Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

CASE Stable with a new diagnosis

Ms. B, age 60, has a history of schizophrenia, which has been stable on clozapine, 500 mg/d, for more than 2 decades. After a series of hospitalizations in her 20s and 30s, clozapine was initiated and she has not required additional inpatient psychiatric care. She has been managed in the outpatient setting with standard biweekly absolute neutrophil count (ANC) monitoring. She lives independently and is an active member in her church.

After experiencing rectal bleeding, Ms. B is diagnosed with rectal carcinoma and is scheduled to undergo chemotherapy and radiation treatment.

[polldaddy:9754786]

The authors’ observations

Both clozapine and chemotherapy carry the risk of immunosuppression, presenting a clinical challenge when choosing an appropriate management strategy. However, the risks of stopping clozapine after a long period of symptom stability are substantial, with a relapse rate up to 50%.¹ Among patients taking clozapine, the risk of agranulocytosis and neutropenia are approximately 0.8% and 3%, respectively, and >80% of agranulocyotis cases occur within the first 18 weeks of treatment.^2,3 Although both clozapine and chemotherapy can lead to neutropenia and agranulocytosis, there currently is no evidence of a synergistic effect on bone marrow suppression with simultaneous use of these therapies² nor is there evidence of the combination leading to sustained marrow suppression.⁴

Because of Ms. B’s positive response to clozapine, the risks associated with discontinuing the medication, and the relatively low risk of clozapine contributing to neutropenia after a long period of stabilization, her outpatient psychiatric providers decide to increase ANC monitoring to weekly while she undergoes cancer treatment.

TREATMENT Neutropenia, psychosis

Ms. B continues clozapine during radiation and chemotherapy, but develops leukopenia and neutropenia with a low of 1,220/μL white blood cells and an ANC of 610/μL. Clozapine is stopped, consistent with current recommendations to hold the drug if the neutrophil count is <1,000/μL in a patient without benign ethnic neutropenia, and her outpatient provider monitors her closely. The treatment team does not restart an antipsychotic immediately after discontinuing clozapine because of the risk that other antipsychotics can cause hematologic toxicity or prolong granulocytopenia associated with clozapine.⁵

Approximately 2 weeks later, Ms. B is admitted to a different hospital for altered mental status and is found to have hypo­natremia and rectal bleeding. The workup suggests that her rectal carcinoma has not fully responded to initial therapies, and she likely will require further treatment. Her mental status improves after hyponatremia resolves, but she reports auditory hallucinations and paranoia. Risperidone, 4 mg/d, is initiated to target psychosis.

After discharge, Ms. B develops bilateral upper extremity tremor, which she finds intolerable and attributes to risperidone. She refuses to continue risperidone or try adjunctive medications to address the tremor, but is willing to consider a different antipsychotic. Olanzapine, 10 mg/d, is initiated and risperidone is slowly tapered. During this time, Ms. B experiences increased paranoia and believes that the Internal Revenue Service is calling her. She misses her next appointment.

Later, the fire department finds Ms. B wandering the streets and brings her to the psychiatric emergency room. During the examination, she is disheveled and withdrawn, and unable to reply to simple questions about diet and sleep. When asked why she was in the street, she says that she left her apartment because it was “too messy.” The treatment team learns that she had walked at least 10 miles from her apartment before sitting down by the side of the road and being picked up by the fire department. She reveals that she left her apartment and continued walking because “a man” told her to do so and threatened to harm her if she stopped.

When Ms. B is admitted to the psychiatric service, she is paranoid, disorganized, and guarded. She remains in her room for most of the day and either refuses to talk to providers or curses at them. She often is seen wearing soiled clothing with her hair mussed. She denies having rectal carcinoma, although she expressed understanding of her medical condition <2 months earlier.

[polldaddy:9754787]

The authors’ observations

Clozapine is considered the most efficacious agent for treatment-resistant schizophrenia.⁶ Although non-compliance is the most common reason for discontinuing clozapine, >20% of patients stop clozapine because of adverse effects.⁷ Clozapine often is a drug of last resort because of the need for frequent monitoring and significant side effects; therefore deciding on a next step when clozapine fails or cannot be continued because of other factors can pose a challenge.

Ms. B’s treatment team gave serious consideration to restarting clozapine. However, because it was likely that Ms. B would undergo another round of chemotherapy and possibly radiation, the risk of neutropenia recurring was considered too high. Lithium has been used successfully to manage neutropenia in patients taking clozapine and, for some, adding lithium could help boost white cell count and allow a successful rechallenge with clozapine.^3,8 However, because of Ms. B’s medical comorbidities, including cancer and chronic kidney disease, adding lithium was not thought to be clinically prudent at that time and the treatment team considered other options.

Olanzapine. Although research is limited, studies suggest olanzapine is the most commonly prescribed medication when a patient has to discontinue clozapine,⁷ with comparable response rates in those with refractory schizophrenia.⁹ Therefore, Ms. B was initially maintained on olanzapine, and the dosage increased to 30 mg over the course of 16 days in the hospital. However, she did not respond to the medication, remaining disorganized and paranoid without any notable improvement in her symptoms therefore other treatment options were explored.

Loxapine. Previous limited case reports have shown loxapine to be effective in treating individuals with refractory schizophrenia, either alone or in combination with other antipsychotics.^10,11 FDA-approved in 1975, loxapine was among the last of the typical antipsychotics brought to the U.S. market before the introduction of clozapine, the first atypical.¹² Loxapine is a dibenzoxazepine that has a molecular structure similar to clozapine.¹³ Unlike clozapine, however, loxapine is not known to cause agranulocytosis.¹⁴ Research suggests that although clozapine is oxidized to metabolites that are cytotoxic, loxapine is not, potentially accounting for their different effects on neutrophils.¹⁵

The efficacy of loxapine has shown to be similar to other typical and atypical antipsychotics, with approximately 70% of patients showing improvement.¹⁴ However, loxapine may be overlooked as an option, possibly because it was not included in the CATIE trial and was the last typical antipsychotic to be approved before atypicals were introduced.¹² First available in oral and IM formulations, there has been increased interest in loxapine recently because of the approval of an inhaled formulation in 2012.¹⁶

Although classified as a typical anti­psychotic, studies have suggested that loxapine acts as an atypical at low dosages.^17,18 Previous work suggests, however, that the side effect profile of loxapine is similar to typical antipsychotics.¹⁴ At dosages <50 mg, it results in fewer cases of extrapyramidal side effects than expected with a typical antipsychotic.¹⁸

Loxapine’s binding profile seems to exist along this spectrum of typical to atypical. Tissue-based binding studies have shown a higher 5-HT2 affinity relative to D2, consistent with atypical antipsychotics.¹⁹ Positron emission tomography studies in humans show 5-HT2 saturation of loxapine to be close to equal to D2 binding in loxapine, thus a slightly lower ratio of 5-HT2 to D2 relative to atypicals, but more than that seen with typical antipsychotics.²⁰ These differences between in vitro and in vivo studies may be secondary to the binding of loxapine’s active metabolites, particularly 7- and 8-hydroxyloxapine, which have more dopaminergic activity. In addition to increased 5-HT2A binding compared with typical antipsychotics, loxapine also has a high affinity for the D4 receptors, as well as interacting with other serotonin receptors 5-HT3, 5-HT6, and 5-HT7. Of note this is a similar pattern of binding affinity as seen in clozapine.¹⁹

It should be noted, however, that loxapine may not be an appropriate treatment in all forms of cancer. Similar to other first-generation antipsychotics, it increases prolactin levels, and thus may have a negative clinical impact on patients with prolactin receptor positive breast cancers.^21,22 Finally, although clozapine can result in significant weight gain, dyslipidemia, and hyperglycemia, unlike many antipsychotics, loxapine has been shown to be weight neutral or result in weight loss,¹⁴ making it an option to consider for patients with type 2 diabetes mellitus, metabolic syndrome, dyslipidemia, or cardiovascular disease.

