Doug Brunk

LAS VEGAS – In the clinical opinion of Dr. David Mischoulon, certain complementary and alternative medicine therapies such as St. John’s wort and omega-3 fatty acids may benefit some patients with mild to moderate depression.

At the annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Mischoulon said more than 70% of people worldwide have used some form of complementary therapy at some point in their lives.

“They often don’t have as many severe side effects as synthetic medication,” he said. “However, the body of knowledge about these therapies is limited. We don’t have as much systematic research or rigorous clinical trials of these treatments, so as clinicians who are put in the position of making recommendations, we don’t know how effective these treatments are compared to placebo or standard therapies.”

Then there’s the common public misconception that just because something is “natural” or can be bought over the counter, it’s automatically safe. “That isn’t the case,” said Dr. Mischoulon, director of research for the Depression Clinical & Research Program at Massachusetts General Hospital, Boston. “There have been a number of cases of adverse reactions when these natural products are taken along with standard medications. Another problem is that these products have different manufacturers that may use different techniques for preparing them, so the purity may vary. Also, most of these natural therapies are not covered by health insurance.”

He highlighted the following natural agents that are used to treat depression:

• St. John’s wort. He described this as “probably the most popular herbal remedy for depression,” with about 40 published trials to date: 26 placebo controlled, and 14 with standard antidepressant comparators. Studies have been limited by short duration, he said, and appear to favor its use for mild to moderate depression. Hypericin, hyperforin, and adhyperforin contained in St. John’s wort are thought to be the key ingredients.

“It’s thought that they might interact with cytokine production through the [hypothalamic-pituitary-adrenal] axis,” Dr. Mischoulon explained. “Consequently, this interaction could result in decreased cortisol production, which may attenuate depression.”

Side effects from using St. John’s wort are similar to those found with antidepressants, including dry mouth, dizziness, and constipation. “It’s generally thought to be safe,” he said. Phototoxicity can be an issue for some, and using St. John’s wort with selective serotonin reuptake inhibitors is not advised because of the potential for developing serotonin syndrome. Several cases of colic, drowsiness, and lethargy have been reported in breastfed infants whose mothers were taking St. John’s wort, and low birth weight from in utero exposure has been demonstrated in animal studies.

Dr. Mischoulon noted that St. John’s wort induces CYP3A4 expression, which reduces the therapeutic activity of numerous drugs, including warfarin, cyclosporine, oral contraceptives, digoxin, zolpidem, and olanzapine. Caution is required in HIV-positive, cancer, and organ transplant patients. “Overall the results for St. John’s wort as reported in the literature are encouraging but with some inconsistencies,” he said. “The best individuals for St. John’s wort are individuals with mild to moderate depression, and less so individuals with more severe depression.” He recommends a dose of 900-1,200 mg per day, “but do remember that different preparations of St. John’s wort may vary in potency, so in some cases you may need to go to a higher dose.”

• S-adenosylmethionine (SAMe). Present in all living beings, this substance is required for neurotransmitter synthesis, and depends on folate and B12 levels to function optimally. According to Dr. Mischoulon, SAMe has been evaluated in more than 45 randomized clinical trials involving various routes of administration in doses of 200-1,600 mg/day. In eight placebo-controlled studies, SAMe was superior to placebo in six trials and had similar efficacy in the other two. In eight studies that compared SAMe with tricyclic antidepressants, six demonstrated similar efficacy with TCAs and one demonstrated benefit of SAMe over imipramine. The other trial, led by Dr. Mischoulon, compared SAMe with escitalopram and placebo in 189 patients in three treatment arms over a course of 12 weeks (J Clin Psychiatry. 2014;75[4]:370-6). The researchers observed a benefit in all treatment arms (a drop of 5-6 points on the 17-item Hamilton Depression Rating Scale [HDRS-17]), but no statistically significant differences were found between the groups. The most common side effect in the SAMe arm was related to gastrointestinal issues, mainly stomach discomfort and diarrhea.

One of the appeals of SAMe is that it’s safe to use in combination with other medicines, including tricyclic antidepressants (TCAs). “It may even boost and accelerate the effect of TCAs,” Dr. Mischoulon said. “It’s also been combined successfully with SSRIs and” [selective serotonin norepinephrine inhibitors]. In one study of 30 patients who were partial or nonresponders to SSRIs, augmentation with SAMe led to a response rate of 50% and a remission rate of 43% at 6 weeks (J Clin Psychopharmacol. 2004;24[6]:661-4), “which is very encouraging for our treatment-resistant population,” he said. In a 2010 trial, researchers investigated augmentation with SAMe 800 mg b.i.d. or placebo for 6 weeks in 73 serotonin reuptake inhibitor nonresponders with major depressive disorder (Am J Psychiatry 2010;167[8]:942-8). The response rate was 36.1% in the SAMe group, compared with 17.6% in the placebo group.

The medical literature generally supports the use of SAMe in doses of 400-1,600 mg/day. “It’s generally well tolerated.” Dr. Mischoulon said. Side effects tend to resemble the usual ones clinicians see with antidepressants: insomnia, anorexia, constipation, nausea, dry mouth, sweating, dizziness, and anxiety. “There have been cases of mania or hypomania developing in patients with bipolar depression, so be careful about [using this] in people with bipolar disorder,” he said.

Pregnancy tends to decrease methylation and SAMe activity, “so theoretically it should be beneficial in pregnant women with intrahepatic cholestasis, but we have limited prospective safety data on SAMe in pregnant women, so we advise caution.”

Cost may be a barrier for some patients, he said, since a 400-mg tablet may cost as much as $1.25. “So if you’re one of those people who need a dose in the range of 2,000-3,000 mg, the costs can be quite significant. Discuss this with your patient before you decide to embark on a trial of SAMe.”

• L-methylfolate (Deplin). Dr. Mischoulon was part of a multicenter research team that carried out a study of L-methylfolate 15 mg/day versus placebo in 223 adult patients with SSRI-resistant major depressive disorder (Am J Psychiatry. 2010 Aug;167[8]:942-8). They conducted the study in two 30-day treatment phases using a sequential parallel comparator design, and found that the mean change from baseline on the Quick Inventory of Depressive Symptomatology–Self Report (QIDS-SR) was significantly greater with L-methylfolate, compared with placebo. Similar results were observed with the HDRS-17, the HDRS-28, and the Clinical Global Impression–Severity scale (CGI-S).

• Omega-3 fatty acids (DHA and EPA). Primarily found in fish oil and other marine sources, omega-3 fatty acids are believed to promote neuronal membrane stabilization and anti-inflammatory effects. To date, more than 30 randomized, controlled trials of fatty acids for the treatment of depression have been conducted, mostly omega-3 fatty acids as an adjunct to standard antidepressant therapy. Most of the studies have involved EPA by itself or EPA in combination with DHA, he said, at a dose of 1-2 g per day. There’s also evidence that EPA may have a role in prophylactic preinterferon therapy in patients with hepatitis C.

Dr. Mischoulon and his associates recently carried out a trial of EPA 1,000 mg/day or DHA 1,000 mg/day, or placebo for 8 weeks in 196 patients (J Clin Psychiatry. 2015;76[1]:54-61). All treatment arms showed improvement, but neither treatment outperformed placebo. Response rates were in the range of 40%-50% for each arm, and the remission rates were in the 30% range. Though the initial results “were discouraging,” a secondary analysis revealed that EPA may benefit individuals with abnormal levels of two or more of the following inflammatory biomarkers at baseline: human C-reactive protein, interleukin-6, interleukin-1 receptor antagonist, leptin, and adiponectin. A new study underway “will examine depressed patients with obesity and elevated inflammatory status at baseline to enhance signal detection,” he said.

For the time being, he said, it’s best to use omega-3 fatty acids in patients with unipolar depression, in a dose of 1-2 g/day of an EPA/DHA combination that contains at least 60% EPA. In patients with bipolar disorder, he uses doses in the range of 6-10 g/day, “but watch out for cycling, which is a common problem in people with bipolar illness.”

Side effects from use may include stomach upset and fishy taste, “although most preparations today are highly purified, so we tend to get fewer complaints about that.” Published studies suggest a benefit of omega-3 fatty acids to expectant mothers, the fetus, and infants, particularly for neural development, “but the safe upper limit in pregnancy is unknown, so we need to advise caution.”

Dr. Mischoulon reported that he has received research support from the Bowman Family Foundation, Fisher Wallace, Nordic Naturals, Methylation Sciences, and PharmoRx Therapeutics. He also has received honoraria for consulting, speaking, and writing from Pamlab and the Massachusetts General Hospital Psychiatry Academy.

[email protected]

LAS VEGAS – In the clinical opinion of Dr. David Mischoulon, certain complementary and alternative medicine therapies such as St. John’s wort and omega-3 fatty acids may benefit some patients with mild to moderate depression.

At the annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Mischoulon said more than 70% of people worldwide have used some form of complementary therapy at some point in their lives.

“They often don’t have as many severe side effects as synthetic medication,” he said. “However, the body of knowledge about these therapies is limited. We don’t have as much systematic research or rigorous clinical trials of these treatments, so as clinicians who are put in the position of making recommendations, we don’t know how effective these treatments are compared to placebo or standard therapies.”

Then there’s the common public misconception that just because something is “natural” or can be bought over the counter, it’s automatically safe. “That isn’t the case,” said Dr. Mischoulon, director of research for the Depression Clinical & Research Program at Massachusetts General Hospital, Boston. “There have been a number of cases of adverse reactions when these natural products are taken along with standard medications. Another problem is that these products have different manufacturers that may use different techniques for preparing them, so the purity may vary. Also, most of these natural therapies are not covered by health insurance.”

He highlighted the following natural agents that are used to treat depression:

• St. John’s wort. He described this as “probably the most popular herbal remedy for depression,” with about 40 published trials to date: 26 placebo controlled, and 14 with standard antidepressant comparators. Studies have been limited by short duration, he said, and appear to favor its use for mild to moderate depression. Hypericin, hyperforin, and adhyperforin contained in St. John’s wort are thought to be the key ingredients.

“It’s thought that they might interact with cytokine production through the [hypothalamic-pituitary-adrenal] axis,” Dr. Mischoulon explained. “Consequently, this interaction could result in decreased cortisol production, which may attenuate depression.”

Side effects from using St. John’s wort are similar to those found with antidepressants, including dry mouth, dizziness, and constipation. “It’s generally thought to be safe,” he said. Phototoxicity can be an issue for some, and using St. John’s wort with selective serotonin reuptake inhibitors is not advised because of the potential for developing serotonin syndrome. Several cases of colic, drowsiness, and lethargy have been reported in breastfed infants whose mothers were taking St. John’s wort, and low birth weight from in utero exposure has been demonstrated in animal studies.

Dr. Mischoulon noted that St. John’s wort induces CYP3A4 expression, which reduces the therapeutic activity of numerous drugs, including warfarin, cyclosporine, oral contraceptives, digoxin, zolpidem, and olanzapine. Caution is required in HIV-positive, cancer, and organ transplant patients. “Overall the results for St. John’s wort as reported in the literature are encouraging but with some inconsistencies,” he said. “The best individuals for St. John’s wort are individuals with mild to moderate depression, and less so individuals with more severe depression.” He recommends a dose of 900-1,200 mg per day, “but do remember that different preparations of St. John’s wort may vary in potency, so in some cases you may need to go to a higher dose.”

• S-adenosylmethionine (SAMe). Present in all living beings, this substance is required for neurotransmitter synthesis, and depends on folate and B12 levels to function optimally. According to Dr. Mischoulon, SAMe has been evaluated in more than 45 randomized clinical trials involving various routes of administration in doses of 200-1,600 mg/day. In eight placebo-controlled studies, SAMe was superior to placebo in six trials and had similar efficacy in the other two. In eight studies that compared SAMe with tricyclic antidepressants, six demonstrated similar efficacy with TCAs and one demonstrated benefit of SAMe over imipramine. The other trial, led by Dr. Mischoulon, compared SAMe with escitalopram and placebo in 189 patients in three treatment arms over a course of 12 weeks (J Clin Psychiatry. 2014;75[4]:370-6). The researchers observed a benefit in all treatment arms (a drop of 5-6 points on the 17-item Hamilton Depression Rating Scale [HDRS-17]), but no statistically significant differences were found between the groups. The most common side effect in the SAMe arm was related to gastrointestinal issues, mainly stomach discomfort and diarrhea.

One of the appeals of SAMe is that it’s safe to use in combination with other medicines, including tricyclic antidepressants (TCAs). “It may even boost and accelerate the effect of TCAs,” Dr. Mischoulon said. “It’s also been combined successfully with SSRIs and” [selective serotonin norepinephrine inhibitors]. In one study of 30 patients who were partial or nonresponders to SSRIs, augmentation with SAMe led to a response rate of 50% and a remission rate of 43% at 6 weeks (J Clin Psychopharmacol. 2004;24[6]:661-4), “which is very encouraging for our treatment-resistant population,” he said. In a 2010 trial, researchers investigated augmentation with SAMe 800 mg b.i.d. or placebo for 6 weeks in 73 serotonin reuptake inhibitor nonresponders with major depressive disorder (Am J Psychiatry 2010;167[8]:942-8). The response rate was 36.1% in the SAMe group, compared with 17.6% in the placebo group.

The medical literature generally supports the use of SAMe in doses of 400-1,600 mg/day. “It’s generally well tolerated.” Dr. Mischoulon said. Side effects tend to resemble the usual ones clinicians see with antidepressants: insomnia, anorexia, constipation, nausea, dry mouth, sweating, dizziness, and anxiety. “There have been cases of mania or hypomania developing in patients with bipolar depression, so be careful about [using this] in people with bipolar disorder,” he said.

Pregnancy tends to decrease methylation and SAMe activity, “so theoretically it should be beneficial in pregnant women with intrahepatic cholestasis, but we have limited prospective safety data on SAMe in pregnant women, so we advise caution.”

Cost may be a barrier for some patients, he said, since a 400-mg tablet may cost as much as $1.25. “So if you’re one of those people who need a dose in the range of 2,000-3,000 mg, the costs can be quite significant. Discuss this with your patient before you decide to embark on a trial of SAMe.”

• L-methylfolate (Deplin). Dr. Mischoulon was part of a multicenter research team that carried out a study of L-methylfolate 15 mg/day versus placebo in 223 adult patients with SSRI-resistant major depressive disorder (Am J Psychiatry. 2010 Aug;167[8]:942-8). They conducted the study in two 30-day treatment phases using a sequential parallel comparator design, and found that the mean change from baseline on the Quick Inventory of Depressive Symptomatology–Self Report (QIDS-SR) was significantly greater with L-methylfolate, compared with placebo. Similar results were observed with the HDRS-17, the HDRS-28, and the Clinical Global Impression–Severity scale (CGI-S).

• Omega-3 fatty acids (DHA and EPA). Primarily found in fish oil and other marine sources, omega-3 fatty acids are believed to promote neuronal membrane stabilization and anti-inflammatory effects. To date, more than 30 randomized, controlled trials of fatty acids for the treatment of depression have been conducted, mostly omega-3 fatty acids as an adjunct to standard antidepressant therapy. Most of the studies have involved EPA by itself or EPA in combination with DHA, he said, at a dose of 1-2 g per day. There’s also evidence that EPA may have a role in prophylactic preinterferon therapy in patients with hepatitis C.

