surgeons.”

In the cross-sectional study, published in Annals of Surgery, Dr. Miller and colleagues surveyed surgeons in all specialties working in the United Kingdom who had at least 1 year of postgraduate surgical training.

Of a total of 631 responses received, 523 (83%) were included in the analysis. The median age of those who responded was 41.2 years, and the mean duration of surgical experience was 15.3 years (range, 1-52 years). Among them, 62% were men, and 52% were of consultant/attending grade.

All of the respondents – 100% – said they believed that performance anxiety affected surgeons, 87% reported having experienced it themselves, and 65% said they felt that performance anxiety had an effect on their surgical performance.

Both male and female surgeons who reported experiencing performance anxiety had significantly worse mental well-being, as assessed using the Short Warwick Edinburgh Mental Wellbeing Scale, compared with those who did not have performance anxiety (P < .0001 for men and P < .001 for women).

Overall, however, male surgeons had significantly better mental well-being, compared with female surgeons (P = .003), yet both genders had significantly lower mental well-being scores compared with U.K. population norms (P = .0019 for men and P = .0001 for women).

The gender differences are “clearly an important topic, which is likely multifactorial,” Dr. Miller told this news organization. “The gender well-being gap requires more in-depth research, and qualitative work involving female surgeons is critical.”

Surgical perfectionism was significantly more common among respondents who did have performance anxiety in comparison with those who did not (P < .0001).

“Although perfectionism may be a beneficial trait in surgery, our findings from hierarchical multiple regression analysis also indicate that perfectionism, [as well as] sex and experience, may drive surgical performance anxiety and help predict those experiencing [the anxiety],” the authors noted.
 

Performing in presence of colleagues a key trigger

By far, the leading trigger that was identified as prompting surgeon performance anxiety was the presence – and scrutiny – of colleagues within the parent specialty. This was reported by 151 respondents. Other triggers were having to perform on highly complex or high-risk cases (66 responses) and a lack of experience (30 responses).

Next to planning and preparation, opening up and talking about the anxiety and shedding light on the issue was seen as a leading strategy to help with the problem, but very few respondents reported openly sharing their struggles. Only 9% reported that they had shared it openly; 27% said they had confided in someone, and 47% did not respond to the question.

“I wish we talked about it more and shared our insecurities,” one respondent lamented. “Most of my colleagues pretend they are living gods.”

Only about 45% of respondents reported a specific technique for overcoming their anxiety. In addition to being open about the problem, other techniques included self-care, such as exercise; and distraction outside of work to get perspective; relaxation techniques such as deep or controlled breathing; music; mindfulness; and positive self-statements.

About 9% said they had received psychological counseling for performance anxiety, and only 3% reported using medication for the problem.
 

Anxiety a positive factor?

Surprisingly, 70% of respondents reported feeling that surgical performance anxiety could have a positive impact on surgical performance, which the authors noted is consistent with some theories.

“This may be explained by the traditional bell-curve relationship between arousal and performance, which describes a dose-dependent relationship between performance and arousal until a ‘tipping point,’ after which performance declines,” the authors explained. “A heightened awareness secondary to anxiety may be beneficial, but at high doses, anxiety can negatively affect attentional control and cause somatic symptoms.”

They noted that “the challenge would be to reap the benefits of low-level stimulation without incurring possible adverse effects.”

Dr. Miller said that, in determining whether selection bias had a role in the results, a detailed analysis showed that “our respondents were not skewed to those with only high levels of trait anxiety.

“We also had a good spread of consultants versus trainees [about half and half], and different specialties, so we feel this is likely to be a representative sample,” he told this news organization.

That being said, the results underscore the need for increased awareness – and open discussion – of the issue of surgical performance anxiety.

“Within other professions, particularly the performing arts and sports, performance psychology is becoming an integral part of training and development,” Dr. Miller said. “We feel surgeons should be supported in a similar manner.

“Surgical performance anxiety is normal for surgeons at all levels and not something to be ashamed about,” Dr. Miller added. “Talk about it, acknowledge it, and be supportive to your colleagues.”
 

Many keep it to themselves in ‘prevailing culture of stoicism’

Commenting on the study, Carter C. Lebares, MD, an associate professor of surgery and director of the Center for Mindfulness in Surgery, department of surgery, University of California, San Francisco, said she was not surprised to see the high rates of performance anxiety among surgeons.

“As surgeons, no matter how hard we train or how thoroughly we prepare our intellectual understanding or the patient, the disease process, and the operation, there may be surprises, unforeseen challenges, or off days,” Dr. Lebares said.

“And whatever we encounter, we are managing these things directly under the scrutiny of others – people who can affect our reputation, operating privileges, and mental health. So, I am not surprised this is a prevalent and widely recognized issue.”

Dr. Lebares noted that the reluctance to share the anxiety is part of a “challenging and recognized conundrum in both medicine and surgery and is a matter of the prevailing culture of stoicism.

“We often are called to shoulder tremendous weight intraoperatively (having perseverance, self-confidence, or sustained focus), and in owning the weight of complications (which eventually we all will have),” she said.

“So, we do need to be strong and not complain, [but] we also need to be able to set that aside [when appropriate] and ask for help or allow others to shoulder the weight for a while, and this is not [yet] a common part of surgical culture.”

Dr. Lebares added that randomized, controlled trials have shown benefits of mindfulness interventions on burnout and anxiety.

“We have observed positive effects on mental noise, self-perception, conflict resolution, and resilience in surgical residents trained in mindfulness-based cognitive skills,” she said. “[Residents] report applying these skills in the OR, in their home lives, and in how they approach their training/education.”

The authors disclosed no relevant financial relationships. Dr. Lebares has developed mindfulness-based cognitive skills training for surgeons but receives no financial compensation for the activities.

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

Most surgeons report being affected by performance anxiety in relation to their work, with the anxiety frequently having a negative effect on well-being, a new study of surgeons in the United Kingdom shows.

“Performance anxiety or stage fright is a widely recognized problem in music and sports, and there are many similarities between these arenas and the operating theater,” first author Robert Miller, MRCS, of the Surgical Psychology and Performance Group and the department of plastic and reconstructive surgery at St. George’s Hospital NHS Trust, London, said in an interview. “We were aware of it anecdotally in a surgical context, but for one reason or another, perhaps professional pride and fear of negative perception, this is rarely openly discussed amongst surgeons.”

In the cross-sectional study, published in Annals of Surgery, Dr. Miller and colleagues surveyed surgeons in all specialties working in the United Kingdom who had at least 1 year of postgraduate surgical training.

Of a total of 631 responses received, 523 (83%) were included in the analysis. The median age of those who responded was 41.2 years, and the mean duration of surgical experience was 15.3 years (range, 1-52 years). Among them, 62% were men, and 52% were of consultant/attending grade.

All of the respondents – 100% – said they believed that performance anxiety affected surgeons, 87% reported having experienced it themselves, and 65% said they felt that performance anxiety had an effect on their surgical performance.

Both male and female surgeons who reported experiencing performance anxiety had significantly worse mental well-being, as assessed using the Short Warwick Edinburgh Mental Wellbeing Scale, compared with those who did not have performance anxiety (P < .0001 for men and P < .001 for women).

Overall, however, male surgeons had significantly better mental well-being, compared with female surgeons (P = .003), yet both genders had significantly lower mental well-being scores compared with U.K. population norms (P = .0019 for men and P = .0001 for women).

The gender differences are “clearly an important topic, which is likely multifactorial,” Dr. Miller told this news organization. “The gender well-being gap requires more in-depth research, and qualitative work involving female surgeons is critical.”

Surgical perfectionism was significantly more common among respondents who did have performance anxiety in comparison with those who did not (P < .0001).

“Although perfectionism may be a beneficial trait in surgery, our findings from hierarchical multiple regression analysis also indicate that perfectionism, [as well as] sex and experience, may drive surgical performance anxiety and help predict those experiencing [the anxiety],” the authors noted.
 

Performing in presence of colleagues a key trigger

By far, the leading trigger that was identified as prompting surgeon performance anxiety was the presence – and scrutiny – of colleagues within the parent specialty. This was reported by 151 respondents. Other triggers were having to perform on highly complex or high-risk cases (66 responses) and a lack of experience (30 responses).

Next to planning and preparation, opening up and talking about the anxiety and shedding light on the issue was seen as a leading strategy to help with the problem, but very few respondents reported openly sharing their struggles. Only 9% reported that they had shared it openly; 27% said they had confided in someone, and 47% did not respond to the question.

“I wish we talked about it more and shared our insecurities,” one respondent lamented. “Most of my colleagues pretend they are living gods.”

Only about 45% of respondents reported a specific technique for overcoming their anxiety. In addition to being open about the problem, other techniques included self-care, such as exercise; and distraction outside of work to get perspective; relaxation techniques such as deep or controlled breathing; music; mindfulness; and positive self-statements.

About 9% said they had received psychological counseling for performance anxiety, and only 3% reported using medication for the problem.
 

Anxiety a positive factor?

Surprisingly, 70% of respondents reported feeling that surgical performance anxiety could have a positive impact on surgical performance, which the authors noted is consistent with some theories.

“This may be explained by the traditional bell-curve relationship between arousal and performance, which describes a dose-dependent relationship between performance and arousal until a ‘tipping point,’ after which performance declines,” the authors explained. “A heightened awareness secondary to anxiety may be beneficial, but at high doses, anxiety can negatively affect attentional control and cause somatic symptoms.”

They noted that “the challenge would be to reap the benefits of low-level stimulation without incurring possible adverse effects.”

Dr. Miller said that, in determining whether selection bias had a role in the results, a detailed analysis showed that “our respondents were not skewed to those with only high levels of trait anxiety.

“We also had a good spread of consultants versus trainees [about half and half], and different specialties, so we feel this is likely to be a representative sample,” he told this news organization.

That being said, the results underscore the need for increased awareness – and open discussion – of the issue of surgical performance anxiety.

“Within other professions, particularly the performing arts and sports, performance psychology is becoming an integral part of training and development,” Dr. Miller said. “We feel surgeons should be supported in a similar manner.

“Surgical performance anxiety is normal for surgeons at all levels and not something to be ashamed about,” Dr. Miller added. “Talk about it, acknowledge it, and be supportive to your colleagues.”
 

Many keep it to themselves in ‘prevailing culture of stoicism’

Commenting on the study, Carter C. Lebares, MD, an associate professor of surgery and director of the Center for Mindfulness in Surgery, department of surgery, University of California, San Francisco, said she was not surprised to see the high rates of performance anxiety among surgeons.

“As surgeons, no matter how hard we train or how thoroughly we prepare our intellectual understanding or the patient, the disease process, and the operation, there may be surprises, unforeseen challenges, or off days,” Dr. Lebares said.

“And whatever we encounter, we are managing these things directly under the scrutiny of others – people who can affect our reputation, operating privileges, and mental health. So, I am not surprised this is a prevalent and widely recognized issue.”

Dr. Lebares noted that the reluctance to share the anxiety is part of a “challenging and recognized conundrum in both medicine and surgery and is a matter of the prevailing culture of stoicism.

“We often are called to shoulder tremendous weight intraoperatively (having perseverance, self-confidence, or sustained focus), and in owning the weight of complications (which eventually we all will have),” she said.

“So, we do need to be strong and not complain, [but] we also need to be able to set that aside [when appropriate] and ask for help or allow others to shoulder the weight for a while, and this is not [yet] a common part of surgical culture.”

Dr. Lebares added that randomized, controlled trials have shown benefits of mindfulness interventions on burnout and anxiety.

“We have observed positive effects on mental noise, self-perception, conflict resolution, and resilience in surgical residents trained in mindfulness-based cognitive skills,” she said. “[Residents] report applying these skills in the OR, in their home lives, and in how they approach their training/education.”

The authors disclosed no relevant financial relationships. Dr. Lebares has developed mindfulness-based cognitive skills training for surgeons but receives no financial compensation for the activities.

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

It’s tough being on the receiving end of care. I’ve tried to avoid it as much as possible, being ever mindful of the law from Samuel Shem’s The House of God: “They can always hurt you more.”

I recently had several medical encounters at three different facilities, highlighting systemic problems in medical care. Fortunately, each procedure went more smoothly than the prior one.

The first was not so elective. I had some uncomfortable symptoms while exercising and, not wanting to totally be in denial, contacted my doctor to ensure that it was not cardiac in origin since symptoms are often atypical in women.

My physician promptly saw me, then scheduled a nuclear stress test. There was a series of needless glitches. Registration at the diagnostic center had me on their schedule but did not have an order. They would have canceled the procedure had I not been able to get hold of the doctor’s office. Why isn’t an order automatically entered when the physician schedules the test?

While I was given the euphemistic “Patient Rights” brochure, asking to have reports sent to a physician outside of the University of Pittsburgh Medical Center empire is apparently not included.

The staff canceled the stress test because I was not fasting. I had received no instructions from diagnostic cardiology. They suggested it was my internist’s responsibility.

I deliberately ate (2 hours earlier) because my trainer always wants me to eat a light meal so I don’t get hypoglycemic during our workouts, and an exercise stress test, is, of course, a workout. The nurse practitioner said that they were concerned I would vomit. I offered to sign a waiver. She parried, saying they would not be able to get adequate images, so I was out of luck.

When I expressed concern about getting hypoglycemic and having difficulty with the test if fasting, the tech said I should bring a soda and snack. Who tells a “borderline” diabetic to bring a soda?

The tech also said she had called our home to give instructions but encountered a busy signal and had not had time to call back. I had not left the house during the prior week (or most of the past 2 years), so this was a pretty lame excuse.

I suggested to the administration that the hospital offer to email the patient instructions well ahead of time (and perhaps ask for confirmation of receipt). If calling, they should try more than once. They should also have patient instruction sheets at the physician’s office and perhaps have them on their website.

It turns out that the hospital mailed me instructions, not on the date it was ordered, but with the postmark being the day of the procedure itself. With Trump donor Louis DeJoy in charge of the U.S. Postal Service, mail across town now has to travel to Baltimore, 3 hours away, be sorted, and returned.

I did finally have the stress test, which was reassuringly normal. I was not surprised, given that the fury I felt on the first attempt had not precipitated symptoms. The hospital sent a patient ombudsman to meet me there to discuss my previous complaints. I have no idea if they implemented any of the changes I had suggested. In 2021, when I urgently had to take my husband to the ED, I couldn’t see the sign pointing toward the ED and had to ask for directions at the main entrance. They said they would fix that promptly but still have not improved the signage. How I miss the friendly community hospital we had before!

Next was trigger-finger surgery. I had developed that in 1978 from using crutches after a fall. I figured that the relative lull in COVID and my activities made it as good a time as any to finally have it fixed. The surgicenter was great; the surgeon was someone I had worked with and respected for decades. The only glitch was not really knowing how long I was going to be out of commission.

The third encounter (at yet another institution) went really well, despite some early administrative glitches. My major complaint was with the lack of communication between preoperative anesthesia and the operating room and the lack of personalization of preoperative instructions. Despite EPIC, medicines were not correctly reconciled between the different encounters, even on the same day!

After about 15 years of diplopia, which has been gradually worsening, my eye doc had suggested that I consider strabismus surgery as a sort of last-ditch effort to improve my quality of life.

Anesthesiology has stock instructions, which they made no effort to individualize. For example, there is no reason to stop NSAIDs a week before such minor surgery. That’s a problem if you depend on NSAIDs for pain control. Similarly, nothing by mouth after midnight is passé and could be tailored for the patient. I felt particularly inconvenienced that I had to go out of town for the preoperative visit and then have a redundant preoperative clearance by my physician.

The nurses in the preoperative area made me feel quite comfortable and as relaxed as I could be under the circumstances. They had a good sense of humor, which helped too. And from the time I met him a few weeks earlier, I instantly liked my surgeon and felt very comfortable with him and had complete trust.

I was pleased that the chief anesthesiologist responded promptly and undefensively to my letter expressing concerns. I do believe that he will try to improve the systemic problems.

The best part: The surgery appears to have been successful and I should have a significantly improved quality of life.

Hospitals could do so much better by improving communications with patients and by viewing them as customers whose loyalty they must earn and will value. With monopolies growing, memories of such care are quickly fading, soon to be as extinct as the family doc who made house calls.

Dr. Stone is an infectious disease specialist and author of Resilience: One Family’s Story of Hope and Triumph over Evil and Conducting Clinical Research: A Practical Guide. She disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

It’s tough being on the receiving end of care. I’ve tried to avoid it as much as possible, being ever mindful of the law from Samuel Shem’s The House of God: “They can always hurt you more.”

I recently had several medical encounters at three different facilities, highlighting systemic problems in medical care. Fortunately, each procedure went more smoothly than the prior one.

The first was not so elective. I had some uncomfortable symptoms while exercising and, not wanting to totally be in denial, contacted my doctor to ensure that it was not cardiac in origin since symptoms are often atypical in women.

My physician promptly saw me, then scheduled a nuclear stress test. There was a series of needless glitches. Registration at the diagnostic center had me on their schedule but did not have an order. They would have canceled the procedure had I not been able to get hold of the doctor’s office. Why isn’t an order automatically entered when the physician schedules the test?

While I was given the euphemistic “Patient Rights” brochure, asking to have reports sent to a physician outside of the University of Pittsburgh Medical Center empire is apparently not included.

The staff canceled the stress test because I was not fasting. I had received no instructions from diagnostic cardiology. They suggested it was my internist’s responsibility.

I deliberately ate (2 hours earlier) because my trainer always wants me to eat a light meal so I don’t get hypoglycemic during our workouts, and an exercise stress test, is, of course, a workout. The nurse practitioner said that they were concerned I would vomit. I offered to sign a waiver. She parried, saying they would not be able to get adequate images, so I was out of luck.

When I expressed concern about getting hypoglycemic and having difficulty with the test if fasting, the tech said I should bring a soda and snack. Who tells a “borderline” diabetic to bring a soda?

The tech also said she had called our home to give instructions but encountered a busy signal and had not had time to call back. I had not left the house during the prior week (or most of the past 2 years), so this was a pretty lame excuse.

I suggested to the administration that the hospital offer to email the patient instructions well ahead of time (and perhaps ask for confirmation of receipt). If calling, they should try more than once. They should also have patient instruction sheets at the physician’s office and perhaps have them on their website.

It turns out that the hospital mailed me instructions, not on the date it was ordered, but with the postmark being the day of the procedure itself. With Trump donor Louis DeJoy in charge of the U.S. Postal Service, mail across town now has to travel to Baltimore, 3 hours away, be sorted, and returned.

I did finally have the stress test, which was reassuringly normal. I was not surprised, given that the fury I felt on the first attempt had not precipitated symptoms. The hospital sent a patient ombudsman to meet me there to discuss my previous complaints. I have no idea if they implemented any of the changes I had suggested. In 2021, when I urgently had to take my husband to the ED, I couldn’t see the sign pointing toward the ED and had to ask for directions at the main entrance. They said they would fix that promptly but still have not improved the signage. How I miss the friendly community hospital we had before!

Next was trigger-finger surgery. I had developed that in 1978 from using crutches after a fall. I figured that the relative lull in COVID and my activities made it as good a time as any to finally have it fixed. The surgicenter was great; the surgeon was someone I had worked with and respected for decades. The only glitch was not really knowing how long I was going to be out of commission.

The third encounter (at yet another institution) went really well, despite some early administrative glitches. My major complaint was with the lack of communication between preoperative anesthesia and the operating room and the lack of personalization of preoperative instructions. Despite EPIC, medicines were not correctly reconciled between the different encounters, even on the same day!

After about 15 years of diplopia, which has been gradually worsening, my eye doc had suggested that I consider strabismus surgery as a sort of last-ditch effort to improve my quality of life.

Anesthesiology has stock instructions, which they made no effort to individualize. For example, there is no reason to stop NSAIDs a week before such minor surgery. That’s a problem if you depend on NSAIDs for pain control. Similarly, nothing by mouth after midnight is passé and could be tailored for the patient. I felt particularly inconvenienced that I had to go out of town for the preoperative visit and then have a redundant preoperative clearance by my physician.

The nurses in the preoperative area made me feel quite comfortable and as relaxed as I could be under the circumstances. They had a good sense of humor, which helped too. And from the time I met him a few weeks earlier, I instantly liked my surgeon and felt very comfortable with him and had complete trust.

I was pleased that the chief anesthesiologist responded promptly and undefensively to my letter expressing concerns. I do believe that he will try to improve the systemic problems.

The best part: The surgery appears to have been successful and I should have a significantly improved quality of life.

Hospitals could do so much better by improving communications with patients and by viewing them as customers whose loyalty they must earn and will value. With monopolies growing, memories of such care are quickly fading, soon to be as extinct as the family doc who made house calls.

Dr. Stone is an infectious disease specialist and author of Resilience: One Family’s Story of Hope and Triumph over Evil and Conducting Clinical Research: A Practical Guide. She disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

It’s tough being on the receiving end of care. I’ve tried to avoid it as much as possible, being ever mindful of the law from Samuel Shem’s The House of God: “They can always hurt you more.”

I recently had several medical encounters at three different facilities, highlighting systemic problems in medical care. Fortunately, each procedure went more smoothly than the prior one.

The first was not so elective. I had some uncomfortable symptoms while exercising and, not wanting to totally be in denial, contacted my doctor to ensure that it was not cardiac in origin since symptoms are often atypical in women.

My physician promptly saw me, then scheduled a nuclear stress test. There was a series of needless glitches. Registration at the diagnostic center had me on their schedule but did not have an order. They would have canceled the procedure had I not been able to get hold of the doctor’s office. Why isn’t an order automatically entered when the physician schedules the test?

While I was given the euphemistic “Patient Rights” brochure, asking to have reports sent to a physician outside of the University of Pittsburgh Medical Center empire is apparently not included.

The staff canceled the stress test because I was not fasting. I had received no instructions from diagnostic cardiology. They suggested it was my internist’s responsibility.

I deliberately ate (2 hours earlier) because my trainer always wants me to eat a light meal so I don’t get hypoglycemic during our workouts, and an exercise stress test, is, of course, a workout. The nurse practitioner said that they were concerned I would vomit. I offered to sign a waiver. She parried, saying they would not be able to get adequate images, so I was out of luck.

When I expressed concern about getting hypoglycemic and having difficulty with the test if fasting, the tech said I should bring a soda and snack. Who tells a “borderline” diabetic to bring a soda?

The tech also said she had called our home to give instructions but encountered a busy signal and had not had time to call back. I had not left the house during the prior week (or most of the past 2 years), so this was a pretty lame excuse.

I suggested to the administration that the hospital offer to email the patient instructions well ahead of time (and perhaps ask for confirmation of receipt). If calling, they should try more than once. They should also have patient instruction sheets at the physician’s office and perhaps have them on their website.

It turns out that the hospital mailed me instructions, not on the date it was ordered, but with the postmark being the day of the procedure itself. With Trump donor Louis DeJoy in charge of the U.S. Postal Service, mail across town now has to travel to Baltimore, 3 hours away, be sorted, and returned.

I did finally have the stress test, which was reassuringly normal. I was not surprised, given that the fury I felt on the first attempt had not precipitated symptoms. The hospital sent a patient ombudsman to meet me there to discuss my previous complaints. I have no idea if they implemented any of the changes I had suggested. In 2021, when I urgently had to take my husband to the ED, I couldn’t see the sign pointing toward the ED and had to ask for directions at the main entrance. They said they would fix that promptly but still have not improved the signage. How I miss the friendly community hospital we had before!

Next was trigger-finger surgery. I had developed that in 1978 from using crutches after a fall. I figured that the relative lull in COVID and my activities made it as good a time as any to finally have it fixed. The surgicenter was great; the surgeon was someone I had worked with and respected for decades. The only glitch was not really knowing how long I was going to be out of commission.

