Pearls

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Many economically disadvantaged psychiatric patients donate plasma for financial incentive. However, plasmapheresis (PP)—separation of plasma and cellular components of blood—can increase drug clearance, which may affect how you manage patients who donate plasma frequently.

Donated plasma is used to help patients with hemophilia and other blood disorders and burn victims. It’s also valuable for medical research. Typically, donors cannot be taking lithium, experiencing active hallucinations, receiving ≥3 psychotropic medications, or have had a psychiatric hospitalization in the past 12 months. Patients can donate while taking antidepressants, mood stabilizers, antipsychotics, and anticonvulsants.¹

Pharmacotherapeutic concerns

During PP, solutes in plasma such as drugs can be removed, increasing drug clearance by 30%.^2,3 PP affects both protein-bound and free drug concentrations. PP effectively clears drugs that are highly protein bound and have a small volume of distribution. As a result, serum levels of psychotropics are lowered. Most psychotropics except lithium are bound to plasma protein. Because of high protein binding, plasma concentrations of psychotropics may rebound after PP. Antipsychotics are highly protein bound—85% to 90%—and highly lipophilic. For a list of protein binding percentages of commonly used psychotropics, see the Table.⁴

Table

Protein binding percentages of common psychotropics

Plasma is regenerated 24 to 48 hours after PP; therefore, the clinical effect on daily psychotropic dosing should be small unless the donations are frequent. Long-term and regular plasma donation may result in hypoalbuminemia and hypocholesterolemia⁵; however, the effects of hypoalbuminemia on psychotropics routinely bound to serum proteins are unknown. Patients with an acute infection or malnourishment could have further decreased albumin production or increased catabolism, resulting in a significant decrease in serum albumin concentration, which may affect psychotropic pharmacokinetics.⁵

Other concerns

Beware of financial incentives because economically disadvantaged psychiatric patients are vulnerable to coercion. Some plasma donor centers will pay donors a specific amount—ranging from $20 to $30— for their first 2 donations and offer monthly bonuses if a patient donates 8 times a month.

The amount of plasma a patient can donate is based on their weight; patients who weigh more get paid more. This may conflict with your attempts to motivate patients to lose weight.

Disclosures

Dr. Selvaraj receives an internal grant from Creighton University.

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

Acknowledgement

The authors would like to thank Darrel E. Willoughby, Librarian, Omaha Veterans Affairs Medical Center, Omaha, NE, for his assistance with this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

Many economically disadvantaged psychiatric patients donate plasma for financial incentive. However, plasmapheresis (PP)—separation of plasma and cellular components of blood—can increase drug clearance, which may affect how you manage patients who donate plasma frequently.

Donated plasma is used to help patients with hemophilia and other blood disorders and burn victims. It’s also valuable for medical research. Typically, donors cannot be taking lithium, experiencing active hallucinations, receiving ≥3 psychotropic medications, or have had a psychiatric hospitalization in the past 12 months. Patients can donate while taking antidepressants, mood stabilizers, antipsychotics, and anticonvulsants.¹

Pharmacotherapeutic concerns

During PP, solutes in plasma such as drugs can be removed, increasing drug clearance by 30%.^2,3 PP affects both protein-bound and free drug concentrations. PP effectively clears drugs that are highly protein bound and have a small volume of distribution. As a result, serum levels of psychotropics are lowered. Most psychotropics except lithium are bound to plasma protein. Because of high protein binding, plasma concentrations of psychotropics may rebound after PP. Antipsychotics are highly protein bound—85% to 90%—and highly lipophilic. For a list of protein binding percentages of commonly used psychotropics, see the Table.⁴

Table

Protein binding percentages of common psychotropics

Plasma is regenerated 24 to 48 hours after PP; therefore, the clinical effect on daily psychotropic dosing should be small unless the donations are frequent. Long-term and regular plasma donation may result in hypoalbuminemia and hypocholesterolemia⁵; however, the effects of hypoalbuminemia on psychotropics routinely bound to serum proteins are unknown. Patients with an acute infection or malnourishment could have further decreased albumin production or increased catabolism, resulting in a significant decrease in serum albumin concentration, which may affect psychotropic pharmacokinetics.⁵

Other concerns

Beware of financial incentives because economically disadvantaged psychiatric patients are vulnerable to coercion. Some plasma donor centers will pay donors a specific amount—ranging from $20 to $30— for their first 2 donations and offer monthly bonuses if a patient donates 8 times a month.