Dr. Mischoulon and his associates recently carried out a trial of EPA 1,000 mg/day or DHA 1,000 mg/day, or placebo for 8 weeks in 196 patients (J Clin Psychiatry. 2015;76[1]:54-61). All treatment arms showed improvement, but neither treatment outperformed placebo. Response rates were in the range of 40%-50% for each arm, and the remission rates were in the 30% range. Though the initial results “were discouraging,” a secondary analysis revealed that EPA may benefit individuals with abnormal levels of two or more of the following inflammatory biomarkers at baseline: human C-reactive protein, interleukin-6, interleukin-1 receptor antagonist, leptin, and adiponectin. A new study underway “will examine depressed patients with obesity and elevated inflammatory status at baseline to enhance signal detection,” he said.

For the time being, he said, it’s best to use omega-3 fatty acids in patients with unipolar depression, in a dose of 1-2 g/day of an EPA/DHA combination that contains at least 60% EPA. In patients with bipolar disorder, he uses doses in the range of 6-10 g/day, “but watch out for cycling, which is a common problem in people with bipolar illness.”

Side effects from use may include stomach upset and fishy taste, “although most preparations today are highly purified, so we tend to get fewer complaints about that.” Published studies suggest a benefit of omega-3 fatty acids to expectant mothers, the fetus, and infants, particularly for neural development, “but the safe upper limit in pregnancy is unknown, so we need to advise caution.”

Dr. Mischoulon reported that he has received research support from the Bowman Family Foundation, Fisher Wallace, Nordic Naturals, Methylation Sciences, and PharmoRx Therapeutics. He also has received honoraria for consulting, speaking, and writing from Pamlab and the Massachusetts General Hospital Psychiatry Academy.

[email protected]

LAS VEGAS – In the clinical opinion of Dr. David Mischoulon, certain complementary and alternative medicine therapies such as St. John’s wort and omega-3 fatty acids may benefit some patients with mild to moderate depression.

At the annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Mischoulon said more than 70% of people worldwide have used some form of complementary therapy at some point in their lives.

“They often don’t have as many severe side effects as synthetic medication,” he said. “However, the body of knowledge about these therapies is limited. We don’t have as much systematic research or rigorous clinical trials of these treatments, so as clinicians who are put in the position of making recommendations, we don’t know how effective these treatments are compared to placebo or standard therapies.”

Then there’s the common public misconception that just because something is “natural” or can be bought over the counter, it’s automatically safe. “That isn’t the case,” said Dr. Mischoulon, director of research for the Depression Clinical & Research Program at Massachusetts General Hospital, Boston. “There have been a number of cases of adverse reactions when these natural products are taken along with standard medications. Another problem is that these products have different manufacturers that may use different techniques for preparing them, so the purity may vary. Also, most of these natural therapies are not covered by health insurance.”

He highlighted the following natural agents that are used to treat depression:

• St. John’s wort. He described this as “probably the most popular herbal remedy for depression,” with about 40 published trials to date: 26 placebo controlled, and 14 with standard antidepressant comparators. Studies have been limited by short duration, he said, and appear to favor its use for mild to moderate depression. Hypericin, hyperforin, and adhyperforin contained in St. John’s wort are thought to be the key ingredients.

“It’s thought that they might interact with cytokine production through the [hypothalamic-pituitary-adrenal] axis,” Dr. Mischoulon explained. “Consequently, this interaction could result in decreased cortisol production, which may attenuate depression.”

Side effects from using St. John’s wort are similar to those found with antidepressants, including dry mouth, dizziness, and constipation. “It’s generally thought to be safe,” he said. Phototoxicity can be an issue for some, and using St. John’s wort with selective serotonin reuptake inhibitors is not advised because of the potential for developing serotonin syndrome. Several cases of colic, drowsiness, and lethargy have been reported in breastfed infants whose mothers were taking St. John’s wort, and low birth weight from in utero exposure has been demonstrated in animal studies.

Dr. Mischoulon noted that St. John’s wort induces CYP3A4 expression, which reduces the therapeutic activity of numerous drugs, including warfarin, cyclosporine, oral contraceptives, digoxin, zolpidem, and olanzapine. Caution is required in HIV-positive, cancer, and organ transplant patients. “Overall the results for St. John’s wort as reported in the literature are encouraging but with some inconsistencies,” he said. “The best individuals for St. John’s wort are individuals with mild to moderate depression, and less so individuals with more severe depression.” He recommends a dose of 900-1,200 mg per day, “but do remember that different preparations of St. John’s wort may vary in potency, so in some cases you may need to go to a higher dose.”

• S-adenosylmethionine (SAMe). Present in all living beings, this substance is required for neurotransmitter synthesis, and depends on folate and B12 levels to function optimally. According to Dr. Mischoulon, SAMe has been evaluated in more than 45 randomized clinical trials involving various routes of administration in doses of 200-1,600 mg/day. In eight placebo-controlled studies, SAMe was superior to placebo in six trials and had similar efficacy in the other two. In eight studies that compared SAMe with tricyclic antidepressants, six demonstrated similar efficacy with TCAs and one demonstrated benefit of SAMe over imipramine. The other trial, led by Dr. Mischoulon, compared SAMe with escitalopram and placebo in 189 patients in three treatment arms over a course of 12 weeks (J Clin Psychiatry. 2014;75[4]:370-6). The researchers observed a benefit in all treatment arms (a drop of 5-6 points on the 17-item Hamilton Depression Rating Scale [HDRS-17]), but no statistically significant differences were found between the groups. The most common side effect in the SAMe arm was related to gastrointestinal issues, mainly stomach discomfort and diarrhea.

One of the appeals of SAMe is that it’s safe to use in combination with other medicines, including tricyclic antidepressants (TCAs). “It may even boost and accelerate the effect of TCAs,” Dr. Mischoulon said. “It’s also been combined successfully with SSRIs and” [selective serotonin norepinephrine inhibitors]. In one study of 30 patients who were partial or nonresponders to SSRIs, augmentation with SAMe led to a response rate of 50% and a remission rate of 43% at 6 weeks (J Clin Psychopharmacol. 2004;24[6]:661-4), “which is very encouraging for our treatment-resistant population,” he said. In a 2010 trial, researchers investigated augmentation with SAMe 800 mg b.i.d. or placebo for 6 weeks in 73 serotonin reuptake inhibitor nonresponders with major depressive disorder (Am J Psychiatry 2010;167[8]:942-8). The response rate was 36.1% in the SAMe group, compared with 17.6% in the placebo group.

The medical literature generally supports the use of SAMe in doses of 400-1,600 mg/day. “It’s generally well tolerated.” Dr. Mischoulon said. Side effects tend to resemble the usual ones clinicians see with antidepressants: insomnia, anorexia, constipation, nausea, dry mouth, sweating, dizziness, and anxiety. “There have been cases of mania or hypomania developing in patients with bipolar depression, so be careful about [using this] in people with bipolar disorder,” he said.

Pregnancy tends to decrease methylation and SAMe activity, “so theoretically it should be beneficial in pregnant women with intrahepatic cholestasis, but we have limited prospective safety data on SAMe in pregnant women, so we advise caution.”

Cost may be a barrier for some patients, he said, since a 400-mg tablet may cost as much as $1.25. “So if you’re one of those people who need a dose in the range of 2,000-3,000 mg, the costs can be quite significant. Discuss this with your patient before you decide to embark on a trial of SAMe.”

• L-methylfolate (Deplin). Dr. Mischoulon was part of a multicenter research team that carried out a study of L-methylfolate 15 mg/day versus placebo in 223 adult patients with SSRI-resistant major depressive disorder (Am J Psychiatry. 2010 Aug;167[8]:942-8). They conducted the study in two 30-day treatment phases using a sequential parallel comparator design, and found that the mean change from baseline on the Quick Inventory of Depressive Symptomatology–Self Report (QIDS-SR) was significantly greater with L-methylfolate, compared with placebo. Similar results were observed with the HDRS-17, the HDRS-28, and the Clinical Global Impression–Severity scale (CGI-S).

• Omega-3 fatty acids (DHA and EPA). Primarily found in fish oil and other marine sources, omega-3 fatty acids are believed to promote neuronal membrane stabilization and anti-inflammatory effects. To date, more than 30 randomized, controlled trials of fatty acids for the treatment of depression have been conducted, mostly omega-3 fatty acids as an adjunct to standard antidepressant therapy. Most of the studies have involved EPA by itself or EPA in combination with DHA, he said, at a dose of 1-2 g per day. There’s also evidence that EPA may have a role in prophylactic preinterferon therapy in patients with hepatitis C.

Dr. Mischoulon and his associates recently carried out a trial of EPA 1,000 mg/day or DHA 1,000 mg/day, or placebo for 8 weeks in 196 patients (J Clin Psychiatry. 2015;76[1]:54-61). All treatment arms showed improvement, but neither treatment outperformed placebo. Response rates were in the range of 40%-50% for each arm, and the remission rates were in the 30% range. Though the initial results “were discouraging,” a secondary analysis revealed that EPA may benefit individuals with abnormal levels of two or more of the following inflammatory biomarkers at baseline: human C-reactive protein, interleukin-6, interleukin-1 receptor antagonist, leptin, and adiponectin. A new study underway “will examine depressed patients with obesity and elevated inflammatory status at baseline to enhance signal detection,” he said.

For the time being, he said, it’s best to use omega-3 fatty acids in patients with unipolar depression, in a dose of 1-2 g/day of an EPA/DHA combination that contains at least 60% EPA. In patients with bipolar disorder, he uses doses in the range of 6-10 g/day, “but watch out for cycling, which is a common problem in people with bipolar illness.”

Side effects from use may include stomach upset and fishy taste, “although most preparations today are highly purified, so we tend to get fewer complaints about that.” Published studies suggest a benefit of omega-3 fatty acids to expectant mothers, the fetus, and infants, particularly for neural development, “but the safe upper limit in pregnancy is unknown, so we need to advise caution.”

Dr. Mischoulon reported that he has received research support from the Bowman Family Foundation, Fisher Wallace, Nordic Naturals, Methylation Sciences, and PharmoRx Therapeutics. He also has received honoraria for consulting, speaking, and writing from Pamlab and the Massachusetts General Hospital Psychiatry Academy.

[email protected]

LAS VEGAS – For patients who present with complaints of insomnia, consider using the principles of the Brief Behavioral Treatment of Insomnia tool as your frontline approach.

“It’s a pragmatic approach to treating insomnia complaints but also provides a useful foundation for the behavioral management of sleep disorders generally, when combined with other pharmacologic approaches,” Dr. Charles F. Reynolds III said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “It involves relatively little time on the part of the clinician to apply.”

Part of the Brief Behavioral Treatment of Insomnia (BBTI), which was developed by Dr. Daniel J. Buysse and his colleagues at the University of Pittsburgh (Arch Intern Med. 2011;171[10]:887-95 and Behav Sleep Med. 2012;10[4]:266-79), involves education about lifestyle choices and practices that can be helpful to sleep, such as physical activity, stability of daily routines, treating medical problems that can interfere with sleep, having a comfortable sleep environment, and keeping the bed only for sleep and sexual intimacy.

The BBTI also educates the patient about practices that can be harmful to sleep, including alcohol, caffeine, worries, a poor sleep environment, or using the bed for things other than sleep or sex. “You can go a long way toward helping people with sleep-wake problems if they’re well educated about these issues, and if they keep a diary so that they can engage in self-monitoring,” Dr. Reynolds said.

He went on to note that the principles of the BBTI are grounded within an understanding of the physiological factors that regulate sleep. “One factor that controls sleep is how long you’ve been awake, the so-called homeostatic drive to sleep,” said Dr. Reynolds, Endowed Professor of Geriatric Psychiatry at the University of Pittsburgh. “Another factor is the biological clock, the circadian rhythms deep within the brain stem that govern the timing of sleep onset and offset. These two physiological processes provide the basis for the behavioral prescriptions that we make in brief behavioral treatment for insomnia.”

The four steps of the BBTI involve the following:

• Reduce time in bed. This doesn’t mean decreasing the amount of sleep per se, but rather the amount of wakefulness that can occur during a night. “By reducing time in bed we’re trying to increase the homeostatic drive to sleep,” said Dr. Reynolds, also director of the University of Pittsburgh Medical Center Aging Institute. “Being awake longer leads to quicker, deeper, more solid sleep.”

• Get up at the same time every day of the week. This practice “provides a kind of circadian anchor to the brain’s sleep wave rhythms, and reinforces those rhythms, and hence the efficiency of sleep,” he explained. “Even if you’ve slept poorly, getting up at the same time helps you to sleep better the next night.”

• Don’t go to bed unless sleepy. This strategy helps to increase sleep drive by keeping you awake longer. “Going to bed when you’re not sleepy can lead to frustration and gives your brain the wrong message,” he said. “The principles of stimulus control and temporal control are at the behavioral root of BBTI prescriptions.”

• Don’t stay in bed unless asleep. “We are teaching patients how to associate lying in bed with sleeping, and not with worrying or other activities that may lead to frustration or hyperarousal,” he said.

Studies have demonstrated that BBTI produces improvement in 70%-80% of patients. “It is a briefer, less complicated approach than traditional cognitive-behavioral therapy for insomnia,” Dr. Reynolds said. “BBTI also provides a wonderful behavioral foundation for intelligent evidence-based pharmacotherapy for common sleep disorders.”

If it’s determined that pharmacologic treatment for insomnia is indicated, Dr. Reynolds cautioned that the margin of safety for benzodiazepines such as temazepam is wide. Contraindications include obstructive sleep apnea, substance abuse disorders, and advanced liver disease. Side effects may include daytime sedation, anterograde amnesia, sleepwalking, sleep-related eating disorder, respiratory depression, and in some cases, rebound insomnia.

“In my practice, I tend to use shorter-acting agents often as an augmentation pharmacotherapy,” he said. “For example, if I’m treating an older adult with depression, I may use an antidepressant as the primary pharmacotherapy and then add a low-dose benzodiazepine to help keep them more comfortable and help them sleep better during the initial phases of treatment.”

Studies of the orexin receptor antagonist suvorexant have shown improved sleep time, falling asleep faster, staying asleep longer, and sleeping more throughout the night. However, “there are some possibilities for daytime hangover,” Dr. Reynolds said. “I’m also not clear on how well suvorexant’s effects on breathing during sleep have been evaluated. In my view, that remains a somewhat open question.”

The two most widely used sedating antidepressants for insomnia problems include doxepin and trazodone. “They can be particularly helpful in patients with co-occurring depression,” he said. Doxepin in low doses is approved for sleep maintenance insomnia.

Ramelteon is the first melatonin receptor agonist approved for the treatment of insomnia. Contraindications include a history of angioedema with concurrent use of fluvoxamine.

“In general, I recommend to my colleagues not to use sedative antipsychotics like quetiapine or olanzapine, particularly in the context of elderly with dementing disorders and sleep-wake disturbances,” he said.

Dr. Reynolds reported having no relevant financial conflicts.

[email protected]

LAS VEGAS – For patients who present with complaints of insomnia, consider using the principles of the Brief Behavioral Treatment of Insomnia tool as your frontline approach.

“It’s a pragmatic approach to treating insomnia complaints but also provides a useful foundation for the behavioral management of sleep disorders generally, when combined with other pharmacologic approaches,” Dr. Charles F. Reynolds III said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “It involves relatively little time on the part of the clinician to apply.”