OUTCOME Improvement, stability

Ms. B begins taking loxapine, 10 mg/d, gradually cross-tapered with olanzapine, increasing loxapine by 10 mg every 2 to 3 days (Figure). After 8 days, when the dosage has reached 40 mg/d, Ms. B’s treatment team begins to observe a consistent change in her behavior. Ms. B comes into the interview room, where previously the team had to see her in her own room because she refused to come out. She also tolerates an extensive interview, even sharing parts of her history without prompting, and is able to discuss her treatment. Ms. B continues to express some paranoia regarding the treatment team. On day 12, receiving loxapine, 50 mg/d, Ms. B says that she likes the new medication and feels she is doing well with it. She becomes less reclusive and begins socializing with other patients. By day 19, receiving loxapine, 80 mg/d, a nurse, who knows Ms. B from the outpatient facility, visits the unit and reports that Ms. B is at her baseline.

At discharge, Ms. B is noted to be “bright,” well organized, neatly dressed, and wearing makeup. Her paranoia and auditory hallucinations have almost completely resolved. She is social, engages appropriately with the treatment team, and is able to describe a plan for self-care after discharge including following up with her oncologist. Her white blood cell counts were carefully monitored throughout her admission and are within normal limits when she is discharged.

One year later, Ms. B remains taking loxapine, 70 mg/d. Although she continues to report mild paranoia, she is living independently in her apartment and attends church regularly.

CASE Stable with a new diagnosis

Ms. B, age 60, has a history of schizophrenia, which has been stable on clozapine, 500 mg/d, for more than 2 decades. After a series of hospitalizations in her 20s and 30s, clozapine was initiated and she has not required additional inpatient psychiatric care. She has been managed in the outpatient setting with standard biweekly absolute neutrophil count (ANC) monitoring. She lives independently and is an active member in her church.

After experiencing rectal bleeding, Ms. B is diagnosed with rectal carcinoma and is scheduled to undergo chemotherapy and radiation treatment.

[polldaddy:9754786]

The authors’ observations

Both clozapine and chemotherapy carry the risk of immunosuppression, presenting a clinical challenge when choosing an appropriate management strategy. However, the risks of stopping clozapine after a long period of symptom stability are substantial, with a relapse rate up to 50%.¹ Among patients taking clozapine, the risk of agranulocytosis and neutropenia are approximately 0.8% and 3%, respectively, and >80% of agranulocyotis cases occur within the first 18 weeks of treatment.^2,3 Although both clozapine and chemotherapy can lead to neutropenia and agranulocytosis, there currently is no evidence of a synergistic effect on bone marrow suppression with simultaneous use of these therapies² nor is there evidence of the combination leading to sustained marrow suppression.⁴

Because of Ms. B’s positive response to clozapine, the risks associated with discontinuing the medication, and the relatively low risk of clozapine contributing to neutropenia after a long period of stabilization, her outpatient psychiatric providers decide to increase ANC monitoring to weekly while she undergoes cancer treatment.

TREATMENT Neutropenia, psychosis

Ms. B continues clozapine during radiation and chemotherapy, but develops leukopenia and neutropenia with a low of 1,220/μL white blood cells and an ANC of 610/μL. Clozapine is stopped, consistent with current recommendations to hold the drug if the neutrophil count is <1,000/μL in a patient without benign ethnic neutropenia, and her outpatient provider monitors her closely. The treatment team does not restart an antipsychotic immediately after discontinuing clozapine because of the risk that other antipsychotics can cause hematologic toxicity or prolong granulocytopenia associated with clozapine.⁵

Approximately 2 weeks later, Ms. B is admitted to a different hospital for altered mental status and is found to have hypo­natremia and rectal bleeding. The workup suggests that her rectal carcinoma has not fully responded to initial therapies, and she likely will require further treatment. Her mental status improves after hyponatremia resolves, but she reports auditory hallucinations and paranoia. Risperidone, 4 mg/d, is initiated to target psychosis.

After discharge, Ms. B develops bilateral upper extremity tremor, which she finds intolerable and attributes to risperidone. She refuses to continue risperidone or try adjunctive medications to address the tremor, but is willing to consider a different antipsychotic. Olanzapine, 10 mg/d, is initiated and risperidone is slowly tapered. During this time, Ms. B experiences increased paranoia and believes that the Internal Revenue Service is calling her. She misses her next appointment.

Later, the fire department finds Ms. B wandering the streets and brings her to the psychiatric emergency room. During the examination, she is disheveled and withdrawn, and unable to reply to simple questions about diet and sleep. When asked why she was in the street, she says that she left her apartment because it was “too messy.” The treatment team learns that she had walked at least 10 miles from her apartment before sitting down by the side of the road and being picked up by the fire department. She reveals that she left her apartment and continued walking because “a man” told her to do so and threatened to harm her if she stopped.

When Ms. B is admitted to the psychiatric service, she is paranoid, disorganized, and guarded. She remains in her room for most of the day and either refuses to talk to providers or curses at them. She often is seen wearing soiled clothing with her hair mussed. She denies having rectal carcinoma, although she expressed understanding of her medical condition <2 months earlier.

[polldaddy:9754787]

The authors’ observations

Clozapine is considered the most efficacious agent for treatment-resistant schizophrenia.⁶ Although non-compliance is the most common reason for discontinuing clozapine, >20% of patients stop clozapine because of adverse effects.⁷ Clozapine often is a drug of last resort because of the need for frequent monitoring and significant side effects; therefore deciding on a next step when clozapine fails or cannot be continued because of other factors can pose a challenge.

Ms. B’s treatment team gave serious consideration to restarting clozapine. However, because it was likely that Ms. B would undergo another round of chemotherapy and possibly radiation, the risk of neutropenia recurring was considered too high. Lithium has been used successfully to manage neutropenia in patients taking clozapine and, for some, adding lithium could help boost white cell count and allow a successful rechallenge with clozapine.^3,8 However, because of Ms. B’s medical comorbidities, including cancer and chronic kidney disease, adding lithium was not thought to be clinically prudent at that time and the treatment team considered other options.

