Current Psychiatry

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Although many states have substantial health services in urban areas, these services—particularly mental health care—are relatively scarce in rural areas.¹ Telepsychiatry, in which clinicians provide mental health care from a distance in real time by using interactive, 2-way, audio-video communication (videoconferencing), could mitigate workforce shortages that affect remote and underserved areas.² Psychiatry is one of the biggest users of telemedicine, which refers to any combination of communication technology and medicine.^3-5 This article discusses telepsychiatry’s effectiveness in providing psychiatric diagnosis and treatment, and the clinical implications of this technology, including improving access, cost, and quality of mental health services.

Outcomes comparable to face-to-face care

Telepsychiatry is used primarily in rural areas or correctional institutions or with underserved populations such as veterans with posttraumatic stress disorder or children. Although the literature generally is weak, there has been more research on psychiatry than other medical specialties because psychiatric clinicians rely on mental status examinations and verbal communications, not physical exams. Telepsychiatry can be considered a part of an evolving “connected health” system that offers many benefits to patients and clinicians (Table).

Table

Benefits of telepsychiatry as part of a ‘connected health’ system

Barriers to implementation

Although telepsychiatry offers tremendous promise, implementation has not been widespread or easy. Potential barriers to implementation, such as cost and resistance to change, are associated with acceptance of new technology or practice in health care. In addition, there are several legal, regulatory, and technical barriers.

Institutional barriers. Physicians and other providers may not have access to timely, evidence-based information and may face challenges, such as time constraints, access to technical support, and complexity of large health care institutions, when integrating this information into clinical practice.¹⁶ Two studies¹⁷ found that after controlling for other barriers—eg, reimbursement and regulatory issues—providers are the most significant initial gatekeepers that affect telemedicine use. When designing a telemedicine system, project managers should prioritize providers’ needs, such as ease of use and incentives.¹⁸

States do not cover services provided by other mental health providers, except for Utah’s coverage for social workers. The American Psychiatric Association has 2 suggestions regarding this issue³:

• reimbursement for telepsychiatry services should follow customary charges for delivering the appropriate current procedural terminology code(s)
  
• a structure for reimbursement of collateral charges, such as technician and line time, should be identified.
  

Licensure. A physician conducting a telemedicine session with a patient in another state must be licensed in both his or her state and the patient’s state. Nurses and other allied health professionals have similar state licensing constraints. Sanders²² suggests 3 potential solutions:

• establishing a national licensing system
  
• assigning the responsibility of care to the referring physician, with the consulting physician’s opinion serving as “recommendation only”
  
• determining that the patient is being “electronically transmitted” to the consultant’s state.
  

Box

Individual states also have developed funding streams to support telemedicine. The Centers for Medicare and Medicaid Services will pay a facility site fee to the host site (where the patient is located), but only if the site is in a rural area. Providers can charge patients a fee to support telepsychiatry infrastructure and maintenance, but typically this arrangement is not affordable and is not standard practice.

The future

Telepsychiatry’s ability to improve access to mental health care to underserved populations is becoming more evident. Technology is adequate for most uses and is constantly advancing. Numerous applications already have been defined, and more are ripe for exploration. Barriers to implementation are primarily of the human variety and will require a combination of consumer, provider, and governmental advocacy to overcome.

Related Resources

• American Telemedicine Association. www.americantelemed.org.
  
• International Society for Telemedicine & eHealth. www.isfteh.org.
  
• American Psychiatric Association. Telepsychiatry internet resources. www.psychiatry.org/practice/professional-interests/underserved-communities/telepsychiatry-internet-resources.
  
• Mossman D. Practicing psychiatry via Skype: Medicolegal considerations. Current Psychiatry. 2011;10(12):30-32,39.
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Although many states have substantial health services in urban areas, these services—particularly mental health care—are relatively scarce in rural areas.¹ Telepsychiatry, in which clinicians provide mental health care from a distance in real time by using interactive, 2-way, audio-video communication (videoconferencing), could mitigate workforce shortages that affect remote and underserved areas.² Psychiatry is one of the biggest users of telemedicine, which refers to any combination of communication technology and medicine.^3-5 This article discusses telepsychiatry’s effectiveness in providing psychiatric diagnosis and treatment, and the clinical implications of this technology, including improving access, cost, and quality of mental health services.

Outcomes comparable to face-to-face care

Telepsychiatry is used primarily in rural areas or correctional institutions or with underserved populations such as veterans with posttraumatic stress disorder or children. Although the literature generally is weak, there has been more research on psychiatry than other medical specialties because psychiatric clinicians rely on mental status examinations and verbal communications, not physical exams. Telepsychiatry can be considered a part of an evolving “connected health” system that offers many benefits to patients and clinicians (Table).

Table

Benefits of telepsychiatry as part of a ‘connected health’ system

Barriers to implementation

Although telepsychiatry offers tremendous promise, implementation has not been widespread or easy. Potential barriers to implementation, such as cost and resistance to change, are associated with acceptance of new technology or practice in health care. In addition, there are several legal, regulatory, and technical barriers.

Institutional barriers. Physicians and other providers may not have access to timely, evidence-based information and may face challenges, such as time constraints, access to technical support, and complexity of large health care institutions, when integrating this information into clinical practice.¹⁶ Two studies¹⁷ found that after controlling for other barriers—eg, reimbursement and regulatory issues—providers are the most significant initial gatekeepers that affect telemedicine use. When designing a telemedicine system, project managers should prioritize providers’ needs, such as ease of use and incentives.¹⁸

States do not cover services provided by other mental health providers, except for Utah’s coverage for social workers. The American Psychiatric Association has 2 suggestions regarding this issue³:

• reimbursement for telepsychiatry services should follow customary charges for delivering the appropriate current procedural terminology code(s)
  
• a structure for reimbursement of collateral charges, such as technician and line time, should be identified.
  

Licensure. A physician conducting a telemedicine session with a patient in another state must be licensed in both his or her state and the patient’s state. Nurses and other allied health professionals have similar state licensing constraints. Sanders²² suggests 3 potential solutions:

• establishing a national licensing system
  
• assigning the responsibility of care to the referring physician, with the consulting physician’s opinion serving as “recommendation only”
  
• determining that the patient is being “electronically transmitted” to the consultant’s state.
  

Box

Individual states also have developed funding streams to support telemedicine. The Centers for Medicare and Medicaid Services will pay a facility site fee to the host site (where the patient is located), but only if the site is in a rural area. Providers can charge patients a fee to support telepsychiatry infrastructure and maintenance, but typically this arrangement is not affordable and is not standard practice.

The future

Telepsychiatry’s ability to improve access to mental health care to underserved populations is becoming more evident. Technology is adequate for most uses and is constantly advancing. Numerous applications already have been defined, and more are ripe for exploration. Barriers to implementation are primarily of the human variety and will require a combination of consumer, provider, and governmental advocacy to overcome.

Related Resources

• American Telemedicine Association. www.americantelemed.org.
  
• International Society for Telemedicine & eHealth. www.isfteh.org.
  
• American Psychiatric Association. Telepsychiatry internet resources. www.psychiatry.org/practice/professional-interests/underserved-communities/telepsychiatry-internet-resources.
  
• Mossman D. Practicing psychiatry via Skype: Medicolegal considerations. Current Psychiatry. 2011;10(12):30-32,39.
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Although many states have substantial health services in urban areas, these services—particularly mental health care—are relatively scarce in rural areas.¹ Telepsychiatry, in which clinicians provide mental health care from a distance in real time by using interactive, 2-way, audio-video communication (videoconferencing), could mitigate workforce shortages that affect remote and underserved areas.² Psychiatry is one of the biggest users of telemedicine, which refers to any combination of communication technology and medicine.^3-5 This article discusses telepsychiatry’s effectiveness in providing psychiatric diagnosis and treatment, and the clinical implications of this technology, including improving access, cost, and quality of mental health services.

Outcomes comparable to face-to-face care

Telepsychiatry is used primarily in rural areas or correctional institutions or with underserved populations such as veterans with posttraumatic stress disorder or children. Although the literature generally is weak, there has been more research on psychiatry than other medical specialties because psychiatric clinicians rely on mental status examinations and verbal communications, not physical exams. Telepsychiatry can be considered a part of an evolving “connected health” system that offers many benefits to patients and clinicians (Table).

Table

Benefits of telepsychiatry as part of a ‘connected health’ system

Barriers to implementation

Although telepsychiatry offers tremendous promise, implementation has not been widespread or easy. Potential barriers to implementation, such as cost and resistance to change, are associated with acceptance of new technology or practice in health care. In addition, there are several legal, regulatory, and technical barriers.

Institutional barriers. Physicians and other providers may not have access to timely, evidence-based information and may face challenges, such as time constraints, access to technical support, and complexity of large health care institutions, when integrating this information into clinical practice.¹⁶ Two studies¹⁷ found that after controlling for other barriers—eg, reimbursement and regulatory issues—providers are the most significant initial gatekeepers that affect telemedicine use. When designing a telemedicine system, project managers should prioritize providers’ needs, such as ease of use and incentives.¹⁸

States do not cover services provided by other mental health providers, except for Utah’s coverage for social workers. The American Psychiatric Association has 2 suggestions regarding this issue³:

• reimbursement for telepsychiatry services should follow customary charges for delivering the appropriate current procedural terminology code(s)
  
• a structure for reimbursement of collateral charges, such as technician and line time, should be identified.
  

Licensure. A physician conducting a telemedicine session with a patient in another state must be licensed in both his or her state and the patient’s state. Nurses and other allied health professionals have similar state licensing constraints. Sanders²² suggests 3 potential solutions:

• establishing a national licensing system
  
• assigning the responsibility of care to the referring physician, with the consulting physician’s opinion serving as “recommendation only”
  
• determining that the patient is being “electronically transmitted” to the consultant’s state.
  

Box

Individual states also have developed funding streams to support telemedicine. The Centers for Medicare and Medicaid Services will pay a facility site fee to the host site (where the patient is located), but only if the site is in a rural area. Providers can charge patients a fee to support telepsychiatry infrastructure and maintenance, but typically this arrangement is not affordable and is not standard practice.

The future

Telepsychiatry’s ability to improve access to mental health care to underserved populations is becoming more evident. Technology is adequate for most uses and is constantly advancing. Numerous applications already have been defined, and more are ripe for exploration. Barriers to implementation are primarily of the human variety and will require a combination of consumer, provider, and governmental advocacy to overcome.

Related Resources

• American Telemedicine Association. www.americantelemed.org.
  
• International Society for Telemedicine & eHealth. www.isfteh.org.
  
• American Psychiatric Association. Telepsychiatry internet resources. www.psychiatry.org/practice/professional-interests/underserved-communities/telepsychiatry-internet-resources.
  
• Mossman D. Practicing psychiatry via Skype: Medicolegal considerations. Current Psychiatry. 2011;10(12):30-32,39.
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

For patients with major depressive disorder (MDD), monoamine oxidase inhibitors (MAOIs) have efficacy comparable to that of other antidepressants. However, concerns about side effects—particularly hypertensive crisis—and drug-drug interactions have led clinicians to prescribe MAOIs less often than newer antidepressants. A 1999 survey of 573 Michigan psychiatrists found that 30% had not prescribed an MAOI within the past 3 years, and 12% had never prescribed an MAOI.¹ Although there are challenges to using these agents, we prefer prescribing MAOIs to depressed patients who have not responded to previous antidepressant trials over trying untested antidepressant combinations.

Currently, MAOIs are used primarily for patients who have not responded to other antidepressant trials and are considered treatment resistant. Treatment-resistant depression (TRD) typically is defined as nonresponse to ≥3 adequate antidepressant trials. TRD is a major cause of disability and loss of productivity. These patients tend to do poorly over the long term, with high rates of hospitalization and suicide attempts. Several controlled trials have shown that patients who fail other antidepressants may respond to MAOIs.^2-4

Our knowledge regarding MAOIs has grown considerably. We have learned more about depression subtypes that MAOIs may help. As we learned more about dietary restrictions for patients taking MAOIs, the list of “forbidden foods” has decreased. Advances in treating a hypertensive crisis have decreased the need for hospitalization. By educating ourselves and our patients about MAOIs, we can provide another option for treating MDD.

An older antidepressant class

MAOIs were introduced approximately 60 years ago. Their potential for treating depression was discovered when a tuberculosis treatment—iproniazid—was found to reduce depressive symptoms. Researchers determined iproniazid’s antidepressant effects were the result of blocking removal of the amine group by monoamine oxidase (MAO) from dopamine, norepinephrine, and serotonin.⁵ A second MAOI, tranylcypromine, was discovered when it was found to be ineffective for treating decongestion.⁶

MAOI use in psychiatric practice has undergone significant changes since these medications were introduced. The discovery of hypertensive crises related to tyramine consumption led to decreased MAOI use, as did the rise of tricyclic antidepressants (TCAs) shortly thereafter. In the 1960s, research compared the relative efficacy of MAOIs to TCAs, and they became second-line antidepressants after the TCAs. In the late 1980s, the introduction of fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) resulted in a significant drop-off in MAOI use.

Pharmacologic effects

MAO is a class of enzymes that initiate oxidation of extracellular neurotransmitters such as serotonin, norepinephrine, and dopamine. MAOIs can be classified based on their relative affinity to MAO as well as their enzyme selectivity. The first distinguishing characteristic is whether the drug binds to MAO in a reversible or irreversible manner. Currently, all MAOIs that are FDA-approved for treating depression bind irreversibly to MAO. As a result, the body must renew its MAO levels before a patient is no longer at risk for a hypertensive crisis, a process that may take up to 2 weeks. Clinicians must take care to ensure their patients avoid foods that contain tyramine and medications contraindicated with MAOIs during this period.