Part of the Brief Behavioral Treatment of Insomnia (BBTI), which was developed by Dr. Daniel J. Buysse and his colleagues at the University of Pittsburgh (Arch Intern Med. 2011;171[10]:887-95 and Behav Sleep Med. 2012;10[4]:266-79), involves education about lifestyle choices and practices that can be helpful to sleep, such as physical activity, stability of daily routines, treating medical problems that can interfere with sleep, having a comfortable sleep environment, and keeping the bed only for sleep and sexual intimacy.

The BBTI also educates the patient about practices that can be harmful to sleep, including alcohol, caffeine, worries, a poor sleep environment, or using the bed for things other than sleep or sex. “You can go a long way toward helping people with sleep-wake problems if they’re well educated about these issues, and if they keep a diary so that they can engage in self-monitoring,” Dr. Reynolds said.

He went on to note that the principles of the BBTI are grounded within an understanding of the physiological factors that regulate sleep. “One factor that controls sleep is how long you’ve been awake, the so-called homeostatic drive to sleep,” said Dr. Reynolds, Endowed Professor of Geriatric Psychiatry at the University of Pittsburgh. “Another factor is the biological clock, the circadian rhythms deep within the brain stem that govern the timing of sleep onset and offset. These two physiological processes provide the basis for the behavioral prescriptions that we make in brief behavioral treatment for insomnia.”

The four steps of the BBTI involve the following:

• Reduce time in bed. This doesn’t mean decreasing the amount of sleep per se, but rather the amount of wakefulness that can occur during a night. “By reducing time in bed we’re trying to increase the homeostatic drive to sleep,” said Dr. Reynolds, also director of the University of Pittsburgh Medical Center Aging Institute. “Being awake longer leads to quicker, deeper, more solid sleep.”

• Get up at the same time every day of the week. This practice “provides a kind of circadian anchor to the brain’s sleep wave rhythms, and reinforces those rhythms, and hence the efficiency of sleep,” he explained. “Even if you’ve slept poorly, getting up at the same time helps you to sleep better the next night.”

• Don’t go to bed unless sleepy. This strategy helps to increase sleep drive by keeping you awake longer. “Going to bed when you’re not sleepy can lead to frustration and gives your brain the wrong message,” he said. “The principles of stimulus control and temporal control are at the behavioral root of BBTI prescriptions.”

• Don’t stay in bed unless asleep. “We are teaching patients how to associate lying in bed with sleeping, and not with worrying or other activities that may lead to frustration or hyperarousal,” he said.

Studies have demonstrated that BBTI produces improvement in 70%-80% of patients. “It is a briefer, less complicated approach than traditional cognitive-behavioral therapy for insomnia,” Dr. Reynolds said. “BBTI also provides a wonderful behavioral foundation for intelligent evidence-based pharmacotherapy for common sleep disorders.”

If it’s determined that pharmacologic treatment for insomnia is indicated, Dr. Reynolds cautioned that the margin of safety for benzodiazepines such as temazepam is wide. Contraindications include obstructive sleep apnea, substance abuse disorders, and advanced liver disease. Side effects may include daytime sedation, anterograde amnesia, sleepwalking, sleep-related eating disorder, respiratory depression, and in some cases, rebound insomnia.

“In my practice, I tend to use shorter-acting agents often as an augmentation pharmacotherapy,” he said. “For example, if I’m treating an older adult with depression, I may use an antidepressant as the primary pharmacotherapy and then add a low-dose benzodiazepine to help keep them more comfortable and help them sleep better during the initial phases of treatment.”

Studies of the orexin receptor antagonist suvorexant have shown improved sleep time, falling asleep faster, staying asleep longer, and sleeping more throughout the night. However, “there are some possibilities for daytime hangover,” Dr. Reynolds said. “I’m also not clear on how well suvorexant’s effects on breathing during sleep have been evaluated. In my view, that remains a somewhat open question.”

The two most widely used sedating antidepressants for insomnia problems include doxepin and trazodone. “They can be particularly helpful in patients with co-occurring depression,” he said. Doxepin in low doses is approved for sleep maintenance insomnia.

Ramelteon is the first melatonin receptor agonist approved for the treatment of insomnia. Contraindications include a history of angioedema with concurrent use of fluvoxamine.

“In general, I recommend to my colleagues not to use sedative antipsychotics like quetiapine or olanzapine, particularly in the context of elderly with dementing disorders and sleep-wake disturbances,” he said.

Dr. Reynolds reported having no relevant financial conflicts.

[email protected]

LAS VEGAS – For patients who present with complaints of insomnia, consider using the principles of the Brief Behavioral Treatment of Insomnia tool as your frontline approach.

“It’s a pragmatic approach to treating insomnia complaints but also provides a useful foundation for the behavioral management of sleep disorders generally, when combined with other pharmacologic approaches,” Dr. Charles F. Reynolds III said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “It involves relatively little time on the part of the clinician to apply.”

Part of the Brief Behavioral Treatment of Insomnia (BBTI), which was developed by Dr. Daniel J. Buysse and his colleagues at the University of Pittsburgh (Arch Intern Med. 2011;171[10]:887-95 and Behav Sleep Med. 2012;10[4]:266-79), involves education about lifestyle choices and practices that can be helpful to sleep, such as physical activity, stability of daily routines, treating medical problems that can interfere with sleep, having a comfortable sleep environment, and keeping the bed only for sleep and sexual intimacy.

The BBTI also educates the patient about practices that can be harmful to sleep, including alcohol, caffeine, worries, a poor sleep environment, or using the bed for things other than sleep or sex. “You can go a long way toward helping people with sleep-wake problems if they’re well educated about these issues, and if they keep a diary so that they can engage in self-monitoring,” Dr. Reynolds said.

He went on to note that the principles of the BBTI are grounded within an understanding of the physiological factors that regulate sleep. “One factor that controls sleep is how long you’ve been awake, the so-called homeostatic drive to sleep,” said Dr. Reynolds, Endowed Professor of Geriatric Psychiatry at the University of Pittsburgh. “Another factor is the biological clock, the circadian rhythms deep within the brain stem that govern the timing of sleep onset and offset. These two physiological processes provide the basis for the behavioral prescriptions that we make in brief behavioral treatment for insomnia.”

The four steps of the BBTI involve the following:

• Reduce time in bed. This doesn’t mean decreasing the amount of sleep per se, but rather the amount of wakefulness that can occur during a night. “By reducing time in bed we’re trying to increase the homeostatic drive to sleep,” said Dr. Reynolds, also director of the University of Pittsburgh Medical Center Aging Institute. “Being awake longer leads to quicker, deeper, more solid sleep.”

• Get up at the same time every day of the week. This practice “provides a kind of circadian anchor to the brain’s sleep wave rhythms, and reinforces those rhythms, and hence the efficiency of sleep,” he explained. “Even if you’ve slept poorly, getting up at the same time helps you to sleep better the next night.”

• Don’t go to bed unless sleepy. This strategy helps to increase sleep drive by keeping you awake longer. “Going to bed when you’re not sleepy can lead to frustration and gives your brain the wrong message,” he said. “The principles of stimulus control and temporal control are at the behavioral root of BBTI prescriptions.”

• Don’t stay in bed unless asleep. “We are teaching patients how to associate lying in bed with sleeping, and not with worrying or other activities that may lead to frustration or hyperarousal,” he said.

Studies have demonstrated that BBTI produces improvement in 70%-80% of patients. “It is a briefer, less complicated approach than traditional cognitive-behavioral therapy for insomnia,” Dr. Reynolds said. “BBTI also provides a wonderful behavioral foundation for intelligent evidence-based pharmacotherapy for common sleep disorders.”

If it’s determined that pharmacologic treatment for insomnia is indicated, Dr. Reynolds cautioned that the margin of safety for benzodiazepines such as temazepam is wide. Contraindications include obstructive sleep apnea, substance abuse disorders, and advanced liver disease. Side effects may include daytime sedation, anterograde amnesia, sleepwalking, sleep-related eating disorder, respiratory depression, and in some cases, rebound insomnia.

“In my practice, I tend to use shorter-acting agents often as an augmentation pharmacotherapy,” he said. “For example, if I’m treating an older adult with depression, I may use an antidepressant as the primary pharmacotherapy and then add a low-dose benzodiazepine to help keep them more comfortable and help them sleep better during the initial phases of treatment.”

Studies of the orexin receptor antagonist suvorexant have shown improved sleep time, falling asleep faster, staying asleep longer, and sleeping more throughout the night. However, “there are some possibilities for daytime hangover,” Dr. Reynolds said. “I’m also not clear on how well suvorexant’s effects on breathing during sleep have been evaluated. In my view, that remains a somewhat open question.”

The two most widely used sedating antidepressants for insomnia problems include doxepin and trazodone. “They can be particularly helpful in patients with co-occurring depression,” he said. Doxepin in low doses is approved for sleep maintenance insomnia.

Ramelteon is the first melatonin receptor agonist approved for the treatment of insomnia. Contraindications include a history of angioedema with concurrent use of fluvoxamine.

“In general, I recommend to my colleagues not to use sedative antipsychotics like quetiapine or olanzapine, particularly in the context of elderly with dementing disorders and sleep-wake disturbances,” he said.

Dr. Reynolds reported having no relevant financial conflicts.

[email protected]

Las Vegas – Electroconvulsive therapy is useful for many patients, particularly those with more severe depressive symptoms and more treatment resistance, according to Dr. Bruce J. Cohen.

However, a survey of 116 psychiatrists in Virginia shows that clinician experience with electroconvulsive therapy (ECT) varies widely. In fact, 8% of respondents reported having no experience with ECT, 41% observed it in residency, 38% performed it while supervised in residency, 35% had performed ECT but are not currently using it, and only 11% indicated that they currently perform ECT (J ECT. 2011;27[3]:232-5). “While most psychiatrists had a basic understanding of ECT and favorable attitude, a lesser fund of knowledge about ECT was associated with both a less favorable attitude toward ECT and fewer referrals,” Dr. Cohen, one of the study authors, said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “Those who viewed ECT as a treatment of last resort made fewer referrals.”

Dr. Cohen of the department of psychiatry and neurobehavioral sciences at the University of Virginia, Charlottesville, said the most common indications for ECT are major depressive episodes both in unipolar and bipolar disorders, including medication-resistant depression; manic or mixed states; inability to tolerate medication side effects; and the need for more rapid and/or certain response.

“You might have a situation with an inpatient where the acuity of the depression is so high that you move to ECT almost immediately,” he said. Other indications include a previous good response to ECT, catatonia, refractory schizophrenia, more severe mood disorder in pregnancy, and neuroleptic malignant syndrome.

Before he meets with patients to discuss ECT, Dr. Cohen said he determines whether the focus will be on prescreening for ECT or a broader consultation about treatment-resistant depression in which he and the patient explore other treatment options besides ECT. “That’s the approach that I favor, because a patient might decide after talking to me that they don’t want ECT, or they might say, ‘I’m glad I talked to you, but I’m not quite ready for ECT at this point,’ ” he said.

Other factors could be contributing to the patient’s current depressive state, he said, perhaps someone “who’s on a very high dose of lithium that’s causing fatigue and apathy or cognitive disturbance. Or maybe the patient has had treatment-resistant psychosis, and the more you talk to them, the more you realize it may be obsessive-compulsive disorder, and not psychotic depression at all, and they’ve tried treatment with various antipsychotic agents but never with a higher dose of [a selective serotonin reuptake inhibitor].”

During the consultation, he said he emphasizes that ECT is not effective for all patients. “This is important, because some patients will come in and say, ‘ECT is my last hope,’ he said. “They might have already decided that if they don’t respond to ECT, they’re going to kill themselves. I share anecdotes and let them know that even if they end up not responding to ECT, there are other treatments out there, and not all treatments have been exhausted.” He also discusses options should ECT be successful for the patient, including the potential for maintenance therapy with ECT or a medication regimen.

Having a family member or a friend accompany the patient to the consultation is helpful. “These are the people who may bring them back and forth to treatments,” he said. “These are also the people who could sabotage treatment. If they don’t know what to expect in terms of transient confusion or memory problems or even coming out of the treatment room looking flushed, you could see where a family member or friend might be frightened. So the family member can be your best ally.”

There are no absolute medical contraindications to ECT, Dr. Cohen said, but medical conditions to be stabilized include cardiac pacemakers, hypertension, pulmonary disease, cardiovascular disease, liver disease, diabetes, skull defects, pregnancy, and CNS conditions that increase the risk of delirium, including dementia, stroke, head injury, Parkinson’s disease, and multiple sclerosis. “Sometimes we’re asking for clearance on a person who has a brain aneurysm,” he said. “I want to get a detailed medical history. At our facility, usually anesthesia will consult with the patient shortly before the treatment rather than as a whole separate outpatient visit.”

Labs to consider prior to performing ECT will include an EKG, blood count, chemistry panel, chest X-ray, spine films, and neuroimaging, “but those things aren’t obligatory or required,” he said. “But just like in any case of refractory depression, you’d want to order those things as appropriate.”

Prior to ECT, Dr. Cohen said he considers discontinuing or minimizing medications that have anticonvulsant effects, such as carbamazepine and lamotrigine and benzodiazepines. “On the other hand, you don’t want the patient relapsing right as you’re starting your treatment, so it might be that you can’t get them off benzodiazepines completely,” he said.

According to a recent meta-analysis of 32 studies, the most robust predictors of poor response to ECT were longer depressive episode duration and medication resistance, while age, psychosis, and melancholic features were not found to be as clinically useful (J Clin Psychiatry. 2015;76[10]:1374-84). Dr. Cohen noted that a major consideration during a pre-ECT consultation is working out any potential logistical difficulties in advance. For example, during an acute course of ECT, he said he advises patients not to drive, even on nontreatment days.

“If you live in a city with good public transportation, it may not be a big deal, but it can be difficult in more rural areas,” he said. “It’s not that ECT makes you lose the memory of how to drive a car, but could give you subtle cognitive slowing or decreased reaction times. Therefore, arranging to have an adequate support system throughout the course of ECT is essential.”

Dr. Cohen reported having no relevant financial conflicts.

[email protected]

Las Vegas – Electroconvulsive therapy is useful for many patients, particularly those with more severe depressive symptoms and more treatment resistance, according to Dr. Bruce J. Cohen.

However, a survey of 116 psychiatrists in Virginia shows that clinician experience with electroconvulsive therapy (ECT) varies widely. In fact, 8% of respondents reported having no experience with ECT, 41% observed it in residency, 38% performed it while supervised in residency, 35% had performed ECT but are not currently using it, and only 11% indicated that they currently perform ECT (J ECT. 2011;27[3]:232-5). “While most psychiatrists had a basic understanding of ECT and favorable attitude, a lesser fund of knowledge about ECT was associated with both a less favorable attitude toward ECT and fewer referrals,” Dr. Cohen, one of the study authors, said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “Those who viewed ECT as a treatment of last resort made fewer referrals.”

Dr. Cohen of the department of psychiatry and neurobehavioral sciences at the University of Virginia, Charlottesville, said the most common indications for ECT are major depressive episodes both in unipolar and bipolar disorders, including medication-resistant depression; manic or mixed states; inability to tolerate medication side effects; and the need for more rapid and/or certain response.