Olanzapine. Although research is limited, studies suggest olanzapine is the most commonly prescribed medication when a patient has to discontinue clozapine,⁷ with comparable response rates in those with refractory schizophrenia.⁹ Therefore, Ms. B was initially maintained on olanzapine, and the dosage increased to 30 mg over the course of 16 days in the hospital. However, she did not respond to the medication, remaining disorganized and paranoid without any notable improvement in her symptoms therefore other treatment options were explored.

Loxapine. Previous limited case reports have shown loxapine to be effective in treating individuals with refractory schizophrenia, either alone or in combination with other antipsychotics.^10,11 FDA-approved in 1975, loxapine was among the last of the typical antipsychotics brought to the U.S. market before the introduction of clozapine, the first atypical.¹² Loxapine is a dibenzoxazepine that has a molecular structure similar to clozapine.¹³ Unlike clozapine, however, loxapine is not known to cause agranulocytosis.¹⁴ Research suggests that although clozapine is oxidized to metabolites that are cytotoxic, loxapine is not, potentially accounting for their different effects on neutrophils.¹⁵

The efficacy of loxapine has shown to be similar to other typical and atypical antipsychotics, with approximately 70% of patients showing improvement.¹⁴ However, loxapine may be overlooked as an option, possibly because it was not included in the CATIE trial and was the last typical antipsychotic to be approved before atypicals were introduced.¹² First available in oral and IM formulations, there has been increased interest in loxapine recently because of the approval of an inhaled formulation in 2012.¹⁶

Although classified as a typical anti­psychotic, studies have suggested that loxapine acts as an atypical at low dosages.^17,18 Previous work suggests, however, that the side effect profile of loxapine is similar to typical antipsychotics.¹⁴ At dosages <50 mg, it results in fewer cases of extrapyramidal side effects than expected with a typical antipsychotic.¹⁸

Loxapine’s binding profile seems to exist along this spectrum of typical to atypical. Tissue-based binding studies have shown a higher 5-HT2 affinity relative to D2, consistent with atypical antipsychotics.¹⁹ Positron emission tomography studies in humans show 5-HT2 saturation of loxapine to be close to equal to D2 binding in loxapine, thus a slightly lower ratio of 5-HT2 to D2 relative to atypicals, but more than that seen with typical antipsychotics.²⁰ These differences between in vitro and in vivo studies may be secondary to the binding of loxapine’s active metabolites, particularly 7- and 8-hydroxyloxapine, which have more dopaminergic activity. In addition to increased 5-HT2A binding compared with typical antipsychotics, loxapine also has a high affinity for the D4 receptors, as well as interacting with other serotonin receptors 5-HT3, 5-HT6, and 5-HT7. Of note this is a similar pattern of binding affinity as seen in clozapine.¹⁹

It should be noted, however, that loxapine may not be an appropriate treatment in all forms of cancer. Similar to other first-generation antipsychotics, it increases prolactin levels, and thus may have a negative clinical impact on patients with prolactin receptor positive breast cancers.^21,22 Finally, although clozapine can result in significant weight gain, dyslipidemia, and hyperglycemia, unlike many antipsychotics, loxapine has been shown to be weight neutral or result in weight loss,¹⁴ making it an option to consider for patients with type 2 diabetes mellitus, metabolic syndrome, dyslipidemia, or cardiovascular disease.

OUTCOME Improvement, stability

Ms. B begins taking loxapine, 10 mg/d, gradually cross-tapered with olanzapine, increasing loxapine by 10 mg every 2 to 3 days (Figure). After 8 days, when the dosage has reached 40 mg/d, Ms. B’s treatment team begins to observe a consistent change in her behavior. Ms. B comes into the interview room, where previously the team had to see her in her own room because she refused to come out. She also tolerates an extensive interview, even sharing parts of her history without prompting, and is able to discuss her treatment. Ms. B continues to express some paranoia regarding the treatment team. On day 12, receiving loxapine, 50 mg/d, Ms. B says that she likes the new medication and feels she is doing well with it. She becomes less reclusive and begins socializing with other patients. By day 19, receiving loxapine, 80 mg/d, a nurse, who knows Ms. B from the outpatient facility, visits the unit and reports that Ms. B is at her baseline.

At discharge, Ms. B is noted to be “bright,” well organized, neatly dressed, and wearing makeup. Her paranoia and auditory hallucinations have almost completely resolved. She is social, engages appropriately with the treatment team, and is able to describe a plan for self-care after discharge including following up with her oncologist. Her white blood cell counts were carefully monitored throughout her admission and are within normal limits when she is discharged.

One year later, Ms. B remains taking loxapine, 70 mg/d. Although she continues to report mild paranoia, she is living independently in her apartment and attends church regularly.

CASE Stable with a new diagnosis

Ms. B, age 60, has a history of schizophrenia, which has been stable on clozapine, 500 mg/d, for more than 2 decades. After a series of hospitalizations in her 20s and 30s, clozapine was initiated and she has not required additional inpatient psychiatric care. She has been managed in the outpatient setting with standard biweekly absolute neutrophil count (ANC) monitoring. She lives independently and is an active member in her church.

After experiencing rectal bleeding, Ms. B is diagnosed with rectal carcinoma and is scheduled to undergo chemotherapy and radiation treatment.

[polldaddy:9754786]

The authors’ observations

Both clozapine and chemotherapy carry the risk of immunosuppression, presenting a clinical challenge when choosing an appropriate management strategy. However, the risks of stopping clozapine after a long period of symptom stability are substantial, with a relapse rate up to 50%.¹ Among patients taking clozapine, the risk of agranulocytosis and neutropenia are approximately 0.8% and 3%, respectively, and >80% of agranulocyotis cases occur within the first 18 weeks of treatment.^2,3 Although both clozapine and chemotherapy can lead to neutropenia and agranulocytosis, there currently is no evidence of a synergistic effect on bone marrow suppression with simultaneous use of these therapies² nor is there evidence of the combination leading to sustained marrow suppression.⁴

Because of Ms. B’s positive response to clozapine, the risks associated with discontinuing the medication, and the relatively low risk of clozapine contributing to neutropenia after a long period of stabilization, her outpatient psychiatric providers decide to increase ANC monitoring to weekly while she undergoes cancer treatment.

TREATMENT Neutropenia, psychosis

Ms. B continues clozapine during radiation and chemotherapy, but develops leukopenia and neutropenia with a low of 1,220/μL white blood cells and an ANC of 610/μL. Clozapine is stopped, consistent with current recommendations to hold the drug if the neutrophil count is <1,000/μL in a patient without benign ethnic neutropenia, and her outpatient provider monitors her closely. The treatment team does not restart an antipsychotic immediately after discontinuing clozapine because of the risk that other antipsychotics can cause hematologic toxicity or prolong granulocytopenia associated with clozapine.⁵

Approximately 2 weeks later, Ms. B is admitted to a different hospital for altered mental status and is found to have hypo­natremia and rectal bleeding. The workup suggests that her rectal carcinoma has not fully responded to initial therapies, and she likely will require further treatment. Her mental status improves after hyponatremia resolves, but she reports auditory hallucinations and paranoia. Risperidone, 4 mg/d, is initiated to target psychosis.