The third encounter (at yet another institution) went really well, despite some early administrative glitches. My major complaint was with the lack of communication between preoperative anesthesia and the operating room and the lack of personalization of preoperative instructions. Despite EPIC, medicines were not correctly reconciled between the different encounters, even on the same day!

After about 15 years of diplopia, which has been gradually worsening, my eye doc had suggested that I consider strabismus surgery as a sort of last-ditch effort to improve my quality of life.

Anesthesiology has stock instructions, which they made no effort to individualize. For example, there is no reason to stop NSAIDs a week before such minor surgery. That’s a problem if you depend on NSAIDs for pain control. Similarly, nothing by mouth after midnight is passé and could be tailored for the patient. I felt particularly inconvenienced that I had to go out of town for the preoperative visit and then have a redundant preoperative clearance by my physician.

The nurses in the preoperative area made me feel quite comfortable and as relaxed as I could be under the circumstances. They had a good sense of humor, which helped too. And from the time I met him a few weeks earlier, I instantly liked my surgeon and felt very comfortable with him and had complete trust.

I was pleased that the chief anesthesiologist responded promptly and undefensively to my letter expressing concerns. I do believe that he will try to improve the systemic problems.

The best part: The surgery appears to have been successful and I should have a significantly improved quality of life.

Hospitals could do so much better by improving communications with patients and by viewing them as customers whose loyalty they must earn and will value. With monopolies growing, memories of such care are quickly fading, soon to be as extinct as the family doc who made house calls.

Dr. Stone is an infectious disease specialist and author of Resilience: One Family’s Story of Hope and Triumph over Evil and Conducting Clinical Research: A Practical Guide. She disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

The 5 days that she spent at her mother’s bedside were eye-opening for an oncologist used to being on the other side of the clinician–patient relationship.

“As a physician, I thought I had a unique perspective of things that were done well – and things that were not,” commented Pamela Kunz, MD.

Dr. Kunz, who was named the 2021 Woman Oncologist of the Year, is director of the Center for Gastrointestinal Cancers at Smilow Cancer Hospital and of the Yale Cancer Center, New Haven, Conn.

But she was propelled into quite a different role when her mother was admitted to the hospital.

Her mom, who has trouble hearing, was easily confused by jargon and by “all of the people coming in and out with no introductions,” she explained.

“She needed someone to translate what was going on because she didn’t feel well,” she added.

Seeing inpatient care through her mother’s eyes was enlightening, and at times it was “shocking to be on the other side.”

Physicians get used to “checking boxes, getting through the day,” she said. “It’s easy to forget the human side.”

“Seeing a loved one sick, [struggling] through this – I just wished I had seen things done differently,” added Dr. Kunz.

The experience prompted Dr. Kunz to share several “communication pearls” via Twitter. Her thread has since garnered thousands of “likes” and scores of comments and retweets.

She began the Twitter thread explaining what prompted her comments:

“I spent many hours last week observing the practice of medicine while sitting at my mom’s hospital bedside and was reminded of some important communication pearls. Some musings ...”

“1. Introduce yourself by full name, role, and team and have ID badges visible. It can get very confusing for [patients] and family members with the number of people in and out of rooms. E.g. ‘My name is Dr. X. I’m the intern on the primary internal medicine team.’

2.  End your patient visit with a summary of the plan for the day.

3. Avoid medical jargon & speak slowly, clearly, and logically. Remember you are a teacher for your [patients] and their family.

4. Masks make it harder to hear, especially for [patients] with hearing loss (and they no longer have the aid of lip reading).

5. Many older [patients] get confused in the hospital. Repetition is a good thing.

6. Speak to a family member at least once per day to relay the plan.

7. Try to avoid last minute or surprise discharges – they make [patients] and family members anxious. Talk about discharge planning from day 1 and what milestones must occur prior to a safe discharge. ‘In order for you to leave the hospital, X, Y, X must happen.’

8. Talk with your [patients] about something other than what brought them to the hospital (a tip I once learned from a wise mentor).

9.  When possible, sit at eye level with your patient (I love these stools from @YNHH).

10. Take time to listen.”

Dr. Kunz closed with her golden rule: “Lastly, treat your patients how you would want your own family member treated.”

Twitter user @BrunaPellini replied: “I love this, especially ‘Treat your patients how you would want your own family member treated.’ My mom and grandma always said that to me since I was a med student, and this is definitely one of my core values.”

Other clinicians shared similar experiences, and some added to Dr. Kunz’s list.

“Agree entirely, love the list – and while none of us can always practice perfectly, my experiences with my own mother’s illness taught me an enormous amount about communication,” @hoperugo responded.

Twitter user @mariejacork added: “Everyone in health care please read ... if you are lucky enough to not have had a loved one unwell in hospital, these may get forgotten. Having sat with my dad for a few days before he died a few years ago, I felt a lot of these, and it changed my practice forever.”

@bjcohenmd provided additional advice: “And use the dry erase board that should be in every room. Never start a medication without explaining it. Many docs will see the patient and then go to the computer, decide to order a med, but never go back to explain it.”

Patients also shared experiences and offered suggestions.

“As a chronic pain patient I’d add – we know it’s frustrating you can’t cure us but PLEASE do not SIGH if we say something didn’t work or [tell] us to be more positive. Just say ‘I know this is very hard, I’m here to listen.’ We don’t expect a cure, we do expect to be believed,” said @ppenguinsmt. “It makes me feel like I’m causing distress to you if I say the pain has been unrelenting. I leave feeling worse. ...You may have heard 10 [people] in pain before me but this is MY only [appointment].”

Twitter user @KatieCahoots added: “These are perfect. I wish doctors would do this not only in the hospital but in the doctor’s office, as well. I would add one caveat: When you try not to use medical jargon, don’t dumb it down as though I don’t know anything about science or haven’t done any of my own research.”

Dr. Kunz said she was taken aback but pleased by the response to her Tweet.

“It’s an example of the human side of medicine, so it resonates with physicians and with patients,” she commented. Seeing through her mom’s eyes how care was provided made her realize that medical training should include more emphasis on communication, including “real-time feedback to interns, residents, fellows, and students.”

Yes, it takes time, and “we don’t all have a lot of extra time,” she acknowledged.

“But some of these elements don’t take that much more time to do. They can help build trust and can, in the long run, actually save time if patients understand and family members feel engaged and like they are participants,” she said. “I think a little time investment will go a long way.”

In her case, she very much appreciated the one trainee who tried to call her and update her about her mother’s care each afternoon. “I really valued that,” she said.

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

The 5 days that she spent at her mother’s bedside were eye-opening for an oncologist used to being on the other side of the clinician–patient relationship.

“As a physician, I thought I had a unique perspective of things that were done well – and things that were not,” commented Pamela Kunz, MD.

Dr. Kunz, who was named the 2021 Woman Oncologist of the Year, is director of the Center for Gastrointestinal Cancers at Smilow Cancer Hospital and of the Yale Cancer Center, New Haven, Conn.

But she was propelled into quite a different role when her mother was admitted to the hospital.

Her mom, who has trouble hearing, was easily confused by jargon and by “all of the people coming in and out with no introductions,” she explained.

“She needed someone to translate what was going on because she didn’t feel well,” she added.

Seeing inpatient care through her mother’s eyes was enlightening, and at times it was “shocking to be on the other side.”

Physicians get used to “checking boxes, getting through the day,” she said. “It’s easy to forget the human side.”

“Seeing a loved one sick, [struggling] through this – I just wished I had seen things done differently,” added Dr. Kunz.

The experience prompted Dr. Kunz to share several “communication pearls” via Twitter. Her thread has since garnered thousands of “likes” and scores of comments and retweets.

She began the Twitter thread explaining what prompted her comments:

“I spent many hours last week observing the practice of medicine while sitting at my mom’s hospital bedside and was reminded of some important communication pearls. Some musings ...”

“1. Introduce yourself by full name, role, and team and have ID badges visible. It can get very confusing for [patients] and family members with the number of people in and out of rooms. E.g. ‘My name is Dr. X. I’m the intern on the primary internal medicine team.’

2.  End your patient visit with a summary of the plan for the day.

3. Avoid medical jargon & speak slowly, clearly, and logically. Remember you are a teacher for your [patients] and their family.

4. Masks make it harder to hear, especially for [patients] with hearing loss (and they no longer have the aid of lip reading).

5. Many older [patients] get confused in the hospital. Repetition is a good thing.

6. Speak to a family member at least once per day to relay the plan.

7. Try to avoid last minute or surprise discharges – they make [patients] and family members anxious. Talk about discharge planning from day 1 and what milestones must occur prior to a safe discharge. ‘In order for you to leave the hospital, X, Y, X must happen.’

8. Talk with your [patients] about something other than what brought them to the hospital (a tip I once learned from a wise mentor).

9.  When possible, sit at eye level with your patient (I love these stools from @YNHH).

10. Take time to listen.”

Dr. Kunz closed with her golden rule: “Lastly, treat your patients how you would want your own family member treated.”

Twitter user @BrunaPellini replied: “I love this, especially ‘Treat your patients how you would want your own family member treated.’ My mom and grandma always said that to me since I was a med student, and this is definitely one of my core values.”

Other clinicians shared similar experiences, and some added to Dr. Kunz’s list.

“Agree entirely, love the list – and while none of us can always practice perfectly, my experiences with my own mother’s illness taught me an enormous amount about communication,” @hoperugo responded.

Twitter user @mariejacork added: “Everyone in health care please read ... if you are lucky enough to not have had a loved one unwell in hospital, these may get forgotten. Having sat with my dad for a few days before he died a few years ago, I felt a lot of these, and it changed my practice forever.”

@bjcohenmd provided additional advice: “And use the dry erase board that should be in every room. Never start a medication without explaining it. Many docs will see the patient and then go to the computer, decide to order a med, but never go back to explain it.”

Patients also shared experiences and offered suggestions.

“As a chronic pain patient I’d add – we know it’s frustrating you can’t cure us but PLEASE do not SIGH if we say something didn’t work or [tell] us to be more positive. Just say ‘I know this is very hard, I’m here to listen.’ We don’t expect a cure, we do expect to be believed,” said @ppenguinsmt. “It makes me feel like I’m causing distress to you if I say the pain has been unrelenting. I leave feeling worse. ...You may have heard 10 [people] in pain before me but this is MY only [appointment].”

Twitter user @KatieCahoots added: “These are perfect. I wish doctors would do this not only in the hospital but in the doctor’s office, as well. I would add one caveat: When you try not to use medical jargon, don’t dumb it down as though I don’t know anything about science or haven’t done any of my own research.”

Dr. Kunz said she was taken aback but pleased by the response to her Tweet.

“It’s an example of the human side of medicine, so it resonates with physicians and with patients,” she commented. Seeing through her mom’s eyes how care was provided made her realize that medical training should include more emphasis on communication, including “real-time feedback to interns, residents, fellows, and students.”

Yes, it takes time, and “we don’t all have a lot of extra time,” she acknowledged.

“But some of these elements don’t take that much more time to do. They can help build trust and can, in the long run, actually save time if patients understand and family members feel engaged and like they are participants,” she said. “I think a little time investment will go a long way.”

In her case, she very much appreciated the one trainee who tried to call her and update her about her mother’s care each afternoon. “I really valued that,” she said.

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

The 5 days that she spent at her mother’s bedside were eye-opening for an oncologist used to being on the other side of the clinician–patient relationship.

“As a physician, I thought I had a unique perspective of things that were done well – and things that were not,” commented Pamela Kunz, MD.

Dr. Kunz, who was named the 2021 Woman Oncologist of the Year, is director of the Center for Gastrointestinal Cancers at Smilow Cancer Hospital and of the Yale Cancer Center, New Haven, Conn.

But she was propelled into quite a different role when her mother was admitted to the hospital.

Her mom, who has trouble hearing, was easily confused by jargon and by “all of the people coming in and out with no introductions,” she explained.

“She needed someone to translate what was going on because she didn’t feel well,” she added.

Seeing inpatient care through her mother’s eyes was enlightening, and at times it was “shocking to be on the other side.”

Physicians get used to “checking boxes, getting through the day,” she said. “It’s easy to forget the human side.”

“Seeing a loved one sick, [struggling] through this – I just wished I had seen things done differently,” added Dr. Kunz.

The experience prompted Dr. Kunz to share several “communication pearls” via Twitter. Her thread has since garnered thousands of “likes” and scores of comments and retweets.

She began the Twitter thread explaining what prompted her comments:

“I spent many hours last week observing the practice of medicine while sitting at my mom’s hospital bedside and was reminded of some important communication pearls. Some musings ...”

“1. Introduce yourself by full name, role, and team and have ID badges visible. It can get very confusing for [patients] and family members with the number of people in and out of rooms. E.g. ‘My name is Dr. X. I’m the intern on the primary internal medicine team.’

2.  End your patient visit with a summary of the plan for the day.

3. Avoid medical jargon & speak slowly, clearly, and logically. Remember you are a teacher for your [patients] and their family.

4. Masks make it harder to hear, especially for [patients] with hearing loss (and they no longer have the aid of lip reading).

5. Many older [patients] get confused in the hospital. Repetition is a good thing.

6. Speak to a family member at least once per day to relay the plan.

7. Try to avoid last minute or surprise discharges – they make [patients] and family members anxious. Talk about discharge planning from day 1 and what milestones must occur prior to a safe discharge. ‘In order for you to leave the hospital, X, Y, X must happen.’

8. Talk with your [patients] about something other than what brought them to the hospital (a tip I once learned from a wise mentor).

9.  When possible, sit at eye level with your patient (I love these stools from @YNHH).

10. Take time to listen.”

Dr. Kunz closed with her golden rule: “Lastly, treat your patients how you would want your own family member treated.”

Twitter user @BrunaPellini replied: “I love this, especially ‘Treat your patients how you would want your own family member treated.’ My mom and grandma always said that to me since I was a med student, and this is definitely one of my core values.”

Other clinicians shared similar experiences, and some added to Dr. Kunz’s list.

“Agree entirely, love the list – and while none of us can always practice perfectly, my experiences with my own mother’s illness taught me an enormous amount about communication,” @hoperugo responded.

Twitter user @mariejacork added: “Everyone in health care please read ... if you are lucky enough to not have had a loved one unwell in hospital, these may get forgotten. Having sat with my dad for a few days before he died a few years ago, I felt a lot of these, and it changed my practice forever.”

@bjcohenmd provided additional advice: “And use the dry erase board that should be in every room. Never start a medication without explaining it. Many docs will see the patient and then go to the computer, decide to order a med, but never go back to explain it.”

Patients also shared experiences and offered suggestions.

“As a chronic pain patient I’d add – we know it’s frustrating you can’t cure us but PLEASE do not SIGH if we say something didn’t work or [tell] us to be more positive. Just say ‘I know this is very hard, I’m here to listen.’ We don’t expect a cure, we do expect to be believed,” said @ppenguinsmt. “It makes me feel like I’m causing distress to you if I say the pain has been unrelenting. I leave feeling worse. ...You may have heard 10 [people] in pain before me but this is MY only [appointment].”

Twitter user @KatieCahoots added: “These are perfect. I wish doctors would do this not only in the hospital but in the doctor’s office, as well. I would add one caveat: When you try not to use medical jargon, don’t dumb it down as though I don’t know anything about science or haven’t done any of my own research.”

Dr. Kunz said she was taken aback but pleased by the response to her Tweet.

“It’s an example of the human side of medicine, so it resonates with physicians and with patients,” she commented. Seeing through her mom’s eyes how care was provided made her realize that medical training should include more emphasis on communication, including “real-time feedback to interns, residents, fellows, and students.”

Yes, it takes time, and “we don’t all have a lot of extra time,” she acknowledged.

“But some of these elements don’t take that much more time to do. They can help build trust and can, in the long run, actually save time if patients understand and family members feel engaged and like they are participants,” she said. “I think a little time investment will go a long way.”

In her case, she very much appreciated the one trainee who tried to call her and update her about her mother’s care each afternoon. “I really valued that,” she said.

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

There is a two-lane bridge in my town. It is quaint and picturesque, and when we first moved here, I would gaze out at the water as I drove, letting my mind wander along with the seagulls drifting alongside the car. Until one day, crossing back over, I passed a school bus stopped in the other lane, and instead of waving back, the driver gave me such a fierce look of disapproval I felt like I’d been to the principal’s office. What had I done?

I started paying more attention to the pattern of the other cars on the bridge. Although it appeared to be a standard two-lane width, the lanes weren’t quite wide enough if a school bus or large truck needed to cross at the same time as a car coming from the opposite direction. They had to wait until the other lane was clear. It was an unwritten rule of the town that if you saw a school bus on the other side, you stopped your car and yielded the bridge to the bus. It took me weeks to figure this out. When I did, I felt like I finally belonged in the community. Before, I’d been an outsider.

This got me thinking about culture. Every place has its unwritten rules, whether a community or a workplace. But how do we know the culture of a place? It’s pretty much impossible until we experience it for ourselves.

When I did figure out the bridge, I had a little bit of anger, to be honest. How was I supposed to know about the lanes? There weren’t any signs. Geez.

Now, when I approach the bridge, I don’t even think about it. I know what to do if I see a bus coming.

But sometimes I remember that time of confusion before I deciphered the unwritten rule. I still have a twinge of guilt for having done something wrong, even though it hadn’t been my fault.

It reminded me of a memory from medical training. I was an MS4, and my ER rotation was in a busy county hospital with a level I trauma center. To say that the place was chaotic would be an understatement.

On the first morning, I was shown the chart rack (yes, this was back in the day of paper charts). Charts were placed in the order that patients arrived. Med students and residents were to take a chart in chronological order, go triage and assess the patient, and then find an attending. Once finished, you put the chart back on the rack and picked up the next one. This was the extent of my orientation to the ER.

The days and weeks of the rotation flew by. It was a busy and exciting time. By the end of the month, I’d come to feel a part of the team.

Until one day, after finishing discharging a patient, an attending asked me, “Where’s the billing sheet?”

I had no idea what she was talking about. No one had ever shown me a billing sheet. But by this point, as an MS4, I knew well that if an attending asked you something you didn’t know the answer to, you shouldn’t just say that you didn’t know. You should try to figure out if you could at least approximate an answer first.

As I scrambled in my mind to figure out what she was asking me, she took one look at the apprehension in my eyes and asked again, raising her voice, “You haven’t been doing the billing sheets?”

I thought back to the first day of the rotation. The cursory 30-second orientation. Chart rack. Take one. See the patient. Put it back. See the next patient. Nothing about billing sheets.

“No,” I said. “No one ever told me about – ”

But the attending didn’t care that I hadn’t been instructed on the billing sheets. She ripped into me, yelling about how she couldn’t believe I’d been working there the entire month and was not doing the billing sheets. She showed me what they were and where they were supposed to be going and, in front of the whole staff, treated me like not only the biggest idiot she’d ever worked with but that the hospital had ever seen.

As she berated me, I thought about all the patients I’d seen that month. All the billing sheets I hadn’t placed in the pile. All the attendings who hadn’t gotten credit for the patients they’d staffed with me.

But how could I have known? I wanted to ask. How could I have known if nobody showed me or told me?

It was like the bridge. I was in a new environment and somehow expected to know the rules without anyone telling me; and when I didn’t know, people treated me like I’d done it the wrong way on purpose.

I didn’t end up saying anything more to that attending. What could I have said? She had already unleashed a mountain of her pent-up anger at me.

What I did decide in that moment was that I would never be an attending like that.

Like the bridge, this memory years later can still make me feel guilt and shame for doing something wrong. Even though it wasn’t my fault.

I was thinking about this recently with the Match. Thousands of freshly graduated medical students embarking on their new positions as interns in teaching hospitals across the country.

For anyone who, like me, struggled with the unwritten rules of the medical culture with each new rotation, remember to be kind to yourself. If someone treats you poorly for not knowing something, you are not an idiot. You’ve worked incredibly hard to get where you are, and you deserve to be there.

For attendings and more senior trainees, remember what it was like to be starting in a new place. We all make mistakes, and often it’s simply because of a lack of information.

Trainees shouldn’t have to suffer and be made to feel like outsiders until they figure out the unwritten rules of the place. They belong.
 

Dr. Lycette is medical director of Providence Oncology and Hematology Care Clinic, Seaside, Ore. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

There is a two-lane bridge in my town. It is quaint and picturesque, and when we first moved here, I would gaze out at the water as I drove, letting my mind wander along with the seagulls drifting alongside the car. Until one day, crossing back over, I passed a school bus stopped in the other lane, and instead of waving back, the driver gave me such a fierce look of disapproval I felt like I’d been to the principal’s office. What had I done?

I started paying more attention to the pattern of the other cars on the bridge. Although it appeared to be a standard two-lane width, the lanes weren’t quite wide enough if a school bus or large truck needed to cross at the same time as a car coming from the opposite direction. They had to wait until the other lane was clear. It was an unwritten rule of the town that if you saw a school bus on the other side, you stopped your car and yielded the bridge to the bus. It took me weeks to figure this out. When I did, I felt like I finally belonged in the community. Before, I’d been an outsider.

This got me thinking about culture. Every place has its unwritten rules, whether a community or a workplace. But how do we know the culture of a place? It’s pretty much impossible until we experience it for ourselves.

When I did figure out the bridge, I had a little bit of anger, to be honest. How was I supposed to know about the lanes? There weren’t any signs. Geez.

Now, when I approach the bridge, I don’t even think about it. I know what to do if I see a bus coming.

But sometimes I remember that time of confusion before I deciphered the unwritten rule. I still have a twinge of guilt for having done something wrong, even though it hadn’t been my fault.

It reminded me of a memory from medical training. I was an MS4, and my ER rotation was in a busy county hospital with a level I trauma center. To say that the place was chaotic would be an understatement.

On the first morning, I was shown the chart rack (yes, this was back in the day of paper charts). Charts were placed in the order that patients arrived. Med students and residents were to take a chart in chronological order, go triage and assess the patient, and then find an attending. Once finished, you put the chart back on the rack and picked up the next one. This was the extent of my orientation to the ER.

The days and weeks of the rotation flew by. It was a busy and exciting time. By the end of the month, I’d come to feel a part of the team.

Until one day, after finishing discharging a patient, an attending asked me, “Where’s the billing sheet?”

I had no idea what she was talking about. No one had ever shown me a billing sheet. But by this point, as an MS4, I knew well that if an attending asked you something you didn’t know the answer to, you shouldn’t just say that you didn’t know. You should try to figure out if you could at least approximate an answer first.

As I scrambled in my mind to figure out what she was asking me, she took one look at the apprehension in my eyes and asked again, raising her voice, “You haven’t been doing the billing sheets?”

I thought back to the first day of the rotation. The cursory 30-second orientation. Chart rack. Take one. See the patient. Put it back. See the next patient. Nothing about billing sheets.

“No,” I said. “No one ever told me about – ”

But the attending didn’t care that I hadn’t been instructed on the billing sheets. She ripped into me, yelling about how she couldn’t believe I’d been working there the entire month and was not doing the billing sheets. She showed me what they were and where they were supposed to be going and, in front of the whole staff, treated me like not only the biggest idiot she’d ever worked with but that the hospital had ever seen.

As she berated me, I thought about all the patients I’d seen that month. All the billing sheets I hadn’t placed in the pile. All the attendings who hadn’t gotten credit for the patients they’d staffed with me.

But how could I have known? I wanted to ask. How could I have known if nobody showed me or told me?

It was like the bridge. I was in a new environment and somehow expected to know the rules without anyone telling me; and when I didn’t know, people treated me like I’d done it the wrong way on purpose.