“You might have a situation with an inpatient where the acuity of the depression is so high that you move to ECT almost immediately,” he said. Other indications include a previous good response to ECT, catatonia, refractory schizophrenia, more severe mood disorder in pregnancy, and neuroleptic malignant syndrome.

Before he meets with patients to discuss ECT, Dr. Cohen said he determines whether the focus will be on prescreening for ECT or a broader consultation about treatment-resistant depression in which he and the patient explore other treatment options besides ECT. “That’s the approach that I favor, because a patient might decide after talking to me that they don’t want ECT, or they might say, ‘I’m glad I talked to you, but I’m not quite ready for ECT at this point,’ ” he said.

Other factors could be contributing to the patient’s current depressive state, he said, perhaps someone “who’s on a very high dose of lithium that’s causing fatigue and apathy or cognitive disturbance. Or maybe the patient has had treatment-resistant psychosis, and the more you talk to them, the more you realize it may be obsessive-compulsive disorder, and not psychotic depression at all, and they’ve tried treatment with various antipsychotic agents but never with a higher dose of [a selective serotonin reuptake inhibitor].”

During the consultation, he said he emphasizes that ECT is not effective for all patients. “This is important, because some patients will come in and say, ‘ECT is my last hope,’ he said. “They might have already decided that if they don’t respond to ECT, they’re going to kill themselves. I share anecdotes and let them know that even if they end up not responding to ECT, there are other treatments out there, and not all treatments have been exhausted.” He also discusses options should ECT be successful for the patient, including the potential for maintenance therapy with ECT or a medication regimen.

Having a family member or a friend accompany the patient to the consultation is helpful. “These are the people who may bring them back and forth to treatments,” he said. “These are also the people who could sabotage treatment. If they don’t know what to expect in terms of transient confusion or memory problems or even coming out of the treatment room looking flushed, you could see where a family member or friend might be frightened. So the family member can be your best ally.”

There are no absolute medical contraindications to ECT, Dr. Cohen said, but medical conditions to be stabilized include cardiac pacemakers, hypertension, pulmonary disease, cardiovascular disease, liver disease, diabetes, skull defects, pregnancy, and CNS conditions that increase the risk of delirium, including dementia, stroke, head injury, Parkinson’s disease, and multiple sclerosis. “Sometimes we’re asking for clearance on a person who has a brain aneurysm,” he said. “I want to get a detailed medical history. At our facility, usually anesthesia will consult with the patient shortly before the treatment rather than as a whole separate outpatient visit.”

Labs to consider prior to performing ECT will include an EKG, blood count, chemistry panel, chest X-ray, spine films, and neuroimaging, “but those things aren’t obligatory or required,” he said. “But just like in any case of refractory depression, you’d want to order those things as appropriate.”

Prior to ECT, Dr. Cohen said he considers discontinuing or minimizing medications that have anticonvulsant effects, such as carbamazepine and lamotrigine and benzodiazepines. “On the other hand, you don’t want the patient relapsing right as you’re starting your treatment, so it might be that you can’t get them off benzodiazepines completely,” he said.

According to a recent meta-analysis of 32 studies, the most robust predictors of poor response to ECT were longer depressive episode duration and medication resistance, while age, psychosis, and melancholic features were not found to be as clinically useful (J Clin Psychiatry. 2015;76[10]:1374-84). Dr. Cohen noted that a major consideration during a pre-ECT consultation is working out any potential logistical difficulties in advance. For example, during an acute course of ECT, he said he advises patients not to drive, even on nontreatment days.

“If you live in a city with good public transportation, it may not be a big deal, but it can be difficult in more rural areas,” he said. “It’s not that ECT makes you lose the memory of how to drive a car, but could give you subtle cognitive slowing or decreased reaction times. Therefore, arranging to have an adequate support system throughout the course of ECT is essential.”

Dr. Cohen reported having no relevant financial conflicts.

[email protected]

Las Vegas – Electroconvulsive therapy is useful for many patients, particularly those with more severe depressive symptoms and more treatment resistance, according to Dr. Bruce J. Cohen.

However, a survey of 116 psychiatrists in Virginia shows that clinician experience with electroconvulsive therapy (ECT) varies widely. In fact, 8% of respondents reported having no experience with ECT, 41% observed it in residency, 38% performed it while supervised in residency, 35% had performed ECT but are not currently using it, and only 11% indicated that they currently perform ECT (J ECT. 2011;27[3]:232-5). “While most psychiatrists had a basic understanding of ECT and favorable attitude, a lesser fund of knowledge about ECT was associated with both a less favorable attitude toward ECT and fewer referrals,” Dr. Cohen, one of the study authors, said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “Those who viewed ECT as a treatment of last resort made fewer referrals.”

Dr. Cohen of the department of psychiatry and neurobehavioral sciences at the University of Virginia, Charlottesville, said the most common indications for ECT are major depressive episodes both in unipolar and bipolar disorders, including medication-resistant depression; manic or mixed states; inability to tolerate medication side effects; and the need for more rapid and/or certain response.

“You might have a situation with an inpatient where the acuity of the depression is so high that you move to ECT almost immediately,” he said. Other indications include a previous good response to ECT, catatonia, refractory schizophrenia, more severe mood disorder in pregnancy, and neuroleptic malignant syndrome.

Before he meets with patients to discuss ECT, Dr. Cohen said he determines whether the focus will be on prescreening for ECT or a broader consultation about treatment-resistant depression in which he and the patient explore other treatment options besides ECT. “That’s the approach that I favor, because a patient might decide after talking to me that they don’t want ECT, or they might say, ‘I’m glad I talked to you, but I’m not quite ready for ECT at this point,’ ” he said.

Other factors could be contributing to the patient’s current depressive state, he said, perhaps someone “who’s on a very high dose of lithium that’s causing fatigue and apathy or cognitive disturbance. Or maybe the patient has had treatment-resistant psychosis, and the more you talk to them, the more you realize it may be obsessive-compulsive disorder, and not psychotic depression at all, and they’ve tried treatment with various antipsychotic agents but never with a higher dose of [a selective serotonin reuptake inhibitor].”

During the consultation, he said he emphasizes that ECT is not effective for all patients. “This is important, because some patients will come in and say, ‘ECT is my last hope,’ he said. “They might have already decided that if they don’t respond to ECT, they’re going to kill themselves. I share anecdotes and let them know that even if they end up not responding to ECT, there are other treatments out there, and not all treatments have been exhausted.” He also discusses options should ECT be successful for the patient, including the potential for maintenance therapy with ECT or a medication regimen.

Having a family member or a friend accompany the patient to the consultation is helpful. “These are the people who may bring them back and forth to treatments,” he said. “These are also the people who could sabotage treatment. If they don’t know what to expect in terms of transient confusion or memory problems or even coming out of the treatment room looking flushed, you could see where a family member or friend might be frightened. So the family member can be your best ally.”

There are no absolute medical contraindications to ECT, Dr. Cohen said, but medical conditions to be stabilized include cardiac pacemakers, hypertension, pulmonary disease, cardiovascular disease, liver disease, diabetes, skull defects, pregnancy, and CNS conditions that increase the risk of delirium, including dementia, stroke, head injury, Parkinson’s disease, and multiple sclerosis. “Sometimes we’re asking for clearance on a person who has a brain aneurysm,” he said. “I want to get a detailed medical history. At our facility, usually anesthesia will consult with the patient shortly before the treatment rather than as a whole separate outpatient visit.”

Labs to consider prior to performing ECT will include an EKG, blood count, chemistry panel, chest X-ray, spine films, and neuroimaging, “but those things aren’t obligatory or required,” he said. “But just like in any case of refractory depression, you’d want to order those things as appropriate.”

Prior to ECT, Dr. Cohen said he considers discontinuing or minimizing medications that have anticonvulsant effects, such as carbamazepine and lamotrigine and benzodiazepines. “On the other hand, you don’t want the patient relapsing right as you’re starting your treatment, so it might be that you can’t get them off benzodiazepines completely,” he said.

According to a recent meta-analysis of 32 studies, the most robust predictors of poor response to ECT were longer depressive episode duration and medication resistance, while age, psychosis, and melancholic features were not found to be as clinically useful (J Clin Psychiatry. 2015;76[10]:1374-84). Dr. Cohen noted that a major consideration during a pre-ECT consultation is working out any potential logistical difficulties in advance. For example, during an acute course of ECT, he said he advises patients not to drive, even on nontreatment days.

“If you live in a city with good public transportation, it may not be a big deal, but it can be difficult in more rural areas,” he said. “It’s not that ECT makes you lose the memory of how to drive a car, but could give you subtle cognitive slowing or decreased reaction times. Therefore, arranging to have an adequate support system throughout the course of ECT is essential.”

Dr. Cohen reported having no relevant financial conflicts.

[email protected]

Fourteen new reports of possible sexual transmission of Zika virus are being investigated by health officials in the United States, including several that involve pregnant women.

According to a media statement released by the Centers for Disease Control and Prevention on Feb. 23, in 2 of the 14 suspected cases, Zika virus infection “has been confirmed in women whose only known risk factor was sexual contact with an ill male partner who had recently traveled to an area with local Zika virus transmission; testing for the male partners is still pending.”

Confirmatory tests are pending for four additional suspected sexual transmission events, and the investigation is ongoing for an additional eight suspected cases.

“Like previously reported cases of sexual transmission, these cases involve possible transmission of the virus from men to their sex partners,” the statement reads. “At this time, there is no evidence that women can transmit Zika virus to their sex partners; however, more research is needed to understand this issue.”

In a separate announcement on Feb. 23, the CDC added Trinidad and Tobago and the Marshall Islands to the Zika virus travel notices. A full list of affected countries regions can be found at http://wwwnc.cdc.gov/travel/page/zika-information.

[email protected]

Fourteen new reports of possible sexual transmission of Zika virus are being investigated by health officials in the United States, including several that involve pregnant women.

According to a media statement released by the Centers for Disease Control and Prevention on Feb. 23, in 2 of the 14 suspected cases, Zika virus infection “has been confirmed in women whose only known risk factor was sexual contact with an ill male partner who had recently traveled to an area with local Zika virus transmission; testing for the male partners is still pending.”

Confirmatory tests are pending for four additional suspected sexual transmission events, and the investigation is ongoing for an additional eight suspected cases.

“Like previously reported cases of sexual transmission, these cases involve possible transmission of the virus from men to their sex partners,” the statement reads. “At this time, there is no evidence that women can transmit Zika virus to their sex partners; however, more research is needed to understand this issue.”

In a separate announcement on Feb. 23, the CDC added Trinidad and Tobago and the Marshall Islands to the Zika virus travel notices. A full list of affected countries regions can be found at http://wwwnc.cdc.gov/travel/page/zika-information.

[email protected]

Fourteen new reports of possible sexual transmission of Zika virus are being investigated by health officials in the United States, including several that involve pregnant women.

According to a media statement released by the Centers for Disease Control and Prevention on Feb. 23, in 2 of the 14 suspected cases, Zika virus infection “has been confirmed in women whose only known risk factor was sexual contact with an ill male partner who had recently traveled to an area with local Zika virus transmission; testing for the male partners is still pending.”

Confirmatory tests are pending for four additional suspected sexual transmission events, and the investigation is ongoing for an additional eight suspected cases.

“Like previously reported cases of sexual transmission, these cases involve possible transmission of the virus from men to their sex partners,” the statement reads. “At this time, there is no evidence that women can transmit Zika virus to their sex partners; however, more research is needed to understand this issue.”

In a separate announcement on Feb. 23, the CDC added Trinidad and Tobago and the Marshall Islands to the Zika virus travel notices. A full list of affected countries regions can be found at http://wwwnc.cdc.gov/travel/page/zika-information.

[email protected]

LAS VEGAS – Calibration of treatment response is a major challenge in patients with schizophrenia, according to Dr. Peter J. Weiden.

“On some level all of our patients with schizophrenia are both responders and nonresponders to medication at the same time,” Dr. Weiden said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “What I mean is that the vast majority of patients with schizophrenia have fewer symptoms on antipsychotic medication, but very few patients on medicine will be perfectly OK without any symptoms or problems.”

Dr. Weiden, professor of psychiatry at the University of Illinois at Chicago, went on to note that clinicians tend to calibrate medication response as the improvement in psychotic symptoms or stability, compared with how the person would be without medication. But the patient will not see it that way. Instead, the patient will calibrate how he is doing with medication, compared with how he felt before the illness started – or how he is compared with others without a diagnosis of schizophrenia.

“We still don’t cure schizophrenia; patients want to be normal,” he said. “We don’t make them normal with our medications, and medications don’t always work as expected. At the very least, when we talk about response and nonresponse, we need to be respectful of the patient’s point of view.”

The same calibration dilemma happens with the side effect burden from antipsychotics. While the side effect burden from current antipsychotics is much better than it used to be in the preclozapine era, patients are still likely to have to put up with a variety of bothersome side effects. Telling the patient: “You should be grateful, because it used to be a lot worse!” somehow doesn’t come across as helpful.

Factors affecting calibration of treatment include the acuity of the patient’s illness, duration of illness, relative engagement in the treatment process (meaning “our outcomes should be a lot better for patients who are engaged in our treatment, who come to treatment, than those who don’t,” he said), comorbidities that may limit efficacy, the clinician’s philosophy of treatment, and the patient’s access to “best practices” care.

Although all antipsychotics can be used for all phases of schizophrenia, Dr. Weiden cautioned that individual antipsychotics are not interchangeable. “There’s always some efficacy risk when changing from an antipsychotic known to be effective for an individual patient,” he said. “Control of psychotic symptoms is always important. If you work in an inpatient unit, there’s a lot of stress and a lot of drive toward rapid resolution of symptoms in a way that’s easy and a way that’s safe.”

Desirable characteristics of pharmacologic agents for immediate initiation of acute treatment, he continued, include rapid onset of action, low toxicity, availability in multiple routes of administration, ease of use, low potential for drug-drug interactions, and ease of crossover to an oral antipsychotic agent. However, managing the acute psychosis in an ER or hospital setting “isn’t all about the medication,” he said.

“It’s very traumatic to be held down. It’s humiliating. It’s disruptive. Yes, we need to hospitalize people when they’re unsafe, but a lot of nonpharmacologic things we do are very important and will reduce the risk of complications from medication.” These include reassuring the patient, making him or her physically comfortable, reducing triggers that may escalate the situation, contacting the family, and educating the staff about the treatment plan.

In his clinical opinion, the inpatient use of a haloperidol p.r.n. regimen often is unsound and unsafe. “Very often on an inpatient unit, the haloperidol p.r.n. orders are done separately from the standing orders,” Dr. Weiden explained. “So you’ll have a clinician do a careful evaluation and write the standing orders of the medication, but the p.r.n.s are kind of boilerplate, and they get Haldol. The brain cannot ‘tell’ the difference between a standing order and a p.r.n. order of haloperidol. It is dangerous; patients die from this. It’s not common to have a life-threatening reaction to p.r.n. haloperidol, but it’s not rare, either, and the automatic use of haloperidol p.r.n. certainly no longer meets any reasonable standard of safety.”

The same antipsychotic medication can be used acutely and in maintenance, Dr. Weiden said, but if the patient relapses, you might consider changing to another agent. “If you know the patient well, and you know that the last medicine helped keep the patient stable but they still have lots of symptoms and a pretty crummy life, you might want to consider that as an opportunity to change the medicine,” he said. ‘However, if the patient came in because they went out drinking with their buddies and they got intoxicated, you really should not change the medicine, because in this situation, it was not a pharmacologic failure of the medication regimen,” Dr. Weiden said. To change or not to change medication “is a really big issue for someone’s life trajectory.”