The amount of plasma a patient can donate is based on their weight; patients who weigh more get paid more. This may conflict with your attempts to motivate patients to lose weight.

Disclosures

Dr. Selvaraj receives an internal grant from Creighton University.

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

Acknowledgement

The authors would like to thank Darrel E. Willoughby, Librarian, Omaha Veterans Affairs Medical Center, Omaha, NE, for his assistance with this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

Many economically disadvantaged psychiatric patients donate plasma for financial incentive. However, plasmapheresis (PP)—separation of plasma and cellular components of blood—can increase drug clearance, which may affect how you manage patients who donate plasma frequently.

Donated plasma is used to help patients with hemophilia and other blood disorders and burn victims. It’s also valuable for medical research. Typically, donors cannot be taking lithium, experiencing active hallucinations, receiving ≥3 psychotropic medications, or have had a psychiatric hospitalization in the past 12 months. Patients can donate while taking antidepressants, mood stabilizers, antipsychotics, and anticonvulsants.¹

Pharmacotherapeutic concerns

During PP, solutes in plasma such as drugs can be removed, increasing drug clearance by 30%.^2,3 PP affects both protein-bound and free drug concentrations. PP effectively clears drugs that are highly protein bound and have a small volume of distribution. As a result, serum levels of psychotropics are lowered. Most psychotropics except lithium are bound to plasma protein. Because of high protein binding, plasma concentrations of psychotropics may rebound after PP. Antipsychotics are highly protein bound—85% to 90%—and highly lipophilic. For a list of protein binding percentages of commonly used psychotropics, see the Table.⁴

Table

Protein binding percentages of common psychotropics

Plasma is regenerated 24 to 48 hours after PP; therefore, the clinical effect on daily psychotropic dosing should be small unless the donations are frequent. Long-term and regular plasma donation may result in hypoalbuminemia and hypocholesterolemia⁵; however, the effects of hypoalbuminemia on psychotropics routinely bound to serum proteins are unknown. Patients with an acute infection or malnourishment could have further decreased albumin production or increased catabolism, resulting in a significant decrease in serum albumin concentration, which may affect psychotropic pharmacokinetics.⁵

Other concerns

Beware of financial incentives because economically disadvantaged psychiatric patients are vulnerable to coercion. Some plasma donor centers will pay donors a specific amount—ranging from $20 to $30— for their first 2 donations and offer monthly bonuses if a patient donates 8 times a month.

The amount of plasma a patient can donate is based on their weight; patients who weigh more get paid more. This may conflict with your attempts to motivate patients to lose weight.

Disclosures

Dr. Selvaraj receives an internal grant from Creighton University.

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

Acknowledgement

The authors would like to thank Darrel E. Willoughby, Librarian, Omaha Veterans Affairs Medical Center, Omaha, NE, for his assistance with this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

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

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

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

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

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

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

Dr. Christensen 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

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

Dr. Christensen 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

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

Dr. Christensen 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

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

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

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

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

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

Disclosure

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

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

Discuss this article at www.facebook.com/CurrentPsychiatry

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

Discuss this article at www.facebook.com/CurrentPsychiatry

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

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Patients who complain of unpleasant paresthesias present a challenge to psychiatrists who need to differentiate between what could be psychotropic side effects from restless legs syndrome (RLS). Reconizing the differences between the 2 conditions can guide intervention. A previously unknown RLS diagnosis may shed light on a patient’s comorbid sleep disturbances and insomnia.

Signs that suggest RLS

Symptoms consistent with akathisia temporally related to initiating an antipsychotic or antidepressant should not be considered RLS-induced. In less clear cases, subtleties of the symptoms can help you decide.

RLS often presents as discomfort in the legs that patients describe as creeping, crawling, pulling, or itching; movement typically relieves this discomfort. Feelings of akathisia also have been described as an inner restlessness and a need to get up and move to relieve the tension. However, RLS has the following defining characteristics:

• occurs specifically in the lower extremities
• has a circadian rhythm and is worse at night
• can be accompanied by paresthesias and myoclonic jerks while awake.¹

Other factors that support an RLS diagnosis are a family history of RLS,¹ positive response to dopaminergic drugs,¹ and low ferritin levels. Also consider conditions that put patients at risk for RLS, including end stage renal disease, diabetes mellitus, multiple sclerosis, Parkinson’s disease, anemia, rheumatic disease, venous insufficiency, and pregnancy.