I didn’t end up saying anything more to that attending. What could I have said? She had already unleashed a mountain of her pent-up anger at me.

What I did decide in that moment was that I would never be an attending like that.

Like the bridge, this memory years later can still make me feel guilt and shame for doing something wrong. Even though it wasn’t my fault.

I was thinking about this recently with the Match. Thousands of freshly graduated medical students embarking on their new positions as interns in teaching hospitals across the country.

For anyone who, like me, struggled with the unwritten rules of the medical culture with each new rotation, remember to be kind to yourself. If someone treats you poorly for not knowing something, you are not an idiot. You’ve worked incredibly hard to get where you are, and you deserve to be there.

For attendings and more senior trainees, remember what it was like to be starting in a new place. We all make mistakes, and often it’s simply because of a lack of information.

Trainees shouldn’t have to suffer and be made to feel like outsiders until they figure out the unwritten rules of the place. They belong.
 

Dr. Lycette is medical director of Providence Oncology and Hematology Care Clinic, Seaside, Ore. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

There is a two-lane bridge in my town. It is quaint and picturesque, and when we first moved here, I would gaze out at the water as I drove, letting my mind wander along with the seagulls drifting alongside the car. Until one day, crossing back over, I passed a school bus stopped in the other lane, and instead of waving back, the driver gave me such a fierce look of disapproval I felt like I’d been to the principal’s office. What had I done?

I started paying more attention to the pattern of the other cars on the bridge. Although it appeared to be a standard two-lane width, the lanes weren’t quite wide enough if a school bus or large truck needed to cross at the same time as a car coming from the opposite direction. They had to wait until the other lane was clear. It was an unwritten rule of the town that if you saw a school bus on the other side, you stopped your car and yielded the bridge to the bus. It took me weeks to figure this out. When I did, I felt like I finally belonged in the community. Before, I’d been an outsider.

This got me thinking about culture. Every place has its unwritten rules, whether a community or a workplace. But how do we know the culture of a place? It’s pretty much impossible until we experience it for ourselves.

When I did figure out the bridge, I had a little bit of anger, to be honest. How was I supposed to know about the lanes? There weren’t any signs. Geez.

Now, when I approach the bridge, I don’t even think about it. I know what to do if I see a bus coming.

But sometimes I remember that time of confusion before I deciphered the unwritten rule. I still have a twinge of guilt for having done something wrong, even though it hadn’t been my fault.

It reminded me of a memory from medical training. I was an MS4, and my ER rotation was in a busy county hospital with a level I trauma center. To say that the place was chaotic would be an understatement.

On the first morning, I was shown the chart rack (yes, this was back in the day of paper charts). Charts were placed in the order that patients arrived. Med students and residents were to take a chart in chronological order, go triage and assess the patient, and then find an attending. Once finished, you put the chart back on the rack and picked up the next one. This was the extent of my orientation to the ER.

The days and weeks of the rotation flew by. It was a busy and exciting time. By the end of the month, I’d come to feel a part of the team.

Until one day, after finishing discharging a patient, an attending asked me, “Where’s the billing sheet?”

I had no idea what she was talking about. No one had ever shown me a billing sheet. But by this point, as an MS4, I knew well that if an attending asked you something you didn’t know the answer to, you shouldn’t just say that you didn’t know. You should try to figure out if you could at least approximate an answer first.

As I scrambled in my mind to figure out what she was asking me, she took one look at the apprehension in my eyes and asked again, raising her voice, “You haven’t been doing the billing sheets?”

I thought back to the first day of the rotation. The cursory 30-second orientation. Chart rack. Take one. See the patient. Put it back. See the next patient. Nothing about billing sheets.

“No,” I said. “No one ever told me about – ”

But the attending didn’t care that I hadn’t been instructed on the billing sheets. She ripped into me, yelling about how she couldn’t believe I’d been working there the entire month and was not doing the billing sheets. She showed me what they were and where they were supposed to be going and, in front of the whole staff, treated me like not only the biggest idiot she’d ever worked with but that the hospital had ever seen.

As she berated me, I thought about all the patients I’d seen that month. All the billing sheets I hadn’t placed in the pile. All the attendings who hadn’t gotten credit for the patients they’d staffed with me.

But how could I have known? I wanted to ask. How could I have known if nobody showed me or told me?

It was like the bridge. I was in a new environment and somehow expected to know the rules without anyone telling me; and when I didn’t know, people treated me like I’d done it the wrong way on purpose.

I didn’t end up saying anything more to that attending. What could I have said? She had already unleashed a mountain of her pent-up anger at me.

What I did decide in that moment was that I would never be an attending like that.

Like the bridge, this memory years later can still make me feel guilt and shame for doing something wrong. Even though it wasn’t my fault.

I was thinking about this recently with the Match. Thousands of freshly graduated medical students embarking on their new positions as interns in teaching hospitals across the country.

For anyone who, like me, struggled with the unwritten rules of the medical culture with each new rotation, remember to be kind to yourself. If someone treats you poorly for not knowing something, you are not an idiot. You’ve worked incredibly hard to get where you are, and you deserve to be there.

For attendings and more senior trainees, remember what it was like to be starting in a new place. We all make mistakes, and often it’s simply because of a lack of information.

Trainees shouldn’t have to suffer and be made to feel like outsiders until they figure out the unwritten rules of the place. They belong.
 

Dr. Lycette is medical director of Providence Oncology and Hematology Care Clinic, Seaside, Ore. She disclosed no relevant conflicts of interest. A version of this article first appeared on Medscape.com.

U.S. hospitals are being warned to prepare for a potential cyberattack from either the Russian government, criminal gangs resident in Russia, or both, as a result of the invasion of Ukraine and the U.S. and Western countermeasures against the aggressor nation.

The day after President Biden announced that the war had begun, the American Hospital Association (AHA) issued an alert to hospitals. The cybersecurity division of the Department of Health and Human Services (HHS), known as HC3, joined AHA with another public warning to the healthcare system on March 1. The federal government’s Cybersecurity & Infrastructure Security Agency (CISA) issued a “Shield’s Up” alert to private industry, supporting Biden’s March 21 statement about the need to improve domestic cybersecurity.

CISA warned that the Russian invasion of Ukraine could lead to “malicious cyber activity against the U.S. homeland, including as a response to the unprecedented economic costs imposed on Russia by the U.S. and our allies and partners.” The agency noted that the Russian government is currently exploring options for cyberattacks.

John Riggi, the AHA’s national advisor for cybersecurity and risk, and a former senior executive in the FBI’s cyber division, said in an interview, “We are not aware of any cyberattacks related to the current conflict [in Ukraine]. We don’t know of any specific credible threats targeted against U.S. healthcare from the Russian government.”

He added that there have been reports of Russian hackers searching U.S. health IT security systems for weaknesses.
 

Criminal gangs remain a threat

Besides the Russian government, Mr. Riggi said, Russian criminal gangs are another threat to U.S. hospitals and other healthcare providers. Of particular concern, he noted, is the Conti gang, which “has a history of conducting ransomware attacks against U.S. healthcare and the Irish health system.”

On February 25, said Mr. Riggi, the Conti group announced plans “to retaliate against the West for what they viewed as potential cyber aggression by the West against the Russian federation.”

Sophisticated hacker groups like the Conti gang that operate under the protection of the Russian government have “caused the greatest amount of disruption and have cost the most in terms of recovery and lost business,” Mac McMillan, CEO of CynergisTek, a cybersecurity consulting firm, told this news organization.

However, he said, the current threat is greater for two reasons: first, it will likely come directly from the Russian military intelligence service; and second, there are indications that the malware will be more destructive than ransomware. Two new types of malware identified by HC3 — HermeticWiper and WhisperGate — are designed to wipe out the data in their targets’ systems, rather than just encrypting it and disrupting access to data until a ransom is paid.

The Russian military intelligence service, known as the GRU, is extremely capable and dangerous, Mr. McMillan said. He doubts that many healthcare systems, even if they are fairly well prepared, could withstand an attack from this source. And he fully believes that the attack, when it comes, will aim to wipe out data in victims’ systems in order to create as much chaos and disruption as possible in the United States.
 

Hospitals better prepared, but still have gaps

Like Mr. Riggi, Mr. McMillan said that the healthcare industry is better prepared for cyberattacks now than it was in 2017, when the NotPetya assault on Ukraine’s online infrastructure created considerable collateral damage in the United States. However, he said, hospitals still have a long way to go before they can counter and/or recover from a dedicated Russian government cyberattack.

The NotPetya malware, Mr. Riggi said, was of the destructive variety. “That digital virus spread uncontrollably across the globe like a biological virus. All the organizations and institutions that had contact with Ukraine became infected.”

According to an indictment of six GRU officers that the Department of Justice announced in December 2020, NotPetya disrupted operations at a major pharmaceutical company, subsequently revealed to be Merck, and hospitals and other medical facilities in the Heritage Valley Health System in Pennsylvania. In addition, it temporarily shut down the transcription services of Nuance Communications, which lost $98 million as a result. Merck received $1.4 billion from an insurer to cover its NotPetya loss, Bloomberg reported.

That incident prompted the AHA to urge hospitals to use “geo-fencing” to block online communications with Ukraine and neighboring countries. However, Mr. Riggi said, that solution is not too effective because hackers commonly use proxy servers in other countries to forward their malware to the intended target.

The AHA alert included a list of actions that hospitals and health systems could take to reduce their vulnerability to Russian hacking. Besides geo-fencing, the AHA suggested that hospitals:

• Heighten staff awareness of the increased risk of receiving malware-laden phishing emails;
• Identify all international and third-party mission-critical, clinical, and operational services and technology and put in place business continuity plans and downtime procedures;
• Check the redundancy, resiliency, and security of the organization’s network and data backups;
• Document, update, and practice the organization’s incident response plan.

Hospitals increasingly targeted

In recent years, Mr. Riggi noted, hospitals have invested much more in cybersecurity than before, and hospital executives have told him that this is now one of their top priorities, along with COVID-19 and workforce issues. This has been not only because of NotPetya, but also because healthcare facilities are being increasingly attacked by foreign ransomware gangs, he says.

The hospitals’ biggest vulnerabilities, he said, are phishing emails, remote desktop access, and unpatched vulnerabilities, in that order. It’s not easy to remedy the latter, he observed, because hospital networks can include up to 100,000 connected medical devices and other computers that can access the network, both within and outside the hospital.

“With the new work-at-home environment, you may have thousands of employees who are using the network outside the traditional perimeter of the organization,” he pointed out. “There’s no longer that standard firewall that protects everything.” In addition, he said, hospitals also have to depend on vendors to develop patches and implement them.

In Mr. McMillan’s view, the healthcare industry is a decade behind the financial industry and other sectors in cybersecurity. Among other things, he says, “half of our hospitals still don’t have active monitoring on their networks. They don’t have privileged access on their networks. A bunch don’t have segmentation or endpoint protection. There are so many things that hospitals don’t have that they need to fend off these attacks — they’re better off than they were in 2017, but they still aren’t where they need to be.”
 

Physician practices also at risk

Employed physicians, naturally, are in danger of losing access to their electronic health records if their hospital’s network goes down as the result of a cyberattack, he notes. Many community doctors also use the EHR of a local hospital, and they’d be similarly affected, Mr. Riggi noted.

Physician practices might be saved if the attack were directed at the hospital and they could still connect to the EHR through a cloud provider, Mr. McMillan said. But Mr. Riggi stressed that practices still need a plan for their doctors to keep working if they lose access to a hospital EHR.

“The other possibility is that the practice could be targeted,” he added. “As hospitals become more hardened, often these hackers are looking for the weak link. The practices could become victims of increased targeting. And the practice becomes the conduit for malware to go from its system to the hospital and infect the hospital system.”
 

Hackers can hit service suppliers

Hospitals’ mission-critical service suppliers may also be targeted by Russian hackers and others, or they may be the accidental victims of a cyberattack elsewhere, Mr. Riggi noted. In the case of Nuance, he said, the disruption in transcription services affected thousands of U.S. healthcare providers who were unable to access their transcribed notes. This not only harmed patient care, but also meant that hospitals couldn’t fully bill for their services.

Another type of service supplier, he said, was struck with a ransomware attack last year. This was a cloud-based service that operated linear accelerators used in radiation oncology. “So radiation oncology and cancer treatment for patients across the U.S. was disrupted, and radiation oncology was delayed for some patients up to 3 weeks.”

More recently, another cloud-based service called Kronos was struck by ransomware. Because of this incident, payroll and timekeeping services were disrupted across several industries, including healthcare.

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

U.S. hospitals are being warned to prepare for a potential cyberattack from either the Russian government, criminal gangs resident in Russia, or both, as a result of the invasion of Ukraine and the U.S. and Western countermeasures against the aggressor nation.

The day after President Biden announced that the war had begun, the American Hospital Association (AHA) issued an alert to hospitals. The cybersecurity division of the Department of Health and Human Services (HHS), known as HC3, joined AHA with another public warning to the healthcare system on March 1. The federal government’s Cybersecurity & Infrastructure Security Agency (CISA) issued a “Shield’s Up” alert to private industry, supporting Biden’s March 21 statement about the need to improve domestic cybersecurity.

CISA warned that the Russian invasion of Ukraine could lead to “malicious cyber activity against the U.S. homeland, including as a response to the unprecedented economic costs imposed on Russia by the U.S. and our allies and partners.” The agency noted that the Russian government is currently exploring options for cyberattacks.

John Riggi, the AHA’s national advisor for cybersecurity and risk, and a former senior executive in the FBI’s cyber division, said in an interview, “We are not aware of any cyberattacks related to the current conflict [in Ukraine]. We don’t know of any specific credible threats targeted against U.S. healthcare from the Russian government.”

He added that there have been reports of Russian hackers searching U.S. health IT security systems for weaknesses.
 

Criminal gangs remain a threat

Besides the Russian government, Mr. Riggi said, Russian criminal gangs are another threat to U.S. hospitals and other healthcare providers. Of particular concern, he noted, is the Conti gang, which “has a history of conducting ransomware attacks against U.S. healthcare and the Irish health system.”

On February 25, said Mr. Riggi, the Conti group announced plans “to retaliate against the West for what they viewed as potential cyber aggression by the West against the Russian federation.”

Sophisticated hacker groups like the Conti gang that operate under the protection of the Russian government have “caused the greatest amount of disruption and have cost the most in terms of recovery and lost business,” Mac McMillan, CEO of CynergisTek, a cybersecurity consulting firm, told this news organization.

However, he said, the current threat is greater for two reasons: first, it will likely come directly from the Russian military intelligence service; and second, there are indications that the malware will be more destructive than ransomware. Two new types of malware identified by HC3 — HermeticWiper and WhisperGate — are designed to wipe out the data in their targets’ systems, rather than just encrypting it and disrupting access to data until a ransom is paid.

The Russian military intelligence service, known as the GRU, is extremely capable and dangerous, Mr. McMillan said. He doubts that many healthcare systems, even if they are fairly well prepared, could withstand an attack from this source. And he fully believes that the attack, when it comes, will aim to wipe out data in victims’ systems in order to create as much chaos and disruption as possible in the United States.
 

Hospitals better prepared, but still have gaps

Like Mr. Riggi, Mr. McMillan said that the healthcare industry is better prepared for cyberattacks now than it was in 2017, when the NotPetya assault on Ukraine’s online infrastructure created considerable collateral damage in the United States. However, he said, hospitals still have a long way to go before they can counter and/or recover from a dedicated Russian government cyberattack.

The NotPetya malware, Mr. Riggi said, was of the destructive variety. “That digital virus spread uncontrollably across the globe like a biological virus. All the organizations and institutions that had contact with Ukraine became infected.”

According to an indictment of six GRU officers that the Department of Justice announced in December 2020, NotPetya disrupted operations at a major pharmaceutical company, subsequently revealed to be Merck, and hospitals and other medical facilities in the Heritage Valley Health System in Pennsylvania. In addition, it temporarily shut down the transcription services of Nuance Communications, which lost $98 million as a result. Merck received $1.4 billion from an insurer to cover its NotPetya loss, Bloomberg reported.

That incident prompted the AHA to urge hospitals to use “geo-fencing” to block online communications with Ukraine and neighboring countries. However, Mr. Riggi said, that solution is not too effective because hackers commonly use proxy servers in other countries to forward their malware to the intended target.

The AHA alert included a list of actions that hospitals and health systems could take to reduce their vulnerability to Russian hacking. Besides geo-fencing, the AHA suggested that hospitals:

• Heighten staff awareness of the increased risk of receiving malware-laden phishing emails;
• Identify all international and third-party mission-critical, clinical, and operational services and technology and put in place business continuity plans and downtime procedures;
• Check the redundancy, resiliency, and security of the organization’s network and data backups;
• Document, update, and practice the organization’s incident response plan.

Hospitals increasingly targeted

In recent years, Mr. Riggi noted, hospitals have invested much more in cybersecurity than before, and hospital executives have told him that this is now one of their top priorities, along with COVID-19 and workforce issues. This has been not only because of NotPetya, but also because healthcare facilities are being increasingly attacked by foreign ransomware gangs, he says.

The hospitals’ biggest vulnerabilities, he said, are phishing emails, remote desktop access, and unpatched vulnerabilities, in that order. It’s not easy to remedy the latter, he observed, because hospital networks can include up to 100,000 connected medical devices and other computers that can access the network, both within and outside the hospital.

“With the new work-at-home environment, you may have thousands of employees who are using the network outside the traditional perimeter of the organization,” he pointed out. “There’s no longer that standard firewall that protects everything.” In addition, he said, hospitals also have to depend on vendors to develop patches and implement them.

In Mr. McMillan’s view, the healthcare industry is a decade behind the financial industry and other sectors in cybersecurity. Among other things, he says, “half of our hospitals still don’t have active monitoring on their networks. They don’t have privileged access on their networks. A bunch don’t have segmentation or endpoint protection. There are so many things that hospitals don’t have that they need to fend off these attacks — they’re better off than they were in 2017, but they still aren’t where they need to be.”
 

Physician practices also at risk

Employed physicians, naturally, are in danger of losing access to their electronic health records if their hospital’s network goes down as the result of a cyberattack, he notes. Many community doctors also use the EHR of a local hospital, and they’d be similarly affected, Mr. Riggi noted.

Physician practices might be saved if the attack were directed at the hospital and they could still connect to the EHR through a cloud provider, Mr. McMillan said. But Mr. Riggi stressed that practices still need a plan for their doctors to keep working if they lose access to a hospital EHR.

“The other possibility is that the practice could be targeted,” he added. “As hospitals become more hardened, often these hackers are looking for the weak link. The practices could become victims of increased targeting. And the practice becomes the conduit for malware to go from its system to the hospital and infect the hospital system.”
 

Hackers can hit service suppliers

Hospitals’ mission-critical service suppliers may also be targeted by Russian hackers and others, or they may be the accidental victims of a cyberattack elsewhere, Mr. Riggi noted. In the case of Nuance, he said, the disruption in transcription services affected thousands of U.S. healthcare providers who were unable to access their transcribed notes. This not only harmed patient care, but also meant that hospitals couldn’t fully bill for their services.

Another type of service supplier, he said, was struck with a ransomware attack last year. This was a cloud-based service that operated linear accelerators used in radiation oncology. “So radiation oncology and cancer treatment for patients across the U.S. was disrupted, and radiation oncology was delayed for some patients up to 3 weeks.”

More recently, another cloud-based service called Kronos was struck by ransomware. Because of this incident, payroll and timekeeping services were disrupted across several industries, including healthcare.

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

U.S. hospitals are being warned to prepare for a potential cyberattack from either the Russian government, criminal gangs resident in Russia, or both, as a result of the invasion of Ukraine and the U.S. and Western countermeasures against the aggressor nation.

The day after President Biden announced that the war had begun, the American Hospital Association (AHA) issued an alert to hospitals. The cybersecurity division of the Department of Health and Human Services (HHS), known as HC3, joined AHA with another public warning to the healthcare system on March 1. The federal government’s Cybersecurity & Infrastructure Security Agency (CISA) issued a “Shield’s Up” alert to private industry, supporting Biden’s March 21 statement about the need to improve domestic cybersecurity.

CISA warned that the Russian invasion of Ukraine could lead to “malicious cyber activity against the U.S. homeland, including as a response to the unprecedented economic costs imposed on Russia by the U.S. and our allies and partners.” The agency noted that the Russian government is currently exploring options for cyberattacks.

John Riggi, the AHA’s national advisor for cybersecurity and risk, and a former senior executive in the FBI’s cyber division, said in an interview, “We are not aware of any cyberattacks related to the current conflict [in Ukraine]. We don’t know of any specific credible threats targeted against U.S. healthcare from the Russian government.”

He added that there have been reports of Russian hackers searching U.S. health IT security systems for weaknesses.
 

Criminal gangs remain a threat

Besides the Russian government, Mr. Riggi said, Russian criminal gangs are another threat to U.S. hospitals and other healthcare providers. Of particular concern, he noted, is the Conti gang, which “has a history of conducting ransomware attacks against U.S. healthcare and the Irish health system.”

On February 25, said Mr. Riggi, the Conti group announced plans “to retaliate against the West for what they viewed as potential cyber aggression by the West against the Russian federation.”

Sophisticated hacker groups like the Conti gang that operate under the protection of the Russian government have “caused the greatest amount of disruption and have cost the most in terms of recovery and lost business,” Mac McMillan, CEO of CynergisTek, a cybersecurity consulting firm, told this news organization.

However, he said, the current threat is greater for two reasons: first, it will likely come directly from the Russian military intelligence service; and second, there are indications that the malware will be more destructive than ransomware. Two new types of malware identified by HC3 — HermeticWiper and WhisperGate — are designed to wipe out the data in their targets’ systems, rather than just encrypting it and disrupting access to data until a ransom is paid.

The Russian military intelligence service, known as the GRU, is extremely capable and dangerous, Mr. McMillan said. He doubts that many healthcare systems, even if they are fairly well prepared, could withstand an attack from this source. And he fully believes that the attack, when it comes, will aim to wipe out data in victims’ systems in order to create as much chaos and disruption as possible in the United States.
 

Hospitals better prepared, but still have gaps

Like Mr. Riggi, Mr. McMillan said that the healthcare industry is better prepared for cyberattacks now than it was in 2017, when the NotPetya assault on Ukraine’s online infrastructure created considerable collateral damage in the United States. However, he said, hospitals still have a long way to go before they can counter and/or recover from a dedicated Russian government cyberattack.

The NotPetya malware, Mr. Riggi said, was of the destructive variety. “That digital virus spread uncontrollably across the globe like a biological virus. All the organizations and institutions that had contact with Ukraine became infected.”

According to an indictment of six GRU officers that the Department of Justice announced in December 2020, NotPetya disrupted operations at a major pharmaceutical company, subsequently revealed to be Merck, and hospitals and other medical facilities in the Heritage Valley Health System in Pennsylvania. In addition, it temporarily shut down the transcription services of Nuance Communications, which lost $98 million as a result. Merck received $1.4 billion from an insurer to cover its NotPetya loss, Bloomberg reported.

That incident prompted the AHA to urge hospitals to use “geo-fencing” to block online communications with Ukraine and neighboring countries. However, Mr. Riggi said, that solution is not too effective because hackers commonly use proxy servers in other countries to forward their malware to the intended target.

The AHA alert included a list of actions that hospitals and health systems could take to reduce their vulnerability to Russian hacking. Besides geo-fencing, the AHA suggested that hospitals:

• Heighten staff awareness of the increased risk of receiving malware-laden phishing emails;
• Identify all international and third-party mission-critical, clinical, and operational services and technology and put in place business continuity plans and downtime procedures;
• Check the redundancy, resiliency, and security of the organization’s network and data backups;
• Document, update, and practice the organization’s incident response plan.