There are 12 Food and Drug Administration–approved atypical antipsychotics for schizophrenia, which can be overwhelming for clinicians who do not specialize in treating the disorder. “While these meds are not perfect, each of these can help some people who are not helped otherwise, and each of these has a different side effect profile,” Dr. Weiden said. “So while we can’t completely cure schizophrenia, we will have a lot more luck in getting a patient on a medication that is not too burdensome for them. The downside is that we don’t have any biologic predictors as to who will respond to what agent.”

Dr. Weiden said he thinks of recovery from schizophrenia as a process in which the choice of goals is decided primarily by the patient and guided by the clinician. “The good thing is, there’s no shortage of symptoms you can work on,” he said. “You don’t have to fix everything, but you and the patient should come together to goal-set and pick one or two that are the priorities. That will keep you from getting overwhelmed and burned out trying to ‘fix’ everything at once.”

Nonpharmacologic causes of persistent symptoms warrant investigation as well, such as substance comorbidities, medical comorbidities such as obstructive sleep apnea, treatment access barriers, and adherence challenges. While discontinuation of the medication class is not an option, “We have dose adjustment; we can substitute, go from one antipsychotic to another; we have route of delivery, you can add a new medication to the regimen, either within the class or a new class, and we can discontinue one or more medications from the current regimen,” Dr. Weiden said. “That is one strategy we often forget: getting the person off a medication that may be causing a problem.”

When positive symptoms persist, make sure that the patient’s current antipsychotic medicine is optimized. “The dose response of these different antipsychotics is not the same,” he said. “Some meds have a very steep dose response; others are more flat. How far you push may depend on the specific agent. You want to do what’s easy first. So raising the dose for persistent positive symptoms is a good idea, except if you think it’s behavioral toxicity.”

Switching to a new agent takes more work than changing the dose of a current agent. He characterized clozapine as “the anchor” for persistent positive symptoms. “No patient is clearly refractory of positive symptoms until they’ve either failed or refused clozapine,” he said. “Combining antipsychotics is not a substitute for clozapine. It’s a lot easier to do, but it’s not a substitute.

“Should the patient seem to have suboptimal response to a few first-line antipsychotics, it is important to tell the patient and family about clozapine even if you are not ready to recommend it right now. Likewise, it is crucial to inform all stakeholders about the suicide prevention indication of clozapine for any schizophrenia patient with any suicide history, even if the overall circumstances are not yet amenable to starting clozapine right away.”

During a separate presentation, Dr. Weiden encouraged meeting attendees to think about adherence to antipsychotics as not an outcome, but rather as an important mediator of outcome.

“As clinicians, we get stuck on [the notion of] ‘you’re not doing what I recommended,’ ” he said. One indirect consequence of adherence is poor information, which obscures assessment of treatment response, and also creates safety risks. When Dr. Weiden meets with patients for the first time, he tells them, “It’s very important that I know what you’re really doing, both in terms of your drugs and the drugs I’ve prescribed for you,” he said. “I make it safe for them. I say, ‘I may disagree, but I’m not going to get mad.’ I give them advance information about how I would respond, because different clinicians respond differently. Some take it personally and some don’t. I don’t take it personally.

“The other thing I say is that, ‘It’s not just about you’re obeying me, but it’s for your safety. It’s less safe if you don’t tell me.’ Safety is less pejorative than adherence.” Other strategies that can be used to track adherence include recommending long-acting therapies such as routine, supervision of oral therapy, and using pharmacy refill data. “Many patients don’t pick up their medications or don’t fill their prescriptions,” he said.

Gradual dose lowering is a feasible strategy, he said. “It can be successful, but not always. We have to advise patients that even brief medication gaps are a bad thing, but gradual dose lowering may be achievable and helpful.”

Dr. Weiden reported having numerous financial ties to the pharmaceutical industry, as well as being a stockholder of Delpor.

[email protected]

LAS VEGAS – Calibration of treatment response is a major challenge in patients with schizophrenia, according to Dr. Peter J. Weiden.

“On some level all of our patients with schizophrenia are both responders and nonresponders to medication at the same time,” Dr. Weiden said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “What I mean is that the vast majority of patients with schizophrenia have fewer symptoms on antipsychotic medication, but very few patients on medicine will be perfectly OK without any symptoms or problems.”

Dr. Weiden, professor of psychiatry at the University of Illinois at Chicago, went on to note that clinicians tend to calibrate medication response as the improvement in psychotic symptoms or stability, compared with how the person would be without medication. But the patient will not see it that way. Instead, the patient will calibrate how he is doing with medication, compared with how he felt before the illness started – or how he is compared with others without a diagnosis of schizophrenia.

“We still don’t cure schizophrenia; patients want to be normal,” he said. “We don’t make them normal with our medications, and medications don’t always work as expected. At the very least, when we talk about response and nonresponse, we need to be respectful of the patient’s point of view.”

The same calibration dilemma happens with the side effect burden from antipsychotics. While the side effect burden from current antipsychotics is much better than it used to be in the preclozapine era, patients are still likely to have to put up with a variety of bothersome side effects. Telling the patient: “You should be grateful, because it used to be a lot worse!” somehow doesn’t come across as helpful.

Factors affecting calibration of treatment include the acuity of the patient’s illness, duration of illness, relative engagement in the treatment process (meaning “our outcomes should be a lot better for patients who are engaged in our treatment, who come to treatment, than those who don’t,” he said), comorbidities that may limit efficacy, the clinician’s philosophy of treatment, and the patient’s access to “best practices” care.

Although all antipsychotics can be used for all phases of schizophrenia, Dr. Weiden cautioned that individual antipsychotics are not interchangeable. “There’s always some efficacy risk when changing from an antipsychotic known to be effective for an individual patient,” he said. “Control of psychotic symptoms is always important. If you work in an inpatient unit, there’s a lot of stress and a lot of drive toward rapid resolution of symptoms in a way that’s easy and a way that’s safe.”

Desirable characteristics of pharmacologic agents for immediate initiation of acute treatment, he continued, include rapid onset of action, low toxicity, availability in multiple routes of administration, ease of use, low potential for drug-drug interactions, and ease of crossover to an oral antipsychotic agent. However, managing the acute psychosis in an ER or hospital setting “isn’t all about the medication,” he said.

“It’s very traumatic to be held down. It’s humiliating. It’s disruptive. Yes, we need to hospitalize people when they’re unsafe, but a lot of nonpharmacologic things we do are very important and will reduce the risk of complications from medication.” These include reassuring the patient, making him or her physically comfortable, reducing triggers that may escalate the situation, contacting the family, and educating the staff about the treatment plan.

In his clinical opinion, the inpatient use of a haloperidol p.r.n. regimen often is unsound and unsafe. “Very often on an inpatient unit, the haloperidol p.r.n. orders are done separately from the standing orders,” Dr. Weiden explained. “So you’ll have a clinician do a careful evaluation and write the standing orders of the medication, but the p.r.n.s are kind of boilerplate, and they get Haldol. The brain cannot ‘tell’ the difference between a standing order and a p.r.n. order of haloperidol. It is dangerous; patients die from this. It’s not common to have a life-threatening reaction to p.r.n. haloperidol, but it’s not rare, either, and the automatic use of haloperidol p.r.n. certainly no longer meets any reasonable standard of safety.”

The same antipsychotic medication can be used acutely and in maintenance, Dr. Weiden said, but if the patient relapses, you might consider changing to another agent. “If you know the patient well, and you know that the last medicine helped keep the patient stable but they still have lots of symptoms and a pretty crummy life, you might want to consider that as an opportunity to change the medicine,” he said. ‘However, if the patient came in because they went out drinking with their buddies and they got intoxicated, you really should not change the medicine, because in this situation, it was not a pharmacologic failure of the medication regimen,” Dr. Weiden said. To change or not to change medication “is a really big issue for someone’s life trajectory.”

There are 12 Food and Drug Administration–approved atypical antipsychotics for schizophrenia, which can be overwhelming for clinicians who do not specialize in treating the disorder. “While these meds are not perfect, each of these can help some people who are not helped otherwise, and each of these has a different side effect profile,” Dr. Weiden said. “So while we can’t completely cure schizophrenia, we will have a lot more luck in getting a patient on a medication that is not too burdensome for them. The downside is that we don’t have any biologic predictors as to who will respond to what agent.”

Dr. Weiden said he thinks of recovery from schizophrenia as a process in which the choice of goals is decided primarily by the patient and guided by the clinician. “The good thing is, there’s no shortage of symptoms you can work on,” he said. “You don’t have to fix everything, but you and the patient should come together to goal-set and pick one or two that are the priorities. That will keep you from getting overwhelmed and burned out trying to ‘fix’ everything at once.”

Nonpharmacologic causes of persistent symptoms warrant investigation as well, such as substance comorbidities, medical comorbidities such as obstructive sleep apnea, treatment access barriers, and adherence challenges. While discontinuation of the medication class is not an option, “We have dose adjustment; we can substitute, go from one antipsychotic to another; we have route of delivery, you can add a new medication to the regimen, either within the class or a new class, and we can discontinue one or more medications from the current regimen,” Dr. Weiden said. “That is one strategy we often forget: getting the person off a medication that may be causing a problem.”

When positive symptoms persist, make sure that the patient’s current antipsychotic medicine is optimized. “The dose response of these different antipsychotics is not the same,” he said. “Some meds have a very steep dose response; others are more flat. How far you push may depend on the specific agent. You want to do what’s easy first. So raising the dose for persistent positive symptoms is a good idea, except if you think it’s behavioral toxicity.”

Switching to a new agent takes more work than changing the dose of a current agent. He characterized clozapine as “the anchor” for persistent positive symptoms. “No patient is clearly refractory of positive symptoms until they’ve either failed or refused clozapine,” he said. “Combining antipsychotics is not a substitute for clozapine. It’s a lot easier to do, but it’s not a substitute.

“Should the patient seem to have suboptimal response to a few first-line antipsychotics, it is important to tell the patient and family about clozapine even if you are not ready to recommend it right now. Likewise, it is crucial to inform all stakeholders about the suicide prevention indication of clozapine for any schizophrenia patient with any suicide history, even if the overall circumstances are not yet amenable to starting clozapine right away.”

During a separate presentation, Dr. Weiden encouraged meeting attendees to think about adherence to antipsychotics as not an outcome, but rather as an important mediator of outcome.

“As clinicians, we get stuck on [the notion of] ‘you’re not doing what I recommended,’ ” he said. One indirect consequence of adherence is poor information, which obscures assessment of treatment response, and also creates safety risks. When Dr. Weiden meets with patients for the first time, he tells them, “It’s very important that I know what you’re really doing, both in terms of your drugs and the drugs I’ve prescribed for you,” he said. “I make it safe for them. I say, ‘I may disagree, but I’m not going to get mad.’ I give them advance information about how I would respond, because different clinicians respond differently. Some take it personally and some don’t. I don’t take it personally.

“The other thing I say is that, ‘It’s not just about you’re obeying me, but it’s for your safety. It’s less safe if you don’t tell me.’ Safety is less pejorative than adherence.” Other strategies that can be used to track adherence include recommending long-acting therapies such as routine, supervision of oral therapy, and using pharmacy refill data. “Many patients don’t pick up their medications or don’t fill their prescriptions,” he said.

Gradual dose lowering is a feasible strategy, he said. “It can be successful, but not always. We have to advise patients that even brief medication gaps are a bad thing, but gradual dose lowering may be achievable and helpful.”

Dr. Weiden reported having numerous financial ties to the pharmaceutical industry, as well as being a stockholder of Delpor.

[email protected]

LAS VEGAS – Calibration of treatment response is a major challenge in patients with schizophrenia, according to Dr. Peter J. Weiden.

“On some level all of our patients with schizophrenia are both responders and nonresponders to medication at the same time,” Dr. Weiden said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “What I mean is that the vast majority of patients with schizophrenia have fewer symptoms on antipsychotic medication, but very few patients on medicine will be perfectly OK without any symptoms or problems.”

Dr. Weiden, professor of psychiatry at the University of Illinois at Chicago, went on to note that clinicians tend to calibrate medication response as the improvement in psychotic symptoms or stability, compared with how the person would be without medication. But the patient will not see it that way. Instead, the patient will calibrate how he is doing with medication, compared with how he felt before the illness started – or how he is compared with others without a diagnosis of schizophrenia.

“We still don’t cure schizophrenia; patients want to be normal,” he said. “We don’t make them normal with our medications, and medications don’t always work as expected. At the very least, when we talk about response and nonresponse, we need to be respectful of the patient’s point of view.”

The same calibration dilemma happens with the side effect burden from antipsychotics. While the side effect burden from current antipsychotics is much better than it used to be in the preclozapine era, patients are still likely to have to put up with a variety of bothersome side effects. Telling the patient: “You should be grateful, because it used to be a lot worse!” somehow doesn’t come across as helpful.

Factors affecting calibration of treatment include the acuity of the patient’s illness, duration of illness, relative engagement in the treatment process (meaning “our outcomes should be a lot better for patients who are engaged in our treatment, who come to treatment, than those who don’t,” he said), comorbidities that may limit efficacy, the clinician’s philosophy of treatment, and the patient’s access to “best practices” care.

Although all antipsychotics can be used for all phases of schizophrenia, Dr. Weiden cautioned that individual antipsychotics are not interchangeable. “There’s always some efficacy risk when changing from an antipsychotic known to be effective for an individual patient,” he said. “Control of psychotic symptoms is always important. If you work in an inpatient unit, there’s a lot of stress and a lot of drive toward rapid resolution of symptoms in a way that’s easy and a way that’s safe.”

Desirable characteristics of pharmacologic agents for immediate initiation of acute treatment, he continued, include rapid onset of action, low toxicity, availability in multiple routes of administration, ease of use, low potential for drug-drug interactions, and ease of crossover to an oral antipsychotic agent. However, managing the acute psychosis in an ER or hospital setting “isn’t all about the medication,” he said.

“It’s very traumatic to be held down. It’s humiliating. It’s disruptive. Yes, we need to hospitalize people when they’re unsafe, but a lot of nonpharmacologic things we do are very important and will reduce the risk of complications from medication.” These include reassuring the patient, making him or her physically comfortable, reducing triggers that may escalate the situation, contacting the family, and educating the staff about the treatment plan.

In his clinical opinion, the inpatient use of a haloperidol p.r.n. regimen often is unsound and unsafe. “Very often on an inpatient unit, the haloperidol p.r.n. orders are done separately from the standing orders,” Dr. Weiden explained. “So you’ll have a clinician do a careful evaluation and write the standing orders of the medication, but the p.r.n.s are kind of boilerplate, and they get Haldol. The brain cannot ‘tell’ the difference between a standing order and a p.r.n. order of haloperidol. It is dangerous; patients die from this. It’s not common to have a life-threatening reaction to p.r.n. haloperidol, but it’s not rare, either, and the automatic use of haloperidol p.r.n. certainly no longer meets any reasonable standard of safety.”