MAOIs also differ from each other in enzyme selectivity. There are 2 subtypes of MAO enzymes—MAO_A and MAO_B. Generally, the antidepressant activity of MAOIs appears to be directed toward MAO_A inhibition. MAO_A has been found to be more specific for binding to serotonin and norepinephrine and MAO_B to be more specific for phenylethylamine. Dopamine is equally deaminated by both MAO_A and MAO_B.

Reversible MAO_A inhibitors require fewer restrictions on diet or concurrent medications, but efficacy data of reversible MAO_A inhibitors is mixed.

Clinical use of MAOIs

Four MAOIs are available in the United States: tranylcypromine, phenelzine, isocarboxazid, and selegiline. Selegiline is the only MAOI available as a transdermal patch. Transdermal administration results in fewer effects on MAO in the gastrointestinal tract, which means no dietary restrictions at the 6 mg/d starting dose, although the manufacturer recommends patients follow the MAO diet at 9 mg/d and 12 mg/d doses.⁷ Although selegiline is selective for MAO_B at low doses, it becomes nonselective at therapeutic doses for depression. Recommended dosages for MAOIs can be found in Table 1.⁸

Table 1

Recommended dosages of monoamine oxidase inhibitors

Serum monitoring of MAOIs is not clinically indicated and there are no correlations between drug levels and effectiveness.¹⁴ In a study that examined the correlation of inhibiting platelet MAO and MAOIs’ antidepressant effects, researchers found that a higher dose of phenelzine (60 mg/d) was significantly better in treating depression and anxiety than a lower dose (30 mg/d), and only the higher dose achieved 80% of platelet MAO inhibition.¹⁵ Further studies with other MAOIs did not reproduce this effect and platelet MAO inhibition is not regularly used to assess adequate dosing.

A refined view of side effects

In a hypertensive crisis, patients experience significant hypertension, headaches, tachycardia, diaphoresis, and vomiting. Intravenous phentolamine—an α-adrenergic receptor blocker—can be used as an antidote; often a single dose is effective.¹⁶ Alternatively, calcium channel blockers such as nifedipine can be prescribed. A patient can take 10 mg/hour and be observed in the emergency room until symptoms are relieved (usually only 1 or 2 doses are needed) without being admitted to the hospital.

Table 2

Food restrictions with MAOIs

Orthostatic hypotension is a common cardiovascular side effect of MAOIs that may lead to dizziness or syncope. Typically this is seen 2 to 3 weeks after initiating MAOI treatment. If hypotension remains a problem, mineralocorticoids can be prescribed with monitoring of serum potassium for hypokalemia. Increasing doses of tranylcypromine can increase supine—but not standing—diastolic blood pressure.¹⁹ Distinguish this type of blood pressure elevation from a hypertensive crisis by monitoring blood pressure with the patient sitting and standing and before and after he or she walks for 60 seconds.

Insomnia and day-night shifting—sleeping during the day and staying awake at night—are common and patients often cite these as reasons for discontinuing MAOIs. Many patients who respond to MAOIs report periods of substantial sleepiness in the mid to late afternoon. Table 3²⁰ provides a more complete list of reported side effects and their frequencies.

Table 3

MAOIs: Stay vigilant for side effects

Practice guidelines

The American Psychiatric Association’s practice guidelines for treating major depression state that MAOIs are effective in treating subgroups of patients with MDD with atypical features who have failed TCA trials.²¹ These guidelines also state that MAOIs have been shown to be effective treatment for some patients who have failed other antidepressants. However, for TRD patients who have not responded to SSRIs or SNRIs, the effectiveness of MAOIs compared with other strategies is unclear.²²

MAOIs have been used for >6 decades, and published studies continue to document their efficacy and safety when patients are monitored appropriately.^{11,12,14,15,25} However, based on our observations we suspect MAOIs are underutilized in clinical practice today. We are concerned that such practices can trickle down into residency training programs. Psychiatric residents typically do not receive adequate training in prescribing MAOIs, largely because many training faculty are not prescribing MAOIs themselves. Despite MAOIs’ limitations, concerns about an increased risk of suicide in patients with TRD²⁶ and the high likelihood of a poor outcome associated with persistent nonresponse to prior treatments must be weighed against the relatively low risk of a hypertensive event with MAOIs.⁶

• McCabe-Sellers BJ, Staggs CG, Bogle ML. Tyramine in foods and monoamine oxidase inhibitor drugs: a crossroad where medicine, nutrition, pharmacy, and food industry converge. Journal of Food Composition and Analysis. 2006;19(suppl):S58-S65.
  
• Fiedorowicz JG, Swartz KL. The role of monoamine oxidase inhibitors in current psychiatric practice. J Psychiatr Pract. 2004;10(4):239-248.
  

• Clomipramine • Anafranil
  
• Epinephrine • Adrenalin, EpiPen
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Isocarboxazid • Marplan
  
• Lithium • Eskalith, Lithobid
  
• Nifedipine • Adalat, Afeditab
  
• Phenelzine • Nardil
  
• Phentolamine • OraVerse, Regitine
  
• Selegiline • EMSAM
  
• Tranylcypromine • Parnate
  

Dr. Kosinski reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Rothschild receives grant or research support from Cyberonics, the National Institute of Mental Health, St. Jude Medical, and Takeda, and is a consultant to Allergan, Eli Lilly and Company, GlaxoSmithKline, Noven Pharmaceuticals, Pfizer Inc., Shire Pharmaceuticals, and Sunovion.

Discuss this article at www.facebook.com/CurrentPsychiatry

For patients with major depressive disorder (MDD), monoamine oxidase inhibitors (MAOIs) have efficacy comparable to that of other antidepressants. However, concerns about side effects—particularly hypertensive crisis—and drug-drug interactions have led clinicians to prescribe MAOIs less often than newer antidepressants. A 1999 survey of 573 Michigan psychiatrists found that 30% had not prescribed an MAOI within the past 3 years, and 12% had never prescribed an MAOI.¹ Although there are challenges to using these agents, we prefer prescribing MAOIs to depressed patients who have not responded to previous antidepressant trials over trying untested antidepressant combinations.

Currently, MAOIs are used primarily for patients who have not responded to other antidepressant trials and are considered treatment resistant. Treatment-resistant depression (TRD) typically is defined as nonresponse to ≥3 adequate antidepressant trials. TRD is a major cause of disability and loss of productivity. These patients tend to do poorly over the long term, with high rates of hospitalization and suicide attempts. Several controlled trials have shown that patients who fail other antidepressants may respond to MAOIs.^2-4

Our knowledge regarding MAOIs has grown considerably. We have learned more about depression subtypes that MAOIs may help. As we learned more about dietary restrictions for patients taking MAOIs, the list of “forbidden foods” has decreased. Advances in treating a hypertensive crisis have decreased the need for hospitalization. By educating ourselves and our patients about MAOIs, we can provide another option for treating MDD.

An older antidepressant class

MAOIs were introduced approximately 60 years ago. Their potential for treating depression was discovered when a tuberculosis treatment—iproniazid—was found to reduce depressive symptoms. Researchers determined iproniazid’s antidepressant effects were the result of blocking removal of the amine group by monoamine oxidase (MAO) from dopamine, norepinephrine, and serotonin.⁵ A second MAOI, tranylcypromine, was discovered when it was found to be ineffective for treating decongestion.⁶

MAOI use in psychiatric practice has undergone significant changes since these medications were introduced. The discovery of hypertensive crises related to tyramine consumption led to decreased MAOI use, as did the rise of tricyclic antidepressants (TCAs) shortly thereafter. In the 1960s, research compared the relative efficacy of MAOIs to TCAs, and they became second-line antidepressants after the TCAs. In the late 1980s, the introduction of fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) resulted in a significant drop-off in MAOI use.

Pharmacologic effects

MAO is a class of enzymes that initiate oxidation of extracellular neurotransmitters such as serotonin, norepinephrine, and dopamine. MAOIs can be classified based on their relative affinity to MAO as well as their enzyme selectivity. The first distinguishing characteristic is whether the drug binds to MAO in a reversible or irreversible manner. Currently, all MAOIs that are FDA-approved for treating depression bind irreversibly to MAO. As a result, the body must renew its MAO levels before a patient is no longer at risk for a hypertensive crisis, a process that may take up to 2 weeks. Clinicians must take care to ensure their patients avoid foods that contain tyramine and medications contraindicated with MAOIs during this period.

MAOIs also differ from each other in enzyme selectivity. There are 2 subtypes of MAO enzymes—MAO_A and MAO_B. Generally, the antidepressant activity of MAOIs appears to be directed toward MAO_A inhibition. MAO_A has been found to be more specific for binding to serotonin and norepinephrine and MAO_B to be more specific for phenylethylamine. Dopamine is equally deaminated by both MAO_A and MAO_B.

Reversible MAO_A inhibitors require fewer restrictions on diet or concurrent medications, but efficacy data of reversible MAO_A inhibitors is mixed.

Clinical use of MAOIs

Four MAOIs are available in the United States: tranylcypromine, phenelzine, isocarboxazid, and selegiline. Selegiline is the only MAOI available as a transdermal patch. Transdermal administration results in fewer effects on MAO in the gastrointestinal tract, which means no dietary restrictions at the 6 mg/d starting dose, although the manufacturer recommends patients follow the MAO diet at 9 mg/d and 12 mg/d doses.⁷ Although selegiline is selective for MAO_B at low doses, it becomes nonselective at therapeutic doses for depression. Recommended dosages for MAOIs can be found in Table 1.⁸

Table 1

Recommended dosages of monoamine oxidase inhibitors

Serum monitoring of MAOIs is not clinically indicated and there are no correlations between drug levels and effectiveness.¹⁴ In a study that examined the correlation of inhibiting platelet MAO and MAOIs’ antidepressant effects, researchers found that a higher dose of phenelzine (60 mg/d) was significantly better in treating depression and anxiety than a lower dose (30 mg/d), and only the higher dose achieved 80% of platelet MAO inhibition.¹⁵ Further studies with other MAOIs did not reproduce this effect and platelet MAO inhibition is not regularly used to assess adequate dosing.

A refined view of side effects

In a hypertensive crisis, patients experience significant hypertension, headaches, tachycardia, diaphoresis, and vomiting. Intravenous phentolamine—an α-adrenergic receptor blocker—can be used as an antidote; often a single dose is effective.¹⁶ Alternatively, calcium channel blockers such as nifedipine can be prescribed. A patient can take 10 mg/hour and be observed in the emergency room until symptoms are relieved (usually only 1 or 2 doses are needed) without being admitted to the hospital.

Table 2

Food restrictions with MAOIs

Orthostatic hypotension is a common cardiovascular side effect of MAOIs that may lead to dizziness or syncope. Typically this is seen 2 to 3 weeks after initiating MAOI treatment. If hypotension remains a problem, mineralocorticoids can be prescribed with monitoring of serum potassium for hypokalemia. Increasing doses of tranylcypromine can increase supine—but not standing—diastolic blood pressure.¹⁹ Distinguish this type of blood pressure elevation from a hypertensive crisis by monitoring blood pressure with the patient sitting and standing and before and after he or she walks for 60 seconds.

Insomnia and day-night shifting—sleeping during the day and staying awake at night—are common and patients often cite these as reasons for discontinuing MAOIs. Many patients who respond to MAOIs report periods of substantial sleepiness in the mid to late afternoon. Table 3²⁰ provides a more complete list of reported side effects and their frequencies.

Table 3

MAOIs: Stay vigilant for side effects

Practice guidelines

The American Psychiatric Association’s practice guidelines for treating major depression state that MAOIs are effective in treating subgroups of patients with MDD with atypical features who have failed TCA trials.²¹ These guidelines also state that MAOIs have been shown to be effective treatment for some patients who have failed other antidepressants. However, for TRD patients who have not responded to SSRIs or SNRIs, the effectiveness of MAOIs compared with other strategies is unclear.²²

MAOIs have been used for >6 decades, and published studies continue to document their efficacy and safety when patients are monitored appropriately.^{11,12,14,15,25} However, based on our observations we suspect MAOIs are underutilized in clinical practice today. We are concerned that such practices can trickle down into residency training programs. Psychiatric residents typically do not receive adequate training in prescribing MAOIs, largely because many training faculty are not prescribing MAOIs themselves. Despite MAOIs’ limitations, concerns about an increased risk of suicide in patients with TRD²⁶ and the high likelihood of a poor outcome associated with persistent nonresponse to prior treatments must be weighed against the relatively low risk of a hypertensive event with MAOIs.⁶

• McCabe-Sellers BJ, Staggs CG, Bogle ML. Tyramine in foods and monoamine oxidase inhibitor drugs: a crossroad where medicine, nutrition, pharmacy, and food industry converge. Journal of Food Composition and Analysis. 2006;19(suppl):S58-S65.
  
• Fiedorowicz JG, Swartz KL. The role of monoamine oxidase inhibitors in current psychiatric practice. J Psychiatr Pract. 2004;10(4):239-248.
  

• Clomipramine • Anafranil
  
• Epinephrine • Adrenalin, EpiPen
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Isocarboxazid • Marplan
  
• Lithium • Eskalith, Lithobid
  
• Nifedipine • Adalat, Afeditab
  
• Phenelzine • Nardil
  
• Phentolamine • OraVerse, Regitine
  
• Selegiline • EMSAM
  
• Tranylcypromine • Parnate
  

Dr. Kosinski reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Rothschild receives grant or research support from Cyberonics, the National Institute of Mental Health, St. Jude Medical, and Takeda, and is a consultant to Allergan, Eli Lilly and Company, GlaxoSmithKline, Noven Pharmaceuticals, Pfizer Inc., Shire Pharmaceuticals, and Sunovion.