Hospitals increasingly targeted

In recent years, Mr. Riggi noted, hospitals have invested much more in cybersecurity than before, and hospital executives have told him that this is now one of their top priorities, along with COVID-19 and workforce issues. This has been not only because of NotPetya, but also because healthcare facilities are being increasingly attacked by foreign ransomware gangs, he says.

The hospitals’ biggest vulnerabilities, he said, are phishing emails, remote desktop access, and unpatched vulnerabilities, in that order. It’s not easy to remedy the latter, he observed, because hospital networks can include up to 100,000 connected medical devices and other computers that can access the network, both within and outside the hospital.

“With the new work-at-home environment, you may have thousands of employees who are using the network outside the traditional perimeter of the organization,” he pointed out. “There’s no longer that standard firewall that protects everything.” In addition, he said, hospitals also have to depend on vendors to develop patches and implement them.

In Mr. McMillan’s view, the healthcare industry is a decade behind the financial industry and other sectors in cybersecurity. Among other things, he says, “half of our hospitals still don’t have active monitoring on their networks. They don’t have privileged access on their networks. A bunch don’t have segmentation or endpoint protection. There are so many things that hospitals don’t have that they need to fend off these attacks — they’re better off than they were in 2017, but they still aren’t where they need to be.”
 

Physician practices also at risk

Employed physicians, naturally, are in danger of losing access to their electronic health records if their hospital’s network goes down as the result of a cyberattack, he notes. Many community doctors also use the EHR of a local hospital, and they’d be similarly affected, Mr. Riggi noted.

Physician practices might be saved if the attack were directed at the hospital and they could still connect to the EHR through a cloud provider, Mr. McMillan said. But Mr. Riggi stressed that practices still need a plan for their doctors to keep working if they lose access to a hospital EHR.

“The other possibility is that the practice could be targeted,” he added. “As hospitals become more hardened, often these hackers are looking for the weak link. The practices could become victims of increased targeting. And the practice becomes the conduit for malware to go from its system to the hospital and infect the hospital system.”
 

Hackers can hit service suppliers

Hospitals’ mission-critical service suppliers may also be targeted by Russian hackers and others, or they may be the accidental victims of a cyberattack elsewhere, Mr. Riggi noted. In the case of Nuance, he said, the disruption in transcription services affected thousands of U.S. healthcare providers who were unable to access their transcribed notes. This not only harmed patient care, but also meant that hospitals couldn’t fully bill for their services.

Another type of service supplier, he said, was struck with a ransomware attack last year. This was a cloud-based service that operated linear accelerators used in radiation oncology. “So radiation oncology and cancer treatment for patients across the U.S. was disrupted, and radiation oncology was delayed for some patients up to 3 weeks.”

More recently, another cloud-based service called Kronos was struck by ransomware. Because of this incident, payroll and timekeeping services were disrupted across several industries, including healthcare.

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

What prophylactic antibiotic should be administered intrapartum to a pregnant woman who is colonized with group B streptococci but who has a mild allergy to penicillin?

Continue to the answer...

In this situation, the drug of choice is intravenous cefazolin, 2 g initially then 1 g every 8 hours until delivery. For patients with a severe allergy to penicillin, the drugs of choice are either clindamycin, 900 mg intravenously every 8 hours (if sensitivity of the organism is confirmed), or vancomycin, 20 mg/kg intravenously every 8 hours (maximum of 2 g per single dose).

What prophylactic antibiotic should be administered intrapartum to a pregnant woman who is colonized with group B streptococci but who has a mild allergy to penicillin?

Continue to the answer...

In this situation, the drug of choice is intravenous cefazolin, 2 g initially then 1 g every 8 hours until delivery. For patients with a severe allergy to penicillin, the drugs of choice are either clindamycin, 900 mg intravenously every 8 hours (if sensitivity of the organism is confirmed), or vancomycin, 20 mg/kg intravenously every 8 hours (maximum of 2 g per single dose).

What prophylactic antibiotic should be administered intrapartum to a pregnant woman who is colonized with group B streptococci but who has a mild allergy to penicillin?

Continue to the answer...

In this situation, the drug of choice is intravenous cefazolin, 2 g initially then 1 g every 8 hours until delivery. For patients with a severe allergy to penicillin, the drugs of choice are either clindamycin, 900 mg intravenously every 8 hours (if sensitivity of the organism is confirmed), or vancomycin, 20 mg/kg intravenously every 8 hours (maximum of 2 g per single dose).

Ms. P, a 63-year-old woman with a history of schizophrenia whose symptoms have been stable on haloperidol 10 mg/d and ziprasidone 40 mg twice daily, presents to the outpatient clinic for a medication review. She mentions that she has noticed problems with her “memory.” She says she has had difficulty remembering names of people and places as well as difficulty concentrating while reading and writing, which she did months ago with ease. A Montreal Cognitive Assessment (MoCA) is conducted, and Ms. P scores 13/30, indicating moderate cognitive impairment. Visuospatial tasks and clock drawing are intact, but she exhibits impairments in working memory, attention, and concentration. One year ago, Ms. P’s MoCA score was 27/30. She agrees to a neurologic assessment and is referred to neurology for work-up.

Ms. P’s physical examination and routine laboratory tests are all within normal limits. The neurologic exam reveals deficits in working memory, concentration, and attention, but is otherwise unremarkable. MRI reveals mild chronic microvascular changes. The neurology service does not rule out cognitive impairment but recommends adjusting the dosage of Ms. P’s psychiatric medications to elucidate if her impairment of memory and attention is due to medications. However, Ms. P had been managed on her current regimen for several years and had not been hospitalized in many years. Previous attempts to taper her antipsychotics had resulted in worsening symptoms. Ms. P is reluctant to attempt a taper of her antipsychotics because she fears decompensation of her chronic illness. The treating team reviews Ms. P’s medication regimen, and notes that she is receiving benztropine 1 mg twice daily for prophylaxis of extrapyramidal symptoms (EPS). Ms. P denies past or present symptoms of drug-induced parkinsonism, dystonia, or akathisia as well as constipation, sialorrhea, blurry vision, palpitations, or urinary retention.

Benztropine is a tropane alkaloid that was synthetized by combining the tropine portion of atropine with the benzhydryl portion of diphenhydramine hydrochloride. It has anticholinergic and antihistaminic properties¹ and seems to inhibit the dopamine transporter. Benztropine is indicated for all forms of parkinsonism, including antipsychotic-induced parkinsonism, but is also prescribed for many off-label uses, including sialorrhea and akathisia (although many authors do not recommend anticholinergics for this purpose^2,3), and for prophylaxis of EPS. Benztropine can be administered intravenously, intramuscularly, or orally. Given orally, the typical dosing is twice daily with a maximum dose of 6 mg/d. Benztropine is preferred over diphenhydramine and trihexyphenidyl due to adverse effects of sedation or potential for misuse of the medication.¹

Second-generation antipsychotics (SGAs) have been associated with lower rates of neurologic adverse effects compared with first-generation antipsychotics (FGAs). Because SGAs are increasingly prescribed, the use of benztropine (along with other agents such as trihexyphenidyl) for EPS prophylaxis is not an evidence-based practice. However, despite a movement away from prophylactic management of movement disorders, benztropine continues to be prescribed for EPS and/or cholinergic symptoms, despite the peripheral and cognitive adverse effects of this agent and, in many instances, the lack of clear indication for its use.

According to the most recent edition of the American Psychiatric Association’s (APA) Practice Guideline for the Treatment of Patients with Schizophrenia,⁴ anticholinergics should only be used for preventing acute dystonia in conjunction with a long-acting injectable antipsychotic. Furthermore, the APA Guideline states anticholinergics may be used for drug-induced parkinsonism when the dose of an antipsychotic cannot be reduced and an alternative agent is required. However, the first-line agent for drug-induced parkinsonism is amantadine, and benztropine should only be considered if amantadine is contraindicated.⁴ The rationale for this guideline and for judicious use of anticholinergics is that like any pharmacologic treatment, anticholinergics (including benztropine) carry the potential for adverse effects. For benztropine, these range from mild effects such as tachycardia and constipation to paralytic ileus, increased falls, worsening of tardive dyskinesia (TD), and potential cognitive impairment. Literature suggests that the first step in managing cognitive concerns in a patient with schizophrenia should be a close review of medications, and avoidance of agents with anticholinergic properties.⁵

Prescribing benztropine for EPS

EPS, which include dystonia, akathisia, drug-induced parkinsonism, and TD, are very frequent adverse effects noted with antipsychotics. Benztropine has demonstrated benefit in managing acute dystonia and the APA Guideline recommends IM administration of either benztropine 1 mg or diphenhydramine 25 mg for this purpose.⁴ However, in our experience, the most frequent indication for long-term prescribing of benztropine is prophylaxis of antipsychoticinduced dystonia. This use was suggested by some older studies. In a 1987 study by Boyer et al,⁶ patients who were administered benztropine with haloperidol did not develop acute dystonia, while patients who received haloperidol alone developed dystonia. However, this was a small retrospective study with methodological issues. Boyer et al⁶ suggested discontinuing prophylaxis with benztropine within 1 week, as acute dystonia occurred within 2.5 days. Other researchers^7,8 have argued that short-term prophylaxis with benztropine for 1 week may work, especially during treatment with high-potency antipsychotics. However, in a review of the use of anticholinergics in conjunction with antipsychotics, Desmarais et al⁵ concluded that there is no need for prophylaxis and recommended alternative treatments. As we have noticed in Ms. P and other patients treated in our facilities, benztropine is frequently continued indefinitely without a clinical indication for its continuous use. Assessment and indication for continued use of benztropine should be considered regularly, and it should be discontinued when there is no clear indication for its use or when adverse effects emerge.

Prescribing benztropine for TD

TD is a subtype of tardive syndromes associated with the use of antipsychotics. It is characterized by repetitive involuntary movements such as lip smacking, puckering, chewing, or tongue protrusion. Proposed pathophysiological mechanisms include dopamine receptor hypersensitivity, N-methyl-D-aspartate (NMDA) receptor excitotoxicity, and gamma-aminobutyric acid (GABA)-containing neuron activity.

According to the APA Guideline, evidence of benztropine’s efficacy for the prevention of TD is lacking.⁴ A 2018 Cochrane systematic review⁹ was unable to provide a definitive conclusion regarding the effectiveness of benztropine and other anticholinergics for the treatment of antipsychotic-induced TD. While many clinicians believe that benztropine can be used to treat all types of EPS, there are no clear instances in reviewed literature where the efficacy of benztropine for treating TD could be reliably demonstrated. Furthermore, some literature suggests that anticholinergics such as benztropine increase the risk of developing TD.^5,10 The mechanism underlying benztropine’s ability to precipitate or exacerbate abnormal movements is unclear, though it is theorized that anticholinergic medications may inhibit dopamine reuptake into neurons, thus leading to an excess of dopamine in the synaptic cleft that manifests as dyskinesias.¹⁰ Some authors also recommend that the first step in the management of TD should be to gradually discontinue anticholinergics, as this has been associated with improvement in TD.¹¹

Continue to: Prescribing anticholinergics in specific patient populations...

In addition to the adverse effects described above, benztropine can affect cognition, as we observed in Ms. P. The cholinergic system plays a role in human cognition, and blockade of muscarinic receptors has been associated with impairments in working memory and prefrontal tasks.¹² These adverse cognitive effects are more pronounced in certain populations, including patients with schizophrenia and older adults.

Schizophrenia is associated with declining cognitive function, and the cognitive faculties of patients with schizophrenia may be worsened by anticholinergics. In patients with schizophrenia, social interactions and social integration are often impacted by profound negative symptoms such as social withdrawal and poverty of thought and speech.¹³ In a double-blind study by Baker et al,¹⁴ benztropine was found to have an impact on attention and concentration in patients with chronic schizophrenia. Baker et al¹⁴ found that patients with schizophrenia who were switched from benztropine to placebo increased their overall Wechsler Memory Scale scores compared to those maintained on benztropine. One crosssectional analysis found that a higher anticholinergic burden was associated with impairments across all cognitive domains, including memory, attention/control, executive and visuospatial functioning, and motor speed domains.¹⁵ Importantly, a higher anticholinergic medication burden was associated with worse cognitive performance.¹⁵ In addition to impairments in cognitive processing, anticholinergics have been associated with a decreased ability to benefit from psychosocial programs and impaired abilities to manage activities of daily living.⁴ In another study exploring the effects of discontinuing anticholinergics and the impact on movement disorders, Desmarais et al¹⁶ found patients experienced a significant improvement in scores on the Brief Assessment of Cognition in Schizophrenia after discontinuing anticholinergics. Vinogradov et al¹⁷ noted that “serum anticholinergic activity in schizophrenia patients shows a significant association with impaired performance in measures of verbal working memory and verbal learning memory and was significantly associated with a lowered response to an intensive course of computerized cognitive training.” They felt their findings underscored the cognitive cost of medications with high anticholinergic burden.

Geriatric patients. Careful consideration should be given before starting benztropine in patients age ≥65. The 2019 American Geriatric Society’s Beers Criteria¹⁸ recommend avoiding benztropine in geriatric patients; the level of recommendation is strong. Furthermore, the American Geriatric Society designates benztropine as a medication that should be avoided, and a nondrug approach or alternative medication be prescribed independent of the patient’s condition or diagnosis. In a recently published case report, Esang et al¹⁹ highlighted several salient findings from previous studies on the risks associated with anticholinergic use:

• any medications a patient takes with anticholinergic properties contribute to the overall anticholinergic load of a patient’s medication regimen
• the higher the anticholinergic burden, the greater the cognitive deficits
• switching from an FGA to an SGA may decrease the risk of EPS and may limit the need for anticholinergic medications such as benztropine for a particular patient.

One must also consider that the effects of multiple medications with anticholinergic properties is probably cumulative.

Alternatives for treating drug-induced parkinsonism

Antipsychotics exert their effects through antagonism of the D2 receptor, and this is the same mechanism that leads to parkinsonism. Specifically, the mechanism is believed to be D2 receptor antagonism in the striatum leading to disinhibition of striatal neurons containing GABA.¹¹ This disinhibition of medium spiny neurons is propagated when acetylcholine is released from cholinergic interneurons. Anticholinergics such as benztropine can remedy symptoms by blocking the signal of acetylcholine on the M1 receptors on medium spiny neurons. However, benztropine also has the propensity to decrease cholinergic transmission, thereby impairing storage of new information into long-term memory as well as impair perception of time—similar to effects seen with (for instance) diphenhydramine.²⁰

The first step in managing drug-induced parkinsonism is to monitor symptoms. The APA Guideline recommends monitoring for acute-onset EPS at weekly intervals when beginning treatment and until stable for 2 weeks, and then monitoring at every follow-up visit thereafter.⁴ The next recommendation for long-term management of drug-induced parkinsonism is reducing the antipsychotic dose, or replacing the patient’s antipsychotic with an antipsychotic that is less likely to precipitate parkinsonism,4 such as quetiapine, iloperidone, or clozapine.¹¹ If dose reduction is not possible, and the patient’s symptoms are severe, pharmacologic management is indicated. The APA Guideline recommends amantadine as a first-line agent because it is associated with fewer peripheral adverse effects and less impairment in cognition compared with benztropine.⁴ In a small (N = 60) doubleblind crossover trial, Gelenberg et al²⁰ found benztropine 4 mg/d—but not amantadine 200 mg/d—impaired free recall and perception of time, and participants’ perception of their own memory impairment was significantly greater with benztropine. Amantadine has also been compared to biperiden, a relatively selective M1 muscarinic receptor muscarinic agent. In a separate double-blind crossover study of 26 patients with chronic schizophrenia, Silver and Geraisy²¹ found that compared to amantadine, biperiden was associated with worse memory performance. The recommended starting dose of amantadine for parkinsonism is 100 mg in the morning, increased to 100 mg twice a day and titrated to a maximum daily dose of 300 mg/d in divided doses.⁴

Continue to: Alternatives for treating drug-induced akathisia...

Akathisia remains a relatively common adverse effect of SGAs, and the profound physical distress and impaired functioning caused by akathisia necessitates pharmacologic treatment. Despite frequent use in practice for presumed benefit in akathisia, benztropine is not effective for the treatment of akathisia and the APA Guideline recommends that long-term management should begin with an antipsychotic dose reduction, followed by a switch to an agent with less propensity to incite akathisia.⁴ Acute manifestations of akathisia must be treated, and mirtazapine, propranolol, or clonazepam may be considered as alternatives.⁴ Mirtazapine is dosed 7.5 mg to 10 mg nightly for akathisia, though it should be used in caution in patients at risk for mania.⁴ Mirtazapine’s potent 5-HT2A blockade at low doses may contribute to its utility in treating akathisia.² Propranolol, a nonselective lipophilic beta-adrenergic antagonist, also has demonstrated efficacy in managing akathisia, with recommended dosing of 40 mg to 80 mg twice daily.² Benzodiazepines such as clonazepam require judicious use for akathisia because they may also precipitate or exacerbate cognitive impairment.⁴

Alternatives for treating TD

As mentioned above, benztropine is not recommended for the treatment of TD.¹ The Box^4,22,23 outlines potential treatment options for TD.

Box

Discontinuing benztropine

Benztropine is recommended as a firstline agent for the management of acute dystonia, and it may be used temporarily for drug-induced parkinsonism, but it is not recommended to prevent EPS or TD. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic agent such as benztropine. Based on their review of earlier studies, Desmarais et al⁵ suggest a gradual 3-month discontinuation of benztropine. Multiple studies have demonstrated an ability to taper anticholinergics in days to months.⁴ However, gradual discontinuation is advisable to avoid cholinergic rebound and the reemergence of EPS, and to decrease the risk of neuroleptic malignant syndrome associated with sudden discontinuation.⁵ One suggested taper regimen is a decrease of 0.5 mg benztropine every week. Amantadine may be considered if parkinsonism is noted during the taper. Patients on benztropine may develop rebound symptoms, such as vivid dreams/nightmares; if this occurs, the taper rate can be slowed to a decrease of 0.5 mg every 2 weeks.⁴

Continue to: First do no harm...

Psychiatrists commonly prescribe benztropine to prevent EPS and TD, but available literature does not support the efficacy of benztropine for mitigating drug-induced parkinsonism, and studies report benztropine may significantly worsen cognitive processes and exacerbate TD.¹⁶ In addition, benztropine misuse has been correlated with euphoria and psychosis.¹⁶ More than 3 decades ago, the World Health Organization Heads of Centres Collaborating in WHO-Coordinated Studies on Biological Aspects of Mental Illness issued a consensus statement²⁴ discouraging the prophylactic use of anticholinergics for patients receiving antipsychotics, yet we still see patients on an indefinite regimen of benztropine.

As clinicians, our goals should be to optimize a patient’s functioning and quality of life, and to use the lowest dose of medication along with the fewest medications necessary to avoid adverse effects such as EPS. Benztropine is recommended as a first-line agent for the management of acute dystonia, but its continued or indefinite use to prevent antipsychotic-induced adverse effects is not recommended. While all pharmacologic interventions carry a risk of adverse effects, weighing the risk of those effects against the clinical benefits is the prerogative of a skilled clinician. Benztropine and other anticholinergics prescribed for prophylactic purposes have numerous adverse effects, limited clinical utility, and a deleterious effect on quality of life. Furthermore, benztropine prophylaxis of drug-induced parkinsonism does not seem to be warranted, and the risks do not seem to outweigh the harm benztropine may cause, with the possible exception of “prophylactic” treatment of dystonia that is discontinued in a few days, as some researchers have suggested.^6-8 The preventive value of benztropine has not been demonstrated. It is time we took inventory of medications that might cause more harm than good, rely on current treatment guidelines instead of habit, and use these agents judiciously while considering replacement with novel, safer medications whenever possible.

CASE CONTINUED

The clinical team considers benztropine’s ability to cause cognitive effects, and decides to taper and discontinue it over 1 month. Ms. P is seen in an outpatient clinic within 1 month of discontinuing benztropine. She reports that her difficulty remembering words and details has improved. She also says that she is now able to concentrate on writing and reading. The consulting neurologist also notes improvement. Ms. P continues to report improvement in symptoms over the next 2 months of follow-up, and says that her mood improved and she has less apathy.

Bottom Line

Benztropine is a first-line medication for acute dystonia, but its continued or indefinite use for preventing antipsychotic-induced adverse effects is not recommended. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic medication such as benztropine.

Ms. P, a 63-year-old woman with a history of schizophrenia whose symptoms have been stable on haloperidol 10 mg/d and ziprasidone 40 mg twice daily, presents to the outpatient clinic for a medication review. She mentions that she has noticed problems with her “memory.” She says she has had difficulty remembering names of people and places as well as difficulty concentrating while reading and writing, which she did months ago with ease. A Montreal Cognitive Assessment (MoCA) is conducted, and Ms. P scores 13/30, indicating moderate cognitive impairment. Visuospatial tasks and clock drawing are intact, but she exhibits impairments in working memory, attention, and concentration. One year ago, Ms. P’s MoCA score was 27/30. She agrees to a neurologic assessment and is referred to neurology for work-up.

Ms. P’s physical examination and routine laboratory tests are all within normal limits. The neurologic exam reveals deficits in working memory, concentration, and attention, but is otherwise unremarkable. MRI reveals mild chronic microvascular changes. The neurology service does not rule out cognitive impairment but recommends adjusting the dosage of Ms. P’s psychiatric medications to elucidate if her impairment of memory and attention is due to medications. However, Ms. P had been managed on her current regimen for several years and had not been hospitalized in many years. Previous attempts to taper her antipsychotics had resulted in worsening symptoms. Ms. P is reluctant to attempt a taper of her antipsychotics because she fears decompensation of her chronic illness. The treating team reviews Ms. P’s medication regimen, and notes that she is receiving benztropine 1 mg twice daily for prophylaxis of extrapyramidal symptoms (EPS). Ms. P denies past or present symptoms of drug-induced parkinsonism, dystonia, or akathisia as well as constipation, sialorrhea, blurry vision, palpitations, or urinary retention.

Benztropine is a tropane alkaloid that was synthetized by combining the tropine portion of atropine with the benzhydryl portion of diphenhydramine hydrochloride. It has anticholinergic and antihistaminic properties¹ and seems to inhibit the dopamine transporter. Benztropine is indicated for all forms of parkinsonism, including antipsychotic-induced parkinsonism, but is also prescribed for many off-label uses, including sialorrhea and akathisia (although many authors do not recommend anticholinergics for this purpose^2,3), and for prophylaxis of EPS. Benztropine can be administered intravenously, intramuscularly, or orally. Given orally, the typical dosing is twice daily with a maximum dose of 6 mg/d. Benztropine is preferred over diphenhydramine and trihexyphenidyl due to adverse effects of sedation or potential for misuse of the medication.¹

Second-generation antipsychotics (SGAs) have been associated with lower rates of neurologic adverse effects compared with first-generation antipsychotics (FGAs). Because SGAs are increasingly prescribed, the use of benztropine (along with other agents such as trihexyphenidyl) for EPS prophylaxis is not an evidence-based practice. However, despite a movement away from prophylactic management of movement disorders, benztropine continues to be prescribed for EPS and/or cholinergic symptoms, despite the peripheral and cognitive adverse effects of this agent and, in many instances, the lack of clear indication for its use.