The same antipsychotic medication can be used acutely and in maintenance, Dr. Weiden said, but if the patient relapses, you might consider changing to another agent. “If you know the patient well, and you know that the last medicine helped keep the patient stable but they still have lots of symptoms and a pretty crummy life, you might want to consider that as an opportunity to change the medicine,” he said. ‘However, if the patient came in because they went out drinking with their buddies and they got intoxicated, you really should not change the medicine, because in this situation, it was not a pharmacologic failure of the medication regimen,” Dr. Weiden said. To change or not to change medication “is a really big issue for someone’s life trajectory.”

There are 12 Food and Drug Administration–approved atypical antipsychotics for schizophrenia, which can be overwhelming for clinicians who do not specialize in treating the disorder. “While these meds are not perfect, each of these can help some people who are not helped otherwise, and each of these has a different side effect profile,” Dr. Weiden said. “So while we can’t completely cure schizophrenia, we will have a lot more luck in getting a patient on a medication that is not too burdensome for them. The downside is that we don’t have any biologic predictors as to who will respond to what agent.”

Dr. Weiden said he thinks of recovery from schizophrenia as a process in which the choice of goals is decided primarily by the patient and guided by the clinician. “The good thing is, there’s no shortage of symptoms you can work on,” he said. “You don’t have to fix everything, but you and the patient should come together to goal-set and pick one or two that are the priorities. That will keep you from getting overwhelmed and burned out trying to ‘fix’ everything at once.”

Nonpharmacologic causes of persistent symptoms warrant investigation as well, such as substance comorbidities, medical comorbidities such as obstructive sleep apnea, treatment access barriers, and adherence challenges. While discontinuation of the medication class is not an option, “We have dose adjustment; we can substitute, go from one antipsychotic to another; we have route of delivery, you can add a new medication to the regimen, either within the class or a new class, and we can discontinue one or more medications from the current regimen,” Dr. Weiden said. “That is one strategy we often forget: getting the person off a medication that may be causing a problem.”

When positive symptoms persist, make sure that the patient’s current antipsychotic medicine is optimized. “The dose response of these different antipsychotics is not the same,” he said. “Some meds have a very steep dose response; others are more flat. How far you push may depend on the specific agent. You want to do what’s easy first. So raising the dose for persistent positive symptoms is a good idea, except if you think it’s behavioral toxicity.”

Switching to a new agent takes more work than changing the dose of a current agent. He characterized clozapine as “the anchor” for persistent positive symptoms. “No patient is clearly refractory of positive symptoms until they’ve either failed or refused clozapine,” he said. “Combining antipsychotics is not a substitute for clozapine. It’s a lot easier to do, but it’s not a substitute.

“Should the patient seem to have suboptimal response to a few first-line antipsychotics, it is important to tell the patient and family about clozapine even if you are not ready to recommend it right now. Likewise, it is crucial to inform all stakeholders about the suicide prevention indication of clozapine for any schizophrenia patient with any suicide history, even if the overall circumstances are not yet amenable to starting clozapine right away.”

During a separate presentation, Dr. Weiden encouraged meeting attendees to think about adherence to antipsychotics as not an outcome, but rather as an important mediator of outcome.

“As clinicians, we get stuck on [the notion of] ‘you’re not doing what I recommended,’ ” he said. One indirect consequence of adherence is poor information, which obscures assessment of treatment response, and also creates safety risks. When Dr. Weiden meets with patients for the first time, he tells them, “It’s very important that I know what you’re really doing, both in terms of your drugs and the drugs I’ve prescribed for you,” he said. “I make it safe for them. I say, ‘I may disagree, but I’m not going to get mad.’ I give them advance information about how I would respond, because different clinicians respond differently. Some take it personally and some don’t. I don’t take it personally.

“The other thing I say is that, ‘It’s not just about you’re obeying me, but it’s for your safety. It’s less safe if you don’t tell me.’ Safety is less pejorative than adherence.” Other strategies that can be used to track adherence include recommending long-acting therapies such as routine, supervision of oral therapy, and using pharmacy refill data. “Many patients don’t pick up their medications or don’t fill their prescriptions,” he said.

Gradual dose lowering is a feasible strategy, he said. “It can be successful, but not always. We have to advise patients that even brief medication gaps are a bad thing, but gradual dose lowering may be achievable and helpful.”

Dr. Weiden reported having numerous financial ties to the pharmaceutical industry, as well as being a stockholder of Delpor.

[email protected]

LAS VEGAS – The way Dr. Barry Eliot Cole sees it, one of the best things general psychiatrists can do to protect their patients and themselves is to stop writing prescriptions for opioids.

“Unless you have a fellowship in addiction or pain medicine, unless you’ve received specialized training in the management of noncancer pain, and unless you remain active in a national pain organization, as a general adult or child psychiatrist, I beg you: Please do not prescribe opioids any longer,” he said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “If you’re working in psycho-oncology or helping a hospice, or if you’ve decided you want to be a palliative medicine specialist, that’s wonderful. You are way ahead of the class.”

Key challenges in managing noncancer pain, he said, include the fact that patients have become sick from adverse events directly related to opioids, and 44 people in the United States die each day from overdose of prescription opioids.

“Like it or not, opioids are gateway drugs, just like marijuana, just like alcohol,” said Dr. Cole, a psychiatrist who practices in Las Vegas. “In many patients’ minds, the prescription opioids are fantastic. They’re predictable; they’re reliable.” Moreover, prescribing challenges are going up rapidly, documentation requirements “are getting outrageous,” and criminal prosecution – not malpractice claims – now awaits “bad faith” prescribers.

Serious adverse events from opioids can include respiratory depression/arrest/apnea, circulatory depression/hypotension/shock, seizures, and withdrawal/neonatal opioid withdrawal, and endocrine suppression.

“Starting opioid therapy is basically inducing menopause and andropause,” he said. “You ask yourself, what does it mean for a 30-year-old to start demineralizing their bones at age 30? What does it mean to accelerate their cardiovascular disease? What about the mood changes? Sexual performance changes? Difficulty with fertility? What are we doing about these kinds of people? What about the implications of immune suppression from use of opioids?”

According to data from the Centers for Disease Control and Prevention, among those who died from prescription opioid overdoses between 1999 and 2013, most were between the ages of 24 and 54, the majority were non-Hispanic whites, and more than half were men, but the mortality gap between men and women is closing. Key risk factors for opioid abuse and overdose identified by the CDC include obtaining overlapping prescriptions from multiple physicians and multiple pharmacies, living in a rural area and being part of a lower socioeconomic class, and taking high daily dosages.

“The definition of high dose has been falling like the stock market,” Dr. Cole said. “Five years ago, I would have said 200 mg of morphine equivalent a day. Now we’re talking about 50 mg of morphine equivalent a day. The proxy for a lot of this turns out to be a personal or family history of mental illness, or a personal or family history of some kind of an addiction.”

According to the Substance Abuse and Mental Health Services Administration (SAMHSA), more patients die from prescriptions of methadone than from any other prescription painkiller. “That’s fascinating because most insurance companies would love us to prescribe methadone,” said Dr. Cole, who served as executive director for the American Society of Pain Educators from 2004 to 2010. “It’s the least expensive opioid we can prescribe. The problem is, it’s the most toxic to prescribe. It screws up QT interval so we get all kinds of interesting corollaries.” The next most potentially lethal painkiller is morphine, followed by fentanyl, then oxycodone.

CDC data indicate that the amount of prescription painkillers prescribed and sold in the United States quadrupled from 1999 to 2013, yet there has not been an overall change in the amount of pain that Americans report. At the same time, SAMHSA data from 2005 through 2011 suggest that emergency department visits involving prescriptions for oxycodone and hydrocodone “are leveling off if not going down,” Dr. Cole said. “ED visits involving methadone and buprenorphine were never exponentially growing the way oxycodone and hydrocodone were.”

Buprenorphine, he continued, has a ceiling effect for respiratory depression but not analgesia, and has emerged as a frontline analgesic in the management of pain. It treats a broader array of pain phenotypes with less analgesic tolerance, and can be combined with other mu agonists. It also produces less constipation and causes less cognitive impairment, compared with other opioids (J Support Oncol. 2012;10[6]:209-19). “In addition, it does not adversely affect the HPA axis or cause hypogonadism, does not significantly prolong the QTc interval, and is safe and effective for the elderly,” Dr. Cole said. “Like methadone, you can use this in complete renal failure. Most opioids always have to be corrected for renal or hepatic failure.”

Current problems with opioid prescribing, he said, include the fact that the medication may fall into the hands of someone other than the intended patient, the wrong medication may be given for the situation, or the wrong dose or dose formulation may be used.

“We know that prescribing the lowest effective dose would be right, and we need to think about when to stop prescribing,” Dr. Cole said. “If you’ve gone to the dentist for a root canal, you probably take home 30 or 40 analgesic opioid tablets. You maybe took five or 10, but what did you do with the rest? Did you dispose of them in a responsible way? Or did you put them up in the medicine shelf, because you might need them 5 years from now? That’s what happens to a lot of these meds: they become long lived. They just don’t go away. We have to plan with people when we’re going to stop [opioid] treatment, how, and get into the discussion of how to store and dispose of opioids.”

He recommends a stepwise approach to the management of neuropathic pain (Pain. 2007;132[3]:237-51) and noted that many nonopioid agents – including anticonvulsants, antidepressants, antipsychotics, anxiolytics, and lithium – have a role in managing people with chronic pain conditions. For clinicians who elect to prescribe opioids, Dr. Cole recommends defining what the goals are and establishing an exit strategy, so you can say “in case this doesn’t work in 3-4 weeks, or whatever the time frame is, this is what we’re going to do. Discuss the risk-benefit ratio with the patient.”

The least amount of medicine should be prescribed for the shortest period possible. “Review the prescription monitoring program to make sure that no one else is prescribing besides you,” he advised. “It’s an ugly day in your life when you realize you’re one of a dozen people who are prescribing for a patient.”

Dr. Cole noted that there are several potential roles for psychiatrists looking to grow their practice without prescribing opioids, including helping to establish goals of care with colleagues in anesthesia and interventional radiology.

“You can help the decision-making capacity, because not everybody makes great decisions,” he said. “We can certainly identify anxious, depressed, and perhaps even psychotic people, who seemingly get by people in anesthesia, physical medicine and rehabilitation, and interventional radiology. Going a little further, we know how to use adjuvant medication. We can predict adverse events before they happen. Market yourself as being able to help identify at-risk people, either for adverse events from procedures or adverse events from opioid therapy, maybe supervising long-term recovery and negotiating goals for treatment. We need to think of risk as a moving target.”

Not all risk screening tools are the same, he said. The Diagnosis, Intractability, Risk, Efficacy (DIRE) tool, Opioid Risk Tool (ORT), and the Screener and Opioid Assessment for Patients with Pain (SOAPP) best address substance abuse potential among those being considered for long-term opioid therapy.

The Current Opioid Misuse Measure (COMM), the Prescription Drug Use Questionnaire (PDUQ), and the Pain Medication Questionnaire (PMQ) aim to capture the degree of medication misuse or aberrant behavior that characterizes a patient’s opioid use once opioids are started.

The Cut Down, Annoyed, Guilty, Eye-Opener/Adjusted to Include Drugs (CAGE/CAGE-AID); Drug Abuse Screening Test (DAST); PMQ; PDUQ; Car, Relax, Alone, Forget, Friends, Trouble (CRAFFT); Substance Abuse Subtle Screening Inventory (SASSI); and others are more suitable for assessing current alcohol and/or drug abuse than potential for such abuse.

“Don’t forget about urine drug testing,” Dr. Cole said. “Get past the dipstick to order more comprehensive testing if you really want to know what’s going on.”

In his opinion, the success of opioid treatment is indicated by activities such as getting up, showering, grooming, going for walks, and doing household chores. “It is not focusing on your pain intensity,” he said.

Dr. Cole reported that he was a consultant for Mundipharma in 2015.

[email protected]

LAS VEGAS – The way Dr. Barry Eliot Cole sees it, one of the best things general psychiatrists can do to protect their patients and themselves is to stop writing prescriptions for opioids.

“Unless you have a fellowship in addiction or pain medicine, unless you’ve received specialized training in the management of noncancer pain, and unless you remain active in a national pain organization, as a general adult or child psychiatrist, I beg you: Please do not prescribe opioids any longer,” he said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “If you’re working in psycho-oncology or helping a hospice, or if you’ve decided you want to be a palliative medicine specialist, that’s wonderful. You are way ahead of the class.”

Key challenges in managing noncancer pain, he said, include the fact that patients have become sick from adverse events directly related to opioids, and 44 people in the United States die each day from overdose of prescription opioids.

“Like it or not, opioids are gateway drugs, just like marijuana, just like alcohol,” said Dr. Cole, a psychiatrist who practices in Las Vegas. “In many patients’ minds, the prescription opioids are fantastic. They’re predictable; they’re reliable.” Moreover, prescribing challenges are going up rapidly, documentation requirements “are getting outrageous,” and criminal prosecution – not malpractice claims – now awaits “bad faith” prescribers.

Serious adverse events from opioids can include respiratory depression/arrest/apnea, circulatory depression/hypotension/shock, seizures, and withdrawal/neonatal opioid withdrawal, and endocrine suppression.

“Starting opioid therapy is basically inducing menopause and andropause,” he said. “You ask yourself, what does it mean for a 30-year-old to start demineralizing their bones at age 30? What does it mean to accelerate their cardiovascular disease? What about the mood changes? Sexual performance changes? Difficulty with fertility? What are we doing about these kinds of people? What about the implications of immune suppression from use of opioids?”

According to data from the Centers for Disease Control and Prevention, among those who died from prescription opioid overdoses between 1999 and 2013, most were between the ages of 24 and 54, the majority were non-Hispanic whites, and more than half were men, but the mortality gap between men and women is closing. Key risk factors for opioid abuse and overdose identified by the CDC include obtaining overlapping prescriptions from multiple physicians and multiple pharmacies, living in a rural area and being part of a lower socioeconomic class, and taking high daily dosages.

“The definition of high dose has been falling like the stock market,” Dr. Cole said. “Five years ago, I would have said 200 mg of morphine equivalent a day. Now we’re talking about 50 mg of morphine equivalent a day. The proxy for a lot of this turns out to be a personal or family history of mental illness, or a personal or family history of some kind of an addiction.”

According to the Substance Abuse and Mental Health Services Administration (SAMHSA), more patients die from prescriptions of methadone than from any other prescription painkiller. “That’s fascinating because most insurance companies would love us to prescribe methadone,” said Dr. Cole, who served as executive director for the American Society of Pain Educators from 2004 to 2010. “It’s the least expensive opioid we can prescribe. The problem is, it’s the most toxic to prescribe. It screws up QT interval so we get all kinds of interesting corollaries.” The next most potentially lethal painkiller is morphine, followed by fentanyl, then oxycodone.

CDC data indicate that the amount of prescription painkillers prescribed and sold in the United States quadrupled from 1999 to 2013, yet there has not been an overall change in the amount of pain that Americans report. At the same time, SAMHSA data from 2005 through 2011 suggest that emergency department visits involving prescriptions for oxycodone and hydrocodone “are leveling off if not going down,” Dr. Cole said. “ED visits involving methadone and buprenorphine were never exponentially growing the way oxycodone and hydrocodone were.”