Discuss this article at www.facebook.com/CurrentPsychiatry

For patients with major depressive disorder (MDD), monoamine oxidase inhibitors (MAOIs) have efficacy comparable to that of other antidepressants. However, concerns about side effects—particularly hypertensive crisis—and drug-drug interactions have led clinicians to prescribe MAOIs less often than newer antidepressants. A 1999 survey of 573 Michigan psychiatrists found that 30% had not prescribed an MAOI within the past 3 years, and 12% had never prescribed an MAOI.¹ Although there are challenges to using these agents, we prefer prescribing MAOIs to depressed patients who have not responded to previous antidepressant trials over trying untested antidepressant combinations.

Currently, MAOIs are used primarily for patients who have not responded to other antidepressant trials and are considered treatment resistant. Treatment-resistant depression (TRD) typically is defined as nonresponse to ≥3 adequate antidepressant trials. TRD is a major cause of disability and loss of productivity. These patients tend to do poorly over the long term, with high rates of hospitalization and suicide attempts. Several controlled trials have shown that patients who fail other antidepressants may respond to MAOIs.^2-4

Our knowledge regarding MAOIs has grown considerably. We have learned more about depression subtypes that MAOIs may help. As we learned more about dietary restrictions for patients taking MAOIs, the list of “forbidden foods” has decreased. Advances in treating a hypertensive crisis have decreased the need for hospitalization. By educating ourselves and our patients about MAOIs, we can provide another option for treating MDD.

An older antidepressant class

MAOIs were introduced approximately 60 years ago. Their potential for treating depression was discovered when a tuberculosis treatment—iproniazid—was found to reduce depressive symptoms. Researchers determined iproniazid’s antidepressant effects were the result of blocking removal of the amine group by monoamine oxidase (MAO) from dopamine, norepinephrine, and serotonin.⁵ A second MAOI, tranylcypromine, was discovered when it was found to be ineffective for treating decongestion.⁶

MAOI use in psychiatric practice has undergone significant changes since these medications were introduced. The discovery of hypertensive crises related to tyramine consumption led to decreased MAOI use, as did the rise of tricyclic antidepressants (TCAs) shortly thereafter. In the 1960s, research compared the relative efficacy of MAOIs to TCAs, and they became second-line antidepressants after the TCAs. In the late 1980s, the introduction of fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) resulted in a significant drop-off in MAOI use.

Pharmacologic effects

MAO is a class of enzymes that initiate oxidation of extracellular neurotransmitters such as serotonin, norepinephrine, and dopamine. MAOIs can be classified based on their relative affinity to MAO as well as their enzyme selectivity. The first distinguishing characteristic is whether the drug binds to MAO in a reversible or irreversible manner. Currently, all MAOIs that are FDA-approved for treating depression bind irreversibly to MAO. As a result, the body must renew its MAO levels before a patient is no longer at risk for a hypertensive crisis, a process that may take up to 2 weeks. Clinicians must take care to ensure their patients avoid foods that contain tyramine and medications contraindicated with MAOIs during this period.

MAOIs also differ from each other in enzyme selectivity. There are 2 subtypes of MAO enzymes—MAO_A and MAO_B. Generally, the antidepressant activity of MAOIs appears to be directed toward MAO_A inhibition. MAO_A has been found to be more specific for binding to serotonin and norepinephrine and MAO_B to be more specific for phenylethylamine. Dopamine is equally deaminated by both MAO_A and MAO_B.

Reversible MAO_A inhibitors require fewer restrictions on diet or concurrent medications, but efficacy data of reversible MAO_A inhibitors is mixed.

Clinical use of MAOIs

Four MAOIs are available in the United States: tranylcypromine, phenelzine, isocarboxazid, and selegiline. Selegiline is the only MAOI available as a transdermal patch. Transdermal administration results in fewer effects on MAO in the gastrointestinal tract, which means no dietary restrictions at the 6 mg/d starting dose, although the manufacturer recommends patients follow the MAO diet at 9 mg/d and 12 mg/d doses.⁷ Although selegiline is selective for MAO_B at low doses, it becomes nonselective at therapeutic doses for depression. Recommended dosages for MAOIs can be found in Table 1.⁸

Table 1

Recommended dosages of monoamine oxidase inhibitors

Serum monitoring of MAOIs is not clinically indicated and there are no correlations between drug levels and effectiveness.¹⁴ In a study that examined the correlation of inhibiting platelet MAO and MAOIs’ antidepressant effects, researchers found that a higher dose of phenelzine (60 mg/d) was significantly better in treating depression and anxiety than a lower dose (30 mg/d), and only the higher dose achieved 80% of platelet MAO inhibition.¹⁵ Further studies with other MAOIs did not reproduce this effect and platelet MAO inhibition is not regularly used to assess adequate dosing.

A refined view of side effects

In a hypertensive crisis, patients experience significant hypertension, headaches, tachycardia, diaphoresis, and vomiting. Intravenous phentolamine—an α-adrenergic receptor blocker—can be used as an antidote; often a single dose is effective.¹⁶ Alternatively, calcium channel blockers such as nifedipine can be prescribed. A patient can take 10 mg/hour and be observed in the emergency room until symptoms are relieved (usually only 1 or 2 doses are needed) without being admitted to the hospital.

Table 2

Food restrictions with MAOIs

Orthostatic hypotension is a common cardiovascular side effect of MAOIs that may lead to dizziness or syncope. Typically this is seen 2 to 3 weeks after initiating MAOI treatment. If hypotension remains a problem, mineralocorticoids can be prescribed with monitoring of serum potassium for hypokalemia. Increasing doses of tranylcypromine can increase supine—but not standing—diastolic blood pressure.¹⁹ Distinguish this type of blood pressure elevation from a hypertensive crisis by monitoring blood pressure with the patient sitting and standing and before and after he or she walks for 60 seconds.

Insomnia and day-night shifting—sleeping during the day and staying awake at night—are common and patients often cite these as reasons for discontinuing MAOIs. Many patients who respond to MAOIs report periods of substantial sleepiness in the mid to late afternoon. Table 3²⁰ provides a more complete list of reported side effects and their frequencies.

Table 3

MAOIs: Stay vigilant for side effects

Practice guidelines

The American Psychiatric Association’s practice guidelines for treating major depression state that MAOIs are effective in treating subgroups of patients with MDD with atypical features who have failed TCA trials.²¹ These guidelines also state that MAOIs have been shown to be effective treatment for some patients who have failed other antidepressants. However, for TRD patients who have not responded to SSRIs or SNRIs, the effectiveness of MAOIs compared with other strategies is unclear.²²

MAOIs have been used for >6 decades, and published studies continue to document their efficacy and safety when patients are monitored appropriately.^{11,12,14,15,25} However, based on our observations we suspect MAOIs are underutilized in clinical practice today. We are concerned that such practices can trickle down into residency training programs. Psychiatric residents typically do not receive adequate training in prescribing MAOIs, largely because many training faculty are not prescribing MAOIs themselves. Despite MAOIs’ limitations, concerns about an increased risk of suicide in patients with TRD²⁶ and the high likelihood of a poor outcome associated with persistent nonresponse to prior treatments must be weighed against the relatively low risk of a hypertensive event with MAOIs.⁶

• McCabe-Sellers BJ, Staggs CG, Bogle ML. Tyramine in foods and monoamine oxidase inhibitor drugs: a crossroad where medicine, nutrition, pharmacy, and food industry converge. Journal of Food Composition and Analysis. 2006;19(suppl):S58-S65.
  
• Fiedorowicz JG, Swartz KL. The role of monoamine oxidase inhibitors in current psychiatric practice. J Psychiatr Pract. 2004;10(4):239-248.
  

• Clomipramine • Anafranil
  
• Epinephrine • Adrenalin, EpiPen
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Isocarboxazid • Marplan
  
• Lithium • Eskalith, Lithobid
  
• Nifedipine • Adalat, Afeditab
  
• Phenelzine • Nardil
  
• Phentolamine • OraVerse, Regitine
  
• Selegiline • EMSAM
  
• Tranylcypromine • Parnate
  

Dr. Kosinski reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Rothschild receives grant or research support from Cyberonics, the National Institute of Mental Health, St. Jude Medical, and Takeda, and is a consultant to Allergan, Eli Lilly and Company, GlaxoSmithKline, Noven Pharmaceuticals, Pfizer Inc., Shire Pharmaceuticals, and Sunovion.

Discuss this article at www.facebook.com/CurrentPsychiatry

Research indicates that even brief physician advice on a regular basis can increase quit rates for patients who smoke.¹ This is particularly important in mental health settings, where there are more smokers than in the general population (50% to 90% vs 25% to 27%, respectively) but quit rates are lower.²

There is no “one size fits all” solution to quitting smoking; there are many individual factors to take into account for each patient. In addition to environmental factors that can make quitting smoking more challenging—eg, the patient’s partner also smokes—a patient’s genetic makeup can make it easier or harder to become addicted or to quit smoking, and can make pharmacologic approaches to cessation more or less successful.^3,4 A patient’s failed attempt to quit in the past does not indicate that quitting is impossible.

Although we encourage the use of traditional mnemonics such as the “5 A’s”⁵ and the “5 R’s,”⁵ we introduce QUIT as an easy-to-remember, compassionate, realistic way of discussing smoking cessation with patients.

Question each patient to understand the pros and cons of quitting. Ask your patients about the “benefits” of smoking and understand what role cigarettes serve in their lives. Remind patients of immediate benefits that would make quitting smoking a “trade” rather than a loss—eg, how would they use the extra $200 a month they would save by giving up cigarettes?

If patients say they are not interested in quitting, find out why they are not motivated to quit and collaborate with them to try to address their concerns. Additionally, ask if they would be comfortable discussing smoking cessation at each visit, even if they are not expressing interest.

Understand the nature of addiction. The trajectory of tobacco dependence—similar to other addictions—involves a chronic and relapsing course. Most patients require multiple quit attempts using several strategies before they succeed. Find out what they have tried in the past and build on previous successes. Be persistent in offering evidence-based treatments to help patients quit, even when motivation is low and patients have multiple failed attempts.

Keep in mind that only 4% to 7% of unaided quit attempts are successful.⁶ Most patients require counseling and/or medication, as well as help from a caring physician. By understanding the nature of addiction, you can be optimistic and supportive of your patients as they face the often disheartening process of quitting.

Identify risk factors and triggers. Studies have demonstrated that stimuli related to smoking increase a patient’s craving to smoke; this response is stronger than triggers encountered by patients addicted to alcohol or opiates.⁷ A plan for handling cravings and avoiding triggers can empower your patients and help them stay on track.

Talk with—not to—your patient. Discussing smoking can help clarify your patient’s feelings rather than avoiding them. Although patients may aspire to eventually quit smoking, the unspoken concerns they harbor combined with the “benefits” of smoking may lead to a failure to act.

Talk is powerful and with training, physicians can move patients toward change. Motivational interviewing is evidence-based and offers techniques that enable physicians to use conversation with their patients as a way of overcoming ambivalence about unhealthy behaviors and eliciting talk about changing these behaviors, and eventually help them to change.

You can make an impact

Physicians need to recognize their potential impact on this life-threatening behavior. Through an active, conversational style, develop a big-picture understanding of your patient’s pros and cons of quitting smoking; strengths and weaknesses; past failures and successes; barriers to success; available supports; etc. This information, combined with encouragement, support, and knowledge of evidence-based practices, can yield a thorough plan for quitting.

Although quitting smoking can be extremely challenging for clinicians and patients, expanding your knowledge in this area will allow you to help your patients make life-saving changes. The best care comes from direct communication and unconditional support.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Research indicates that even brief physician advice on a regular basis can increase quit rates for patients who smoke.¹ This is particularly important in mental health settings, where there are more smokers than in the general population (50% to 90% vs 25% to 27%, respectively) but quit rates are lower.²

There is no “one size fits all” solution to quitting smoking; there are many individual factors to take into account for each patient. In addition to environmental factors that can make quitting smoking more challenging—eg, the patient’s partner also smokes—a patient’s genetic makeup can make it easier or harder to become addicted or to quit smoking, and can make pharmacologic approaches to cessation more or less successful.^3,4 A patient’s failed attempt to quit in the past does not indicate that quitting is impossible.

Although we encourage the use of traditional mnemonics such as the “5 A’s”⁵ and the “5 R’s,”⁵ we introduce QUIT as an easy-to-remember, compassionate, realistic way of discussing smoking cessation with patients.

Question each patient to understand the pros and cons of quitting. Ask your patients about the “benefits” of smoking and understand what role cigarettes serve in their lives. Remind patients of immediate benefits that would make quitting smoking a “trade” rather than a loss—eg, how would they use the extra $200 a month they would save by giving up cigarettes?

If patients say they are not interested in quitting, find out why they are not motivated to quit and collaborate with them to try to address their concerns. Additionally, ask if they would be comfortable discussing smoking cessation at each visit, even if they are not expressing interest.

Understand the nature of addiction. The trajectory of tobacco dependence—similar to other addictions—involves a chronic and relapsing course. Most patients require multiple quit attempts using several strategies before they succeed. Find out what they have tried in the past and build on previous successes. Be persistent in offering evidence-based treatments to help patients quit, even when motivation is low and patients have multiple failed attempts.

Keep in mind that only 4% to 7% of unaided quit attempts are successful.⁶ Most patients require counseling and/or medication, as well as help from a caring physician. By understanding the nature of addiction, you can be optimistic and supportive of your patients as they face the often disheartening process of quitting.

Identify risk factors and triggers. Studies have demonstrated that stimuli related to smoking increase a patient’s craving to smoke; this response is stronger than triggers encountered by patients addicted to alcohol or opiates.⁷ A plan for handling cravings and avoiding triggers can empower your patients and help them stay on track.

Talk with—not to—your patient. Discussing smoking can help clarify your patient’s feelings rather than avoiding them. Although patients may aspire to eventually quit smoking, the unspoken concerns they harbor combined with the “benefits” of smoking may lead to a failure to act.