After discharge, Ms. B develops bilateral upper extremity tremor, which she finds intolerable and attributes to risperidone. She refuses to continue risperidone or try adjunctive medications to address the tremor, but is willing to consider a different antipsychotic. Olanzapine, 10 mg/d, is initiated and risperidone is slowly tapered. During this time, Ms. B experiences increased paranoia and believes that the Internal Revenue Service is calling her. She misses her next appointment.

Later, the fire department finds Ms. B wandering the streets and brings her to the psychiatric emergency room. During the examination, she is disheveled and withdrawn, and unable to reply to simple questions about diet and sleep. When asked why she was in the street, she says that she left her apartment because it was “too messy.” The treatment team learns that she had walked at least 10 miles from her apartment before sitting down by the side of the road and being picked up by the fire department. She reveals that she left her apartment and continued walking because “a man” told her to do so and threatened to harm her if she stopped.

When Ms. B is admitted to the psychiatric service, she is paranoid, disorganized, and guarded. She remains in her room for most of the day and either refuses to talk to providers or curses at them. She often is seen wearing soiled clothing with her hair mussed. She denies having rectal carcinoma, although she expressed understanding of her medical condition <2 months earlier.

[polldaddy:9754787]

The authors’ observations

Clozapine is considered the most efficacious agent for treatment-resistant schizophrenia.⁶ Although non-compliance is the most common reason for discontinuing clozapine, >20% of patients stop clozapine because of adverse effects.⁷ Clozapine often is a drug of last resort because of the need for frequent monitoring and significant side effects; therefore deciding on a next step when clozapine fails or cannot be continued because of other factors can pose a challenge.

Ms. B’s treatment team gave serious consideration to restarting clozapine. However, because it was likely that Ms. B would undergo another round of chemotherapy and possibly radiation, the risk of neutropenia recurring was considered too high. Lithium has been used successfully to manage neutropenia in patients taking clozapine and, for some, adding lithium could help boost white cell count and allow a successful rechallenge with clozapine.^3,8 However, because of Ms. B’s medical comorbidities, including cancer and chronic kidney disease, adding lithium was not thought to be clinically prudent at that time and the treatment team considered other options.

Olanzapine. Although research is limited, studies suggest olanzapine is the most commonly prescribed medication when a patient has to discontinue clozapine,⁷ with comparable response rates in those with refractory schizophrenia.⁹ Therefore, Ms. B was initially maintained on olanzapine, and the dosage increased to 30 mg over the course of 16 days in the hospital. However, she did not respond to the medication, remaining disorganized and paranoid without any notable improvement in her symptoms therefore other treatment options were explored.

Loxapine. Previous limited case reports have shown loxapine to be effective in treating individuals with refractory schizophrenia, either alone or in combination with other antipsychotics.^10,11 FDA-approved in 1975, loxapine was among the last of the typical antipsychotics brought to the U.S. market before the introduction of clozapine, the first atypical.¹² Loxapine is a dibenzoxazepine that has a molecular structure similar to clozapine.¹³ Unlike clozapine, however, loxapine is not known to cause agranulocytosis.¹⁴ Research suggests that although clozapine is oxidized to metabolites that are cytotoxic, loxapine is not, potentially accounting for their different effects on neutrophils.¹⁵

The efficacy of loxapine has shown to be similar to other typical and atypical antipsychotics, with approximately 70% of patients showing improvement.¹⁴ However, loxapine may be overlooked as an option, possibly because it was not included in the CATIE trial and was the last typical antipsychotic to be approved before atypicals were introduced.¹² First available in oral and IM formulations, there has been increased interest in loxapine recently because of the approval of an inhaled formulation in 2012.¹⁶

Although classified as a typical anti­psychotic, studies have suggested that loxapine acts as an atypical at low dosages.^17,18 Previous work suggests, however, that the side effect profile of loxapine is similar to typical antipsychotics.¹⁴ At dosages <50 mg, it results in fewer cases of extrapyramidal side effects than expected with a typical antipsychotic.¹⁸

Loxapine’s binding profile seems to exist along this spectrum of typical to atypical. Tissue-based binding studies have shown a higher 5-HT2 affinity relative to D2, consistent with atypical antipsychotics.¹⁹ Positron emission tomography studies in humans show 5-HT2 saturation of loxapine to be close to equal to D2 binding in loxapine, thus a slightly lower ratio of 5-HT2 to D2 relative to atypicals, but more than that seen with typical antipsychotics.²⁰ These differences between in vitro and in vivo studies may be secondary to the binding of loxapine’s active metabolites, particularly 7- and 8-hydroxyloxapine, which have more dopaminergic activity. In addition to increased 5-HT2A binding compared with typical antipsychotics, loxapine also has a high affinity for the D4 receptors, as well as interacting with other serotonin receptors 5-HT3, 5-HT6, and 5-HT7. Of note this is a similar pattern of binding affinity as seen in clozapine.¹⁹

It should be noted, however, that loxapine may not be an appropriate treatment in all forms of cancer. Similar to other first-generation antipsychotics, it increases prolactin levels, and thus may have a negative clinical impact on patients with prolactin receptor positive breast cancers.^21,22 Finally, although clozapine can result in significant weight gain, dyslipidemia, and hyperglycemia, unlike many antipsychotics, loxapine has been shown to be weight neutral or result in weight loss,¹⁴ making it an option to consider for patients with type 2 diabetes mellitus, metabolic syndrome, dyslipidemia, or cardiovascular disease.

OUTCOME Improvement, stability

Ms. B begins taking loxapine, 10 mg/d, gradually cross-tapered with olanzapine, increasing loxapine by 10 mg every 2 to 3 days (Figure). After 8 days, when the dosage has reached 40 mg/d, Ms. B’s treatment team begins to observe a consistent change in her behavior. Ms. B comes into the interview room, where previously the team had to see her in her own room because she refused to come out. She also tolerates an extensive interview, even sharing parts of her history without prompting, and is able to discuss her treatment. Ms. B continues to express some paranoia regarding the treatment team. On day 12, receiving loxapine, 50 mg/d, Ms. B says that she likes the new medication and feels she is doing well with it. She becomes less reclusive and begins socializing with other patients. By day 19, receiving loxapine, 80 mg/d, a nurse, who knows Ms. B from the outpatient facility, visits the unit and reports that Ms. B is at her baseline.

At discharge, Ms. B is noted to be “bright,” well organized, neatly dressed, and wearing makeup. Her paranoia and auditory hallucinations have almost completely resolved. She is social, engages appropriately with the treatment team, and is able to describe a plan for self-care after discharge including following up with her oncologist. Her white blood cell counts were carefully monitored throughout her admission and are within normal limits when she is discharged.

One year later, Ms. B remains taking loxapine, 70 mg/d. Although she continues to report mild paranoia, she is living independently in her apartment and attends church regularly.