Buprenorphine, he continued, has a ceiling effect for respiratory depression but not analgesia, and has emerged as a frontline analgesic in the management of pain. It treats a broader array of pain phenotypes with less analgesic tolerance, and can be combined with other mu agonists. It also produces less constipation and causes less cognitive impairment, compared with other opioids (J Support Oncol. 2012;10[6]:209-19). “In addition, it does not adversely affect the HPA axis or cause hypogonadism, does not significantly prolong the QTc interval, and is safe and effective for the elderly,” Dr. Cole said. “Like methadone, you can use this in complete renal failure. Most opioids always have to be corrected for renal or hepatic failure.”

Current problems with opioid prescribing, he said, include the fact that the medication may fall into the hands of someone other than the intended patient, the wrong medication may be given for the situation, or the wrong dose or dose formulation may be used.

“We know that prescribing the lowest effective dose would be right, and we need to think about when to stop prescribing,” Dr. Cole said. “If you’ve gone to the dentist for a root canal, you probably take home 30 or 40 analgesic opioid tablets. You maybe took five or 10, but what did you do with the rest? Did you dispose of them in a responsible way? Or did you put them up in the medicine shelf, because you might need them 5 years from now? That’s what happens to a lot of these meds: they become long lived. They just don’t go away. We have to plan with people when we’re going to stop [opioid] treatment, how, and get into the discussion of how to store and dispose of opioids.”

He recommends a stepwise approach to the management of neuropathic pain (Pain. 2007;132[3]:237-51) and noted that many nonopioid agents – including anticonvulsants, antidepressants, antipsychotics, anxiolytics, and lithium – have a role in managing people with chronic pain conditions. For clinicians who elect to prescribe opioids, Dr. Cole recommends defining what the goals are and establishing an exit strategy, so you can say “in case this doesn’t work in 3-4 weeks, or whatever the time frame is, this is what we’re going to do. Discuss the risk-benefit ratio with the patient.”

The least amount of medicine should be prescribed for the shortest period possible. “Review the prescription monitoring program to make sure that no one else is prescribing besides you,” he advised. “It’s an ugly day in your life when you realize you’re one of a dozen people who are prescribing for a patient.”

Dr. Cole noted that there are several potential roles for psychiatrists looking to grow their practice without prescribing opioids, including helping to establish goals of care with colleagues in anesthesia and interventional radiology.

“You can help the decision-making capacity, because not everybody makes great decisions,” he said. “We can certainly identify anxious, depressed, and perhaps even psychotic people, who seemingly get by people in anesthesia, physical medicine and rehabilitation, and interventional radiology. Going a little further, we know how to use adjuvant medication. We can predict adverse events before they happen. Market yourself as being able to help identify at-risk people, either for adverse events from procedures or adverse events from opioid therapy, maybe supervising long-term recovery and negotiating goals for treatment. We need to think of risk as a moving target.”

Not all risk screening tools are the same, he said. The Diagnosis, Intractability, Risk, Efficacy (DIRE) tool, Opioid Risk Tool (ORT), and the Screener and Opioid Assessment for Patients with Pain (SOAPP) best address substance abuse potential among those being considered for long-term opioid therapy.

The Current Opioid Misuse Measure (COMM), the Prescription Drug Use Questionnaire (PDUQ), and the Pain Medication Questionnaire (PMQ) aim to capture the degree of medication misuse or aberrant behavior that characterizes a patient’s opioid use once opioids are started.

The Cut Down, Annoyed, Guilty, Eye-Opener/Adjusted to Include Drugs (CAGE/CAGE-AID); Drug Abuse Screening Test (DAST); PMQ; PDUQ; Car, Relax, Alone, Forget, Friends, Trouble (CRAFFT); Substance Abuse Subtle Screening Inventory (SASSI); and others are more suitable for assessing current alcohol and/or drug abuse than potential for such abuse.

“Don’t forget about urine drug testing,” Dr. Cole said. “Get past the dipstick to order more comprehensive testing if you really want to know what’s going on.”

In his opinion, the success of opioid treatment is indicated by activities such as getting up, showering, grooming, going for walks, and doing household chores. “It is not focusing on your pain intensity,” he said.

Dr. Cole reported that he was a consultant for Mundipharma in 2015.

[email protected]

LAS VEGAS – The way Dr. Barry Eliot Cole sees it, one of the best things general psychiatrists can do to protect their patients and themselves is to stop writing prescriptions for opioids.

“Unless you have a fellowship in addiction or pain medicine, unless you’ve received specialized training in the management of noncancer pain, and unless you remain active in a national pain organization, as a general adult or child psychiatrist, I beg you: Please do not prescribe opioids any longer,” he said at the annual psychopharmacology update held by the Nevada Psychiatric Association. “If you’re working in psycho-oncology or helping a hospice, or if you’ve decided you want to be a palliative medicine specialist, that’s wonderful. You are way ahead of the class.”

Key challenges in managing noncancer pain, he said, include the fact that patients have become sick from adverse events directly related to opioids, and 44 people in the United States die each day from overdose of prescription opioids.

“Like it or not, opioids are gateway drugs, just like marijuana, just like alcohol,” said Dr. Cole, a psychiatrist who practices in Las Vegas. “In many patients’ minds, the prescription opioids are fantastic. They’re predictable; they’re reliable.” Moreover, prescribing challenges are going up rapidly, documentation requirements “are getting outrageous,” and criminal prosecution – not malpractice claims – now awaits “bad faith” prescribers.

Serious adverse events from opioids can include respiratory depression/arrest/apnea, circulatory depression/hypotension/shock, seizures, and withdrawal/neonatal opioid withdrawal, and endocrine suppression.

“Starting opioid therapy is basically inducing menopause and andropause,” he said. “You ask yourself, what does it mean for a 30-year-old to start demineralizing their bones at age 30? What does it mean to accelerate their cardiovascular disease? What about the mood changes? Sexual performance changes? Difficulty with fertility? What are we doing about these kinds of people? What about the implications of immune suppression from use of opioids?”

According to data from the Centers for Disease Control and Prevention, among those who died from prescription opioid overdoses between 1999 and 2013, most were between the ages of 24 and 54, the majority were non-Hispanic whites, and more than half were men, but the mortality gap between men and women is closing. Key risk factors for opioid abuse and overdose identified by the CDC include obtaining overlapping prescriptions from multiple physicians and multiple pharmacies, living in a rural area and being part of a lower socioeconomic class, and taking high daily dosages.

“The definition of high dose has been falling like the stock market,” Dr. Cole said. “Five years ago, I would have said 200 mg of morphine equivalent a day. Now we’re talking about 50 mg of morphine equivalent a day. The proxy for a lot of this turns out to be a personal or family history of mental illness, or a personal or family history of some kind of an addiction.”

According to the Substance Abuse and Mental Health Services Administration (SAMHSA), more patients die from prescriptions of methadone than from any other prescription painkiller. “That’s fascinating because most insurance companies would love us to prescribe methadone,” said Dr. Cole, who served as executive director for the American Society of Pain Educators from 2004 to 2010. “It’s the least expensive opioid we can prescribe. The problem is, it’s the most toxic to prescribe. It screws up QT interval so we get all kinds of interesting corollaries.” The next most potentially lethal painkiller is morphine, followed by fentanyl, then oxycodone.

CDC data indicate that the amount of prescription painkillers prescribed and sold in the United States quadrupled from 1999 to 2013, yet there has not been an overall change in the amount of pain that Americans report. At the same time, SAMHSA data from 2005 through 2011 suggest that emergency department visits involving prescriptions for oxycodone and hydrocodone “are leveling off if not going down,” Dr. Cole said. “ED visits involving methadone and buprenorphine were never exponentially growing the way oxycodone and hydrocodone were.”

Buprenorphine, he continued, has a ceiling effect for respiratory depression but not analgesia, and has emerged as a frontline analgesic in the management of pain. It treats a broader array of pain phenotypes with less analgesic tolerance, and can be combined with other mu agonists. It also produces less constipation and causes less cognitive impairment, compared with other opioids (J Support Oncol. 2012;10[6]:209-19). “In addition, it does not adversely affect the HPA axis or cause hypogonadism, does not significantly prolong the QTc interval, and is safe and effective for the elderly,” Dr. Cole said. “Like methadone, you can use this in complete renal failure. Most opioids always have to be corrected for renal or hepatic failure.”

Current problems with opioid prescribing, he said, include the fact that the medication may fall into the hands of someone other than the intended patient, the wrong medication may be given for the situation, or the wrong dose or dose formulation may be used.

“We know that prescribing the lowest effective dose would be right, and we need to think about when to stop prescribing,” Dr. Cole said. “If you’ve gone to the dentist for a root canal, you probably take home 30 or 40 analgesic opioid tablets. You maybe took five or 10, but what did you do with the rest? Did you dispose of them in a responsible way? Or did you put them up in the medicine shelf, because you might need them 5 years from now? That’s what happens to a lot of these meds: they become long lived. They just don’t go away. We have to plan with people when we’re going to stop [opioid] treatment, how, and get into the discussion of how to store and dispose of opioids.”

He recommends a stepwise approach to the management of neuropathic pain (Pain. 2007;132[3]:237-51) and noted that many nonopioid agents – including anticonvulsants, antidepressants, antipsychotics, anxiolytics, and lithium – have a role in managing people with chronic pain conditions. For clinicians who elect to prescribe opioids, Dr. Cole recommends defining what the goals are and establishing an exit strategy, so you can say “in case this doesn’t work in 3-4 weeks, or whatever the time frame is, this is what we’re going to do. Discuss the risk-benefit ratio with the patient.”

The least amount of medicine should be prescribed for the shortest period possible. “Review the prescription monitoring program to make sure that no one else is prescribing besides you,” he advised. “It’s an ugly day in your life when you realize you’re one of a dozen people who are prescribing for a patient.”

Dr. Cole noted that there are several potential roles for psychiatrists looking to grow their practice without prescribing opioids, including helping to establish goals of care with colleagues in anesthesia and interventional radiology.

“You can help the decision-making capacity, because not everybody makes great decisions,” he said. “We can certainly identify anxious, depressed, and perhaps even psychotic people, who seemingly get by people in anesthesia, physical medicine and rehabilitation, and interventional radiology. Going a little further, we know how to use adjuvant medication. We can predict adverse events before they happen. Market yourself as being able to help identify at-risk people, either for adverse events from procedures or adverse events from opioid therapy, maybe supervising long-term recovery and negotiating goals for treatment. We need to think of risk as a moving target.”

Not all risk screening tools are the same, he said. The Diagnosis, Intractability, Risk, Efficacy (DIRE) tool, Opioid Risk Tool (ORT), and the Screener and Opioid Assessment for Patients with Pain (SOAPP) best address substance abuse potential among those being considered for long-term opioid therapy.

The Current Opioid Misuse Measure (COMM), the Prescription Drug Use Questionnaire (PDUQ), and the Pain Medication Questionnaire (PMQ) aim to capture the degree of medication misuse or aberrant behavior that characterizes a patient’s opioid use once opioids are started.

The Cut Down, Annoyed, Guilty, Eye-Opener/Adjusted to Include Drugs (CAGE/CAGE-AID); Drug Abuse Screening Test (DAST); PMQ; PDUQ; Car, Relax, Alone, Forget, Friends, Trouble (CRAFFT); Substance Abuse Subtle Screening Inventory (SASSI); and others are more suitable for assessing current alcohol and/or drug abuse than potential for such abuse.

“Don’t forget about urine drug testing,” Dr. Cole said. “Get past the dipstick to order more comprehensive testing if you really want to know what’s going on.”

In his opinion, the success of opioid treatment is indicated by activities such as getting up, showering, grooming, going for walks, and doing household chores. “It is not focusing on your pain intensity,” he said.

Dr. Cole reported that he was a consultant for Mundipharma in 2015.

[email protected]

PHOENIX – In the clinical opinion of Dr. Nevin M. Katz, caring for critical care patients after cardiothoracic surgery requires a multidisciplinary team.

“It used to be just the surgeons and the residents and anesthesiologists, but in this era, it’s a broad team,” Dr. Katz said at the annual meeting of the Society of Thoracic Surgeons. “Coordination of the team, which includes surgeons, anesthesiologists, physician assistants, bedside nurses, nurse practitioners, perfusionists, pharmacists, respiratory therapists, and nutritionists is very important, and it’s important that members of the team be on the same page.”

Dr. Katz, a cardiovascular surgeon/intensivist at Johns Hopkins University, Baltimore, went on to offer tips for managing right ventricular failure in cardiac surgical patients. He recommends that clinicians consider five basic parameters of hemodynamic management: the heart rate and rhythm; the preload; the afterload; contractility; and the surgical result, including the potential for an anatomic problem and the risk of cardiac tamponade. “One must also consider a cardiac assist device,” he said.

He recommended that the cardiac index goal for cardiovascular patients in the ICU be in the range of 2.2-4.4 L per min/m². The recommended hemodynamic goals also included systemic blood pressure ranges with a systolic pressure of 90-140 mm Hg and a mean arterial pressure of 70-90 mm Hg; a left arterial pressure or pulmonary capillary wedge pressure of 5-18 mm Hg, a right arterial pressure or central venous pressure of 5-15 mm Hg, and a systemic vascular resistance of 800-1,200 dynes per sec/cm⁵. “When treating right ventricular failure or complex patients, I think advanced PA [pulmonary artery] catheters are valuable, although they’re not absolutely necessary,” he said.

Complementary technologies available in most ICUs can help clinicians manage these patients, particularly ultrasound. With ultrasound, “we can determine where the patient is on the ventricular function curve, regional versus global dysfunction, right ventricular versus left ventricular dysfunction, valve dysfunction, and cardiac tamponade,” said Dr. Katz, who also created the Foundation for the Advancement of Cardiothoracic Care, also known as FACTS-Care. “It’s a very important monitoring modality.”

An important goal in managing patients with right ventricular failure is to establish an optimal heart rate and rhythm. “We have modalities to treat bradycardia and heart block,” he said. “Loss of atrial contraction is very important. If we can avoid atrial fibrillation, that’s good. Ventricular arrhythmias can be a problem, and nowadays we can treat atrioventricular and ventricular dyssynchrony.”

Optimal preload requires a focus on volume responsiveness, Dr. Katz continued. “Where is the patient on that ventricular function curve?” he asked. “With the advanced PA catheters, there are ways to look at that. You would like to be on the ascending part of that curve.” Clinicians can also use pulsus paradoxus, a variation of systemic arterial pulse volume. “That will indicate that perhaps you’re low in volume, but you can use stroke volume variation with an advanced PA catheter,” he said. “If your stroke volume variation is greater than 15% you’re on the ascending part of the curve. But if your stroke volume variation is less than 15%, your volume is probably optimal and you’re not going to be volume responsive.”

Clinicians who lack the benefit of an advanced PA catheter can assess volume responsiveness with passive leg raising.

Low preload causes of RV failure include hypovolemia, bleeding, third-spacing, high urine output, and cardiac tamponade. High preload can be a problem, too, from excess fluid administration, tricuspid or pulmonary valve regurgitation, or from left to right shunting.

Overall, optimal management of RV failure depends on the coordination of the multidisciplinary critical care team.

Dr. Katz reported having no financial disclosures.

[email protected]

PHOENIX – In the clinical opinion of Dr. Nevin M. Katz, caring for critical care patients after cardiothoracic surgery requires a multidisciplinary team.