Talk is powerful and with training, physicians can move patients toward change. Motivational interviewing is evidence-based and offers techniques that enable physicians to use conversation with their patients as a way of overcoming ambivalence about unhealthy behaviors and eliciting talk about changing these behaviors, and eventually help them to change.

You can make an impact

Physicians need to recognize their potential impact on this life-threatening behavior. Through an active, conversational style, develop a big-picture understanding of your patient’s pros and cons of quitting smoking; strengths and weaknesses; past failures and successes; barriers to success; available supports; etc. This information, combined with encouragement, support, and knowledge of evidence-based practices, can yield a thorough plan for quitting.

Although quitting smoking can be extremely challenging for clinicians and patients, expanding your knowledge in this area will allow you to help your patients make life-saving changes. The best care comes from direct communication and unconditional support.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Research indicates that even brief physician advice on a regular basis can increase quit rates for patients who smoke.¹ This is particularly important in mental health settings, where there are more smokers than in the general population (50% to 90% vs 25% to 27%, respectively) but quit rates are lower.²

There is no “one size fits all” solution to quitting smoking; there are many individual factors to take into account for each patient. In addition to environmental factors that can make quitting smoking more challenging—eg, the patient’s partner also smokes—a patient’s genetic makeup can make it easier or harder to become addicted or to quit smoking, and can make pharmacologic approaches to cessation more or less successful.^3,4 A patient’s failed attempt to quit in the past does not indicate that quitting is impossible.

Although we encourage the use of traditional mnemonics such as the “5 A’s”⁵ and the “5 R’s,”⁵ we introduce QUIT as an easy-to-remember, compassionate, realistic way of discussing smoking cessation with patients.

Question each patient to understand the pros and cons of quitting. Ask your patients about the “benefits” of smoking and understand what role cigarettes serve in their lives. Remind patients of immediate benefits that would make quitting smoking a “trade” rather than a loss—eg, how would they use the extra $200 a month they would save by giving up cigarettes?

If patients say they are not interested in quitting, find out why they are not motivated to quit and collaborate with them to try to address their concerns. Additionally, ask if they would be comfortable discussing smoking cessation at each visit, even if they are not expressing interest.

Understand the nature of addiction. The trajectory of tobacco dependence—similar to other addictions—involves a chronic and relapsing course. Most patients require multiple quit attempts using several strategies before they succeed. Find out what they have tried in the past and build on previous successes. Be persistent in offering evidence-based treatments to help patients quit, even when motivation is low and patients have multiple failed attempts.

Keep in mind that only 4% to 7% of unaided quit attempts are successful.⁶ Most patients require counseling and/or medication, as well as help from a caring physician. By understanding the nature of addiction, you can be optimistic and supportive of your patients as they face the often disheartening process of quitting.

Identify risk factors and triggers. Studies have demonstrated that stimuli related to smoking increase a patient’s craving to smoke; this response is stronger than triggers encountered by patients addicted to alcohol or opiates.⁷ A plan for handling cravings and avoiding triggers can empower your patients and help them stay on track.

Talk with—not to—your patient. Discussing smoking can help clarify your patient’s feelings rather than avoiding them. Although patients may aspire to eventually quit smoking, the unspoken concerns they harbor combined with the “benefits” of smoking may lead to a failure to act.

Talk is powerful and with training, physicians can move patients toward change. Motivational interviewing is evidence-based and offers techniques that enable physicians to use conversation with their patients as a way of overcoming ambivalence about unhealthy behaviors and eliciting talk about changing these behaviors, and eventually help them to change.

You can make an impact

Physicians need to recognize their potential impact on this life-threatening behavior. Through an active, conversational style, develop a big-picture understanding of your patient’s pros and cons of quitting smoking; strengths and weaknesses; past failures and successes; barriers to success; available supports; etc. This information, combined with encouragement, support, and knowledge of evidence-based practices, can yield a thorough plan for quitting.

Although quitting smoking can be extremely challenging for clinicians and patients, expanding your knowledge in this area will allow you to help your patients make life-saving changes. The best care comes from direct communication and unconditional support.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Children and adolescents who have unrestricted use of the internet and cell phones are at increased risk for being exposed to sexually explicit material. One study found almost 1 in 5 high school students have “sexted”—sending a text message with sexually explicit pictures—and almost twice as many reported that they had received a sexually explicit picture via cell phone.¹ More than 25% of students acknowledged forwarding a sexually explicit picture to others; >33% did so despite knowing the legal consequences, including being arrested and facing pornography charges.¹

Concerned parents may seek advice on how to prevent their child from receiving or sending sexually inappropriate material on the internet or on their cell phones. You can help parents keep their children safe by sharing the following tips from The American Academy of Pediatrics (AAP)²:

Keep up with technology. Advise parents to become familiar with popular social networking websites such as Facebook. Creating their own Facebook page and “friending” their child may help them facilitate a conversation about their individual online experiences.

Enable privacy features. Instruct parents to install parental controls on their child’s computer. Explain to parents that these monitoring systems can help them check their child’s e-mail, chat records, and instant messages. Many social networking sites have privacy features that can help block unwanted users from contacting a child.

Check up on your children. Parents should let children know they are aware of their online presence and will be keeping an eye on them. They should periodically check a child’s chat logs, messages, e-mails, and social networking profiles for inappropriate content, friends, messages, and images. Instruct parents to teach their children that nothing is private once it’s posted on the internet. Suggest keeping the child’s computer in a public location such as the family room or kitchen.

Limit time spent online. Explain to parents that they should limit their child’s internet and cell phone access.

Combating ‘sexting’

Suggest to parents that they explain to their child in an age-appropriate manner what sexting is before giving their child a cell phone. The AAP² recommends that parents make sure their children understand the legal ramifications of sexting. A child who is caught sexting could be arrested, which may hurt his or her chances of being accepted into college or getting a job. A simple way to reduce a child’s opportunities for sexting is to restrict his or her access to a cell phone during social situations where peer pressure could influence behavior.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Children and adolescents who have unrestricted use of the internet and cell phones are at increased risk for being exposed to sexually explicit material. One study found almost 1 in 5 high school students have “sexted”—sending a text message with sexually explicit pictures—and almost twice as many reported that they had received a sexually explicit picture via cell phone.¹ More than 25% of students acknowledged forwarding a sexually explicit picture to others; >33% did so despite knowing the legal consequences, including being arrested and facing pornography charges.¹

Concerned parents may seek advice on how to prevent their child from receiving or sending sexually inappropriate material on the internet or on their cell phones. You can help parents keep their children safe by sharing the following tips from The American Academy of Pediatrics (AAP)²:

Keep up with technology. Advise parents to become familiar with popular social networking websites such as Facebook. Creating their own Facebook page and “friending” their child may help them facilitate a conversation about their individual online experiences.

Enable privacy features. Instruct parents to install parental controls on their child’s computer. Explain to parents that these monitoring systems can help them check their child’s e-mail, chat records, and instant messages. Many social networking sites have privacy features that can help block unwanted users from contacting a child.

Check up on your children. Parents should let children know they are aware of their online presence and will be keeping an eye on them. They should periodically check a child’s chat logs, messages, e-mails, and social networking profiles for inappropriate content, friends, messages, and images. Instruct parents to teach their children that nothing is private once it’s posted on the internet. Suggest keeping the child’s computer in a public location such as the family room or kitchen.

Limit time spent online. Explain to parents that they should limit their child’s internet and cell phone access.

Combating ‘sexting’

Suggest to parents that they explain to their child in an age-appropriate manner what sexting is before giving their child a cell phone. The AAP² recommends that parents make sure their children understand the legal ramifications of sexting. A child who is caught sexting could be arrested, which may hurt his or her chances of being accepted into college or getting a job. A simple way to reduce a child’s opportunities for sexting is to restrict his or her access to a cell phone during social situations where peer pressure could influence behavior.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Children and adolescents who have unrestricted use of the internet and cell phones are at increased risk for being exposed to sexually explicit material. One study found almost 1 in 5 high school students have “sexted”—sending a text message with sexually explicit pictures—and almost twice as many reported that they had received a sexually explicit picture via cell phone.¹ More than 25% of students acknowledged forwarding a sexually explicit picture to others; >33% did so despite knowing the legal consequences, including being arrested and facing pornography charges.¹

Concerned parents may seek advice on how to prevent their child from receiving or sending sexually inappropriate material on the internet or on their cell phones. You can help parents keep their children safe by sharing the following tips from The American Academy of Pediatrics (AAP)²:

Keep up with technology. Advise parents to become familiar with popular social networking websites such as Facebook. Creating their own Facebook page and “friending” their child may help them facilitate a conversation about their individual online experiences.

Enable privacy features. Instruct parents to install parental controls on their child’s computer. Explain to parents that these monitoring systems can help them check their child’s e-mail, chat records, and instant messages. Many social networking sites have privacy features that can help block unwanted users from contacting a child.

Check up on your children. Parents should let children know they are aware of their online presence and will be keeping an eye on them. They should periodically check a child’s chat logs, messages, e-mails, and social networking profiles for inappropriate content, friends, messages, and images. Instruct parents to teach their children that nothing is private once it’s posted on the internet. Suggest keeping the child’s computer in a public location such as the family room or kitchen.

Limit time spent online. Explain to parents that they should limit their child’s internet and cell phone access.

Combating ‘sexting’

Suggest to parents that they explain to their child in an age-appropriate manner what sexting is before giving their child a cell phone. The AAP² recommends that parents make sure their children understand the legal ramifications of sexting. A child who is caught sexting could be arrested, which may hurt his or her chances of being accepted into college or getting a job. A simple way to reduce a child’s opportunities for sexting is to restrict his or her access to a cell phone during social situations where peer pressure could influence behavior.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Since September 11, 2001, many Arab Americans have faced increased discrimination, which puts them at greater risk for depression and low self-esteem.¹ Children and adolescents in particular have been the victims of teasing and taunts. Many Muslim Arab Americans turned to their imams—a mosque’s spiritual leader—rather than a mental health clinician to help them deal with the national tragedy and the fallout that followed.²

Arab Americans may struggle to bridge their personal identity with their cultural one. Traditional Arab values stress the importance of family—both immediate and extended—loyalty to parents, religious adherence, and respect for elders and authority. Adapting those values to typical American values can cause dissonance as Arab Americans grapple to find a balance between renouncing their Arab culture in hopes of fitting in and feeling like outcasts in the country they call home.

Understanding cultural nuances

Be aware of the stigma of mental illness within Arab American communities. Unlike diabetes or heart disease, psychiatric disorders can carry a negative connotation for many Arab Americans.³ They may view mental illness as a personal shortcoming or ascribe their symptoms to supernatural spirits. The fear of being discriminated against for being culturally different and mentally ill may delay or prevent individuals from seeking care.

Understanding these dynamics, as well as Arab American culture, is the first step to evaluating these patients. Being aware of cultural nuances also is important. Patients may say they don’t smoke, but some prodding may reveal that they use a tobacco water pipe, or hookah.

Be cognizant of any preconceived notions that can seep into an assessment. It’s easy to assume that Arab American patients fall into stereotypical gender roles or are unhappy with what may be perceived as inadequate assimilation. Conversely, a patient’s appearance, devotion to cultural and religious values, and family support may lead to an assumption that the patient does not abuse substances or engage in high-risk behavior.

In addition, note that Arab Americans tend to present their mental illness as somatic complaints, which may make them more comfortable seeing a primary care physician than a psychiatrist.

Adjusting treatment

Many Arab Americans’ first choice is to seek support from family, friends, and religious leaders.⁴ A patient may need to be convinced to take psychotropics the same as they would other medications. Therefore, it may be necessary to involve family members to ensure treatment compliance. Clinicians may need to spend more time with Arab American patients, which can help the clinician grasp the complexity of their issues and allow patients to feel that they’re being cared for by a clinician who respects their cultural and religious beliefs. In conjunction, these steps will help you provide culturally sensitive care that best addresses Arab Americans’ mental health needs.

Since September 11, 2001, many Arab Americans have faced increased discrimination, which puts them at greater risk for depression and low self-esteem.¹ Children and adolescents in particular have been the victims of teasing and taunts. Many Muslim Arab Americans turned to their imams—a mosque’s spiritual leader—rather than a mental health clinician to help them deal with the national tragedy and the fallout that followed.²

Arab Americans may struggle to bridge their personal identity with their cultural one. Traditional Arab values stress the importance of family—both immediate and extended—loyalty to parents, religious adherence, and respect for elders and authority. Adapting those values to typical American values can cause dissonance as Arab Americans grapple to find a balance between renouncing their Arab culture in hopes of fitting in and feeling like outcasts in the country they call home.

Understanding cultural nuances

Be aware of the stigma of mental illness within Arab American communities. Unlike diabetes or heart disease, psychiatric disorders can carry a negative connotation for many Arab Americans.³ They may view mental illness as a personal shortcoming or ascribe their symptoms to supernatural spirits. The fear of being discriminated against for being culturally different and mentally ill may delay or prevent individuals from seeking care.

Understanding these dynamics, as well as Arab American culture, is the first step to evaluating these patients. Being aware of cultural nuances also is important. Patients may say they don’t smoke, but some prodding may reveal that they use a tobacco water pipe, or hookah.

Be cognizant of any preconceived notions that can seep into an assessment. It’s easy to assume that Arab American patients fall into stereotypical gender roles or are unhappy with what may be perceived as inadequate assimilation. Conversely, a patient’s appearance, devotion to cultural and religious values, and family support may lead to an assumption that the patient does not abuse substances or engage in high-risk behavior.

In addition, note that Arab Americans tend to present their mental illness as somatic complaints, which may make them more comfortable seeing a primary care physician than a psychiatrist.

Adjusting treatment

Many Arab Americans’ first choice is to seek support from family, friends, and religious leaders.⁴ A patient may need to be convinced to take psychotropics the same as they would other medications. Therefore, it may be necessary to involve family members to ensure treatment compliance. Clinicians may need to spend more time with Arab American patients, which can help the clinician grasp the complexity of their issues and allow patients to feel that they’re being cared for by a clinician who respects their cultural and religious beliefs. In conjunction, these steps will help you provide culturally sensitive care that best addresses Arab Americans’ mental health needs.