Ms. X, age 41, has a history of bipolar disorder and presents with extreme sleepiness, constipation with mild abdominal cramping, occasional dizziness, and “palpitations.” Although usually she is quite articulate, Ms. X seems to have trouble describing her symptoms and reports that they have been worsening over 4 to 6 days. She is worried because she is making mistakes at work and repeatedly misunderstanding directions.

Ms. X has a family history of hyperlipidemia, heart disease, and diabetes, and she has been employing a healthy diet, exercise, and use of supplements for cardiovascular health since her early 20s. Her medication regimen includes lithium, 600 mg, twice a day, quetiapine, 1,200 mg/d, a multivitamin and mineral tablet once a day, a brand name garlic supplement (garlic powder, 300 mg, vitamin C, 80 mg, vitamin E, 20 IU, vitamin A, 2,640 IU) twice a day, and fish oil, 2 g/d, at bedtime. Lithium levels consistently have been 0.8 to 0.9 mEq/L for the last 3 years.

Factors of drug–supplement interactions

Because an interaction is possible doesn’t always mean that a drug and an offending botanical cannot be used together. With awareness and planning, possible interactions can be safely managed (Table 1). Such was the case of Ms. X, who was stable on a higher-than-usual dosage of quetiapine (average target is 600 mg/d for bipolar disorder) because of presumed moderate enzyme induction by the brand name garlic supplement. Ms. X did not want to stop taking this supplement when she started quetiapine. Although garlic is listed as a possible moderate cytochrome P450 (CYP) 3A4 inducer, there is conflicting evidence.¹ Ms. X’s clinician advised her to avoid changes in dosage, because it could affect her quetiapine levels. However, the change in the botanical preparation from dried, powdered garlic to garlic oil likely removed the CYP3A4 enzyme induction, leading to a lower rate of metabolism and accumulation of the drug to toxic levels.

Drug metabolism. Practitioners are increasingly aware that St. John’s wort can significantly affect concomitantly administered drug levels by induction of the CYP isoenzyme 3A4 and more resources are listing this same possible induction for garlic.¹ However, what is less understood is the extent to which different preparations of the same plant possess different chemical profiles (Table 2).

Clinical studies with different garlic preparations—dried powder, aqueous extracts, deodorized preparations, oils—have demonstrated diverse and highly variable results in tests of effects on CYP isoenzymes and other metabolism activities.² There also is contradictory evidence between in vitro and in vivo studies, with 1 in vitro study of garlic extract demonstrating marked CYP3A4 effects up to 30%, while another study using a water-soluble, aged garlic extract noted little or no effects.³

• pain
• influenza
• rheumatoid arthritis
• asthma
• loss of appetite
• stimulating peristalsis.⁶

Animal studies have demonstrated anti-inflammatory, anticonvulsant, anticarcinogenic, and antioxidant effects, as well as stimulation of digestion via digestive enzyme secretion and increased gastromotility.^3,6

Because piperine is known to increase intestinal absorption by various mechanisms, it often is added to botanical medicines to increase bioavailability of active components. BioPerine is a 95% piperine extract marketed to be included in vitamin and herbal supplements for that purpose.³ This allows use of lower dosages to achieve outcomes, which, for expensive botanicals, could be a cost savings for the manufacturer. Studies examining piperine’s influence on drug absorption have demonstrated significant increases in carbamazepine, rifampin, phenytoin, nevirapine, and many other drugs.^7,8 These increases are caused by several mechanisms, but the 2 most important may be inhibition of intestinal P-glycoprotein and increases in small intestine absorption surfaces (Table 2).^6-9

In addition to increased absorption, piperine seems to be a non-specific general inhibitor of CYP isoenzymes; IV phenytoin levels also were higher among test participants.^6,8 Piperine reduces intestinal glucuronidation via uridine 5’-diphospho-glucuronosyltransferase inhibition, and the small or moderate effects on lithium levels seem to be the result of diuretic activities.^3,7

Patients often are motivated to control at least 1 aspect of their medical treatment, such as the supplements they choose to take. Being open to patient use of non-harmful or low-risk supplements, even when they are unlikely to have any medicinal benefit, helps preserve a relationship in which patients are more likely to consider your recommendation to avoid a harmful or high-risk supplement.

Related Resources

Ms. X, age 41, has a history of bipolar disorder and presents with extreme sleepiness, constipation with mild abdominal cramping, occasional dizziness, and “palpitations.” Although usually she is quite articulate, Ms. X seems to have trouble describing her symptoms and reports that they have been worsening over 4 to 6 days. She is worried because she is making mistakes at work and repeatedly misunderstanding directions.

Ms. X has a family history of hyperlipidemia, heart disease, and diabetes, and she has been employing a healthy diet, exercise, and use of supplements for cardiovascular health since her early 20s. Her medication regimen includes lithium, 600 mg, twice a day, quetiapine, 1,200 mg/d, a multivitamin and mineral tablet once a day, a brand name garlic supplement (garlic powder, 300 mg, vitamin C, 80 mg, vitamin E, 20 IU, vitamin A, 2,640 IU) twice a day, and fish oil, 2 g/d, at bedtime. Lithium levels consistently have been 0.8 to 0.9 mEq/L for the last 3 years.

Factors of drug–supplement interactions

Because an interaction is possible doesn’t always mean that a drug and an offending botanical cannot be used together. With awareness and planning, possible interactions can be safely managed (Table 1). Such was the case of Ms. X, who was stable on a higher-than-usual dosage of quetiapine (average target is 600 mg/d for bipolar disorder) because of presumed moderate enzyme induction by the brand name garlic supplement. Ms. X did not want to stop taking this supplement when she started quetiapine. Although garlic is listed as a possible moderate cytochrome P450 (CYP) 3A4 inducer, there is conflicting evidence.¹ Ms. X’s clinician advised her to avoid changes in dosage, because it could affect her quetiapine levels. However, the change in the botanical preparation from dried, powdered garlic to garlic oil likely removed the CYP3A4 enzyme induction, leading to a lower rate of metabolism and accumulation of the drug to toxic levels.

Drug metabolism. Practitioners are increasingly aware that St. John’s wort can significantly affect concomitantly administered drug levels by induction of the CYP isoenzyme 3A4 and more resources are listing this same possible induction for garlic.¹ However, what is less understood is the extent to which different preparations of the same plant possess different chemical profiles (Table 2).