“It used to be just the surgeons and the residents and anesthesiologists, but in this era, it’s a broad team,” Dr. Katz said at the annual meeting of the Society of Thoracic Surgeons. “Coordination of the team, which includes surgeons, anesthesiologists, physician assistants, bedside nurses, nurse practitioners, perfusionists, pharmacists, respiratory therapists, and nutritionists is very important, and it’s important that members of the team be on the same page.”

Dr. Katz, a cardiovascular surgeon/intensivist at Johns Hopkins University, Baltimore, went on to offer tips for managing right ventricular failure in cardiac surgical patients. He recommends that clinicians consider five basic parameters of hemodynamic management: the heart rate and rhythm; the preload; the afterload; contractility; and the surgical result, including the potential for an anatomic problem and the risk of cardiac tamponade. “One must also consider a cardiac assist device,” he said.

He recommended that the cardiac index goal for cardiovascular patients in the ICU be in the range of 2.2-4.4 L per min/m². The recommended hemodynamic goals also included systemic blood pressure ranges with a systolic pressure of 90-140 mm Hg and a mean arterial pressure of 70-90 mm Hg; a left arterial pressure or pulmonary capillary wedge pressure of 5-18 mm Hg, a right arterial pressure or central venous pressure of 5-15 mm Hg, and a systemic vascular resistance of 800-1,200 dynes per sec/cm⁵. “When treating right ventricular failure or complex patients, I think advanced PA [pulmonary artery] catheters are valuable, although they’re not absolutely necessary,” he said.

Complementary technologies available in most ICUs can help clinicians manage these patients, particularly ultrasound. With ultrasound, “we can determine where the patient is on the ventricular function curve, regional versus global dysfunction, right ventricular versus left ventricular dysfunction, valve dysfunction, and cardiac tamponade,” said Dr. Katz, who also created the Foundation for the Advancement of Cardiothoracic Care, also known as FACTS-Care. “It’s a very important monitoring modality.”

An important goal in managing patients with right ventricular failure is to establish an optimal heart rate and rhythm. “We have modalities to treat bradycardia and heart block,” he said. “Loss of atrial contraction is very important. If we can avoid atrial fibrillation, that’s good. Ventricular arrhythmias can be a problem, and nowadays we can treat atrioventricular and ventricular dyssynchrony.”

Optimal preload requires a focus on volume responsiveness, Dr. Katz continued. “Where is the patient on that ventricular function curve?” he asked. “With the advanced PA catheters, there are ways to look at that. You would like to be on the ascending part of that curve.” Clinicians can also use pulsus paradoxus, a variation of systemic arterial pulse volume. “That will indicate that perhaps you’re low in volume, but you can use stroke volume variation with an advanced PA catheter,” he said. “If your stroke volume variation is greater than 15% you’re on the ascending part of the curve. But if your stroke volume variation is less than 15%, your volume is probably optimal and you’re not going to be volume responsive.”

Clinicians who lack the benefit of an advanced PA catheter can assess volume responsiveness with passive leg raising.

Low preload causes of RV failure include hypovolemia, bleeding, third-spacing, high urine output, and cardiac tamponade. High preload can be a problem, too, from excess fluid administration, tricuspid or pulmonary valve regurgitation, or from left to right shunting.

Overall, optimal management of RV failure depends on the coordination of the multidisciplinary critical care team.

Dr. Katz reported having no financial disclosures.

[email protected]

PHOENIX – In the clinical opinion of Dr. Nevin M. Katz, caring for critical care patients after cardiothoracic surgery requires a multidisciplinary team.

“It used to be just the surgeons and the residents and anesthesiologists, but in this era, it’s a broad team,” Dr. Katz said at the annual meeting of the Society of Thoracic Surgeons. “Coordination of the team, which includes surgeons, anesthesiologists, physician assistants, bedside nurses, nurse practitioners, perfusionists, pharmacists, respiratory therapists, and nutritionists is very important, and it’s important that members of the team be on the same page.”

Dr. Katz, a cardiovascular surgeon/intensivist at Johns Hopkins University, Baltimore, went on to offer tips for managing right ventricular failure in cardiac surgical patients. He recommends that clinicians consider five basic parameters of hemodynamic management: the heart rate and rhythm; the preload; the afterload; contractility; and the surgical result, including the potential for an anatomic problem and the risk of cardiac tamponade. “One must also consider a cardiac assist device,” he said.

He recommended that the cardiac index goal for cardiovascular patients in the ICU be in the range of 2.2-4.4 L per min/m². The recommended hemodynamic goals also included systemic blood pressure ranges with a systolic pressure of 90-140 mm Hg and a mean arterial pressure of 70-90 mm Hg; a left arterial pressure or pulmonary capillary wedge pressure of 5-18 mm Hg, a right arterial pressure or central venous pressure of 5-15 mm Hg, and a systemic vascular resistance of 800-1,200 dynes per sec/cm⁵. “When treating right ventricular failure or complex patients, I think advanced PA [pulmonary artery] catheters are valuable, although they’re not absolutely necessary,” he said.

Complementary technologies available in most ICUs can help clinicians manage these patients, particularly ultrasound. With ultrasound, “we can determine where the patient is on the ventricular function curve, regional versus global dysfunction, right ventricular versus left ventricular dysfunction, valve dysfunction, and cardiac tamponade,” said Dr. Katz, who also created the Foundation for the Advancement of Cardiothoracic Care, also known as FACTS-Care. “It’s a very important monitoring modality.”

An important goal in managing patients with right ventricular failure is to establish an optimal heart rate and rhythm. “We have modalities to treat bradycardia and heart block,” he said. “Loss of atrial contraction is very important. If we can avoid atrial fibrillation, that’s good. Ventricular arrhythmias can be a problem, and nowadays we can treat atrioventricular and ventricular dyssynchrony.”

Optimal preload requires a focus on volume responsiveness, Dr. Katz continued. “Where is the patient on that ventricular function curve?” he asked. “With the advanced PA catheters, there are ways to look at that. You would like to be on the ascending part of that curve.” Clinicians can also use pulsus paradoxus, a variation of systemic arterial pulse volume. “That will indicate that perhaps you’re low in volume, but you can use stroke volume variation with an advanced PA catheter,” he said. “If your stroke volume variation is greater than 15% you’re on the ascending part of the curve. But if your stroke volume variation is less than 15%, your volume is probably optimal and you’re not going to be volume responsive.”

Clinicians who lack the benefit of an advanced PA catheter can assess volume responsiveness with passive leg raising.

Low preload causes of RV failure include hypovolemia, bleeding, third-spacing, high urine output, and cardiac tamponade. High preload can be a problem, too, from excess fluid administration, tricuspid or pulmonary valve regurgitation, or from left to right shunting.

Overall, optimal management of RV failure depends on the coordination of the multidisciplinary critical care team.

Dr. Katz reported having no financial disclosures.

[email protected]

PHOENIX – Patients with a history of head and neck, lung, bladder, and hematologic malignancies had increased rates of subsequent non–small cell lung cancer (NSCLC), a large analysis of national data found.

“It is unclear to what extent the higher rate of primary NSCLC in these patients may be attributed to smoking, previous cancer history, or other lung cancer risk factors,” researchers led by Dr. Geena Wu wrote in an abstract presented during a poster session at the annual meeting of the Society of Thoracic Surgeons. “Further research using individual smoking data may better delineate who is at increased risk of NSCLC based on prior cancer site and smoking history.”

Doug Brunk/Frontline Medical News

In a study that Dr. Wu led during a research fellowship at the City of Hope National Medical Center, Duarte, Calif., she and her associates used the Surveillance, Epidemiology, and End Results (SEER) 1992-2007 dataset to identify 32,058 patients with a prior malignancy who subsequently developed primary lung cancer at 6 months or more after their initial cancer. They calculated standardized incidence ratios (SIRs) for NSCLC as a rate of observed to expected NSCLC cases adjusted by person-years at risk, age, gender, and time of diagnosis.

The researchers found that patients with a history of the following cancers had higher rates of second primary NSCLC than expected: head and neck (SIR, 4.00), colon and rectum (SIR, 1.16), pancreas (SIR, 1.44), lung (SIR, 4.88), bladder (SIR, 1.97), kidney (SIR, 1.21), breast (SIR, 1.09), and leukemia or lymphoma (SIR, 1.40).

At the same time, patients with a history of pancreatic or breast cancer who were treated with radiation had a higher incidence of second primary NSCLC (SIR of 2.54 and SIR of 1.14, respectively), while those who were not treated with radiation did not.

Although the SEER database does not contain information about patient smoking history, the researchers evaluated adult smoking rates by state by using a national map from the Centers for Disease Control and Prevention’s 2013 Behavioral Risk Factor Surveillance System. Smoking rates were low (defined as 13.7% or less) in California, Hawaii, and Utah, and were higher in all other states, especially in Southeastern states. Dr. Wu and her associates found that patients from high smoking areas who had previous cancers of the colon and rectum, pancreas, kidney, thyroid, and breast had higher rates of a primary NSCLC, while those from low smoking areas did not. Interestingly, patients from high smoking areas who previously had uterine cancer, prostate, or melanoma had did not have higher rates of a primary NSCLC.

“Just because someone has a previous history of cancer, they’re not necessarily at increased risk of a second lung cancer,” Dr. Wu, who is now a fourth-year general surgery resident at Maricopa County Hospital in Phoenix said in an interview at the meeting. “You have to look at what kind of cancer they had and what their smoking history is – whether or not they continue to smoke, because smoking is such an important risk factor.”

Another limitation of the SEER database is that it lacks details about the type of chemotherapy patients receive, “so whether or not chemotherapy plays an impact in the elevated risk of lung cancer we can’t say.”

Dr. Wu reported having no financial disclosures.

[email protected]

PHOENIX – Patients with a history of head and neck, lung, bladder, and hematologic malignancies had increased rates of subsequent non–small cell lung cancer (NSCLC), a large analysis of national data found.

“It is unclear to what extent the higher rate of primary NSCLC in these patients may be attributed to smoking, previous cancer history, or other lung cancer risk factors,” researchers led by Dr. Geena Wu wrote in an abstract presented during a poster session at the annual meeting of the Society of Thoracic Surgeons. “Further research using individual smoking data may better delineate who is at increased risk of NSCLC based on prior cancer site and smoking history.”

Doug Brunk/Frontline Medical News

In a study that Dr. Wu led during a research fellowship at the City of Hope National Medical Center, Duarte, Calif., she and her associates used the Surveillance, Epidemiology, and End Results (SEER) 1992-2007 dataset to identify 32,058 patients with a prior malignancy who subsequently developed primary lung cancer at 6 months or more after their initial cancer. They calculated standardized incidence ratios (SIRs) for NSCLC as a rate of observed to expected NSCLC cases adjusted by person-years at risk, age, gender, and time of diagnosis.

The researchers found that patients with a history of the following cancers had higher rates of second primary NSCLC than expected: head and neck (SIR, 4.00), colon and rectum (SIR, 1.16), pancreas (SIR, 1.44), lung (SIR, 4.88), bladder (SIR, 1.97), kidney (SIR, 1.21), breast (SIR, 1.09), and leukemia or lymphoma (SIR, 1.40).

At the same time, patients with a history of pancreatic or breast cancer who were treated with radiation had a higher incidence of second primary NSCLC (SIR of 2.54 and SIR of 1.14, respectively), while those who were not treated with radiation did not.

Although the SEER database does not contain information about patient smoking history, the researchers evaluated adult smoking rates by state by using a national map from the Centers for Disease Control and Prevention’s 2013 Behavioral Risk Factor Surveillance System. Smoking rates were low (defined as 13.7% or less) in California, Hawaii, and Utah, and were higher in all other states, especially in Southeastern states. Dr. Wu and her associates found that patients from high smoking areas who had previous cancers of the colon and rectum, pancreas, kidney, thyroid, and breast had higher rates of a primary NSCLC, while those from low smoking areas did not. Interestingly, patients from high smoking areas who previously had uterine cancer, prostate, or melanoma had did not have higher rates of a primary NSCLC.

“Just because someone has a previous history of cancer, they’re not necessarily at increased risk of a second lung cancer,” Dr. Wu, who is now a fourth-year general surgery resident at Maricopa County Hospital in Phoenix said in an interview at the meeting. “You have to look at what kind of cancer they had and what their smoking history is – whether or not they continue to smoke, because smoking is such an important risk factor.”

Another limitation of the SEER database is that it lacks details about the type of chemotherapy patients receive, “so whether or not chemotherapy plays an impact in the elevated risk of lung cancer we can’t say.”

Dr. Wu reported having no financial disclosures.

[email protected]

PHOENIX – Patients with a history of head and neck, lung, bladder, and hematologic malignancies had increased rates of subsequent non–small cell lung cancer (NSCLC), a large analysis of national data found.

“It is unclear to what extent the higher rate of primary NSCLC in these patients may be attributed to smoking, previous cancer history, or other lung cancer risk factors,” researchers led by Dr. Geena Wu wrote in an abstract presented during a poster session at the annual meeting of the Society of Thoracic Surgeons. “Further research using individual smoking data may better delineate who is at increased risk of NSCLC based on prior cancer site and smoking history.”

Doug Brunk/Frontline Medical News

In a study that Dr. Wu led during a research fellowship at the City of Hope National Medical Center, Duarte, Calif., she and her associates used the Surveillance, Epidemiology, and End Results (SEER) 1992-2007 dataset to identify 32,058 patients with a prior malignancy who subsequently developed primary lung cancer at 6 months or more after their initial cancer. They calculated standardized incidence ratios (SIRs) for NSCLC as a rate of observed to expected NSCLC cases adjusted by person-years at risk, age, gender, and time of diagnosis.

The researchers found that patients with a history of the following cancers had higher rates of second primary NSCLC than expected: head and neck (SIR, 4.00), colon and rectum (SIR, 1.16), pancreas (SIR, 1.44), lung (SIR, 4.88), bladder (SIR, 1.97), kidney (SIR, 1.21), breast (SIR, 1.09), and leukemia or lymphoma (SIR, 1.40).

At the same time, patients with a history of pancreatic or breast cancer who were treated with radiation had a higher incidence of second primary NSCLC (SIR of 2.54 and SIR of 1.14, respectively), while those who were not treated with radiation did not.

Although the SEER database does not contain information about patient smoking history, the researchers evaluated adult smoking rates by state by using a national map from the Centers for Disease Control and Prevention’s 2013 Behavioral Risk Factor Surveillance System. Smoking rates were low (defined as 13.7% or less) in California, Hawaii, and Utah, and were higher in all other states, especially in Southeastern states. Dr. Wu and her associates found that patients from high smoking areas who had previous cancers of the colon and rectum, pancreas, kidney, thyroid, and breast had higher rates of a primary NSCLC, while those from low smoking areas did not. Interestingly, patients from high smoking areas who previously had uterine cancer, prostate, or melanoma had did not have higher rates of a primary NSCLC.

“Just because someone has a previous history of cancer, they’re not necessarily at increased risk of a second lung cancer,” Dr. Wu, who is now a fourth-year general surgery resident at Maricopa County Hospital in Phoenix said in an interview at the meeting. “You have to look at what kind of cancer they had and what their smoking history is – whether or not they continue to smoke, because smoking is such an important risk factor.”

Another limitation of the SEER database is that it lacks details about the type of chemotherapy patients receive, “so whether or not chemotherapy plays an impact in the elevated risk of lung cancer we can’t say.”

Dr. Wu reported having no financial disclosures.

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