Since September 11, 2001, many Arab Americans have faced increased discrimination, which puts them at greater risk for depression and low self-esteem.¹ Children and adolescents in particular have been the victims of teasing and taunts. Many Muslim Arab Americans turned to their imams—a mosque’s spiritual leader—rather than a mental health clinician to help them deal with the national tragedy and the fallout that followed.²

Arab Americans may struggle to bridge their personal identity with their cultural one. Traditional Arab values stress the importance of family—both immediate and extended—loyalty to parents, religious adherence, and respect for elders and authority. Adapting those values to typical American values can cause dissonance as Arab Americans grapple to find a balance between renouncing their Arab culture in hopes of fitting in and feeling like outcasts in the country they call home.

Understanding cultural nuances

Be aware of the stigma of mental illness within Arab American communities. Unlike diabetes or heart disease, psychiatric disorders can carry a negative connotation for many Arab Americans.³ They may view mental illness as a personal shortcoming or ascribe their symptoms to supernatural spirits. The fear of being discriminated against for being culturally different and mentally ill may delay or prevent individuals from seeking care.

Understanding these dynamics, as well as Arab American culture, is the first step to evaluating these patients. Being aware of cultural nuances also is important. Patients may say they don’t smoke, but some prodding may reveal that they use a tobacco water pipe, or hookah.

Be cognizant of any preconceived notions that can seep into an assessment. It’s easy to assume that Arab American patients fall into stereotypical gender roles or are unhappy with what may be perceived as inadequate assimilation. Conversely, a patient’s appearance, devotion to cultural and religious values, and family support may lead to an assumption that the patient does not abuse substances or engage in high-risk behavior.

In addition, note that Arab Americans tend to present their mental illness as somatic complaints, which may make them more comfortable seeing a primary care physician than a psychiatrist.

Adjusting treatment

Many Arab Americans’ first choice is to seek support from family, friends, and religious leaders.⁴ A patient may need to be convinced to take psychotropics the same as they would other medications. Therefore, it may be necessary to involve family members to ensure treatment compliance. Clinicians may need to spend more time with Arab American patients, which can help the clinician grasp the complexity of their issues and allow patients to feel that they’re being cared for by a clinician who respects their cultural and religious beliefs. In conjunction, these steps will help you provide culturally sensitive care that best addresses Arab Americans’ mental health needs.

The vast majority of psychiatrists and psychiatric nurse practitioners in the United States are aware of the following facts:

• The unhealthy lifestyle of persons with chronic psychotic disorders (sedentary living, smoking, poor diet) is conducive to weight gain, metabolic disorders, high cardiovascular risk, and premature mortality. ¹
• Second-generation antipsychotics (SGAs) are associated with metabolic dysregulation, including obesity, diabetes, dyslipidemia, and hypertension.²
• The dramatic increase in diabetes, diabetic ketoacidosis, and death in the late 1990s and early 2000s prompted the FDA in August 2003 to apply a class warning to the labels of all SGAs and require that practitioners monitor metabolic parameters in patients receiving SGAs, before and after initiating therapy.³
• The consensus statement published by the American Psychiatric Association (APA) and American Diabetes Association (ADA) in February 2004 reviewed the metabolic side-effects literature of SGAs and included guidelines for monitoring the metabolic status of patients at baseline and after initiating treatment, including family history of metabolic disorders, body mass index, waist circumference, blood pressure, fasting glucose, and fasting lipids.^4,5
• The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study⁶ confirmed the APA/ADA findings and indicated that 43% of 1,460 outpatients with schizophrenia met criteria for metabolic syndrome⁷ when they enrolled in the study and the prevalence of metabolic syndrome increased over the duration of the study.⁸
• The CATIE study also reported that a substantial proportion of patients with schizophrenia had no access to primary care and never received standard treatment for hyperlipidemia, hypertension, and diabetes,⁹ prompting an angry Current Psychiatry editorial.¹⁰

And now for the grim facts. It is simply shocking that many practitioners are not monitoring the metabolic status of their patients consistently or at all. A recent systematic review and meta-analysis of 48 published studies showed that clinicians who prescribed antipsychotics are not abiding by guidelines to monitor metabolic risk in their seriously ill psychotic patients.¹¹ The inconsistent monitoring was evident not only in the United States but also in Canada, the United Kingdom, Australia, and Spain. Thirty-nine of those studies were conducted on the pattern of monitoring before any guidelines were published and 9 were conducted after monitoring guidelines were published. All of them were equally dismal in their findings.

The most urgent question is why aren’t practitioners monitoring vulnerable, seriously mentally ill patients to protect them from potential iatrogenic harm? If we don’t do it, who will? Wouldn’t we be outraged if a family member was not receiving standard clinical monitoring for a serious medical condition? The language that the FDA inserted in SGA labels specifically states that intervention is required if hyperglycemia emerges during monitoring, including treatment or switch to a metabolically more benign antipsychotic agent. How can an intervention be implemented if the monitoring is not done in a timely manner?

Persons suffering from psychotic disorders such as schizophrenia are compromised mentally and physically. They rely on us to give them proper treatment and follow-up, driven by evidence as well as compassion and commitment. Our guiding principle is to treat while doing no harm. The potential benefit of antipsychotic pharmacotherapy is widely accepted and the potential harm also is well recognized; published guidelines help protect patients via early detection of metabolic dysregulation. There is absolutely no excuse for failing to provide patients who need antipsychotics with consistent, guideline-based monitoring. No excuses. None.

The vast majority of psychiatrists and psychiatric nurse practitioners in the United States are aware of the following facts:

• The unhealthy lifestyle of persons with chronic psychotic disorders (sedentary living, smoking, poor diet) is conducive to weight gain, metabolic disorders, high cardiovascular risk, and premature mortality. ¹
• Second-generation antipsychotics (SGAs) are associated with metabolic dysregulation, including obesity, diabetes, dyslipidemia, and hypertension.²
• The dramatic increase in diabetes, diabetic ketoacidosis, and death in the late 1990s and early 2000s prompted the FDA in August 2003 to apply a class warning to the labels of all SGAs and require that practitioners monitor metabolic parameters in patients receiving SGAs, before and after initiating therapy.³
• The consensus statement published by the American Psychiatric Association (APA) and American Diabetes Association (ADA) in February 2004 reviewed the metabolic side-effects literature of SGAs and included guidelines for monitoring the metabolic status of patients at baseline and after initiating treatment, including family history of metabolic disorders, body mass index, waist circumference, blood pressure, fasting glucose, and fasting lipids.^4,5
• The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study⁶ confirmed the APA/ADA findings and indicated that 43% of 1,460 outpatients with schizophrenia met criteria for metabolic syndrome⁷ when they enrolled in the study and the prevalence of metabolic syndrome increased over the duration of the study.⁸
• The CATIE study also reported that a substantial proportion of patients with schizophrenia had no access to primary care and never received standard treatment for hyperlipidemia, hypertension, and diabetes,⁹ prompting an angry Current Psychiatry editorial.¹⁰

And now for the grim facts. It is simply shocking that many practitioners are not monitoring the metabolic status of their patients consistently or at all. A recent systematic review and meta-analysis of 48 published studies showed that clinicians who prescribed antipsychotics are not abiding by guidelines to monitor metabolic risk in their seriously ill psychotic patients.¹¹ The inconsistent monitoring was evident not only in the United States but also in Canada, the United Kingdom, Australia, and Spain. Thirty-nine of those studies were conducted on the pattern of monitoring before any guidelines were published and 9 were conducted after monitoring guidelines were published. All of them were equally dismal in their findings.

The most urgent question is why aren’t practitioners monitoring vulnerable, seriously mentally ill patients to protect them from potential iatrogenic harm? If we don’t do it, who will? Wouldn’t we be outraged if a family member was not receiving standard clinical monitoring for a serious medical condition? The language that the FDA inserted in SGA labels specifically states that intervention is required if hyperglycemia emerges during monitoring, including treatment or switch to a metabolically more benign antipsychotic agent. How can an intervention be implemented if the monitoring is not done in a timely manner?

Persons suffering from psychotic disorders such as schizophrenia are compromised mentally and physically. They rely on us to give them proper treatment and follow-up, driven by evidence as well as compassion and commitment. Our guiding principle is to treat while doing no harm. The potential benefit of antipsychotic pharmacotherapy is widely accepted and the potential harm also is well recognized; published guidelines help protect patients via early detection of metabolic dysregulation. There is absolutely no excuse for failing to provide patients who need antipsychotics with consistent, guideline-based monitoring. No excuses. None.

The vast majority of psychiatrists and psychiatric nurse practitioners in the United States are aware of the following facts:

• The unhealthy lifestyle of persons with chronic psychotic disorders (sedentary living, smoking, poor diet) is conducive to weight gain, metabolic disorders, high cardiovascular risk, and premature mortality. ¹
• Second-generation antipsychotics (SGAs) are associated with metabolic dysregulation, including obesity, diabetes, dyslipidemia, and hypertension.²
• The dramatic increase in diabetes, diabetic ketoacidosis, and death in the late 1990s and early 2000s prompted the FDA in August 2003 to apply a class warning to the labels of all SGAs and require that practitioners monitor metabolic parameters in patients receiving SGAs, before and after initiating therapy.³
• The consensus statement published by the American Psychiatric Association (APA) and American Diabetes Association (ADA) in February 2004 reviewed the metabolic side-effects literature of SGAs and included guidelines for monitoring the metabolic status of patients at baseline and after initiating treatment, including family history of metabolic disorders, body mass index, waist circumference, blood pressure, fasting glucose, and fasting lipids.^4,5
• The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study⁶ confirmed the APA/ADA findings and indicated that 43% of 1,460 outpatients with schizophrenia met criteria for metabolic syndrome⁷ when they enrolled in the study and the prevalence of metabolic syndrome increased over the duration of the study.⁸
• The CATIE study also reported that a substantial proportion of patients with schizophrenia had no access to primary care and never received standard treatment for hyperlipidemia, hypertension, and diabetes,⁹ prompting an angry Current Psychiatry editorial.¹⁰

And now for the grim facts. It is simply shocking that many practitioners are not monitoring the metabolic status of their patients consistently or at all. A recent systematic review and meta-analysis of 48 published studies showed that clinicians who prescribed antipsychotics are not abiding by guidelines to monitor metabolic risk in their seriously ill psychotic patients.¹¹ The inconsistent monitoring was evident not only in the United States but also in Canada, the United Kingdom, Australia, and Spain. Thirty-nine of those studies were conducted on the pattern of monitoring before any guidelines were published and 9 were conducted after monitoring guidelines were published. All of them were equally dismal in their findings.

The most urgent question is why aren’t practitioners monitoring vulnerable, seriously mentally ill patients to protect them from potential iatrogenic harm? If we don’t do it, who will? Wouldn’t we be outraged if a family member was not receiving standard clinical monitoring for a serious medical condition? The language that the FDA inserted in SGA labels specifically states that intervention is required if hyperglycemia emerges during monitoring, including treatment or switch to a metabolically more benign antipsychotic agent. How can an intervention be implemented if the monitoring is not done in a timely manner?

Persons suffering from psychotic disorders such as schizophrenia are compromised mentally and physically. They rely on us to give them proper treatment and follow-up, driven by evidence as well as compassion and commitment. Our guiding principle is to treat while doing no harm. The potential benefit of antipsychotic pharmacotherapy is widely accepted and the potential harm also is well recognized; published guidelines help protect patients via early detection of metabolic dysregulation. There is absolutely no excuse for failing to provide patients who need antipsychotics with consistent, guideline-based monitoring. No excuses. None.

Acute psychosis is a symptom that can be caused by many psychiatric and medical conditions. Psychotic patients might be unable to provide a history or participate in treatment if they are agitated, hostile, or violent. An appropriate workup may reveal the etiology of the psychosis; secondary causes, such as medical illness and substance use, are prevalent in the emergency room (ER) setting. If the patient has an underlying primary psychotic disorder, such as schizophrenia or mania, illness-specific intervention will help acutely and long-term. With agitated and uncooperative psychotic patients, clinicians often have to intervene quickly to ensure the safety of the patient and those nearby.

This article focuses on the initial evaluation and treatment of psychotic patients in the ER, either by a psychiatric emergency service or a psychiatric consultant. This process can be broken down into:

• triage or initial clinical assessment
• initial psychiatric stabilization, including pharmacologic interventions and agitation management
• diagnostic workup to evaluate medical and psychiatric conditions
• further psychiatric evaluation
• determining safe disposition.¹

Triage determines the next step

Initial clinical assessment and triage are necessary to select the appropriate immediate intervention. When a patient arrives in the ER, determine if he or she requires urgent medical attention. Basic initial screening should include:

• vital signs
• finger stick blood glucose
• medical history
• signs or symptoms of intoxication or withdrawal
• signs of trauma (eg, neck ligature marks, gunshot wounds, lacerations)
• asking the patient to give a brief history leading up to the current presentation.

A review of medical records may reveal patients’ medical and psychiatric history and allergies. Collateral documentation—such as ambulance run sheets or police reports—may provide additional information. If no immediate medical intervention is warranted, determine if the patient can wait in an open, unlocked waiting area or if he or she needs to be in an unlocked area with a sitter, a locked open area, or a secluded room with access to restraints. In general, psychotic patients who pose a threat of harm to themselves or others or cannot care for themselves because of their psychosis need locked areas or observation.