Clinical studies with different garlic preparations—dried powder, aqueous extracts, deodorized preparations, oils—have demonstrated diverse and highly variable results in tests of effects on CYP isoenzymes and other metabolism activities.² There also is contradictory evidence between in vitro and in vivo studies, with 1 in vitro study of garlic extract demonstrating marked CYP3A4 effects up to 30%, while another study using a water-soluble, aged garlic extract noted little or no effects.³

• pain
• influenza
• rheumatoid arthritis
• asthma
• loss of appetite
• stimulating peristalsis.⁶

Animal studies have demonstrated anti-inflammatory, anticonvulsant, anticarcinogenic, and antioxidant effects, as well as stimulation of digestion via digestive enzyme secretion and increased gastromotility.^3,6

Because piperine is known to increase intestinal absorption by various mechanisms, it often is added to botanical medicines to increase bioavailability of active components. BioPerine is a 95% piperine extract marketed to be included in vitamin and herbal supplements for that purpose.³ This allows use of lower dosages to achieve outcomes, which, for expensive botanicals, could be a cost savings for the manufacturer. Studies examining piperine’s influence on drug absorption have demonstrated significant increases in carbamazepine, rifampin, phenytoin, nevirapine, and many other drugs.^7,8 These increases are caused by several mechanisms, but the 2 most important may be inhibition of intestinal P-glycoprotein and increases in small intestine absorption surfaces (Table 2).^6-9

In addition to increased absorption, piperine seems to be a non-specific general inhibitor of CYP isoenzymes; IV phenytoin levels also were higher among test participants.^6,8 Piperine reduces intestinal glucuronidation via uridine 5’-diphospho-glucuronosyltransferase inhibition, and the small or moderate effects on lithium levels seem to be the result of diuretic activities.^3,7

Patients often are motivated to control at least 1 aspect of their medical treatment, such as the supplements they choose to take. Being open to patient use of non-harmful or low-risk supplements, even when they are unlikely to have any medicinal benefit, helps preserve a relationship in which patients are more likely to consider your recommendation to avoid a harmful or high-risk supplement.

Related Resources

Ms. X, age 41, has a history of bipolar disorder and presents with extreme sleepiness, constipation with mild abdominal cramping, occasional dizziness, and “palpitations.” Although usually she is quite articulate, Ms. X seems to have trouble describing her symptoms and reports that they have been worsening over 4 to 6 days. She is worried because she is making mistakes at work and repeatedly misunderstanding directions.

Ms. X has a family history of hyperlipidemia, heart disease, and diabetes, and she has been employing a healthy diet, exercise, and use of supplements for cardiovascular health since her early 20s. Her medication regimen includes lithium, 600 mg, twice a day, quetiapine, 1,200 mg/d, a multivitamin and mineral tablet once a day, a brand name garlic supplement (garlic powder, 300 mg, vitamin C, 80 mg, vitamin E, 20 IU, vitamin A, 2,640 IU) twice a day, and fish oil, 2 g/d, at bedtime. Lithium levels consistently have been 0.8 to 0.9 mEq/L for the last 3 years.

Factors of drug–supplement interactions

Because an interaction is possible doesn’t always mean that a drug and an offending botanical cannot be used together. With awareness and planning, possible interactions can be safely managed (Table 1). Such was the case of Ms. X, who was stable on a higher-than-usual dosage of quetiapine (average target is 600 mg/d for bipolar disorder) because of presumed moderate enzyme induction by the brand name garlic supplement. Ms. X did not want to stop taking this supplement when she started quetiapine. Although garlic is listed as a possible moderate cytochrome P450 (CYP) 3A4 inducer, there is conflicting evidence.¹ Ms. X’s clinician advised her to avoid changes in dosage, because it could affect her quetiapine levels. However, the change in the botanical preparation from dried, powdered garlic to garlic oil likely removed the CYP3A4 enzyme induction, leading to a lower rate of metabolism and accumulation of the drug to toxic levels.

Drug metabolism. Practitioners are increasingly aware that St. John’s wort can significantly affect concomitantly administered drug levels by induction of the CYP isoenzyme 3A4 and more resources are listing this same possible induction for garlic.¹ However, what is less understood is the extent to which different preparations of the same plant possess different chemical profiles (Table 2).

Clinical studies with different garlic preparations—dried powder, aqueous extracts, deodorized preparations, oils—have demonstrated diverse and highly variable results in tests of effects on CYP isoenzymes and other metabolism activities.² There also is contradictory evidence between in vitro and in vivo studies, with 1 in vitro study of garlic extract demonstrating marked CYP3A4 effects up to 30%, while another study using a water-soluble, aged garlic extract noted little or no effects.³

• pain
• influenza
• rheumatoid arthritis
• asthma
• loss of appetite
• stimulating peristalsis.⁶

Animal studies have demonstrated anti-inflammatory, anticonvulsant, anticarcinogenic, and antioxidant effects, as well as stimulation of digestion via digestive enzyme secretion and increased gastromotility.^3,6

Because piperine is known to increase intestinal absorption by various mechanisms, it often is added to botanical medicines to increase bioavailability of active components. BioPerine is a 95% piperine extract marketed to be included in vitamin and herbal supplements for that purpose.³ This allows use of lower dosages to achieve outcomes, which, for expensive botanicals, could be a cost savings for the manufacturer. Studies examining piperine’s influence on drug absorption have demonstrated significant increases in carbamazepine, rifampin, phenytoin, nevirapine, and many other drugs.^7,8 These increases are caused by several mechanisms, but the 2 most important may be inhibition of intestinal P-glycoprotein and increases in small intestine absorption surfaces (Table 2).^6-9

In addition to increased absorption, piperine seems to be a non-specific general inhibitor of CYP isoenzymes; IV phenytoin levels also were higher among test participants.^6,8 Piperine reduces intestinal glucuronidation via uridine 5’-diphospho-glucuronosyltransferase inhibition, and the small or moderate effects on lithium levels seem to be the result of diuretic activities.^3,7

Patients often are motivated to control at least 1 aspect of their medical treatment, such as the supplements they choose to take. Being open to patient use of non-harmful or low-risk supplements, even when they are unlikely to have any medicinal benefit, helps preserve a relationship in which patients are more likely to consider your recommendation to avoid a harmful or high-risk supplement.

Related Resources

Dear Dr. Mossman,
The clinic where I work initiated a “3 misses and out” policy: If a patient doesn’t show for 3 appointments in a 12-month period, the clinic removes him from the patient rolls. I’ve heard such policies are common, but I worry: Is this abandonment?
Submitted by “Dr. C”

The short answer to Dr. C’s question is, “Handled properly, it’s not abandonment.” But if this response really was satisfactory, Dr. C probably would not have asked the question. Dealing with no-show patients has bothered psychiatrists, other mental health professionals, and other physicians for decades.¹

Clinicians worry when patients miss important follow-up, and unreimbursed office time won’t help pay a clinician’s salary or office expenses.² But a policy such as the one Dr. C describes may not be the best response—clinically or financially—for many patients who miss appointments repeatedly.

If no-show patients worry you or cause problems where you practice, read on as I cover:

• charging for missed appointments
• why patients miss appointments
• evidence-based methods to improve show-up rates
• when ending a treatment relationship unilaterally is not abandonment
• how to dismiss no-show patients from a practice properly.