According to the most recent edition of the American Psychiatric Association’s (APA) Practice Guideline for the Treatment of Patients with Schizophrenia,⁴ anticholinergics should only be used for preventing acute dystonia in conjunction with a long-acting injectable antipsychotic. Furthermore, the APA Guideline states anticholinergics may be used for drug-induced parkinsonism when the dose of an antipsychotic cannot be reduced and an alternative agent is required. However, the first-line agent for drug-induced parkinsonism is amantadine, and benztropine should only be considered if amantadine is contraindicated.⁴ The rationale for this guideline and for judicious use of anticholinergics is that like any pharmacologic treatment, anticholinergics (including benztropine) carry the potential for adverse effects. For benztropine, these range from mild effects such as tachycardia and constipation to paralytic ileus, increased falls, worsening of tardive dyskinesia (TD), and potential cognitive impairment. Literature suggests that the first step in managing cognitive concerns in a patient with schizophrenia should be a close review of medications, and avoidance of agents with anticholinergic properties.⁵

Prescribing benztropine for EPS

EPS, which include dystonia, akathisia, drug-induced parkinsonism, and TD, are very frequent adverse effects noted with antipsychotics. Benztropine has demonstrated benefit in managing acute dystonia and the APA Guideline recommends IM administration of either benztropine 1 mg or diphenhydramine 25 mg for this purpose.⁴ However, in our experience, the most frequent indication for long-term prescribing of benztropine is prophylaxis of antipsychoticinduced dystonia. This use was suggested by some older studies. In a 1987 study by Boyer et al,⁶ patients who were administered benztropine with haloperidol did not develop acute dystonia, while patients who received haloperidol alone developed dystonia. However, this was a small retrospective study with methodological issues. Boyer et al⁶ suggested discontinuing prophylaxis with benztropine within 1 week, as acute dystonia occurred within 2.5 days. Other researchers^7,8 have argued that short-term prophylaxis with benztropine for 1 week may work, especially during treatment with high-potency antipsychotics. However, in a review of the use of anticholinergics in conjunction with antipsychotics, Desmarais et al⁵ concluded that there is no need for prophylaxis and recommended alternative treatments. As we have noticed in Ms. P and other patients treated in our facilities, benztropine is frequently continued indefinitely without a clinical indication for its continuous use. Assessment and indication for continued use of benztropine should be considered regularly, and it should be discontinued when there is no clear indication for its use or when adverse effects emerge.

Prescribing benztropine for TD

TD is a subtype of tardive syndromes associated with the use of antipsychotics. It is characterized by repetitive involuntary movements such as lip smacking, puckering, chewing, or tongue protrusion. Proposed pathophysiological mechanisms include dopamine receptor hypersensitivity, N-methyl-D-aspartate (NMDA) receptor excitotoxicity, and gamma-aminobutyric acid (GABA)-containing neuron activity.

According to the APA Guideline, evidence of benztropine’s efficacy for the prevention of TD is lacking.⁴ A 2018 Cochrane systematic review⁹ was unable to provide a definitive conclusion regarding the effectiveness of benztropine and other anticholinergics for the treatment of antipsychotic-induced TD. While many clinicians believe that benztropine can be used to treat all types of EPS, there are no clear instances in reviewed literature where the efficacy of benztropine for treating TD could be reliably demonstrated. Furthermore, some literature suggests that anticholinergics such as benztropine increase the risk of developing TD.^5,10 The mechanism underlying benztropine’s ability to precipitate or exacerbate abnormal movements is unclear, though it is theorized that anticholinergic medications may inhibit dopamine reuptake into neurons, thus leading to an excess of dopamine in the synaptic cleft that manifests as dyskinesias.¹⁰ Some authors also recommend that the first step in the management of TD should be to gradually discontinue anticholinergics, as this has been associated with improvement in TD.¹¹

Continue to: Prescribing anticholinergics in specific patient populations...

In addition to the adverse effects described above, benztropine can affect cognition, as we observed in Ms. P. The cholinergic system plays a role in human cognition, and blockade of muscarinic receptors has been associated with impairments in working memory and prefrontal tasks.¹² These adverse cognitive effects are more pronounced in certain populations, including patients with schizophrenia and older adults.

Schizophrenia is associated with declining cognitive function, and the cognitive faculties of patients with schizophrenia may be worsened by anticholinergics. In patients with schizophrenia, social interactions and social integration are often impacted by profound negative symptoms such as social withdrawal and poverty of thought and speech.¹³ In a double-blind study by Baker et al,¹⁴ benztropine was found to have an impact on attention and concentration in patients with chronic schizophrenia. Baker et al¹⁴ found that patients with schizophrenia who were switched from benztropine to placebo increased their overall Wechsler Memory Scale scores compared to those maintained on benztropine. One crosssectional analysis found that a higher anticholinergic burden was associated with impairments across all cognitive domains, including memory, attention/control, executive and visuospatial functioning, and motor speed domains.¹⁵ Importantly, a higher anticholinergic medication burden was associated with worse cognitive performance.¹⁵ In addition to impairments in cognitive processing, anticholinergics have been associated with a decreased ability to benefit from psychosocial programs and impaired abilities to manage activities of daily living.⁴ In another study exploring the effects of discontinuing anticholinergics and the impact on movement disorders, Desmarais et al¹⁶ found patients experienced a significant improvement in scores on the Brief Assessment of Cognition in Schizophrenia after discontinuing anticholinergics. Vinogradov et al¹⁷ noted that “serum anticholinergic activity in schizophrenia patients shows a significant association with impaired performance in measures of verbal working memory and verbal learning memory and was significantly associated with a lowered response to an intensive course of computerized cognitive training.” They felt their findings underscored the cognitive cost of medications with high anticholinergic burden.

Geriatric patients. Careful consideration should be given before starting benztropine in patients age ≥65. The 2019 American Geriatric Society’s Beers Criteria¹⁸ recommend avoiding benztropine in geriatric patients; the level of recommendation is strong. Furthermore, the American Geriatric Society designates benztropine as a medication that should be avoided, and a nondrug approach or alternative medication be prescribed independent of the patient’s condition or diagnosis. In a recently published case report, Esang et al¹⁹ highlighted several salient findings from previous studies on the risks associated with anticholinergic use:

• any medications a patient takes with anticholinergic properties contribute to the overall anticholinergic load of a patient’s medication regimen
• the higher the anticholinergic burden, the greater the cognitive deficits
• switching from an FGA to an SGA may decrease the risk of EPS and may limit the need for anticholinergic medications such as benztropine for a particular patient.

One must also consider that the effects of multiple medications with anticholinergic properties is probably cumulative.

Alternatives for treating drug-induced parkinsonism

Antipsychotics exert their effects through antagonism of the D2 receptor, and this is the same mechanism that leads to parkinsonism. Specifically, the mechanism is believed to be D2 receptor antagonism in the striatum leading to disinhibition of striatal neurons containing GABA.¹¹ This disinhibition of medium spiny neurons is propagated when acetylcholine is released from cholinergic interneurons. Anticholinergics such as benztropine can remedy symptoms by blocking the signal of acetylcholine on the M1 receptors on medium spiny neurons. However, benztropine also has the propensity to decrease cholinergic transmission, thereby impairing storage of new information into long-term memory as well as impair perception of time—similar to effects seen with (for instance) diphenhydramine.²⁰

The first step in managing drug-induced parkinsonism is to monitor symptoms. The APA Guideline recommends monitoring for acute-onset EPS at weekly intervals when beginning treatment and until stable for 2 weeks, and then monitoring at every follow-up visit thereafter.⁴ The next recommendation for long-term management of drug-induced parkinsonism is reducing the antipsychotic dose, or replacing the patient’s antipsychotic with an antipsychotic that is less likely to precipitate parkinsonism,4 such as quetiapine, iloperidone, or clozapine.¹¹ If dose reduction is not possible, and the patient’s symptoms are severe, pharmacologic management is indicated. The APA Guideline recommends amantadine as a first-line agent because it is associated with fewer peripheral adverse effects and less impairment in cognition compared with benztropine.⁴ In a small (N = 60) doubleblind crossover trial, Gelenberg et al²⁰ found benztropine 4 mg/d—but not amantadine 200 mg/d—impaired free recall and perception of time, and participants’ perception of their own memory impairment was significantly greater with benztropine. Amantadine has also been compared to biperiden, a relatively selective M1 muscarinic receptor muscarinic agent. In a separate double-blind crossover study of 26 patients with chronic schizophrenia, Silver and Geraisy²¹ found that compared to amantadine, biperiden was associated with worse memory performance. The recommended starting dose of amantadine for parkinsonism is 100 mg in the morning, increased to 100 mg twice a day and titrated to a maximum daily dose of 300 mg/d in divided doses.⁴

Continue to: Alternatives for treating drug-induced akathisia...

Akathisia remains a relatively common adverse effect of SGAs, and the profound physical distress and impaired functioning caused by akathisia necessitates pharmacologic treatment. Despite frequent use in practice for presumed benefit in akathisia, benztropine is not effective for the treatment of akathisia and the APA Guideline recommends that long-term management should begin with an antipsychotic dose reduction, followed by a switch to an agent with less propensity to incite akathisia.⁴ Acute manifestations of akathisia must be treated, and mirtazapine, propranolol, or clonazepam may be considered as alternatives.⁴ Mirtazapine is dosed 7.5 mg to 10 mg nightly for akathisia, though it should be used in caution in patients at risk for mania.⁴ Mirtazapine’s potent 5-HT2A blockade at low doses may contribute to its utility in treating akathisia.² Propranolol, a nonselective lipophilic beta-adrenergic antagonist, also has demonstrated efficacy in managing akathisia, with recommended dosing of 40 mg to 80 mg twice daily.² Benzodiazepines such as clonazepam require judicious use for akathisia because they may also precipitate or exacerbate cognitive impairment.⁴

Alternatives for treating TD

As mentioned above, benztropine is not recommended for the treatment of TD.¹ The Box^4,22,23 outlines potential treatment options for TD.

Box

Discontinuing benztropine

Benztropine is recommended as a firstline agent for the management of acute dystonia, and it may be used temporarily for drug-induced parkinsonism, but it is not recommended to prevent EPS or TD. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic agent such as benztropine. Based on their review of earlier studies, Desmarais et al⁵ suggest a gradual 3-month discontinuation of benztropine. Multiple studies have demonstrated an ability to taper anticholinergics in days to months.⁴ However, gradual discontinuation is advisable to avoid cholinergic rebound and the reemergence of EPS, and to decrease the risk of neuroleptic malignant syndrome associated with sudden discontinuation.⁵ One suggested taper regimen is a decrease of 0.5 mg benztropine every week. Amantadine may be considered if parkinsonism is noted during the taper. Patients on benztropine may develop rebound symptoms, such as vivid dreams/nightmares; if this occurs, the taper rate can be slowed to a decrease of 0.5 mg every 2 weeks.⁴

Continue to: First do no harm...

Psychiatrists commonly prescribe benztropine to prevent EPS and TD, but available literature does not support the efficacy of benztropine for mitigating drug-induced parkinsonism, and studies report benztropine may significantly worsen cognitive processes and exacerbate TD.¹⁶ In addition, benztropine misuse has been correlated with euphoria and psychosis.¹⁶ More than 3 decades ago, the World Health Organization Heads of Centres Collaborating in WHO-Coordinated Studies on Biological Aspects of Mental Illness issued a consensus statement²⁴ discouraging the prophylactic use of anticholinergics for patients receiving antipsychotics, yet we still see patients on an indefinite regimen of benztropine.

As clinicians, our goals should be to optimize a patient’s functioning and quality of life, and to use the lowest dose of medication along with the fewest medications necessary to avoid adverse effects such as EPS. Benztropine is recommended as a first-line agent for the management of acute dystonia, but its continued or indefinite use to prevent antipsychotic-induced adverse effects is not recommended. While all pharmacologic interventions carry a risk of adverse effects, weighing the risk of those effects against the clinical benefits is the prerogative of a skilled clinician. Benztropine and other anticholinergics prescribed for prophylactic purposes have numerous adverse effects, limited clinical utility, and a deleterious effect on quality of life. Furthermore, benztropine prophylaxis of drug-induced parkinsonism does not seem to be warranted, and the risks do not seem to outweigh the harm benztropine may cause, with the possible exception of “prophylactic” treatment of dystonia that is discontinued in a few days, as some researchers have suggested.^6-8 The preventive value of benztropine has not been demonstrated. It is time we took inventory of medications that might cause more harm than good, rely on current treatment guidelines instead of habit, and use these agents judiciously while considering replacement with novel, safer medications whenever possible.

CASE CONTINUED

The clinical team considers benztropine’s ability to cause cognitive effects, and decides to taper and discontinue it over 1 month. Ms. P is seen in an outpatient clinic within 1 month of discontinuing benztropine. She reports that her difficulty remembering words and details has improved. She also says that she is now able to concentrate on writing and reading. The consulting neurologist also notes improvement. Ms. P continues to report improvement in symptoms over the next 2 months of follow-up, and says that her mood improved and she has less apathy.

Bottom Line

Benztropine is a first-line medication for acute dystonia, but its continued or indefinite use for preventing antipsychotic-induced adverse effects is not recommended. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic medication such as benztropine.

Ms. P, a 63-year-old woman with a history of schizophrenia whose symptoms have been stable on haloperidol 10 mg/d and ziprasidone 40 mg twice daily, presents to the outpatient clinic for a medication review. She mentions that she has noticed problems with her “memory.” She says she has had difficulty remembering names of people and places as well as difficulty concentrating while reading and writing, which she did months ago with ease. A Montreal Cognitive Assessment (MoCA) is conducted, and Ms. P scores 13/30, indicating moderate cognitive impairment. Visuospatial tasks and clock drawing are intact, but she exhibits impairments in working memory, attention, and concentration. One year ago, Ms. P’s MoCA score was 27/30. She agrees to a neurologic assessment and is referred to neurology for work-up.

Ms. P’s physical examination and routine laboratory tests are all within normal limits. The neurologic exam reveals deficits in working memory, concentration, and attention, but is otherwise unremarkable. MRI reveals mild chronic microvascular changes. The neurology service does not rule out cognitive impairment but recommends adjusting the dosage of Ms. P’s psychiatric medications to elucidate if her impairment of memory and attention is due to medications. However, Ms. P had been managed on her current regimen for several years and had not been hospitalized in many years. Previous attempts to taper her antipsychotics had resulted in worsening symptoms. Ms. P is reluctant to attempt a taper of her antipsychotics because she fears decompensation of her chronic illness. The treating team reviews Ms. P’s medication regimen, and notes that she is receiving benztropine 1 mg twice daily for prophylaxis of extrapyramidal symptoms (EPS). Ms. P denies past or present symptoms of drug-induced parkinsonism, dystonia, or akathisia as well as constipation, sialorrhea, blurry vision, palpitations, or urinary retention.

Benztropine is a tropane alkaloid that was synthetized by combining the tropine portion of atropine with the benzhydryl portion of diphenhydramine hydrochloride. It has anticholinergic and antihistaminic properties¹ and seems to inhibit the dopamine transporter. Benztropine is indicated for all forms of parkinsonism, including antipsychotic-induced parkinsonism, but is also prescribed for many off-label uses, including sialorrhea and akathisia (although many authors do not recommend anticholinergics for this purpose^2,3), and for prophylaxis of EPS. Benztropine can be administered intravenously, intramuscularly, or orally. Given orally, the typical dosing is twice daily with a maximum dose of 6 mg/d. Benztropine is preferred over diphenhydramine and trihexyphenidyl due to adverse effects of sedation or potential for misuse of the medication.¹

Second-generation antipsychotics (SGAs) have been associated with lower rates of neurologic adverse effects compared with first-generation antipsychotics (FGAs). Because SGAs are increasingly prescribed, the use of benztropine (along with other agents such as trihexyphenidyl) for EPS prophylaxis is not an evidence-based practice. However, despite a movement away from prophylactic management of movement disorders, benztropine continues to be prescribed for EPS and/or cholinergic symptoms, despite the peripheral and cognitive adverse effects of this agent and, in many instances, the lack of clear indication for its use.

According to the most recent edition of the American Psychiatric Association’s (APA) Practice Guideline for the Treatment of Patients with Schizophrenia,⁴ anticholinergics should only be used for preventing acute dystonia in conjunction with a long-acting injectable antipsychotic. Furthermore, the APA Guideline states anticholinergics may be used for drug-induced parkinsonism when the dose of an antipsychotic cannot be reduced and an alternative agent is required. However, the first-line agent for drug-induced parkinsonism is amantadine, and benztropine should only be considered if amantadine is contraindicated.⁴ The rationale for this guideline and for judicious use of anticholinergics is that like any pharmacologic treatment, anticholinergics (including benztropine) carry the potential for adverse effects. For benztropine, these range from mild effects such as tachycardia and constipation to paralytic ileus, increased falls, worsening of tardive dyskinesia (TD), and potential cognitive impairment. Literature suggests that the first step in managing cognitive concerns in a patient with schizophrenia should be a close review of medications, and avoidance of agents with anticholinergic properties.⁵

Prescribing benztropine for EPS

EPS, which include dystonia, akathisia, drug-induced parkinsonism, and TD, are very frequent adverse effects noted with antipsychotics. Benztropine has demonstrated benefit in managing acute dystonia and the APA Guideline recommends IM administration of either benztropine 1 mg or diphenhydramine 25 mg for this purpose.⁴ However, in our experience, the most frequent indication for long-term prescribing of benztropine is prophylaxis of antipsychoticinduced dystonia. This use was suggested by some older studies. In a 1987 study by Boyer et al,⁶ patients who were administered benztropine with haloperidol did not develop acute dystonia, while patients who received haloperidol alone developed dystonia. However, this was a small retrospective study with methodological issues. Boyer et al⁶ suggested discontinuing prophylaxis with benztropine within 1 week, as acute dystonia occurred within 2.5 days. Other researchers^7,8 have argued that short-term prophylaxis with benztropine for 1 week may work, especially during treatment with high-potency antipsychotics. However, in a review of the use of anticholinergics in conjunction with antipsychotics, Desmarais et al⁵ concluded that there is no need for prophylaxis and recommended alternative treatments. As we have noticed in Ms. P and other patients treated in our facilities, benztropine is frequently continued indefinitely without a clinical indication for its continuous use. Assessment and indication for continued use of benztropine should be considered regularly, and it should be discontinued when there is no clear indication for its use or when adverse effects emerge.

Prescribing benztropine for TD

TD is a subtype of tardive syndromes associated with the use of antipsychotics. It is characterized by repetitive involuntary movements such as lip smacking, puckering, chewing, or tongue protrusion. Proposed pathophysiological mechanisms include dopamine receptor hypersensitivity, N-methyl-D-aspartate (NMDA) receptor excitotoxicity, and gamma-aminobutyric acid (GABA)-containing neuron activity.

According to the APA Guideline, evidence of benztropine’s efficacy for the prevention of TD is lacking.⁴ A 2018 Cochrane systematic review⁹ was unable to provide a definitive conclusion regarding the effectiveness of benztropine and other anticholinergics for the treatment of antipsychotic-induced TD. While many clinicians believe that benztropine can be used to treat all types of EPS, there are no clear instances in reviewed literature where the efficacy of benztropine for treating TD could be reliably demonstrated. Furthermore, some literature suggests that anticholinergics such as benztropine increase the risk of developing TD.^5,10 The mechanism underlying benztropine’s ability to precipitate or exacerbate abnormal movements is unclear, though it is theorized that anticholinergic medications may inhibit dopamine reuptake into neurons, thus leading to an excess of dopamine in the synaptic cleft that manifests as dyskinesias.¹⁰ Some authors also recommend that the first step in the management of TD should be to gradually discontinue anticholinergics, as this has been associated with improvement in TD.¹¹

Continue to: Prescribing anticholinergics in specific patient populations...

In addition to the adverse effects described above, benztropine can affect cognition, as we observed in Ms. P. The cholinergic system plays a role in human cognition, and blockade of muscarinic receptors has been associated with impairments in working memory and prefrontal tasks.¹² These adverse cognitive effects are more pronounced in certain populations, including patients with schizophrenia and older adults.

Schizophrenia is associated with declining cognitive function, and the cognitive faculties of patients with schizophrenia may be worsened by anticholinergics. In patients with schizophrenia, social interactions and social integration are often impacted by profound negative symptoms such as social withdrawal and poverty of thought and speech.¹³ In a double-blind study by Baker et al,¹⁴ benztropine was found to have an impact on attention and concentration in patients with chronic schizophrenia. Baker et al¹⁴ found that patients with schizophrenia who were switched from benztropine to placebo increased their overall Wechsler Memory Scale scores compared to those maintained on benztropine. One crosssectional analysis found that a higher anticholinergic burden was associated with impairments across all cognitive domains, including memory, attention/control, executive and visuospatial functioning, and motor speed domains.¹⁵ Importantly, a higher anticholinergic medication burden was associated with worse cognitive performance.¹⁵ In addition to impairments in cognitive processing, anticholinergics have been associated with a decreased ability to benefit from psychosocial programs and impaired abilities to manage activities of daily living.⁴ In another study exploring the effects of discontinuing anticholinergics and the impact on movement disorders, Desmarais et al¹⁶ found patients experienced a significant improvement in scores on the Brief Assessment of Cognition in Schizophrenia after discontinuing anticholinergics. Vinogradov et al¹⁷ noted that “serum anticholinergic activity in schizophrenia patients shows a significant association with impaired performance in measures of verbal working memory and verbal learning memory and was significantly associated with a lowered response to an intensive course of computerized cognitive training.” They felt their findings underscored the cognitive cost of medications with high anticholinergic burden.

Geriatric patients. Careful consideration should be given before starting benztropine in patients age ≥65. The 2019 American Geriatric Society’s Beers Criteria¹⁸ recommend avoiding benztropine in geriatric patients; the level of recommendation is strong. Furthermore, the American Geriatric Society designates benztropine as a medication that should be avoided, and a nondrug approach or alternative medication be prescribed independent of the patient’s condition or diagnosis. In a recently published case report, Esang et al¹⁹ highlighted several salient findings from previous studies on the risks associated with anticholinergic use:

• any medications a patient takes with anticholinergic properties contribute to the overall anticholinergic load of a patient’s medication regimen
• the higher the anticholinergic burden, the greater the cognitive deficits
• switching from an FGA to an SGA may decrease the risk of EPS and may limit the need for anticholinergic medications such as benztropine for a particular patient.

One must also consider that the effects of multiple medications with anticholinergic properties is probably cumulative.

Alternatives for treating drug-induced parkinsonism

Antipsychotics exert their effects through antagonism of the D2 receptor, and this is the same mechanism that leads to parkinsonism. Specifically, the mechanism is believed to be D2 receptor antagonism in the striatum leading to disinhibition of striatal neurons containing GABA.¹¹ This disinhibition of medium spiny neurons is propagated when acetylcholine is released from cholinergic interneurons. Anticholinergics such as benztropine can remedy symptoms by blocking the signal of acetylcholine on the M1 receptors on medium spiny neurons. However, benztropine also has the propensity to decrease cholinergic transmission, thereby impairing storage of new information into long-term memory as well as impair perception of time—similar to effects seen with (for instance) diphenhydramine.²⁰

The first step in managing drug-induced parkinsonism is to monitor symptoms. The APA Guideline recommends monitoring for acute-onset EPS at weekly intervals when beginning treatment and until stable for 2 weeks, and then monitoring at every follow-up visit thereafter.⁴ The next recommendation for long-term management of drug-induced parkinsonism is reducing the antipsychotic dose, or replacing the patient’s antipsychotic with an antipsychotic that is less likely to precipitate parkinsonism,4 such as quetiapine, iloperidone, or clozapine.¹¹ If dose reduction is not possible, and the patient’s symptoms are severe, pharmacologic management is indicated. The APA Guideline recommends amantadine as a first-line agent because it is associated with fewer peripheral adverse effects and less impairment in cognition compared with benztropine.⁴ In a small (N = 60) doubleblind crossover trial, Gelenberg et al²⁰ found benztropine 4 mg/d—but not amantadine 200 mg/d—impaired free recall and perception of time, and participants’ perception of their own memory impairment was significantly greater with benztropine. Amantadine has also been compared to biperiden, a relatively selective M1 muscarinic receptor muscarinic agent. In a separate double-blind crossover study of 26 patients with chronic schizophrenia, Silver and Geraisy²¹ found that compared to amantadine, biperiden was associated with worse memory performance. The recommended starting dose of amantadine for parkinsonism is 100 mg in the morning, increased to 100 mg twice a day and titrated to a maximum daily dose of 300 mg/d in divided doses.⁴

Continue to: Alternatives for treating drug-induced akathisia...