Initial psychiatric stabilization

Agitation is diagnostically unspecific but can occur in patients with psychosis. Psychotic patients can become unpredictably and impulsively aggressive and assaultive. Rapid intervention is necessary to minimize risk of bodily harm to the patient and those around the patient. Physicians often must make quick interventions based on limited clinical information. It is important to recognize early signs and symptoms of agitation, including:

• restlessness (pacing, fidgeting, hand wringing, fist clenching, posturing)
• irritability
• decreased attention
• inappropriate or hostile behaviors.²

Pharmacologic interventions. The initial goals of pharmacologic treatment are to calm the patient without oversedation, thereby allowing the patient to take part in his or her care and begin treatment for the primary psychotic illness.^3,4 Offering oral medications first and a choice of medications may help a patient feel more in control of the situation. If a patient has to be physically restrained, pharmacotherapy may limit the amount of time spent in restraints.

Medication choice depends on several factors, including onset of action, available formulation (eg, IM, liquid, rapidly dissolving), the patient’s previous medication response, side effect profile, allergies or adverse reactions to medications, and medical comorbidities.³ If a patient has a known psychotic illness, it may be helpful to administer the patient’s regular antipsychotic or anxiolytic medication. Some medications, such as lithium, are not effective in the acute setting and should be avoided. Additionally, benzodiazepines other than lorazepam or midazolam should not be administered IM because of erratic absorption.

Antipsychotics can be used for psychotic patients with or without agitation. Benzodiazepines may treat agitation, but are not specific for psychosis. Haloperidol can be used to treat acute psychosis and has proven efficacy for agitation. Benzodiazepines can decrease acute agitation and have efficacy similar to haloperidol, but with more sedation.⁵ A combination of lorazepam and haloperidol is thought to be superior to either medication alone.⁶ Lorazepam helps maintain sedation and decreases potential side effects caused by haloperidol. Consensus guidelines from 2001 and 2005 recommend combined haloperidol and lorazepam for first-line treatment of acute agitation.^3,7 High-potency antipsychotics such as haloperidol have an increased risk for extrapyramidal symptoms (EPS), particularly acute dystonic reactions—involuntary, sustained muscle contractions—in susceptible patients (eg, antipsychotic-naïve patients); consider starting diphenhydramine, 25 to 50 mg, or benztropine, 0.5 to 2 mg, to prevent EPS from high-potency antipsychotics (Algorithm 1).

Algorithm 1: Treating acute psychosis: Choosing pharmacologic agents
EPS: extrapyramidal symptoms; PO: by mouth; SL: sublingual

Second-generation antipsychotics (SGAs) increasingly have been used for managing acute agitation in patients with an underlying psychotic disorder. Guidelines from a 2012 American Association for Emergency Psychiatry workgroup recommend using an SGA as monotherapy or in combination with another medication instead of haloperidol to treat agitated patients with a known psychotic disorder.⁸ Clinical policy guidelines from the American College of Emergency Physicians recommend antipsychotic monotherapy for agitation and initial treatment in patients with a known psychiatric illness for which antipsychotic treatment is indicated (eg, schizophrenia).⁹ For patients with known psychotic illness, expert opinion recommends oral risperidone or olanzapine.^3,8 The combination of oral risperidone plus lorazepam may be as effective as the IM haloperidol and IM lorazepam combination.¹⁰ Patients who are too agitated to take oral doses may require parenteral medications. Ziprasidone, olanzapine, and aripiprazole are available in IM formulations. Ziprasidone, 20 mg IM, is well tolerated and has been shown to be effective in decreasing acute agitation symptoms in patients with psychotic disorders.¹¹ Olanzapine is as effective as haloperidol in decreasing agitation in patients with schizophrenia, with lower rates of EPS.¹² In a double-blind, placebo-controlled trial, psychotic symptoms in patients with schizophrenia or schizoaffective disorder decreased within 2 hours of IM olanzapine administration.¹³ Both IM ziprasidone and olanzapine have a relatively rapid onset of action (within 30 minutes), which makes them reasonable choices in the acute setting. Olanzapine has a long half-life (21 to 50 hours); therefore, patients’ comorbid medical conditions, such as cardiac abnormalities or hypotension, must be considered. If parenteral medication is required, IM olanzapine or IM ziprasidone is recommended.⁸ IM haloperidol with a benzodiazepine also can be considered.³

Coadministration of parenteral olanzapine and a benzodiazepine can lead to severe orthostatic hypotension and cardiac or respiratory depression and should be avoided in geriatric patients.¹⁴ Finally, it is important to rule out presentations that may worsen with antipsychotic treatment, including phencyclidine (PCP) toxicity (could worsen dystonic reactions), anticholinergic delirium, neuroleptic malignant syndrome (NMS), or catatonia.

If a patient does not respond to the initial dose of a medication, the dose may be repeated. However, doses should not be repeated until a patient is so sedated that he or she cannot take part in his or her care, or until he or she has developed significant EPS.

In addition to antipsychotics, consider loading with oral divalproex for patients who are acutely psychotic in the context of a manic episode (Table).^15,16 Higher serum divalproex levels—target serum levels >94 μg/mL—are associated with greater efficacy as measured by change from baseline in Mania Rating Scale or Young Mania Rating Scale scores compared with placebo.¹⁵ For acutely psychotic schizophrenia patients, there is evidence of benefit with initial treatment with divalproex combined with an SGA. In a randomized, double-blind study, patients treated with divalproex plus olanzapine or risperidone showed quicker initial resolution of psychotic symptoms compared with olanzapine or risperidone monotherapy, but no better long-term benefit.¹⁶ Clinicians may consider this well-tolerated combination after an appropriate medical workup. This finding of early benefit was not replicated with divalproex extended-release.¹⁷

Table

Divalproex dosing for patients with acute psychosis and mania

Side effects and adverse reactions. Treatment with antipsychotics may cause QTc interval prolongation, which can lead to increased risk for torsades de pointes and sudden death due to ventricular fibrillation. However, there have been few cases of torsades de pointes after oral haloperidol and none with IM haloperidol compared with at least 30 cases of torsades de pointes after IV haloperidol treatment. Torsades de pointes after risperidone, olanzapine, or ziprasidone treatment has not been reported.¹⁸

Hypotension and bradycardia may occur in patients treated with olanzapine; however, these signs occur less frequently in agitated patients.¹⁸ Antipsychotic treatment increases risk for EPS, including acute dystonia, akathisia (subjective restlessness with desire to move), and parkinsonism (shuffling gait, resting tremor, rigidity and bradykinesia), as well as NMS.

Nonpharmacologic interventions. Verbal intervention to try to de-escalate an agitated, psychotic patient should be attempted first; however, this is not always possible. Other behavioral interventions include offering a meal, blanket, or pillow, or other comforting options to decrease the patient’s anxiety associated with psychosis.² However, if agitated psychotic patients continue to display aggressive behaviors and pose a risk of harm to themselves or those around them, physical restraints should be considered because the clinician must balance protecting the patient’s rights with others’ safety. If physical restraints are used, medication also should be administered. Remove physical restraints as soon as safely possible; the Joint Commission has established standards for minimizing harm when using physical restraints.¹⁹

Diagnostic workup

Once a patient is medically stable in the ER, begin further workup of the etiology of the psychosis (Algorithm 2). All patients should have a physical exam, provided they are calm and in behavioral control. Monitor vital signs; patients at risk of withdrawal from substances should be monitored more frequently. Although there is no established standard for “medical clearance” of a psychiatric patient,²⁰ all patients should undergo basic laboratory tests, including basic metabolic panel, complete blood count, and urine toxicology. The extent of the workup is determined by the clinical situation and suspected cause of psychosis.²¹

Algorithm 2: Diagnostic workup of an acutely psychotic patient
ER: emergency room; EEG: electroencephalography; LP: lumbar puncture; TSH: thyroid-stimulating hormone

If you suspect delirium, the underlying medical etiology must be identified and treated. Up to 40% of hospitalized patients with delirium may have psychosis.²² Psychosis in a delirious patient may be characterized by poorly formed delusions and visual hallucinations. Delirious patients often are inattentive, easily distracted, and disoriented, with a fluctuating clinical course. Patients with psychosis generally do not have impaired attention and are alert with intact memory. However, acutely psychotic patients may be quite disorganized and uncooperative, which makes it difficult to distinguish between these 2 diagnoses. Serial exams may help clarify the clinical picture. It is important to remember that patients with a history of a psychotic disorder may have a superimposed delirium.

In young patients (age 18 to 30) with new-onset psychosis, consider drug-induced psychosis; PCP, lysergic acid diethylamide, and methamphetamine intoxication and withdrawal can lead to psychotic presentations. Additionally, comorbid substance use is common among patients with primary psychotic disorders. One study found 37% of first-episode psychotic patients misused drugs or alcohol, similar to the lifetime rate of patients with chronic psychotic disorders.^23,24 Check urine and serum toxicology screens and obtain relevant substance use history. Brain MRI may be considered for patients with first presentation of psychosis; however, there is little evidence to support head CT imaging unless there is known head trauma.²⁵ Electroencephalography and lumbar puncture can be considered if clinically indicated.

Further psychiatric evaluation

Obtaining a psychiatric history is necessary to determine the etiology of the acute psychotic presentation. The timing and duration of psychotic symptoms are key. Acute symptom onset with fluctuating course and impaired attention suggests a delirious process. A gradual decline in functioning over several months to years in a young person suggests a first episode of a psychotic disorder (eg, schizophrenia). Drug abuse is common among young persons with a psychotic disorder and a positive drug screen for a psychogenic substance does not exclude a primary psychotic disorder.

If a patient has a history of schizophrenia, bipolar disorder, or psychotic depression, acutely worsening psychosis may be considered an acute or chronic presentation. Even in patients diagnosed with a psychotic illness, it is necessary to determine the cause of symptom exacerbation. Medication nonadherence (which can be partial), substance use, psychosocial stressors, or underlying medical illness should be considered. Collateral information from family or friends may be crucial to understanding a patient’s presentation.

Safe disposition

Patients who pose a risk of harm to themselves or others or who are so impaired by their psychosis that they cannot care for themselves generally should be admitted to an inpatient psychiatric facility. For some psychotic patients who are agreeable to treatment and not prone to violence, less restrictive settings—such as a crisis intervention unit or respite facility—may be appropriate. A patient with first-episode psychosis could be admitted for further diagnostic clarification and treatment initiation. Manic patients often have no insight into their illness and may need hospitalization for containment and assurance of medication adherence. Goals of inpatient care include initiating or resuming pharmacologic treatment to reduce psychotic symptoms and beginning the recovery process. Response rates—defined as ≥20% improvement in total score on a psychopathology scale such as the Positive and Negative Syndrome Scale—will vary, but can take ≥4 weeks in some patients with first-episode schizophrenia.²⁶ However, most patients will be stabilized and ready for discharge before 4 weeks. Family education and alliance building with the patient and family are important during hospitalization.

Related Resources

• Schwartz S, Weathers, M. The psychotic patient. In: Riba MB, Ravindranath D, eds. Clinical manual of emergency psychiatry. Arlington, VA: American Psychiatric Publishing, Inc.; 2010:115-140.
• American Association for Emergency Psychiatry. http://emergencypsychiatry.org.

Drug Brand Names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Diphenhydramine • Benadryl
• Divalproex • Depakote
• Haloperidol • Haldol
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Midazolam • Versed
• Olanzapine • Zyprexa
• Risperidone • Risperdal
• Ziprasidone • Geodon

Disclosures

Dr. Freudenreich receives grant or research support from Beacon Health Strategies, Global Medical Education, MGH Psychiatry Academy, Optimal Medicine, Pfizer Inc., and PsychoGenics.

Drs. Brown and Stoklosa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acute psychosis is a symptom that can be caused by many psychiatric and medical conditions. Psychotic patients might be unable to provide a history or participate in treatment if they are agitated, hostile, or violent. An appropriate workup may reveal the etiology of the psychosis; secondary causes, such as medical illness and substance use, are prevalent in the emergency room (ER) setting. If the patient has an underlying primary psychotic disorder, such as schizophrenia or mania, illness-specific intervention will help acutely and long-term. With agitated and uncooperative psychotic patients, clinicians often have to intervene quickly to ensure the safety of the patient and those nearby.

This article focuses on the initial evaluation and treatment of psychotic patients in the ER, either by a psychiatric emergency service or a psychiatric consultant. This process can be broken down into:

• triage or initial clinical assessment
• initial psychiatric stabilization, including pharmacologic interventions and agitation management
• diagnostic workup to evaluate medical and psychiatric conditions
• further psychiatric evaluation
• determining safe disposition.¹

Triage determines the next step

Initial clinical assessment and triage are necessary to select the appropriate immediate intervention. When a patient arrives in the ER, determine if he or she requires urgent medical attention. Basic initial screening should include:

• vital signs
• finger stick blood glucose
• medical history
• signs or symptoms of intoxication or withdrawal
• signs of trauma (eg, neck ligature marks, gunshot wounds, lacerations)
• asking the patient to give a brief history leading up to the current presentation.

A review of medical records may reveal patients’ medical and psychiatric history and allergies. Collateral documentation—such as ambulance run sheets or police reports—may provide additional information. If no immediate medical intervention is warranted, determine if the patient can wait in an open, unlocked waiting area or if he or she needs to be in an unlocked area with a sitter, a locked open area, or a secluded room with access to restraints. In general, psychotic patients who pose a threat of harm to themselves or others or cannot care for themselves because of their psychosis need locked areas or observation.

Initial psychiatric stabilization

Agitation is diagnostically unspecific but can occur in patients with psychosis. Psychotic patients can become unpredictably and impulsively aggressive and assaultive. Rapid intervention is necessary to minimize risk of bodily harm to the patient and those around the patient. Physicians often must make quick interventions based on limited clinical information. It is important to recognize early signs and symptoms of agitation, including:

• restlessness (pacing, fidgeting, hand wringing, fist clenching, posturing)
• irritability
• decreased attention
• inappropriate or hostile behaviors.²

Pharmacologic interventions. The initial goals of pharmacologic treatment are to calm the patient without oversedation, thereby allowing the patient to take part in his or her care and begin treatment for the primary psychotic illness.^3,4 Offering oral medications first and a choice of medications may help a patient feel more in control of the situation. If a patient has to be physically restrained, pharmacotherapy may limit the amount of time spent in restraints.