The traditional response: Charging for no-shows

Before the mid-1980s, most office-based psychiatrists worked in solo or small group and required patients to pay cash for treatment; approximately 40% of psychiatrists still practice this way.³ Often, private practice clinicians require payment for appointments missed without 24 hours’ notice. This well-accepted practice^2,4,5 reinforces the notion that psychotherapy involves making a commitment to work on problems. It also protects clinicians’ financial interests and mitigates possible resentment that might arise if office time committed to a patient went unreimbursed.⁶ Clinicians who charge for missed appointments should inform patients of this at the beginning of treatment, explaining clearly that the patient—not the insurer—will be paying for unused treatment time.^2,4

Since the 1980s, outpatient psychiatrists have increasingly worked in public agencies or other organizational practice settings⁷ where patients—whose care is funded by public monies or third-party payors—cannot afford to pay for missed appointments. If you work in a clinic such as the one where Dr. C provides services, you probably are paid an hourly wage whether your patients show up or not. To pay you and remain solvent, your clinic must find ways other than charging patients to address and reduce no-shows.

Why patients miss appointments

The literature abounds with research on why no-shows occur. But no-shows seem to be more common in psychiatry than in other medical specialties.⁸ The frequency of no-shows varies considerably, but it’s a big problem in some mental health treatment contexts, with reported rates ranging from 12% to 60%.⁹ A recent, comprehensive review reported that approximately 30% of patients refuse, drop out, or prematurely disengage from services after first-episode psychosis.¹⁰ No-shows and drop outs are linked to clinical deterioration¹¹ and heightened risk of hospitalization.¹²

Reducing no-shows: Evidence-based methods

Many medical and mental health articles describe evidence-based methods for lower­ing no-show rates. Studies document the value of assertive outreach, home visits, avoiding scheduling on religious holidays, scheduling appointments in the afternoon rather than the morning, providing assistance with transportation,⁸ sending reminder letters,¹⁶ or making telephone calls.¹⁷ Growing evidence suggests that text messages reduce missed appointments, even among patients with severe disorders (eg, schizophrenia) that compromise cognitive functioning.¹⁸

When dismissing a patient isn’t abandonment

The measures I’ve described won’t prevent every patient from no-showing repeatedly. If you or your employer have tried some of these proven methods and they haven’t reduced a patient’s persistent no-shows, and if it makes sense from a clinical and financial standpoint, then it’s all right to dismiss the patient.

To understand why you are permitted to dismiss a patient from your practice, it helps to understand how the law views the doctor–patient relationship. A doctor has no legal duty to treat anyone—even someone who desperately needs care—unless the doctor has taken some action to establish a treatment relationship with that person. Having previously treated the patient establishes a treatment relationship, as could other actions such as giving specific advice or (in some cases) making an appointment for a person. Once you have a treatment relationship with someone, you usually must continue to provide necessary medical attention until either the treatment episode has concluded or you and the patient agree to end treatment.²⁰

For many chronic mental illnesses, a treatment episode could last years. But this does not force you to continue caring for a patient indefinitely if your circumstances change or if the patient’s behavior causes you to want to withdraw from providing care.

To ethically end care of a patient while a treatment episode is ongoing, you must either transfer care to another competent physician, or give your patient adequate notice and opportunity to obtain appropriate treatment elsewhere.²⁰ If you fail to do either, however, you are guilty of “abandonment” and potentially subject to discipline by state licensing authorities²¹ or, if harm results, a malpractice lawsuit.²²

Dismissing a patient properly

In many states, statutes or regulations describe what you must do to end a treatment relationship properly. Ohio’s rule is typical: You must send the patient a certified letter explaining that the treatment relationship is ending, that you will remain available to provide care for 30 days, and that you will send treatment records to another provider upon receiving the patient’s signed authorization.²¹

One note of caution, however: If you practice in hospitals or groups, or if you or the agency where you work has signed provider contracts, you may have agreed to terms of practice that make dismissing a patient more complicated.²³ Whether you practice individually or in a large organization, it’s usually wise to get advice from an attorney and/or your malpractice carrier to make sure you’re handling a patient dismissal the right way.

Dear Dr. Mossman,
The clinic where I work initiated a “3 misses and out” policy: If a patient doesn’t show for 3 appointments in a 12-month period, the clinic removes him from the patient rolls. I’ve heard such policies are common, but I worry: Is this abandonment?
Submitted by “Dr. C”

The short answer to Dr. C’s question is, “Handled properly, it’s not abandonment.” But if this response really was satisfactory, Dr. C probably would not have asked the question. Dealing with no-show patients has bothered psychiatrists, other mental health professionals, and other physicians for decades.¹

Clinicians worry when patients miss important follow-up, and unreimbursed office time won’t help pay a clinician’s salary or office expenses.² But a policy such as the one Dr. C describes may not be the best response—clinically or financially—for many patients who miss appointments repeatedly.

If no-show patients worry you or cause problems where you practice, read on as I cover:

• charging for missed appointments
• why patients miss appointments
• evidence-based methods to improve show-up rates
• when ending a treatment relationship unilaterally is not abandonment
• how to dismiss no-show patients from a practice properly.

The traditional response: Charging for no-shows

Before the mid-1980s, most office-based psychiatrists worked in solo or small group and required patients to pay cash for treatment; approximately 40% of psychiatrists still practice this way.³ Often, private practice clinicians require payment for appointments missed without 24 hours’ notice. This well-accepted practice^2,4,5 reinforces the notion that psychotherapy involves making a commitment to work on problems. It also protects clinicians’ financial interests and mitigates possible resentment that might arise if office time committed to a patient went unreimbursed.⁶ Clinicians who charge for missed appointments should inform patients of this at the beginning of treatment, explaining clearly that the patient—not the insurer—will be paying for unused treatment time.^2,4

Since the 1980s, outpatient psychiatrists have increasingly worked in public agencies or other organizational practice settings⁷ where patients—whose care is funded by public monies or third-party payors—cannot afford to pay for missed appointments. If you work in a clinic such as the one where Dr. C provides services, you probably are paid an hourly wage whether your patients show up or not. To pay you and remain solvent, your clinic must find ways other than charging patients to address and reduce no-shows.

Why patients miss appointments

The literature abounds with research on why no-shows occur. But no-shows seem to be more common in psychiatry than in other medical specialties.⁸ The frequency of no-shows varies considerably, but it’s a big problem in some mental health treatment contexts, with reported rates ranging from 12% to 60%.⁹ A recent, comprehensive review reported that approximately 30% of patients refuse, drop out, or prematurely disengage from services after first-episode psychosis.¹⁰ No-shows and drop outs are linked to clinical deterioration¹¹ and heightened risk of hospitalization.¹²

Reducing no-shows: Evidence-based methods

Many medical and mental health articles describe evidence-based methods for lower­ing no-show rates. Studies document the value of assertive outreach, home visits, avoiding scheduling on religious holidays, scheduling appointments in the afternoon rather than the morning, providing assistance with transportation,⁸ sending reminder letters,¹⁶ or making telephone calls.¹⁷ Growing evidence suggests that text messages reduce missed appointments, even among patients with severe disorders (eg, schizophrenia) that compromise cognitive functioning.¹⁸

When dismissing a patient isn’t abandonment

The measures I’ve described won’t prevent every patient from no-showing repeatedly. If you or your employer have tried some of these proven methods and they haven’t reduced a patient’s persistent no-shows, and if it makes sense from a clinical and financial standpoint, then it’s all right to dismiss the patient.