Akathisia remains a relatively common adverse effect of SGAs, and the profound physical distress and impaired functioning caused by akathisia necessitates pharmacologic treatment. Despite frequent use in practice for presumed benefit in akathisia, benztropine is not effective for the treatment of akathisia and the APA Guideline recommends that long-term management should begin with an antipsychotic dose reduction, followed by a switch to an agent with less propensity to incite akathisia.⁴ Acute manifestations of akathisia must be treated, and mirtazapine, propranolol, or clonazepam may be considered as alternatives.⁴ Mirtazapine is dosed 7.5 mg to 10 mg nightly for akathisia, though it should be used in caution in patients at risk for mania.⁴ Mirtazapine’s potent 5-HT2A blockade at low doses may contribute to its utility in treating akathisia.² Propranolol, a nonselective lipophilic beta-adrenergic antagonist, also has demonstrated efficacy in managing akathisia, with recommended dosing of 40 mg to 80 mg twice daily.² Benzodiazepines such as clonazepam require judicious use for akathisia because they may also precipitate or exacerbate cognitive impairment.⁴

Alternatives for treating TD

As mentioned above, benztropine is not recommended for the treatment of TD.¹ The Box^4,22,23 outlines potential treatment options for TD.

Box

Discontinuing benztropine

Benztropine is recommended as a firstline agent for the management of acute dystonia, and it may be used temporarily for drug-induced parkinsonism, but it is not recommended to prevent EPS or TD. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic agent such as benztropine. Based on their review of earlier studies, Desmarais et al⁵ suggest a gradual 3-month discontinuation of benztropine. Multiple studies have demonstrated an ability to taper anticholinergics in days to months.⁴ However, gradual discontinuation is advisable to avoid cholinergic rebound and the reemergence of EPS, and to decrease the risk of neuroleptic malignant syndrome associated with sudden discontinuation.⁵ One suggested taper regimen is a decrease of 0.5 mg benztropine every week. Amantadine may be considered if parkinsonism is noted during the taper. Patients on benztropine may develop rebound symptoms, such as vivid dreams/nightmares; if this occurs, the taper rate can be slowed to a decrease of 0.5 mg every 2 weeks.⁴

Continue to: First do no harm...

Psychiatrists commonly prescribe benztropine to prevent EPS and TD, but available literature does not support the efficacy of benztropine for mitigating drug-induced parkinsonism, and studies report benztropine may significantly worsen cognitive processes and exacerbate TD.¹⁶ In addition, benztropine misuse has been correlated with euphoria and psychosis.¹⁶ More than 3 decades ago, the World Health Organization Heads of Centres Collaborating in WHO-Coordinated Studies on Biological Aspects of Mental Illness issued a consensus statement²⁴ discouraging the prophylactic use of anticholinergics for patients receiving antipsychotics, yet we still see patients on an indefinite regimen of benztropine.

As clinicians, our goals should be to optimize a patient’s functioning and quality of life, and to use the lowest dose of medication along with the fewest medications necessary to avoid adverse effects such as EPS. Benztropine is recommended as a first-line agent for the management of acute dystonia, but its continued or indefinite use to prevent antipsychotic-induced adverse effects is not recommended. While all pharmacologic interventions carry a risk of adverse effects, weighing the risk of those effects against the clinical benefits is the prerogative of a skilled clinician. Benztropine and other anticholinergics prescribed for prophylactic purposes have numerous adverse effects, limited clinical utility, and a deleterious effect on quality of life. Furthermore, benztropine prophylaxis of drug-induced parkinsonism does not seem to be warranted, and the risks do not seem to outweigh the harm benztropine may cause, with the possible exception of “prophylactic” treatment of dystonia that is discontinued in a few days, as some researchers have suggested.^6-8 The preventive value of benztropine has not been demonstrated. It is time we took inventory of medications that might cause more harm than good, rely on current treatment guidelines instead of habit, and use these agents judiciously while considering replacement with novel, safer medications whenever possible.

CASE CONTINUED

The clinical team considers benztropine’s ability to cause cognitive effects, and decides to taper and discontinue it over 1 month. Ms. P is seen in an outpatient clinic within 1 month of discontinuing benztropine. She reports that her difficulty remembering words and details has improved. She also says that she is now able to concentrate on writing and reading. The consulting neurologist also notes improvement. Ms. P continues to report improvement in symptoms over the next 2 months of follow-up, and says that her mood improved and she has less apathy.

Bottom Line

Benztropine is a first-line medication for acute dystonia, but its continued or indefinite use for preventing antipsychotic-induced adverse effects is not recommended. Given the multitude of adverse effects and cognitive impairment noted with anticholinergics, tapering should be considered for patients receiving an anticholinergic medication such as benztropine.

SECOND OF 2 PARTS

Evidence supports the crucial role of early intervention and nonpharmacologic approaches

A large percentage of individuals with autism spectrum disorder (ASD) experience persisting significant social deficits in adulthood,¹ which often leads to isolation, depressive symptoms, and poor occupational and relationship functioning.^2,3 Childhood is a vital time for making the most significant and lasting changes that can improve functioning of individuals with ASD. Psychiatrists and other physicians who treat children are in a key role to influence outcomes of children at risk for or diagnosed with ASD.

This article provides updates on various aspects of ASD diagnosis and treatment (based on available evidence up to March 2020). Part 1 (Current Psychiatry, March 2022) focused on early detection and diagnosis. Here in Part 2, I describe an overview of treatment strategies. Given the vast nature of the topic and the abundance of research that has emerged in the field of ASD over the last several years,⁴ providing an exhaustive review of each of the aspects discussed here is not within the scope of this article.

A comprehensive approach is essential

Multiple treatment modalities have been recommended for ASD.⁵ It is essential to address all aspects of ASD through cognitive, developmental, social-communication, sensory-motor, and behavioral interventions. Nonpharmacologic interventions are crucial in improving long-term outcomes of children with ASD.⁶

Nonpharmacologic treatments

Nonpharmacologic interventions commonly utilized for children with ASD include behavioral therapies, other psychological therapies, speech-language therapy, occupational therapy, educational interventions, parent coaching/training, developmental social interventions, and other modalities of therapy that are delivered in school, home, and clinic settings.^5,7

A recent study examining ASD treatment trends via caregivers’ reports (N = 5,122) from the SPARK (Simons Foundation Powering Autism Research for Knowledge) cohort in the United States reported that 80% of children received speech-language therapy or occupational therapy; 52% got both.⁵ The study revealed that approximately one-quarter utilized 3 therapies simultaneously; two-thirds had utilized 3 or more therapies in the previous year.⁵

Interventions for children with ASD need to be individualized.^1,8 Evidence-based behavioral interventions for ASD fall into 2 broad categories: Applied Behavior Analysis (ABA), and Naturalistic Developmental Behavioral Interventions (NDBI). Traditionally, ABA has been a key model, guiding treatment for enhancing social-communicating skills and lowering maladaptive behaviors in ASD.⁹ ABA follows a structured and prescribed format,^10,11 and has been shown to be efficacious.^1,7 More recently, NDBI, in which interventions are “embedded” in the natural environment of the young child and more actively incorporate a developmental perspective, has been shown to be beneficial in improving and generalizing social-communication skills in young children with ASD.^7,11

Early Start Denver Model (ESDM) is an intensive, naturalistic behavioral intervention⁴ that has been shown to be efficacious for enhancing communication and adaptive behavior in children with ASD.^7,8,12 A multisite randomized controlled trial (RCT) by Rogers et al¹² that examined the efficacy of ESDM in 118 children (age 14 to 24 months) with ASD found the treatment was beneficial and superior compared with a “community intervention” group, in regards to language ability measured in time by group analyses.The ESDM intervention in this study involved weekly parent coaching for 3 months, along with 24 months of 15 hours/week of one-on-one treatment provided by therapy professionals.¹²

Reciprocal imitation training (RIT) is another naturalistic intervention that has shown benefit in training children with ASD in imitation skills during play.¹³ Studies have found that both RIT and ESDM can be parent-implemented, after parents receive training.^13,14

Parent-mediated, parent-implemented interventions may have a role in improving outcomes in childhood ASD,^7,15 particularly “better generalization and maintenance of skills than therapist-implemented intervention” for lowering challenging behaviors and enhancing verbal and nonverbal communication.¹⁶

Various social skills interventions have also been found effective for children with ASD.¹ Such interventions are often provided in the school setting.⁷ Coordination with the child’s school to discuss and advocating for adequate and suitable interventions, educational services, and placement is an essential aspect of ASD treatment.⁷

Two other school-based, comprehensive treatment model interventions—Learning Experiences and Alternative Programs for Preschoolers and their Parents (LEAP), and TEACCH—have some evidence of leading to improvement in children with ASD.^7,17

Some studies have found that music therapy may have high efficacy for children with ASD, even with smaller length and intensity of treatment, particularly in improving social interaction, engagement with parents, joint attention, and communication.^3,18 Further research is needed to conclusively establish the efficacy of music therapy for ASD in children and adolescents.

A few studies have assessed the long-term outcomes of interventions for ASD; however, more research is needed.¹⁹ Pickles et al¹⁹ conducted a follow-up to determine the long-term effects of the Preschool Autism Communication Trial (PACT), an RCT of parent-mediated social communication therapy for children age 2 to 4 with ASD. The children’s average age at follow-up was 10 years. The authors found a significant long-term decrease in ASD symptoms and enhancement of social communication with parents (N = 152).¹⁹

Technology-based interventions, including games and robotics, have been investigated in recent years, for treatment of children with ASD (eg, for improving social skills).²⁰

Research suggests that the intensity (number of hours) and duration of nonpharmacologic treatments for ASD is critical to improving outcomes (Box^{1,3,5,7,10,16}).

Box

Continue to: Pharmacotherapy...

Pharmacotherapy

Medications cannot resolve core features of ASD.²¹ However, certain medications may help address associated comorbidities, such as attention-deficit/hyperactivity disorder (ADHD), depression, or others, when these conditions have not responded to nonpharmacologic interventions.^7,22 Common symptoms that are often treated with pharmacotherapy include aggression, irritability, hyperactivity, attentional difficulties, tics, self-injurious behavior, obsessive-compulsive symptoms, and mood dysregulation/lability.²³ Generally speaking, medications might be considered if symptoms are severe and markedly impair functioning. For mild to moderate conditions, psychotherapy and other nonpharmacologic interventions are generally considered first-line. Since none of the medications described below are specific to ASD and psychiatrists generally receive training in prescribing them for other indications, a comprehensive review of their risks and benefits is beyond the scope of this article. No psychotropic medications are known to have robust evidence for safety in preschool children with ASD, and thus are best avoided.

Antipsychotics. Risperidone (for age 5 and older) and aripiprazole (age 6 to 17) are the only medications FDA-approved for use in children and adolescents with ASD, specifically for irritability associated with ASD.^21,24 These 2 second-generation antipsychotics may also assist in lowering aggression in patients with ASD.²⁴ First-generation antipsychotics such as haloperidol have been shown to be effective for irritability and aggression in ASD, but the risk of significant adverse effects such as dyskinesias and extrapyramidal symptoms limit their use.²⁴ Two studies (a double-blind study and an open-label extension of that study) in children and adolescents with ASD found that risperidone was more effective and better tolerated than haloperidol in behavioral measures, impulsivity, and even in the social domain.^25,26 In addition to other adverse effects and risks, increased prolactin secondary to risperidone use requires close monitoring and caution.^24-26 As is the case with the use of other psychotropic medications in children and adolescents, those with ASD who receive antipsychotics should also be periodically reassessed to determine the need for continued use of these medications.²⁷ A multicenter relapse prevention RCT found no statistically significant difference in the time to relapse between aripiprazole and placebo.²⁷ Metabolic syndrome, cardiac risks, and other risks need to be considered before prescribing an antipsychotic.²⁸ Given their serious adverse effects profile, use should be considered only when there is severe impairment or risk of injury, after carefully weighing risks/benefits.

Medications for attentional difficulties. A multisite, randomized, placebo-controlled trial evaluating the use of extended-release guanfacine in children with ASD (N = 62) found the rate of positive response on the Clinical Global Impressions–Improvement scale was 50% for guanfacine vs 9.4% for placebo.²⁹ Clinicians need to monitor for adverse effects of guanfacine, such as fatigue, drowsiness, lightheadedness, lowering of blood pressure and heart rate, and other effects.²⁹ A randomized, double-blind trial of 97 children and adolescents with ASD and ADHD found that atomoxetine had moderate benefit for ADHD symptoms.³⁰ The study reported no serious adverse effects.³⁰ However, it is especially important to monitor for hepatic and cardiac adverse effects (in addition to monitoring for risk of increase in suicidal thoughts/behavior, as in the case of antidepressants) when using atomoxetine, in addition to other side effects and risks. Some evidence suggests that methylphenidate may be effective for attentional difficulties in children and adolescents with ASD²¹ but may pose a higher risk of adverse effects in this population compared with neurotypical patients.³¹

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) are sometimes used to reduce obsessive-compulsive symptoms, repetitive behavior, or depressive symptoms in children with ASD, but are not FDA-approved for children or adolescents with ASD. In general, there is inadequate evidence to support the use of SSRIs for ASD in children.^31-34 In addition, children with ASD may be at a greater risk of adverse effects from SSRIs.^32,34 Despite this, SSRIs are the most commonly prescribed psychotropic medications in children with ASD.³²

An RCT examining the efficacy of fluoxetine in 158 children and adolescents with ASD found no significant difference in Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS) score after 14 weeks of treatment; activation was a common adverse effect.³⁵ A 2005 randomized, double-blind, placebo-controlled trial of 45 children/adolescents with ASD found that low-dose liquid fluoxetine was more effective than placebo for reducing repetitive behaviors in this population.³⁶ Larger studies are warranted to further evaluate the efficacy and safety of fluoxetine (and of SSRIs in general, particularly in the long term) for children and adolescents with ASD.³⁶ A 2009 randomized, placebo-controlled trial of 149 children with ASD revealed no significant difference between citalopram and placebo as measured by Clinical Global Impressions scale or CY-BOCS scores, and noted a significantly elevated likelihood of adverse effects.³⁷

Other antidepressants. There is insufficient evidence to support the use of any other antidepressants in children and adolescents with ASD. A few studies^38,39 have examined the use of venlafaxine in children with ASD; however, further research and controlled studies with large sample sizes are required to conclusively establish its benefits. There is a dearth of evidence examining the use of the tetracyclic antidepressant mirtazapine, or other classes of medications such as tricyclic antidepressants or mood stabilizers, in children with ASD; only a few small studies have assessed the efficacy and adverse effects of these medications for such patients.³¹

Polypharmacy. Although there is no evidence to support polypharmacy in children and adolescents with ASD, the practice appears to be rampant in these patients.^28,40 A 2013 retrospective, observational study of psychotropic medication use in children with ASD (N = 33,565) found that 64% were prescribed psychotropic medications, and 35% exhibited evidence of polypharmacy.⁴⁰ In this study, the total duration of polypharmacy averaged 525 days.⁴⁰ When addressing polypharmacy, systematic deprescribing or simplification of the psychotropic medication regimen may be needed,²⁸ while taking into account the patient’s complete clinical situation, including (but not limited to) tolerability of the medication regimen, presence or absence of current stressors, presence or absence of adequate supports, use of nonpharmacologic treatments where appropriate, and other factors.

More studies assessing the efficacy and safety of psychotropic medications for children and adolescents with ASD are needed,³² especially studies that evaluate the effects of long-term use, because evidence for pharmacologic treatments for children with ASD is mixed and insufficient.³³ There is also a need for evidence-based standards for prescribing psychotropic medications in children and adolescents with ASD.

Psychotropic medications, if used in ASD, should be used only in conjunction with other evidence-based treatment modalities, and not as monotherapy.²¹ Children and adolescents with ASD may be particularly susceptible to side effects or adverse effects of certain psychotropic medications.³¹ When considering medications, carefully weigh the risks and benefits.^7,21,24,28 Starting low and going slow is generally the preferred strategy.^31,32 As always, when recommending medications, discuss in detail with parents the potential side effects, benefits, risks, interactions, and alternatives.

Other agents. Several double-blind, placebo-controlled trials have evaluated using melatonin for sleep difficulties in children and adolescents with ASD.⁴¹ A randomized, placebo-controlled, 12-week trial that assessed 160 children with ASD and insomnia found that melatonin plus cognitive-behavioral therapy (CBT) was superior in efficacy to melatonin alone, CBT alone, or placebo.⁴¹

The evidence regarding oxytocin use for children with ASD is mixed.³¹ Some small studies have associated improvement in the social domain with its use. Guastella et al⁴² conducted a randomized, double-blind, placebo-controlled trial of oxytocin nasal spray for 16 participants (age 12 to 19) with ASD, and found oxytocin enhanced emotional identification. Gordon et al⁴³ conducted a functional MRI study of brain activity with oxytocin use in children with high-functioning ASD (N = 17). They found that oxytocin may augment “salience and hedonic evaluations of socially meaningful stimuli in children with ASD” and thus help social attunement. Further research is needed to evaluate the impact of oxytocin on social behavior.

Complementary and alternative medicine. Although there is limited and inconclusive evidence about the use of complementary and alternative medicine in children and adolescents with ASD, these therapies continue to be commonly used.^44-46 A recent survey of parents (N = 211) of children with ASD from academic ASD outpatient clinics in Germany found that 46% reported their child was using or had used some type of complementary and alternative medicine.⁴⁴ There is inadequate evidence to support the use of a gluten-free, casein-free diet for children/adolescents with ASD.⁴⁶ A recent cross-sectional study assessing supplement use in 210 children with ASD in Canada found that 75% used supplements, such as multivitamins (77.8%), vitamin D (44.9%), omega 3 (42.5%), probiotics (36.5%), and magnesium (28.1%), despite insufficient evidence to support their safety or efficacy for children with ASD.⁴⁷ Importantly, 33.5% of parents in this study reported that they did not inform the physician about all their child’s supplements.⁴⁷ Some of the reasons the parents in this study provided for not disclosing information about supplements to their physicians were “physician lack of knowledge,” “no benefit,” “too time-consuming,” and “scared of judgment.”⁴⁷ Semi-structured interviews of parents of 21 children with ASD in Australia revealed that parents found information on complementary and alternative medicine and therapies complex and often conflicting.⁴⁵ In addition to recommendations from health care professionals, evidence suggests that parents often consider the opinions of media, friends, and family when making a decision on using complementary and alternative medicine modalities for children/adolescents with ASD.⁴⁶ Such findings can inform physician practices regarding supplement use, and highlight the need to educate parents about the evidence regarding these therapies and potential adverse effects and interactions of such therapies,⁴⁶ along with the need to develop a centralized, evidence-based resource for parents regarding their use.⁴⁵

Omega 3 supplementation has in general shown few adverse effects⁴⁷; still, risks/benefits need to be weighed before use. Some evidence suggests that it may decrease hyperactivity in children with ASD.^31,48 However, further research, particularly controlled trials with large sample sizes, are needed for a definitive determination of efficacy.^31,48 A meta-analysis that included 27 RCTs assessing the efficacy of dietary interventions for various ASD symptoms found that omega 3 supplementation was more effective than placebo, but compared with placebo, the effect size was small.⁴⁹ A RCT of 73 children with ASD in New Zealand found that omega 3 long chain polyunsaturated fatty acids may benefit some core symptoms of ASD; the authors suggested that further research is needed to conclusively establish efficacy.⁵⁰

Continue to: A need for advocacy and research..

Physicians who treat children with ASD can not only make appropriate referrals and educate parents, but also educate their patients’ schools and advocate for their patients to get the level of services they need.^23,28

A recent study in the United States found that behavior therapy and speech-language therapy were used less often in the treatment of children with ASD in rural areas compared with those in metro areas.⁵ This suggests that in addition to increasing parents’ awareness and use of ASD services and providing referrals where appropriate, physicians are in a unique position to advocate for public health policies to improve access, coverage, and training for the provision of such services in rural areas.

There is need for ongoing research to further examine the efficacy and nuances of effects of various treatment interventions for ASD, especially long-term studies with larger sample sizes.^11,51 Additionally, research is warranted to better understand the underlying genetic and neurobiological mechanisms of ASD, which would help guide the development of biomarkers,⁵² innovative treatments, and disease-modifying agents for ASD.^7,22 Exploring the effects of potential alliances or joint action between biological and psychosocial interventions for ASD is also an area that needs further research.⁵¹

Bottom Line

A combination of treatment modalities (such as speech-language therapy, social skills training, behavior therapy/other psychotherapy, and occupational therapy for sensory sensitivities) is generally needed to improve the long-term outcomes of children and adolescents with autism spectrum disorder (ASD). In addition to the importance of early intervention, the intensity and duration of nonpharmacologic treatments are vital to improving outcomes in ASD.

SECOND OF 2 PARTS

Evidence supports the crucial role of early intervention and nonpharmacologic approaches

A large percentage of individuals with autism spectrum disorder (ASD) experience persisting significant social deficits in adulthood,¹ which often leads to isolation, depressive symptoms, and poor occupational and relationship functioning.^2,3 Childhood is a vital time for making the most significant and lasting changes that can improve functioning of individuals with ASD. Psychiatrists and other physicians who treat children are in a key role to influence outcomes of children at risk for or diagnosed with ASD.

This article provides updates on various aspects of ASD diagnosis and treatment (based on available evidence up to March 2020). Part 1 (Current Psychiatry, March 2022) focused on early detection and diagnosis. Here in Part 2, I describe an overview of treatment strategies. Given the vast nature of the topic and the abundance of research that has emerged in the field of ASD over the last several years,⁴ providing an exhaustive review of each of the aspects discussed here is not within the scope of this article.