Medication choice depends on several factors, including onset of action, available formulation (eg, IM, liquid, rapidly dissolving), the patient’s previous medication response, side effect profile, allergies or adverse reactions to medications, and medical comorbidities.³ If a patient has a known psychotic illness, it may be helpful to administer the patient’s regular antipsychotic or anxiolytic medication. Some medications, such as lithium, are not effective in the acute setting and should be avoided. Additionally, benzodiazepines other than lorazepam or midazolam should not be administered IM because of erratic absorption.

Antipsychotics can be used for psychotic patients with or without agitation. Benzodiazepines may treat agitation, but are not specific for psychosis. Haloperidol can be used to treat acute psychosis and has proven efficacy for agitation. Benzodiazepines can decrease acute agitation and have efficacy similar to haloperidol, but with more sedation.⁵ A combination of lorazepam and haloperidol is thought to be superior to either medication alone.⁶ Lorazepam helps maintain sedation and decreases potential side effects caused by haloperidol. Consensus guidelines from 2001 and 2005 recommend combined haloperidol and lorazepam for first-line treatment of acute agitation.^3,7 High-potency antipsychotics such as haloperidol have an increased risk for extrapyramidal symptoms (EPS), particularly acute dystonic reactions—involuntary, sustained muscle contractions—in susceptible patients (eg, antipsychotic-naïve patients); consider starting diphenhydramine, 25 to 50 mg, or benztropine, 0.5 to 2 mg, to prevent EPS from high-potency antipsychotics (Algorithm 1).

Algorithm 1: Treating acute psychosis: Choosing pharmacologic agents
EPS: extrapyramidal symptoms; PO: by mouth; SL: sublingual

Second-generation antipsychotics (SGAs) increasingly have been used for managing acute agitation in patients with an underlying psychotic disorder. Guidelines from a 2012 American Association for Emergency Psychiatry workgroup recommend using an SGA as monotherapy or in combination with another medication instead of haloperidol to treat agitated patients with a known psychotic disorder.⁸ Clinical policy guidelines from the American College of Emergency Physicians recommend antipsychotic monotherapy for agitation and initial treatment in patients with a known psychiatric illness for which antipsychotic treatment is indicated (eg, schizophrenia).⁹ For patients with known psychotic illness, expert opinion recommends oral risperidone or olanzapine.^3,8 The combination of oral risperidone plus lorazepam may be as effective as the IM haloperidol and IM lorazepam combination.¹⁰ Patients who are too agitated to take oral doses may require parenteral medications. Ziprasidone, olanzapine, and aripiprazole are available in IM formulations. Ziprasidone, 20 mg IM, is well tolerated and has been shown to be effective in decreasing acute agitation symptoms in patients with psychotic disorders.¹¹ Olanzapine is as effective as haloperidol in decreasing agitation in patients with schizophrenia, with lower rates of EPS.¹² In a double-blind, placebo-controlled trial, psychotic symptoms in patients with schizophrenia or schizoaffective disorder decreased within 2 hours of IM olanzapine administration.¹³ Both IM ziprasidone and olanzapine have a relatively rapid onset of action (within 30 minutes), which makes them reasonable choices in the acute setting. Olanzapine has a long half-life (21 to 50 hours); therefore, patients’ comorbid medical conditions, such as cardiac abnormalities or hypotension, must be considered. If parenteral medication is required, IM olanzapine or IM ziprasidone is recommended.⁸ IM haloperidol with a benzodiazepine also can be considered.³

Coadministration of parenteral olanzapine and a benzodiazepine can lead to severe orthostatic hypotension and cardiac or respiratory depression and should be avoided in geriatric patients.¹⁴ Finally, it is important to rule out presentations that may worsen with antipsychotic treatment, including phencyclidine (PCP) toxicity (could worsen dystonic reactions), anticholinergic delirium, neuroleptic malignant syndrome (NMS), or catatonia.

If a patient does not respond to the initial dose of a medication, the dose may be repeated. However, doses should not be repeated until a patient is so sedated that he or she cannot take part in his or her care, or until he or she has developed significant EPS.

In addition to antipsychotics, consider loading with oral divalproex for patients who are acutely psychotic in the context of a manic episode (Table).^15,16 Higher serum divalproex levels—target serum levels >94 μg/mL—are associated with greater efficacy as measured by change from baseline in Mania Rating Scale or Young Mania Rating Scale scores compared with placebo.¹⁵ For acutely psychotic schizophrenia patients, there is evidence of benefit with initial treatment with divalproex combined with an SGA. In a randomized, double-blind study, patients treated with divalproex plus olanzapine or risperidone showed quicker initial resolution of psychotic symptoms compared with olanzapine or risperidone monotherapy, but no better long-term benefit.¹⁶ Clinicians may consider this well-tolerated combination after an appropriate medical workup. This finding of early benefit was not replicated with divalproex extended-release.¹⁷

Table

Divalproex dosing for patients with acute psychosis and mania

Side effects and adverse reactions. Treatment with antipsychotics may cause QTc interval prolongation, which can lead to increased risk for torsades de pointes and sudden death due to ventricular fibrillation. However, there have been few cases of torsades de pointes after oral haloperidol and none with IM haloperidol compared with at least 30 cases of torsades de pointes after IV haloperidol treatment. Torsades de pointes after risperidone, olanzapine, or ziprasidone treatment has not been reported.¹⁸

Hypotension and bradycardia may occur in patients treated with olanzapine; however, these signs occur less frequently in agitated patients.¹⁸ Antipsychotic treatment increases risk for EPS, including acute dystonia, akathisia (subjective restlessness with desire to move), and parkinsonism (shuffling gait, resting tremor, rigidity and bradykinesia), as well as NMS.

Nonpharmacologic interventions. Verbal intervention to try to de-escalate an agitated, psychotic patient should be attempted first; however, this is not always possible. Other behavioral interventions include offering a meal, blanket, or pillow, or other comforting options to decrease the patient’s anxiety associated with psychosis.² However, if agitated psychotic patients continue to display aggressive behaviors and pose a risk of harm to themselves or those around them, physical restraints should be considered because the clinician must balance protecting the patient’s rights with others’ safety. If physical restraints are used, medication also should be administered. Remove physical restraints as soon as safely possible; the Joint Commission has established standards for minimizing harm when using physical restraints.¹⁹

Diagnostic workup

Once a patient is medically stable in the ER, begin further workup of the etiology of the psychosis (Algorithm 2). All patients should have a physical exam, provided they are calm and in behavioral control. Monitor vital signs; patients at risk of withdrawal from substances should be monitored more frequently. Although there is no established standard for “medical clearance” of a psychiatric patient,²⁰ all patients should undergo basic laboratory tests, including basic metabolic panel, complete blood count, and urine toxicology. The extent of the workup is determined by the clinical situation and suspected cause of psychosis.²¹

Algorithm 2: Diagnostic workup of an acutely psychotic patient
ER: emergency room; EEG: electroencephalography; LP: lumbar puncture; TSH: thyroid-stimulating hormone

If you suspect delirium, the underlying medical etiology must be identified and treated. Up to 40% of hospitalized patients with delirium may have psychosis.²² Psychosis in a delirious patient may be characterized by poorly formed delusions and visual hallucinations. Delirious patients often are inattentive, easily distracted, and disoriented, with a fluctuating clinical course. Patients with psychosis generally do not have impaired attention and are alert with intact memory. However, acutely psychotic patients may be quite disorganized and uncooperative, which makes it difficult to distinguish between these 2 diagnoses. Serial exams may help clarify the clinical picture. It is important to remember that patients with a history of a psychotic disorder may have a superimposed delirium.

In young patients (age 18 to 30) with new-onset psychosis, consider drug-induced psychosis; PCP, lysergic acid diethylamide, and methamphetamine intoxication and withdrawal can lead to psychotic presentations. Additionally, comorbid substance use is common among patients with primary psychotic disorders. One study found 37% of first-episode psychotic patients misused drugs or alcohol, similar to the lifetime rate of patients with chronic psychotic disorders.^23,24 Check urine and serum toxicology screens and obtain relevant substance use history. Brain MRI may be considered for patients with first presentation of psychosis; however, there is little evidence to support head CT imaging unless there is known head trauma.²⁵ Electroencephalography and lumbar puncture can be considered if clinically indicated.

Further psychiatric evaluation

Obtaining a psychiatric history is necessary to determine the etiology of the acute psychotic presentation. The timing and duration of psychotic symptoms are key. Acute symptom onset with fluctuating course and impaired attention suggests a delirious process. A gradual decline in functioning over several months to years in a young person suggests a first episode of a psychotic disorder (eg, schizophrenia). Drug abuse is common among young persons with a psychotic disorder and a positive drug screen for a psychogenic substance does not exclude a primary psychotic disorder.

If a patient has a history of schizophrenia, bipolar disorder, or psychotic depression, acutely worsening psychosis may be considered an acute or chronic presentation. Even in patients diagnosed with a psychotic illness, it is necessary to determine the cause of symptom exacerbation. Medication nonadherence (which can be partial), substance use, psychosocial stressors, or underlying medical illness should be considered. Collateral information from family or friends may be crucial to understanding a patient’s presentation.

Safe disposition

Patients who pose a risk of harm to themselves or others or who are so impaired by their psychosis that they cannot care for themselves generally should be admitted to an inpatient psychiatric facility. For some psychotic patients who are agreeable to treatment and not prone to violence, less restrictive settings—such as a crisis intervention unit or respite facility—may be appropriate. A patient with first-episode psychosis could be admitted for further diagnostic clarification and treatment initiation. Manic patients often have no insight into their illness and may need hospitalization for containment and assurance of medication adherence. Goals of inpatient care include initiating or resuming pharmacologic treatment to reduce psychotic symptoms and beginning the recovery process. Response rates—defined as ≥20% improvement in total score on a psychopathology scale such as the Positive and Negative Syndrome Scale—will vary, but can take ≥4 weeks in some patients with first-episode schizophrenia.²⁶ However, most patients will be stabilized and ready for discharge before 4 weeks. Family education and alliance building with the patient and family are important during hospitalization.

Related Resources

• Schwartz S, Weathers, M. The psychotic patient. In: Riba MB, Ravindranath D, eds. Clinical manual of emergency psychiatry. Arlington, VA: American Psychiatric Publishing, Inc.; 2010:115-140.
• American Association for Emergency Psychiatry. http://emergencypsychiatry.org.

Drug Brand Names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Diphenhydramine • Benadryl
• Divalproex • Depakote
• Haloperidol • Haldol
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Midazolam • Versed
• Olanzapine • Zyprexa
• Risperidone • Risperdal
• Ziprasidone • Geodon

Disclosures

Dr. Freudenreich receives grant or research support from Beacon Health Strategies, Global Medical Education, MGH Psychiatry Academy, Optimal Medicine, Pfizer Inc., and PsychoGenics.

Drs. Brown and Stoklosa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acute psychosis is a symptom that can be caused by many psychiatric and medical conditions. Psychotic patients might be unable to provide a history or participate in treatment if they are agitated, hostile, or violent. An appropriate workup may reveal the etiology of the psychosis; secondary causes, such as medical illness and substance use, are prevalent in the emergency room (ER) setting. If the patient has an underlying primary psychotic disorder, such as schizophrenia or mania, illness-specific intervention will help acutely and long-term. With agitated and uncooperative psychotic patients, clinicians often have to intervene quickly to ensure the safety of the patient and those nearby.

This article focuses on the initial evaluation and treatment of psychotic patients in the ER, either by a psychiatric emergency service or a psychiatric consultant. This process can be broken down into:

• triage or initial clinical assessment
• initial psychiatric stabilization, including pharmacologic interventions and agitation management
• diagnostic workup to evaluate medical and psychiatric conditions
• further psychiatric evaluation
• determining safe disposition.¹

Triage determines the next step

Initial clinical assessment and triage are necessary to select the appropriate immediate intervention. When a patient arrives in the ER, determine if he or she requires urgent medical attention. Basic initial screening should include:

• vital signs
• finger stick blood glucose
• medical history
• signs or symptoms of intoxication or withdrawal
• signs of trauma (eg, neck ligature marks, gunshot wounds, lacerations)
• asking the patient to give a brief history leading up to the current presentation.

A review of medical records may reveal patients’ medical and psychiatric history and allergies. Collateral documentation—such as ambulance run sheets or police reports—may provide additional information. If no immediate medical intervention is warranted, determine if the patient can wait in an open, unlocked waiting area or if he or she needs to be in an unlocked area with a sitter, a locked open area, or a secluded room with access to restraints. In general, psychotic patients who pose a threat of harm to themselves or others or cannot care for themselves because of their psychosis need locked areas or observation.

Initial psychiatric stabilization

Agitation is diagnostically unspecific but can occur in patients with psychosis. Psychotic patients can become unpredictably and impulsively aggressive and assaultive. Rapid intervention is necessary to minimize risk of bodily harm to the patient and those around the patient. Physicians often must make quick interventions based on limited clinical information. It is important to recognize early signs and symptoms of agitation, including:

• restlessness (pacing, fidgeting, hand wringing, fist clenching, posturing)
• irritability
• decreased attention
• inappropriate or hostile behaviors.²

Pharmacologic interventions. The initial goals of pharmacologic treatment are to calm the patient without oversedation, thereby allowing the patient to take part in his or her care and begin treatment for the primary psychotic illness.^3,4 Offering oral medications first and a choice of medications may help a patient feel more in control of the situation. If a patient has to be physically restrained, pharmacotherapy may limit the amount of time spent in restraints.