To understand why you are permitted to dismiss a patient from your practice, it helps to understand how the law views the doctor–patient relationship. A doctor has no legal duty to treat anyone—even someone who desperately needs care—unless the doctor has taken some action to establish a treatment relationship with that person. Having previously treated the patient establishes a treatment relationship, as could other actions such as giving specific advice or (in some cases) making an appointment for a person. Once you have a treatment relationship with someone, you usually must continue to provide necessary medical attention until either the treatment episode has concluded or you and the patient agree to end treatment.²⁰

For many chronic mental illnesses, a treatment episode could last years. But this does not force you to continue caring for a patient indefinitely if your circumstances change or if the patient’s behavior causes you to want to withdraw from providing care.

To ethically end care of a patient while a treatment episode is ongoing, you must either transfer care to another competent physician, or give your patient adequate notice and opportunity to obtain appropriate treatment elsewhere.²⁰ If you fail to do either, however, you are guilty of “abandonment” and potentially subject to discipline by state licensing authorities²¹ or, if harm results, a malpractice lawsuit.²²

Dismissing a patient properly

In many states, statutes or regulations describe what you must do to end a treatment relationship properly. Ohio’s rule is typical: You must send the patient a certified letter explaining that the treatment relationship is ending, that you will remain available to provide care for 30 days, and that you will send treatment records to another provider upon receiving the patient’s signed authorization.²¹

One note of caution, however: If you practice in hospitals or groups, or if you or the agency where you work has signed provider contracts, you may have agreed to terms of practice that make dismissing a patient more complicated.²³ Whether you practice individually or in a large organization, it’s usually wise to get advice from an attorney and/or your malpractice carrier to make sure you’re handling a patient dismissal the right way.

Dear Dr. Mossman,
The clinic where I work initiated a “3 misses and out” policy: If a patient doesn’t show for 3 appointments in a 12-month period, the clinic removes him from the patient rolls. I’ve heard such policies are common, but I worry: Is this abandonment?
Submitted by “Dr. C”

The short answer to Dr. C’s question is, “Handled properly, it’s not abandonment.” But if this response really was satisfactory, Dr. C probably would not have asked the question. Dealing with no-show patients has bothered psychiatrists, other mental health professionals, and other physicians for decades.¹

Clinicians worry when patients miss important follow-up, and unreimbursed office time won’t help pay a clinician’s salary or office expenses.² But a policy such as the one Dr. C describes may not be the best response—clinically or financially—for many patients who miss appointments repeatedly.

If no-show patients worry you or cause problems where you practice, read on as I cover:

• charging for missed appointments
• why patients miss appointments
• evidence-based methods to improve show-up rates
• when ending a treatment relationship unilaterally is not abandonment
• how to dismiss no-show patients from a practice properly.

The traditional response: Charging for no-shows

Before the mid-1980s, most office-based psychiatrists worked in solo or small group and required patients to pay cash for treatment; approximately 40% of psychiatrists still practice this way.³ Often, private practice clinicians require payment for appointments missed without 24 hours’ notice. This well-accepted practice^2,4,5 reinforces the notion that psychotherapy involves making a commitment to work on problems. It also protects clinicians’ financial interests and mitigates possible resentment that might arise if office time committed to a patient went unreimbursed.⁶ Clinicians who charge for missed appointments should inform patients of this at the beginning of treatment, explaining clearly that the patient—not the insurer—will be paying for unused treatment time.^2,4

Since the 1980s, outpatient psychiatrists have increasingly worked in public agencies or other organizational practice settings⁷ where patients—whose care is funded by public monies or third-party payors—cannot afford to pay for missed appointments. If you work in a clinic such as the one where Dr. C provides services, you probably are paid an hourly wage whether your patients show up or not. To pay you and remain solvent, your clinic must find ways other than charging patients to address and reduce no-shows.

Why patients miss appointments

The literature abounds with research on why no-shows occur. But no-shows seem to be more common in psychiatry than in other medical specialties.⁸ The frequency of no-shows varies considerably, but it’s a big problem in some mental health treatment contexts, with reported rates ranging from 12% to 60%.⁹ A recent, comprehensive review reported that approximately 30% of patients refuse, drop out, or prematurely disengage from services after first-episode psychosis.¹⁰ No-shows and drop outs are linked to clinical deterioration¹¹ and heightened risk of hospitalization.¹²

Reducing no-shows: Evidence-based methods

Many medical and mental health articles describe evidence-based methods for lower­ing no-show rates. Studies document the value of assertive outreach, home visits, avoiding scheduling on religious holidays, scheduling appointments in the afternoon rather than the morning, providing assistance with transportation,⁸ sending reminder letters,¹⁶ or making telephone calls.¹⁷ Growing evidence suggests that text messages reduce missed appointments, even among patients with severe disorders (eg, schizophrenia) that compromise cognitive functioning.¹⁸

When dismissing a patient isn’t abandonment

The measures I’ve described won’t prevent every patient from no-showing repeatedly. If you or your employer have tried some of these proven methods and they haven’t reduced a patient’s persistent no-shows, and if it makes sense from a clinical and financial standpoint, then it’s all right to dismiss the patient.

To understand why you are permitted to dismiss a patient from your practice, it helps to understand how the law views the doctor–patient relationship. A doctor has no legal duty to treat anyone—even someone who desperately needs care—unless the doctor has taken some action to establish a treatment relationship with that person. Having previously treated the patient establishes a treatment relationship, as could other actions such as giving specific advice or (in some cases) making an appointment for a person. Once you have a treatment relationship with someone, you usually must continue to provide necessary medical attention until either the treatment episode has concluded or you and the patient agree to end treatment.²⁰

For many chronic mental illnesses, a treatment episode could last years. But this does not force you to continue caring for a patient indefinitely if your circumstances change or if the patient’s behavior causes you to want to withdraw from providing care.

To ethically end care of a patient while a treatment episode is ongoing, you must either transfer care to another competent physician, or give your patient adequate notice and opportunity to obtain appropriate treatment elsewhere.²⁰ If you fail to do either, however, you are guilty of “abandonment” and potentially subject to discipline by state licensing authorities²¹ or, if harm results, a malpractice lawsuit.²²

Dismissing a patient properly

In many states, statutes or regulations describe what you must do to end a treatment relationship properly. Ohio’s rule is typical: You must send the patient a certified letter explaining that the treatment relationship is ending, that you will remain available to provide care for 30 days, and that you will send treatment records to another provider upon receiving the patient’s signed authorization.²¹

One note of caution, however: If you practice in hospitals or groups, or if you or the agency where you work has signed provider contracts, you may have agreed to terms of practice that make dismissing a patient more complicated.²³ Whether you practice individually or in a large organization, it’s usually wise to get advice from an attorney and/or your malpractice carrier to make sure you’re handling a patient dismissal the right way.