A comprehensive approach is essential

Multiple treatment modalities have been recommended for ASD.⁵ It is essential to address all aspects of ASD through cognitive, developmental, social-communication, sensory-motor, and behavioral interventions. Nonpharmacologic interventions are crucial in improving long-term outcomes of children with ASD.⁶

Nonpharmacologic treatments

Nonpharmacologic interventions commonly utilized for children with ASD include behavioral therapies, other psychological therapies, speech-language therapy, occupational therapy, educational interventions, parent coaching/training, developmental social interventions, and other modalities of therapy that are delivered in school, home, and clinic settings.^5,7

A recent study examining ASD treatment trends via caregivers’ reports (N = 5,122) from the SPARK (Simons Foundation Powering Autism Research for Knowledge) cohort in the United States reported that 80% of children received speech-language therapy or occupational therapy; 52% got both.⁵ The study revealed that approximately one-quarter utilized 3 therapies simultaneously; two-thirds had utilized 3 or more therapies in the previous year.⁵

Interventions for children with ASD need to be individualized.^1,8 Evidence-based behavioral interventions for ASD fall into 2 broad categories: Applied Behavior Analysis (ABA), and Naturalistic Developmental Behavioral Interventions (NDBI). Traditionally, ABA has been a key model, guiding treatment for enhancing social-communicating skills and lowering maladaptive behaviors in ASD.⁹ ABA follows a structured and prescribed format,^10,11 and has been shown to be efficacious.^1,7 More recently, NDBI, in which interventions are “embedded” in the natural environment of the young child and more actively incorporate a developmental perspective, has been shown to be beneficial in improving and generalizing social-communication skills in young children with ASD.^7,11

Early Start Denver Model (ESDM) is an intensive, naturalistic behavioral intervention⁴ that has been shown to be efficacious for enhancing communication and adaptive behavior in children with ASD.^7,8,12 A multisite randomized controlled trial (RCT) by Rogers et al¹² that examined the efficacy of ESDM in 118 children (age 14 to 24 months) with ASD found the treatment was beneficial and superior compared with a “community intervention” group, in regards to language ability measured in time by group analyses.The ESDM intervention in this study involved weekly parent coaching for 3 months, along with 24 months of 15 hours/week of one-on-one treatment provided by therapy professionals.¹²

Reciprocal imitation training (RIT) is another naturalistic intervention that has shown benefit in training children with ASD in imitation skills during play.¹³ Studies have found that both RIT and ESDM can be parent-implemented, after parents receive training.^13,14

Parent-mediated, parent-implemented interventions may have a role in improving outcomes in childhood ASD,^7,15 particularly “better generalization and maintenance of skills than therapist-implemented intervention” for lowering challenging behaviors and enhancing verbal and nonverbal communication.¹⁶

Various social skills interventions have also been found effective for children with ASD.¹ Such interventions are often provided in the school setting.⁷ Coordination with the child’s school to discuss and advocating for adequate and suitable interventions, educational services, and placement is an essential aspect of ASD treatment.⁷

Two other school-based, comprehensive treatment model interventions—Learning Experiences and Alternative Programs for Preschoolers and their Parents (LEAP), and TEACCH—have some evidence of leading to improvement in children with ASD.^7,17

Some studies have found that music therapy may have high efficacy for children with ASD, even with smaller length and intensity of treatment, particularly in improving social interaction, engagement with parents, joint attention, and communication.^3,18 Further research is needed to conclusively establish the efficacy of music therapy for ASD in children and adolescents.

A few studies have assessed the long-term outcomes of interventions for ASD; however, more research is needed.¹⁹ Pickles et al¹⁹ conducted a follow-up to determine the long-term effects of the Preschool Autism Communication Trial (PACT), an RCT of parent-mediated social communication therapy for children age 2 to 4 with ASD. The children’s average age at follow-up was 10 years. The authors found a significant long-term decrease in ASD symptoms and enhancement of social communication with parents (N = 152).¹⁹

Technology-based interventions, including games and robotics, have been investigated in recent years, for treatment of children with ASD (eg, for improving social skills).²⁰

Research suggests that the intensity (number of hours) and duration of nonpharmacologic treatments for ASD is critical to improving outcomes (Box^{1,3,5,7,10,16}).

Box

Continue to: Pharmacotherapy...

Pharmacotherapy

Medications cannot resolve core features of ASD.²¹ However, certain medications may help address associated comorbidities, such as attention-deficit/hyperactivity disorder (ADHD), depression, or others, when these conditions have not responded to nonpharmacologic interventions.^7,22 Common symptoms that are often treated with pharmacotherapy include aggression, irritability, hyperactivity, attentional difficulties, tics, self-injurious behavior, obsessive-compulsive symptoms, and mood dysregulation/lability.²³ Generally speaking, medications might be considered if symptoms are severe and markedly impair functioning. For mild to moderate conditions, psychotherapy and other nonpharmacologic interventions are generally considered first-line. Since none of the medications described below are specific to ASD and psychiatrists generally receive training in prescribing them for other indications, a comprehensive review of their risks and benefits is beyond the scope of this article. No psychotropic medications are known to have robust evidence for safety in preschool children with ASD, and thus are best avoided.

Antipsychotics. Risperidone (for age 5 and older) and aripiprazole (age 6 to 17) are the only medications FDA-approved for use in children and adolescents with ASD, specifically for irritability associated with ASD.^21,24 These 2 second-generation antipsychotics may also assist in lowering aggression in patients with ASD.²⁴ First-generation antipsychotics such as haloperidol have been shown to be effective for irritability and aggression in ASD, but the risk of significant adverse effects such as dyskinesias and extrapyramidal symptoms limit their use.²⁴ Two studies (a double-blind study and an open-label extension of that study) in children and adolescents with ASD found that risperidone was more effective and better tolerated than haloperidol in behavioral measures, impulsivity, and even in the social domain.^25,26 In addition to other adverse effects and risks, increased prolactin secondary to risperidone use requires close monitoring and caution.^24-26 As is the case with the use of other psychotropic medications in children and adolescents, those with ASD who receive antipsychotics should also be periodically reassessed to determine the need for continued use of these medications.²⁷ A multicenter relapse prevention RCT found no statistically significant difference in the time to relapse between aripiprazole and placebo.²⁷ Metabolic syndrome, cardiac risks, and other risks need to be considered before prescribing an antipsychotic.²⁸ Given their serious adverse effects profile, use should be considered only when there is severe impairment or risk of injury, after carefully weighing risks/benefits.

Medications for attentional difficulties. A multisite, randomized, placebo-controlled trial evaluating the use of extended-release guanfacine in children with ASD (N = 62) found the rate of positive response on the Clinical Global Impressions–Improvement scale was 50% for guanfacine vs 9.4% for placebo.²⁹ Clinicians need to monitor for adverse effects of guanfacine, such as fatigue, drowsiness, lightheadedness, lowering of blood pressure and heart rate, and other effects.²⁹ A randomized, double-blind trial of 97 children and adolescents with ASD and ADHD found that atomoxetine had moderate benefit for ADHD symptoms.³⁰ The study reported no serious adverse effects.³⁰ However, it is especially important to monitor for hepatic and cardiac adverse effects (in addition to monitoring for risk of increase in suicidal thoughts/behavior, as in the case of antidepressants) when using atomoxetine, in addition to other side effects and risks. Some evidence suggests that methylphenidate may be effective for attentional difficulties in children and adolescents with ASD²¹ but may pose a higher risk of adverse effects in this population compared with neurotypical patients.³¹

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) are sometimes used to reduce obsessive-compulsive symptoms, repetitive behavior, or depressive symptoms in children with ASD, but are not FDA-approved for children or adolescents with ASD. In general, there is inadequate evidence to support the use of SSRIs for ASD in children.^31-34 In addition, children with ASD may be at a greater risk of adverse effects from SSRIs.^32,34 Despite this, SSRIs are the most commonly prescribed psychotropic medications in children with ASD.³²

An RCT examining the efficacy of fluoxetine in 158 children and adolescents with ASD found no significant difference in Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS) score after 14 weeks of treatment; activation was a common adverse effect.³⁵ A 2005 randomized, double-blind, placebo-controlled trial of 45 children/adolescents with ASD found that low-dose liquid fluoxetine was more effective than placebo for reducing repetitive behaviors in this population.³⁶ Larger studies are warranted to further evaluate the efficacy and safety of fluoxetine (and of SSRIs in general, particularly in the long term) for children and adolescents with ASD.³⁶ A 2009 randomized, placebo-controlled trial of 149 children with ASD revealed no significant difference between citalopram and placebo as measured by Clinical Global Impressions scale or CY-BOCS scores, and noted a significantly elevated likelihood of adverse effects.³⁷

Other antidepressants. There is insufficient evidence to support the use of any other antidepressants in children and adolescents with ASD. A few studies^38,39 have examined the use of venlafaxine in children with ASD; however, further research and controlled studies with large sample sizes are required to conclusively establish its benefits. There is a dearth of evidence examining the use of the tetracyclic antidepressant mirtazapine, or other classes of medications such as tricyclic antidepressants or mood stabilizers, in children with ASD; only a few small studies have assessed the efficacy and adverse effects of these medications for such patients.³¹

Polypharmacy. Although there is no evidence to support polypharmacy in children and adolescents with ASD, the practice appears to be rampant in these patients.^28,40 A 2013 retrospective, observational study of psychotropic medication use in children with ASD (N = 33,565) found that 64% were prescribed psychotropic medications, and 35% exhibited evidence of polypharmacy.⁴⁰ In this study, the total duration of polypharmacy averaged 525 days.⁴⁰ When addressing polypharmacy, systematic deprescribing or simplification of the psychotropic medication regimen may be needed,²⁸ while taking into account the patient’s complete clinical situation, including (but not limited to) tolerability of the medication regimen, presence or absence of current stressors, presence or absence of adequate supports, use of nonpharmacologic treatments where appropriate, and other factors.

More studies assessing the efficacy and safety of psychotropic medications for children and adolescents with ASD are needed,³² especially studies that evaluate the effects of long-term use, because evidence for pharmacologic treatments for children with ASD is mixed and insufficient.³³ There is also a need for evidence-based standards for prescribing psychotropic medications in children and adolescents with ASD.

Psychotropic medications, if used in ASD, should be used only in conjunction with other evidence-based treatment modalities, and not as monotherapy.²¹ Children and adolescents with ASD may be particularly susceptible to side effects or adverse effects of certain psychotropic medications.³¹ When considering medications, carefully weigh the risks and benefits.^7,21,24,28 Starting low and going slow is generally the preferred strategy.^31,32 As always, when recommending medications, discuss in detail with parents the potential side effects, benefits, risks, interactions, and alternatives.

Other agents. Several double-blind, placebo-controlled trials have evaluated using melatonin for sleep difficulties in children and adolescents with ASD.⁴¹ A randomized, placebo-controlled, 12-week trial that assessed 160 children with ASD and insomnia found that melatonin plus cognitive-behavioral therapy (CBT) was superior in efficacy to melatonin alone, CBT alone, or placebo.⁴¹

The evidence regarding oxytocin use for children with ASD is mixed.³¹ Some small studies have associated improvement in the social domain with its use. Guastella et al⁴² conducted a randomized, double-blind, placebo-controlled trial of oxytocin nasal spray for 16 participants (age 12 to 19) with ASD, and found oxytocin enhanced emotional identification. Gordon et al⁴³ conducted a functional MRI study of brain activity with oxytocin use in children with high-functioning ASD (N = 17). They found that oxytocin may augment “salience and hedonic evaluations of socially meaningful stimuli in children with ASD” and thus help social attunement. Further research is needed to evaluate the impact of oxytocin on social behavior.

Complementary and alternative medicine. Although there is limited and inconclusive evidence about the use of complementary and alternative medicine in children and adolescents with ASD, these therapies continue to be commonly used.^44-46 A recent survey of parents (N = 211) of children with ASD from academic ASD outpatient clinics in Germany found that 46% reported their child was using or had used some type of complementary and alternative medicine.⁴⁴ There is inadequate evidence to support the use of a gluten-free, casein-free diet for children/adolescents with ASD.⁴⁶ A recent cross-sectional study assessing supplement use in 210 children with ASD in Canada found that 75% used supplements, such as multivitamins (77.8%), vitamin D (44.9%), omega 3 (42.5%), probiotics (36.5%), and magnesium (28.1%), despite insufficient evidence to support their safety or efficacy for children with ASD.⁴⁷ Importantly, 33.5% of parents in this study reported that they did not inform the physician about all their child’s supplements.⁴⁷ Some of the reasons the parents in this study provided for not disclosing information about supplements to their physicians were “physician lack of knowledge,” “no benefit,” “too time-consuming,” and “scared of judgment.”⁴⁷ Semi-structured interviews of parents of 21 children with ASD in Australia revealed that parents found information on complementary and alternative medicine and therapies complex and often conflicting.⁴⁵ In addition to recommendations from health care professionals, evidence suggests that parents often consider the opinions of media, friends, and family when making a decision on using complementary and alternative medicine modalities for children/adolescents with ASD.⁴⁶ Such findings can inform physician practices regarding supplement use, and highlight the need to educate parents about the evidence regarding these therapies and potential adverse effects and interactions of such therapies,⁴⁶ along with the need to develop a centralized, evidence-based resource for parents regarding their use.⁴⁵

Omega 3 supplementation has in general shown few adverse effects⁴⁷; still, risks/benefits need to be weighed before use. Some evidence suggests that it may decrease hyperactivity in children with ASD.^31,48 However, further research, particularly controlled trials with large sample sizes, are needed for a definitive determination of efficacy.^31,48 A meta-analysis that included 27 RCTs assessing the efficacy of dietary interventions for various ASD symptoms found that omega 3 supplementation was more effective than placebo, but compared with placebo, the effect size was small.⁴⁹ A RCT of 73 children with ASD in New Zealand found that omega 3 long chain polyunsaturated fatty acids may benefit some core symptoms of ASD; the authors suggested that further research is needed to conclusively establish efficacy.⁵⁰

Continue to: A need for advocacy and research..

Physicians who treat children with ASD can not only make appropriate referrals and educate parents, but also educate their patients’ schools and advocate for their patients to get the level of services they need.^23,28

A recent study in the United States found that behavior therapy and speech-language therapy were used less often in the treatment of children with ASD in rural areas compared with those in metro areas.⁵ This suggests that in addition to increasing parents’ awareness and use of ASD services and providing referrals where appropriate, physicians are in a unique position to advocate for public health policies to improve access, coverage, and training for the provision of such services in rural areas.

There is need for ongoing research to further examine the efficacy and nuances of effects of various treatment interventions for ASD, especially long-term studies with larger sample sizes.^11,51 Additionally, research is warranted to better understand the underlying genetic and neurobiological mechanisms of ASD, which would help guide the development of biomarkers,⁵² innovative treatments, and disease-modifying agents for ASD.^7,22 Exploring the effects of potential alliances or joint action between biological and psychosocial interventions for ASD is also an area that needs further research.⁵¹

Bottom Line

A combination of treatment modalities (such as speech-language therapy, social skills training, behavior therapy/other psychotherapy, and occupational therapy for sensory sensitivities) is generally needed to improve the long-term outcomes of children and adolescents with autism spectrum disorder (ASD). In addition to the importance of early intervention, the intensity and duration of nonpharmacologic treatments are vital to improving outcomes in ASD.

SECOND OF 2 PARTS

Evidence supports the crucial role of early intervention and nonpharmacologic approaches

A large percentage of individuals with autism spectrum disorder (ASD) experience persisting significant social deficits in adulthood,¹ which often leads to isolation, depressive symptoms, and poor occupational and relationship functioning.^2,3 Childhood is a vital time for making the most significant and lasting changes that can improve functioning of individuals with ASD. Psychiatrists and other physicians who treat children are in a key role to influence outcomes of children at risk for or diagnosed with ASD.

This article provides updates on various aspects of ASD diagnosis and treatment (based on available evidence up to March 2020). Part 1 (Current Psychiatry, March 2022) focused on early detection and diagnosis. Here in Part 2, I describe an overview of treatment strategies. Given the vast nature of the topic and the abundance of research that has emerged in the field of ASD over the last several years,⁴ providing an exhaustive review of each of the aspects discussed here is not within the scope of this article.

A comprehensive approach is essential

Multiple treatment modalities have been recommended for ASD.⁵ It is essential to address all aspects of ASD through cognitive, developmental, social-communication, sensory-motor, and behavioral interventions. Nonpharmacologic interventions are crucial in improving long-term outcomes of children with ASD.⁶

Nonpharmacologic treatments

Nonpharmacologic interventions commonly utilized for children with ASD include behavioral therapies, other psychological therapies, speech-language therapy, occupational therapy, educational interventions, parent coaching/training, developmental social interventions, and other modalities of therapy that are delivered in school, home, and clinic settings.^5,7

A recent study examining ASD treatment trends via caregivers’ reports (N = 5,122) from the SPARK (Simons Foundation Powering Autism Research for Knowledge) cohort in the United States reported that 80% of children received speech-language therapy or occupational therapy; 52% got both.⁵ The study revealed that approximately one-quarter utilized 3 therapies simultaneously; two-thirds had utilized 3 or more therapies in the previous year.⁵

Interventions for children with ASD need to be individualized.^1,8 Evidence-based behavioral interventions for ASD fall into 2 broad categories: Applied Behavior Analysis (ABA), and Naturalistic Developmental Behavioral Interventions (NDBI). Traditionally, ABA has been a key model, guiding treatment for enhancing social-communicating skills and lowering maladaptive behaviors in ASD.⁹ ABA follows a structured and prescribed format,^10,11 and has been shown to be efficacious.^1,7 More recently, NDBI, in which interventions are “embedded” in the natural environment of the young child and more actively incorporate a developmental perspective, has been shown to be beneficial in improving and generalizing social-communication skills in young children with ASD.^7,11

Early Start Denver Model (ESDM) is an intensive, naturalistic behavioral intervention⁴ that has been shown to be efficacious for enhancing communication and adaptive behavior in children with ASD.^7,8,12 A multisite randomized controlled trial (RCT) by Rogers et al¹² that examined the efficacy of ESDM in 118 children (age 14 to 24 months) with ASD found the treatment was beneficial and superior compared with a “community intervention” group, in regards to language ability measured in time by group analyses.The ESDM intervention in this study involved weekly parent coaching for 3 months, along with 24 months of 15 hours/week of one-on-one treatment provided by therapy professionals.¹²

Reciprocal imitation training (RIT) is another naturalistic intervention that has shown benefit in training children with ASD in imitation skills during play.¹³ Studies have found that both RIT and ESDM can be parent-implemented, after parents receive training.^13,14

Parent-mediated, parent-implemented interventions may have a role in improving outcomes in childhood ASD,^7,15 particularly “better generalization and maintenance of skills than therapist-implemented intervention” for lowering challenging behaviors and enhancing verbal and nonverbal communication.¹⁶

Various social skills interventions have also been found effective for children with ASD.¹ Such interventions are often provided in the school setting.⁷ Coordination with the child’s school to discuss and advocating for adequate and suitable interventions, educational services, and placement is an essential aspect of ASD treatment.⁷

Two other school-based, comprehensive treatment model interventions—Learning Experiences and Alternative Programs for Preschoolers and their Parents (LEAP), and TEACCH—have some evidence of leading to improvement in children with ASD.^7,17

Some studies have found that music therapy may have high efficacy for children with ASD, even with smaller length and intensity of treatment, particularly in improving social interaction, engagement with parents, joint attention, and communication.^3,18 Further research is needed to conclusively establish the efficacy of music therapy for ASD in children and adolescents.

A few studies have assessed the long-term outcomes of interventions for ASD; however, more research is needed.¹⁹ Pickles et al¹⁹ conducted a follow-up to determine the long-term effects of the Preschool Autism Communication Trial (PACT), an RCT of parent-mediated social communication therapy for children age 2 to 4 with ASD. The children’s average age at follow-up was 10 years. The authors found a significant long-term decrease in ASD symptoms and enhancement of social communication with parents (N = 152).¹⁹

Technology-based interventions, including games and robotics, have been investigated in recent years, for treatment of children with ASD (eg, for improving social skills).²⁰

Research suggests that the intensity (number of hours) and duration of nonpharmacologic treatments for ASD is critical to improving outcomes (Box^{1,3,5,7,10,16}).

Box

Continue to: Pharmacotherapy...

Pharmacotherapy

Medications cannot resolve core features of ASD.²¹ However, certain medications may help address associated comorbidities, such as attention-deficit/hyperactivity disorder (ADHD), depression, or others, when these conditions have not responded to nonpharmacologic interventions.^7,22 Common symptoms that are often treated with pharmacotherapy include aggression, irritability, hyperactivity, attentional difficulties, tics, self-injurious behavior, obsessive-compulsive symptoms, and mood dysregulation/lability.²³ Generally speaking, medications might be considered if symptoms are severe and markedly impair functioning. For mild to moderate conditions, psychotherapy and other nonpharmacologic interventions are generally considered first-line. Since none of the medications described below are specific to ASD and psychiatrists generally receive training in prescribing them for other indications, a comprehensive review of their risks and benefits is beyond the scope of this article. No psychotropic medications are known to have robust evidence for safety in preschool children with ASD, and thus are best avoided.

Antipsychotics. Risperidone (for age 5 and older) and aripiprazole (age 6 to 17) are the only medications FDA-approved for use in children and adolescents with ASD, specifically for irritability associated with ASD.^21,24 These 2 second-generation antipsychotics may also assist in lowering aggression in patients with ASD.²⁴ First-generation antipsychotics such as haloperidol have been shown to be effective for irritability and aggression in ASD, but the risk of significant adverse effects such as dyskinesias and extrapyramidal symptoms limit their use.²⁴ Two studies (a double-blind study and an open-label extension of that study) in children and adolescents with ASD found that risperidone was more effective and better tolerated than haloperidol in behavioral measures, impulsivity, and even in the social domain.^25,26 In addition to other adverse effects and risks, increased prolactin secondary to risperidone use requires close monitoring and caution.^24-26 As is the case with the use of other psychotropic medications in children and adolescents, those with ASD who receive antipsychotics should also be periodically reassessed to determine the need for continued use of these medications.²⁷ A multicenter relapse prevention RCT found no statistically significant difference in the time to relapse between aripiprazole and placebo.²⁷ Metabolic syndrome, cardiac risks, and other risks need to be considered before prescribing an antipsychotic.²⁸ Given their serious adverse effects profile, use should be considered only when there is severe impairment or risk of injury, after carefully weighing risks/benefits.

Medications for attentional difficulties. A multisite, randomized, placebo-controlled trial evaluating the use of extended-release guanfacine in children with ASD (N = 62) found the rate of positive response on the Clinical Global Impressions–Improvement scale was 50% for guanfacine vs 9.4% for placebo.²⁹ Clinicians need to monitor for adverse effects of guanfacine, such as fatigue, drowsiness, lightheadedness, lowering of blood pressure and heart rate, and other effects.²⁹ A randomized, double-blind trial of 97 children and adolescents with ASD and ADHD found that atomoxetine had moderate benefit for ADHD symptoms.³⁰ The study reported no serious adverse effects.³⁰ However, it is especially important to monitor for hepatic and cardiac adverse effects (in addition to monitoring for risk of increase in suicidal thoughts/behavior, as in the case of antidepressants) when using atomoxetine, in addition to other side effects and risks. Some evidence suggests that methylphenidate may be effective for attentional difficulties in children and adolescents with ASD²¹ but may pose a higher risk of adverse effects in this population compared with neurotypical patients.³¹

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) are sometimes used to reduce obsessive-compulsive symptoms, repetitive behavior, or depressive symptoms in children with ASD, but are not FDA-approved for children or adolescents with ASD. In general, there is inadequate evidence to support the use of SSRIs for ASD in children.^31-34 In addition, children with ASD may be at a greater risk of adverse effects from SSRIs.^32,34 Despite this, SSRIs are the most commonly prescribed psychotropic medications in children with ASD.³²

An RCT examining the efficacy of fluoxetine in 158 children and adolescents with ASD found no significant difference in Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS) score after 14 weeks of treatment; activation was a common adverse effect.³⁵ A 2005 randomized, double-blind, placebo-controlled trial of 45 children/adolescents with ASD found that low-dose liquid fluoxetine was more effective than placebo for reducing repetitive behaviors in this population.³⁶ Larger studies are warranted to further evaluate the efficacy and safety of fluoxetine (and of SSRIs in general, particularly in the long term) for children and adolescents with ASD.³⁶ A 2009 randomized, placebo-controlled trial of 149 children with ASD revealed no significant difference between citalopram and placebo as measured by Clinical Global Impressions scale or CY-BOCS scores, and noted a significantly elevated likelihood of adverse effects.³⁷

Other antidepressants. There is insufficient evidence to support the use of any other antidepressants in children and adolescents with ASD. A few studies^38,39 have examined the use of venlafaxine in children with ASD; however, further research and controlled studies with large sample sizes are required to conclusively establish its benefits. There is a dearth of evidence examining the use of the tetracyclic antidepressant mirtazapine, or other classes of medications such as tricyclic antidepressants or mood stabilizers, in children with ASD; only a few small studies have assessed the efficacy and adverse effects of these medications for such patients.³¹

Polypharmacy. Although there is no evidence to support polypharmacy in children and adolescents with ASD, the practice appears to be rampant in these patients.^28,40 A 2013 retrospective, observational study of psychotropic medication use in children with ASD (N = 33,565) found that 64% were prescribed psychotropic medications, and 35% exhibited evidence of polypharmacy.⁴⁰ In this study, the total duration of polypharmacy averaged 525 days.⁴⁰ When addressing polypharmacy, systematic deprescribing or simplification of the psychotropic medication regimen may be needed,²⁸ while taking into account the patient’s complete clinical situation, including (but not limited to) tolerability of the medication regimen, presence or absence of current stressors, presence or absence of adequate supports, use of nonpharmacologic treatments where appropriate, and other factors.