Medication choice depends on several factors, including onset of action, available formulation (eg, IM, liquid, rapidly dissolving), the patient’s previous medication response, side effect profile, allergies or adverse reactions to medications, and medical comorbidities.³ If a patient has a known psychotic illness, it may be helpful to administer the patient’s regular antipsychotic or anxiolytic medication. Some medications, such as lithium, are not effective in the acute setting and should be avoided. Additionally, benzodiazepines other than lorazepam or midazolam should not be administered IM because of erratic absorption.

Antipsychotics can be used for psychotic patients with or without agitation. Benzodiazepines may treat agitation, but are not specific for psychosis. Haloperidol can be used to treat acute psychosis and has proven efficacy for agitation. Benzodiazepines can decrease acute agitation and have efficacy similar to haloperidol, but with more sedation.⁵ A combination of lorazepam and haloperidol is thought to be superior to either medication alone.⁶ Lorazepam helps maintain sedation and decreases potential side effects caused by haloperidol. Consensus guidelines from 2001 and 2005 recommend combined haloperidol and lorazepam for first-line treatment of acute agitation.^3,7 High-potency antipsychotics such as haloperidol have an increased risk for extrapyramidal symptoms (EPS), particularly acute dystonic reactions—involuntary, sustained muscle contractions—in susceptible patients (eg, antipsychotic-naïve patients); consider starting diphenhydramine, 25 to 50 mg, or benztropine, 0.5 to 2 mg, to prevent EPS from high-potency antipsychotics (Algorithm 1).

Algorithm 1: Treating acute psychosis: Choosing pharmacologic agents
EPS: extrapyramidal symptoms; PO: by mouth; SL: sublingual

Second-generation antipsychotics (SGAs) increasingly have been used for managing acute agitation in patients with an underlying psychotic disorder. Guidelines from a 2012 American Association for Emergency Psychiatry workgroup recommend using an SGA as monotherapy or in combination with another medication instead of haloperidol to treat agitated patients with a known psychotic disorder.⁸ Clinical policy guidelines from the American College of Emergency Physicians recommend antipsychotic monotherapy for agitation and initial treatment in patients with a known psychiatric illness for which antipsychotic treatment is indicated (eg, schizophrenia).⁹ For patients with known psychotic illness, expert opinion recommends oral risperidone or olanzapine.^3,8 The combination of oral risperidone plus lorazepam may be as effective as the IM haloperidol and IM lorazepam combination.¹⁰ Patients who are too agitated to take oral doses may require parenteral medications. Ziprasidone, olanzapine, and aripiprazole are available in IM formulations. Ziprasidone, 20 mg IM, is well tolerated and has been shown to be effective in decreasing acute agitation symptoms in patients with psychotic disorders.¹¹ Olanzapine is as effective as haloperidol in decreasing agitation in patients with schizophrenia, with lower rates of EPS.¹² In a double-blind, placebo-controlled trial, psychotic symptoms in patients with schizophrenia or schizoaffective disorder decreased within 2 hours of IM olanzapine administration.¹³ Both IM ziprasidone and olanzapine have a relatively rapid onset of action (within 30 minutes), which makes them reasonable choices in the acute setting. Olanzapine has a long half-life (21 to 50 hours); therefore, patients’ comorbid medical conditions, such as cardiac abnormalities or hypotension, must be considered. If parenteral medication is required, IM olanzapine or IM ziprasidone is recommended.⁸ IM haloperidol with a benzodiazepine also can be considered.³

Coadministration of parenteral olanzapine and a benzodiazepine can lead to severe orthostatic hypotension and cardiac or respiratory depression and should be avoided in geriatric patients.¹⁴ Finally, it is important to rule out presentations that may worsen with antipsychotic treatment, including phencyclidine (PCP) toxicity (could worsen dystonic reactions), anticholinergic delirium, neuroleptic malignant syndrome (NMS), or catatonia.

If a patient does not respond to the initial dose of a medication, the dose may be repeated. However, doses should not be repeated until a patient is so sedated that he or she cannot take part in his or her care, or until he or she has developed significant EPS.

In addition to antipsychotics, consider loading with oral divalproex for patients who are acutely psychotic in the context of a manic episode (Table).^15,16 Higher serum divalproex levels—target serum levels >94 μg/mL—are associated with greater efficacy as measured by change from baseline in Mania Rating Scale or Young Mania Rating Scale scores compared with placebo.¹⁵ For acutely psychotic schizophrenia patients, there is evidence of benefit with initial treatment with divalproex combined with an SGA. In a randomized, double-blind study, patients treated with divalproex plus olanzapine or risperidone showed quicker initial resolution of psychotic symptoms compared with olanzapine or risperidone monotherapy, but no better long-term benefit.¹⁶ Clinicians may consider this well-tolerated combination after an appropriate medical workup. This finding of early benefit was not replicated with divalproex extended-release.¹⁷

Table

Divalproex dosing for patients with acute psychosis and mania

Side effects and adverse reactions. Treatment with antipsychotics may cause QTc interval prolongation, which can lead to increased risk for torsades de pointes and sudden death due to ventricular fibrillation. However, there have been few cases of torsades de pointes after oral haloperidol and none with IM haloperidol compared with at least 30 cases of torsades de pointes after IV haloperidol treatment. Torsades de pointes after risperidone, olanzapine, or ziprasidone treatment has not been reported.¹⁸

Hypotension and bradycardia may occur in patients treated with olanzapine; however, these signs occur less frequently in agitated patients.¹⁸ Antipsychotic treatment increases risk for EPS, including acute dystonia, akathisia (subjective restlessness with desire to move), and parkinsonism (shuffling gait, resting tremor, rigidity and bradykinesia), as well as NMS.

Nonpharmacologic interventions. Verbal intervention to try to de-escalate an agitated, psychotic patient should be attempted first; however, this is not always possible. Other behavioral interventions include offering a meal, blanket, or pillow, or other comforting options to decrease the patient’s anxiety associated with psychosis.² However, if agitated psychotic patients continue to display aggressive behaviors and pose a risk of harm to themselves or those around them, physical restraints should be considered because the clinician must balance protecting the patient’s rights with others’ safety. If physical restraints are used, medication also should be administered. Remove physical restraints as soon as safely possible; the Joint Commission has established standards for minimizing harm when using physical restraints.¹⁹

Diagnostic workup

Once a patient is medically stable in the ER, begin further workup of the etiology of the psychosis (Algorithm 2). All patients should have a physical exam, provided they are calm and in behavioral control. Monitor vital signs; patients at risk of withdrawal from substances should be monitored more frequently. Although there is no established standard for “medical clearance” of a psychiatric patient,²⁰ all patients should undergo basic laboratory tests, including basic metabolic panel, complete blood count, and urine toxicology. The extent of the workup is determined by the clinical situation and suspected cause of psychosis.²¹

Algorithm 2: Diagnostic workup of an acutely psychotic patient
ER: emergency room; EEG: electroencephalography; LP: lumbar puncture; TSH: thyroid-stimulating hormone

If you suspect delirium, the underlying medical etiology must be identified and treated. Up to 40% of hospitalized patients with delirium may have psychosis.²² Psychosis in a delirious patient may be characterized by poorly formed delusions and visual hallucinations. Delirious patients often are inattentive, easily distracted, and disoriented, with a fluctuating clinical course. Patients with psychosis generally do not have impaired attention and are alert with intact memory. However, acutely psychotic patients may be quite disorganized and uncooperative, which makes it difficult to distinguish between these 2 diagnoses. Serial exams may help clarify the clinical picture. It is important to remember that patients with a history of a psychotic disorder may have a superimposed delirium.

In young patients (age 18 to 30) with new-onset psychosis, consider drug-induced psychosis; PCP, lysergic acid diethylamide, and methamphetamine intoxication and withdrawal can lead to psychotic presentations. Additionally, comorbid substance use is common among patients with primary psychotic disorders. One study found 37% of first-episode psychotic patients misused drugs or alcohol, similar to the lifetime rate of patients with chronic psychotic disorders.^23,24 Check urine and serum toxicology screens and obtain relevant substance use history. Brain MRI may be considered for patients with first presentation of psychosis; however, there is little evidence to support head CT imaging unless there is known head trauma.²⁵ Electroencephalography and lumbar puncture can be considered if clinically indicated.

Further psychiatric evaluation

Obtaining a psychiatric history is necessary to determine the etiology of the acute psychotic presentation. The timing and duration of psychotic symptoms are key. Acute symptom onset with fluctuating course and impaired attention suggests a delirious process. A gradual decline in functioning over several months to years in a young person suggests a first episode of a psychotic disorder (eg, schizophrenia). Drug abuse is common among young persons with a psychotic disorder and a positive drug screen for a psychogenic substance does not exclude a primary psychotic disorder.

If a patient has a history of schizophrenia, bipolar disorder, or psychotic depression, acutely worsening psychosis may be considered an acute or chronic presentation. Even in patients diagnosed with a psychotic illness, it is necessary to determine the cause of symptom exacerbation. Medication nonadherence (which can be partial), substance use, psychosocial stressors, or underlying medical illness should be considered. Collateral information from family or friends may be crucial to understanding a patient’s presentation.

Safe disposition

Patients who pose a risk of harm to themselves or others or who are so impaired by their psychosis that they cannot care for themselves generally should be admitted to an inpatient psychiatric facility. For some psychotic patients who are agreeable to treatment and not prone to violence, less restrictive settings—such as a crisis intervention unit or respite facility—may be appropriate. A patient with first-episode psychosis could be admitted for further diagnostic clarification and treatment initiation. Manic patients often have no insight into their illness and may need hospitalization for containment and assurance of medication adherence. Goals of inpatient care include initiating or resuming pharmacologic treatment to reduce psychotic symptoms and beginning the recovery process. Response rates—defined as ≥20% improvement in total score on a psychopathology scale such as the Positive and Negative Syndrome Scale—will vary, but can take ≥4 weeks in some patients with first-episode schizophrenia.²⁶ However, most patients will be stabilized and ready for discharge before 4 weeks. Family education and alliance building with the patient and family are important during hospitalization.

Related Resources

• Schwartz S, Weathers, M. The psychotic patient. In: Riba MB, Ravindranath D, eds. Clinical manual of emergency psychiatry. Arlington, VA: American Psychiatric Publishing, Inc.; 2010:115-140.
• American Association for Emergency Psychiatry. http://emergencypsychiatry.org.

Drug Brand Names

• Aripiprazole • Abilify
• Benztropine • Cogentin
• Diphenhydramine • Benadryl
• Divalproex • Depakote
• Haloperidol • Haldol
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Midazolam • Versed
• Olanzapine • Zyprexa
• Risperidone • Risperdal
• Ziprasidone • Geodon

Disclosures

Dr. Freudenreich receives grant or research support from Beacon Health Strategies, Global Medical Education, MGH Psychiatry Academy, Optimal Medicine, Pfizer Inc., and PsychoGenics.

Drs. Brown and Stoklosa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Thank you for making your wonderful journal available to all psychiatrists. I look forward to receiving each issue of Current Psychiatry. Please keep this educational, balanced journal coming.

A. Guillermo Pezzarossi, MDPrivate PracticeAlbuquerque, NM

Thank you for making your wonderful journal available to all psychiatrists. I look forward to receiving each issue of Current Psychiatry. Please keep this educational, balanced journal coming.

A. Guillermo Pezzarossi, MDPrivate PracticeAlbuquerque, NM

Thank you for making your wonderful journal available to all psychiatrists. I look forward to receiving each issue of Current Psychiatry. Please keep this educational, balanced journal coming.

A. Guillermo Pezzarossi, MDPrivate PracticeAlbuquerque, NM

For years, I have been telling people what E. Fuller Torrey revealed in his 2010 report and what Dr. Nasrallah wrote about in his October 2012 editorial (“Psychiatry and the politics of incarceration,” From the Editor, Current Psychiatry, October 2012, p. 4-5; http://bit.ly/1JWYa87). It has been my experience that people falsely believe the mentally ill are dangerous and unpredictable or lazy and uncooperative and therefore are properly housed in prisons. Such a false idea seems to have pervaded Americans’ thoughts about the mentally ill to such a degree that a vast educational program would be needed to change this idea.

How sad is it that a nation founded on freedom has come to this.

Roxanne Lewis, PhDAssistant Professor of Behavioral SciencesDestiny University School of Medicine and Health SciencesRodney Bay, St. Lucia

For years, I have been telling people what E. Fuller Torrey revealed in his 2010 report and what Dr. Nasrallah wrote about in his October 2012 editorial (“Psychiatry and the politics of incarceration,” From the Editor, Current Psychiatry, October 2012, p. 4-5; http://bit.ly/1JWYa87). It has been my experience that people falsely believe the mentally ill are dangerous and unpredictable or lazy and uncooperative and therefore are properly housed in prisons. Such a false idea seems to have pervaded Americans’ thoughts about the mentally ill to such a degree that a vast educational program would be needed to change this idea.

How sad is it that a nation founded on freedom has come to this.

Roxanne Lewis, PhDAssistant Professor of Behavioral SciencesDestiny University School of Medicine and Health SciencesRodney Bay, St. Lucia

For years, I have been telling people what E. Fuller Torrey revealed in his 2010 report and what Dr. Nasrallah wrote about in his October 2012 editorial (“Psychiatry and the politics of incarceration,” From the Editor, Current Psychiatry, October 2012, p. 4-5; http://bit.ly/1JWYa87). It has been my experience that people falsely believe the mentally ill are dangerous and unpredictable or lazy and uncooperative and therefore are properly housed in prisons. Such a false idea seems to have pervaded Americans’ thoughts about the mentally ill to such a degree that a vast educational program would be needed to change this idea.

How sad is it that a nation founded on freedom has come to this.

Roxanne Lewis, PhDAssistant Professor of Behavioral SciencesDestiny University School of Medicine and Health SciencesRodney Bay, St. Lucia