More studies assessing the efficacy and safety of psychotropic medications for children and adolescents with ASD are needed,³² especially studies that evaluate the effects of long-term use, because evidence for pharmacologic treatments for children with ASD is mixed and insufficient.³³ There is also a need for evidence-based standards for prescribing psychotropic medications in children and adolescents with ASD.

Psychotropic medications, if used in ASD, should be used only in conjunction with other evidence-based treatment modalities, and not as monotherapy.²¹ Children and adolescents with ASD may be particularly susceptible to side effects or adverse effects of certain psychotropic medications.³¹ When considering medications, carefully weigh the risks and benefits.^7,21,24,28 Starting low and going slow is generally the preferred strategy.^31,32 As always, when recommending medications, discuss in detail with parents the potential side effects, benefits, risks, interactions, and alternatives.

Other agents. Several double-blind, placebo-controlled trials have evaluated using melatonin for sleep difficulties in children and adolescents with ASD.⁴¹ A randomized, placebo-controlled, 12-week trial that assessed 160 children with ASD and insomnia found that melatonin plus cognitive-behavioral therapy (CBT) was superior in efficacy to melatonin alone, CBT alone, or placebo.⁴¹

The evidence regarding oxytocin use for children with ASD is mixed.³¹ Some small studies have associated improvement in the social domain with its use. Guastella et al⁴² conducted a randomized, double-blind, placebo-controlled trial of oxytocin nasal spray for 16 participants (age 12 to 19) with ASD, and found oxytocin enhanced emotional identification. Gordon et al⁴³ conducted a functional MRI study of brain activity with oxytocin use in children with high-functioning ASD (N = 17). They found that oxytocin may augment “salience and hedonic evaluations of socially meaningful stimuli in children with ASD” and thus help social attunement. Further research is needed to evaluate the impact of oxytocin on social behavior.

Complementary and alternative medicine. Although there is limited and inconclusive evidence about the use of complementary and alternative medicine in children and adolescents with ASD, these therapies continue to be commonly used.^44-46 A recent survey of parents (N = 211) of children with ASD from academic ASD outpatient clinics in Germany found that 46% reported their child was using or had used some type of complementary and alternative medicine.⁴⁴ There is inadequate evidence to support the use of a gluten-free, casein-free diet for children/adolescents with ASD.⁴⁶ A recent cross-sectional study assessing supplement use in 210 children with ASD in Canada found that 75% used supplements, such as multivitamins (77.8%), vitamin D (44.9%), omega 3 (42.5%), probiotics (36.5%), and magnesium (28.1%), despite insufficient evidence to support their safety or efficacy for children with ASD.⁴⁷ Importantly, 33.5% of parents in this study reported that they did not inform the physician about all their child’s supplements.⁴⁷ Some of the reasons the parents in this study provided for not disclosing information about supplements to their physicians were “physician lack of knowledge,” “no benefit,” “too time-consuming,” and “scared of judgment.”⁴⁷ Semi-structured interviews of parents of 21 children with ASD in Australia revealed that parents found information on complementary and alternative medicine and therapies complex and often conflicting.⁴⁵ In addition to recommendations from health care professionals, evidence suggests that parents often consider the opinions of media, friends, and family when making a decision on using complementary and alternative medicine modalities for children/adolescents with ASD.⁴⁶ Such findings can inform physician practices regarding supplement use, and highlight the need to educate parents about the evidence regarding these therapies and potential adverse effects and interactions of such therapies,⁴⁶ along with the need to develop a centralized, evidence-based resource for parents regarding their use.⁴⁵

Omega 3 supplementation has in general shown few adverse effects⁴⁷; still, risks/benefits need to be weighed before use. Some evidence suggests that it may decrease hyperactivity in children with ASD.^31,48 However, further research, particularly controlled trials with large sample sizes, are needed for a definitive determination of efficacy.^31,48 A meta-analysis that included 27 RCTs assessing the efficacy of dietary interventions for various ASD symptoms found that omega 3 supplementation was more effective than placebo, but compared with placebo, the effect size was small.⁴⁹ A RCT of 73 children with ASD in New Zealand found that omega 3 long chain polyunsaturated fatty acids may benefit some core symptoms of ASD; the authors suggested that further research is needed to conclusively establish efficacy.⁵⁰

Continue to: A need for advocacy and research..

Physicians who treat children with ASD can not only make appropriate referrals and educate parents, but also educate their patients’ schools and advocate for their patients to get the level of services they need.^23,28

A recent study in the United States found that behavior therapy and speech-language therapy were used less often in the treatment of children with ASD in rural areas compared with those in metro areas.⁵ This suggests that in addition to increasing parents’ awareness and use of ASD services and providing referrals where appropriate, physicians are in a unique position to advocate for public health policies to improve access, coverage, and training for the provision of such services in rural areas.

There is need for ongoing research to further examine the efficacy and nuances of effects of various treatment interventions for ASD, especially long-term studies with larger sample sizes.^11,51 Additionally, research is warranted to better understand the underlying genetic and neurobiological mechanisms of ASD, which would help guide the development of biomarkers,⁵² innovative treatments, and disease-modifying agents for ASD.^7,22 Exploring the effects of potential alliances or joint action between biological and psychosocial interventions for ASD is also an area that needs further research.⁵¹

Bottom Line

A combination of treatment modalities (such as speech-language therapy, social skills training, behavior therapy/other psychotherapy, and occupational therapy for sensory sensitivities) is generally needed to improve the long-term outcomes of children and adolescents with autism spectrum disorder (ASD). In addition to the importance of early intervention, the intensity and duration of nonpharmacologic treatments are vital to improving outcomes in ASD.

Evidence is strong that sexual partners transmit microbiota (bacteria, viruses, fungi, protozoa, and archaea) to each other. While microbial flora are abundant in the gastrointestinal tract, they are also present in the vagina, penis, urethra, mouth, and skin.¹ For better or worse, sexual contact of all types means that participants will acquire each other’s microbiota.

The 39 trillion microbiota in the body (which exceed the 30 trillion cells in the body) are commensal and influence both the larger brain in the skull and the smaller enteric brain in the gut. The microbiota and their microbiome genes (1,000 times larger than the human genome) have been linked to depression, anxiety, psychosis, and autism.^2-4 They produce 90% of the body’s serotonin, as well as catecholamines (norepinephrine, epinephrine, dopamine), make hormones (eg, cortisol), and modulate the immune system. Microbiota have several important functions, including food digestion, synthesis of vitamins, autoimmunity, hypothalamic-pituitary-adrenal axis regulation, and CNS modulation.

Consequences of dysbiosis

Everyone should be concerned about maintaining a healthy diversity of microbiota in their body, with a predominance of beneficial bacteria such as Lactobacillus and Bacteroides, and avoiding acquiring pathogenic bacteria such as Gardnerella, Prevotella, and Atopobium. Sexual activity involving a partner with unhealthy microbiota may increase the risk of dysbiosis, defined as a reduction in microbiota diversity, including a loss of beneficial bacteria and a rise in harmful bacteria.

Dysbiosis is associated with multiple symptoms, including⁵:

• brain “fog,” irritability, mood changes, and anxiety
• bloating, loss of intestinal permeability, and insufficient reclamation of nutrients
• congestion of certain organs, such as the liver, gallbladder, and pancreas
• production of antigen-antibody complexes in response to chemicals in partially digested food
• aggravation of inflammatory disorders such as migraine, arthritis, and autoimmune disorders.

Apart from intimate sexual contact, simply sharing a household with someone leads to sharing of gut microflora. Persons who live together, whether genetically related or not, have similar microbiota. Compared with people living in separate households, cohabiting human pairs, dog pairs, and human-dog pairs share most of their microbiota (especially in the skin).

A consequence of acquiring pathogenic microbiota in the vagina is bacterial vaginosis (BV), which is not an infection but an ecologic imbalance in the composition of the vaginal microbiota. BV is caused by a significant decline in the beneficial vaginal Lactobacillus and a marked increase in the non-Lactobacillus taxa (especially Gardnerella and Atopobium).⁶ It can last for a least 1 week after sexual intercourse. BV is rare or absent among virgins. For a male partner, penile microbiota changes significantly after unprotected sex.⁶

Pathogenic bacteria can be cultivated from the glans, the coronal sulcus, and the prepuce, as well as from the penile skin, semen, urethra, and urine.⁶ Diverse bacteria exist in human semen, regardless if the male is fertile or infertile.⁷Anaerococcus is a biomarker for low sperm quality. Many of the semen bacteria are also found in the vagina of women with BV.⁷ Semen is a medium for the transmission of bacteria and viruses between men and women, and can contribute to sexually transmitted diseases.⁸

There are approximately 21 million cases of BV in the United States each year, and BV can also increase the risk of HIV and poor obstetric outcomes.⁹ The microbiota in the penile skin and urethra in males who have monogamous relationships with females are very similar to the vaginal microbiota of their female partner.

Consequences of BV include:

• decrease in hydrogen peroxide–producing bacilli
• prevalence of anaerobic bacteria (Prevotella, Gardnerella, and Atopobium)
• alkalinization, fishy odor, and gray-white vaginal discharge
• increase in the rate of pelvic inflammatory disease, ectopic pregnancy, endometriosis, preterm birth, and tubal factor infertility.⁹

Circumcision decreases the risk of BV. There is an increased rate of BV bacterial taxa in men with extramarital affairs and in women with multiple partners. Both oral and vaginal sex increase the abundance of Lactobacillus in the male oral and penile microbiota. Gingivitis has also been reported after oral sex.¹⁰

A link to psychiatric disorders

Given that all forms of sexual contact (vaginal, oral, anal, or skin) can transmit microbiota bidirectionally between partners, it is vital to practice safe sex and consider a monogamous relationship rather than indiscriminate promiscuity. Unfortunately, certain psychiatric disorders, such as bipolar disorder, are associated with hypersexuality and multiple partners, which may disrupt the microbiota. This can further disrupt the diversity of an individual’s microbiome and may put them at risk for mood, anxiety, and other psychiatric disorders. Another problem is sexually transmitted infections such as gonorrhea or syphilis require antibiotic therapy. It is well established that antibiotics kill both the bad pathogenic and the good nonpathogenic microbiota, further exacerbating dysbiosis and leading to disruptions in the microbiota-gut-brain (MGB) axis, which then results in psychiatric disorders.

The MGB axis modulates neurological processes via the vagus nerve, the major “highway” connecting the gut and brain for bidirectional traffic. The MGB axis produces microbial metabolites and immune factors that can lead to changes in brain neurotransmitters as well as neuroinflammation and psychiatric symptoms such as depression and anxiety.⁵

Many researchers are focusing on how to exploit the microbiome to develop novel therapeutic strategies, and encouraging advances are emerging.⁵ But the exact mechanisms by which the gut microbiome can impact mental health is still a work in progress. It is highly likely that dysbiosis is associated with mood and anxiety symptoms.

The bottom line: Sexual activity—whether it is heavy kissing, vaginal intercourse, oral sex, anal sex, or extensive skin contact—can lead to the exchange of microbiota. If an individual has dysbiosis, that could impact the mental health of their sexual partner(s). This raises the question of whether counseling patients about avoiding indiscriminate sex and practicing safe sex is as important for mental health as diet and exercise counseling is for physical health.

Evidence is strong that sexual partners transmit microbiota (bacteria, viruses, fungi, protozoa, and archaea) to each other. While microbial flora are abundant in the gastrointestinal tract, they are also present in the vagina, penis, urethra, mouth, and skin.¹ For better or worse, sexual contact of all types means that participants will acquire each other’s microbiota.

The 39 trillion microbiota in the body (which exceed the 30 trillion cells in the body) are commensal and influence both the larger brain in the skull and the smaller enteric brain in the gut. The microbiota and their microbiome genes (1,000 times larger than the human genome) have been linked to depression, anxiety, psychosis, and autism.^2-4 They produce 90% of the body’s serotonin, as well as catecholamines (norepinephrine, epinephrine, dopamine), make hormones (eg, cortisol), and modulate the immune system. Microbiota have several important functions, including food digestion, synthesis of vitamins, autoimmunity, hypothalamic-pituitary-adrenal axis regulation, and CNS modulation.

Consequences of dysbiosis

Everyone should be concerned about maintaining a healthy diversity of microbiota in their body, with a predominance of beneficial bacteria such as Lactobacillus and Bacteroides, and avoiding acquiring pathogenic bacteria such as Gardnerella, Prevotella, and Atopobium. Sexual activity involving a partner with unhealthy microbiota may increase the risk of dysbiosis, defined as a reduction in microbiota diversity, including a loss of beneficial bacteria and a rise in harmful bacteria.

Dysbiosis is associated with multiple symptoms, including⁵:

• brain “fog,” irritability, mood changes, and anxiety
• bloating, loss of intestinal permeability, and insufficient reclamation of nutrients
• congestion of certain organs, such as the liver, gallbladder, and pancreas
• production of antigen-antibody complexes in response to chemicals in partially digested food
• aggravation of inflammatory disorders such as migraine, arthritis, and autoimmune disorders.

Apart from intimate sexual contact, simply sharing a household with someone leads to sharing of gut microflora. Persons who live together, whether genetically related or not, have similar microbiota. Compared with people living in separate households, cohabiting human pairs, dog pairs, and human-dog pairs share most of their microbiota (especially in the skin).

A consequence of acquiring pathogenic microbiota in the vagina is bacterial vaginosis (BV), which is not an infection but an ecologic imbalance in the composition of the vaginal microbiota. BV is caused by a significant decline in the beneficial vaginal Lactobacillus and a marked increase in the non-Lactobacillus taxa (especially Gardnerella and Atopobium).⁶ It can last for a least 1 week after sexual intercourse. BV is rare or absent among virgins. For a male partner, penile microbiota changes significantly after unprotected sex.⁶

Pathogenic bacteria can be cultivated from the glans, the coronal sulcus, and the prepuce, as well as from the penile skin, semen, urethra, and urine.⁶ Diverse bacteria exist in human semen, regardless if the male is fertile or infertile.⁷Anaerococcus is a biomarker for low sperm quality. Many of the semen bacteria are also found in the vagina of women with BV.⁷ Semen is a medium for the transmission of bacteria and viruses between men and women, and can contribute to sexually transmitted diseases.⁸

There are approximately 21 million cases of BV in the United States each year, and BV can also increase the risk of HIV and poor obstetric outcomes.⁹ The microbiota in the penile skin and urethra in males who have monogamous relationships with females are very similar to the vaginal microbiota of their female partner.

Consequences of BV include:

• decrease in hydrogen peroxide–producing bacilli
• prevalence of anaerobic bacteria (Prevotella, Gardnerella, and Atopobium)
• alkalinization, fishy odor, and gray-white vaginal discharge
• increase in the rate of pelvic inflammatory disease, ectopic pregnancy, endometriosis, preterm birth, and tubal factor infertility.⁹

Circumcision decreases the risk of BV. There is an increased rate of BV bacterial taxa in men with extramarital affairs and in women with multiple partners. Both oral and vaginal sex increase the abundance of Lactobacillus in the male oral and penile microbiota. Gingivitis has also been reported after oral sex.¹⁰

A link to psychiatric disorders

Given that all forms of sexual contact (vaginal, oral, anal, or skin) can transmit microbiota bidirectionally between partners, it is vital to practice safe sex and consider a monogamous relationship rather than indiscriminate promiscuity. Unfortunately, certain psychiatric disorders, such as bipolar disorder, are associated with hypersexuality and multiple partners, which may disrupt the microbiota. This can further disrupt the diversity of an individual’s microbiome and may put them at risk for mood, anxiety, and other psychiatric disorders. Another problem is sexually transmitted infections such as gonorrhea or syphilis require antibiotic therapy. It is well established that antibiotics kill both the bad pathogenic and the good nonpathogenic microbiota, further exacerbating dysbiosis and leading to disruptions in the microbiota-gut-brain (MGB) axis, which then results in psychiatric disorders.

The MGB axis modulates neurological processes via the vagus nerve, the major “highway” connecting the gut and brain for bidirectional traffic. The MGB axis produces microbial metabolites and immune factors that can lead to changes in brain neurotransmitters as well as neuroinflammation and psychiatric symptoms such as depression and anxiety.⁵

Many researchers are focusing on how to exploit the microbiome to develop novel therapeutic strategies, and encouraging advances are emerging.⁵ But the exact mechanisms by which the gut microbiome can impact mental health is still a work in progress. It is highly likely that dysbiosis is associated with mood and anxiety symptoms.

The bottom line: Sexual activity—whether it is heavy kissing, vaginal intercourse, oral sex, anal sex, or extensive skin contact—can lead to the exchange of microbiota. If an individual has dysbiosis, that could impact the mental health of their sexual partner(s). This raises the question of whether counseling patients about avoiding indiscriminate sex and practicing safe sex is as important for mental health as diet and exercise counseling is for physical health.

Evidence is strong that sexual partners transmit microbiota (bacteria, viruses, fungi, protozoa, and archaea) to each other. While microbial flora are abundant in the gastrointestinal tract, they are also present in the vagina, penis, urethra, mouth, and skin.¹ For better or worse, sexual contact of all types means that participants will acquire each other’s microbiota.

The 39 trillion microbiota in the body (which exceed the 30 trillion cells in the body) are commensal and influence both the larger brain in the skull and the smaller enteric brain in the gut. The microbiota and their microbiome genes (1,000 times larger than the human genome) have been linked to depression, anxiety, psychosis, and autism.^2-4 They produce 90% of the body’s serotonin, as well as catecholamines (norepinephrine, epinephrine, dopamine), make hormones (eg, cortisol), and modulate the immune system. Microbiota have several important functions, including food digestion, synthesis of vitamins, autoimmunity, hypothalamic-pituitary-adrenal axis regulation, and CNS modulation.

Consequences of dysbiosis

Everyone should be concerned about maintaining a healthy diversity of microbiota in their body, with a predominance of beneficial bacteria such as Lactobacillus and Bacteroides, and avoiding acquiring pathogenic bacteria such as Gardnerella, Prevotella, and Atopobium. Sexual activity involving a partner with unhealthy microbiota may increase the risk of dysbiosis, defined as a reduction in microbiota diversity, including a loss of beneficial bacteria and a rise in harmful bacteria.

Dysbiosis is associated with multiple symptoms, including⁵:

• brain “fog,” irritability, mood changes, and anxiety
• bloating, loss of intestinal permeability, and insufficient reclamation of nutrients
• congestion of certain organs, such as the liver, gallbladder, and pancreas
• production of antigen-antibody complexes in response to chemicals in partially digested food
• aggravation of inflammatory disorders such as migraine, arthritis, and autoimmune disorders.

Apart from intimate sexual contact, simply sharing a household with someone leads to sharing of gut microflora. Persons who live together, whether genetically related or not, have similar microbiota. Compared with people living in separate households, cohabiting human pairs, dog pairs, and human-dog pairs share most of their microbiota (especially in the skin).

A consequence of acquiring pathogenic microbiota in the vagina is bacterial vaginosis (BV), which is not an infection but an ecologic imbalance in the composition of the vaginal microbiota. BV is caused by a significant decline in the beneficial vaginal Lactobacillus and a marked increase in the non-Lactobacillus taxa (especially Gardnerella and Atopobium).⁶ It can last for a least 1 week after sexual intercourse. BV is rare or absent among virgins. For a male partner, penile microbiota changes significantly after unprotected sex.⁶

Pathogenic bacteria can be cultivated from the glans, the coronal sulcus, and the prepuce, as well as from the penile skin, semen, urethra, and urine.⁶ Diverse bacteria exist in human semen, regardless if the male is fertile or infertile.⁷Anaerococcus is a biomarker for low sperm quality. Many of the semen bacteria are also found in the vagina of women with BV.⁷ Semen is a medium for the transmission of bacteria and viruses between men and women, and can contribute to sexually transmitted diseases.⁸

There are approximately 21 million cases of BV in the United States each year, and BV can also increase the risk of HIV and poor obstetric outcomes.⁹ The microbiota in the penile skin and urethra in males who have monogamous relationships with females are very similar to the vaginal microbiota of their female partner.

Consequences of BV include:

• decrease in hydrogen peroxide–producing bacilli
• prevalence of anaerobic bacteria (Prevotella, Gardnerella, and Atopobium)
• alkalinization, fishy odor, and gray-white vaginal discharge
• increase in the rate of pelvic inflammatory disease, ectopic pregnancy, endometriosis, preterm birth, and tubal factor infertility.⁹

Circumcision decreases the risk of BV. There is an increased rate of BV bacterial taxa in men with extramarital affairs and in women with multiple partners. Both oral and vaginal sex increase the abundance of Lactobacillus in the male oral and penile microbiota. Gingivitis has also been reported after oral sex.¹⁰

A link to psychiatric disorders

Given that all forms of sexual contact (vaginal, oral, anal, or skin) can transmit microbiota bidirectionally between partners, it is vital to practice safe sex and consider a monogamous relationship rather than indiscriminate promiscuity. Unfortunately, certain psychiatric disorders, such as bipolar disorder, are associated with hypersexuality and multiple partners, which may disrupt the microbiota. This can further disrupt the diversity of an individual’s microbiome and may put them at risk for mood, anxiety, and other psychiatric disorders. Another problem is sexually transmitted infections such as gonorrhea or syphilis require antibiotic therapy. It is well established that antibiotics kill both the bad pathogenic and the good nonpathogenic microbiota, further exacerbating dysbiosis and leading to disruptions in the microbiota-gut-brain (MGB) axis, which then results in psychiatric disorders.

The MGB axis modulates neurological processes via the vagus nerve, the major “highway” connecting the gut and brain for bidirectional traffic. The MGB axis produces microbial metabolites and immune factors that can lead to changes in brain neurotransmitters as well as neuroinflammation and psychiatric symptoms such as depression and anxiety.⁵

Many researchers are focusing on how to exploit the microbiome to develop novel therapeutic strategies, and encouraging advances are emerging.⁵ But the exact mechanisms by which the gut microbiome can impact mental health is still a work in progress. It is highly likely that dysbiosis is associated with mood and anxiety symptoms.

The bottom line: Sexual activity—whether it is heavy kissing, vaginal intercourse, oral sex, anal sex, or extensive skin contact—can lead to the exchange of microbiota. If an individual has dysbiosis, that could impact the mental health of their sexual partner(s). This raises the question of whether counseling patients about avoiding indiscriminate sex and practicing safe sex is as important for mental health as diet and exercise counseling is for physical health.