3 substances that can worsen RLS

Ask patients about their intake of caffeine, nicotine, and alcohol. Use of these substances is common among psychiatric patients and can worsen RLS symptoms. Making a connection between these substances and RLS symptoms can help motivate patients to temper their use.

In addition to mimicking the subjective experience of RLS, many psychotropics, including antidepressants, neuroleptics, and antihistamines,^2-4 can worsen RLS symptoms in patients with a known RLS diagnosis.

The next step

RLS is a clinical diagnosis that’s usually made based on a patient’s medical history. Polysomnography is not necessary to make an RLS diagnosis but may be helpful if a patient is treatment-resistant or to monitor periodic leg movement disorders. Serum ferritin levels should be checked because normal hemoglobin levels do not rule out iron deficiency.

Disclosure

Dr. Baker 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

Patients who complain of unpleasant paresthesias present a challenge to psychiatrists who need to differentiate between what could be psychotropic side effects from restless legs syndrome (RLS). Reconizing the differences between the 2 conditions can guide intervention. A previously unknown RLS diagnosis may shed light on a patient’s comorbid sleep disturbances and insomnia.

Signs that suggest RLS

Symptoms consistent with akathisia temporally related to initiating an antipsychotic or antidepressant should not be considered RLS-induced. In less clear cases, subtleties of the symptoms can help you decide.

RLS often presents as discomfort in the legs that patients describe as creeping, crawling, pulling, or itching; movement typically relieves this discomfort. Feelings of akathisia also have been described as an inner restlessness and a need to get up and move to relieve the tension. However, RLS has the following defining characteristics:

• occurs specifically in the lower extremities
• has a circadian rhythm and is worse at night
• can be accompanied by paresthesias and myoclonic jerks while awake.¹

Other factors that support an RLS diagnosis are a family history of RLS,¹ positive response to dopaminergic drugs,¹ and low ferritin levels. Also consider conditions that put patients at risk for RLS, including end stage renal disease, diabetes mellitus, multiple sclerosis, Parkinson’s disease, anemia, rheumatic disease, venous insufficiency, and pregnancy.

3 substances that can worsen RLS

Ask patients about their intake of caffeine, nicotine, and alcohol. Use of these substances is common among psychiatric patients and can worsen RLS symptoms. Making a connection between these substances and RLS symptoms can help motivate patients to temper their use.

In addition to mimicking the subjective experience of RLS, many psychotropics, including antidepressants, neuroleptics, and antihistamines,^2-4 can worsen RLS symptoms in patients with a known RLS diagnosis.

The next step

RLS is a clinical diagnosis that’s usually made based on a patient’s medical history. Polysomnography is not necessary to make an RLS diagnosis but may be helpful if a patient is treatment-resistant or to monitor periodic leg movement disorders. Serum ferritin levels should be checked because normal hemoglobin levels do not rule out iron deficiency.

Disclosure

Dr. Baker 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

Patients who complain of unpleasant paresthesias present a challenge to psychiatrists who need to differentiate between what could be psychotropic side effects from restless legs syndrome (RLS). Reconizing the differences between the 2 conditions can guide intervention. A previously unknown RLS diagnosis may shed light on a patient’s comorbid sleep disturbances and insomnia.

Signs that suggest RLS

Symptoms consistent with akathisia temporally related to initiating an antipsychotic or antidepressant should not be considered RLS-induced. In less clear cases, subtleties of the symptoms can help you decide.

RLS often presents as discomfort in the legs that patients describe as creeping, crawling, pulling, or itching; movement typically relieves this discomfort. Feelings of akathisia also have been described as an inner restlessness and a need to get up and move to relieve the tension. However, RLS has the following defining characteristics:

• occurs specifically in the lower extremities
• has a circadian rhythm and is worse at night
• can be accompanied by paresthesias and myoclonic jerks while awake.¹

Other factors that support an RLS diagnosis are a family history of RLS,¹ positive response to dopaminergic drugs,¹ and low ferritin levels. Also consider conditions that put patients at risk for RLS, including end stage renal disease, diabetes mellitus, multiple sclerosis, Parkinson’s disease, anemia, rheumatic disease, venous insufficiency, and pregnancy.

3 substances that can worsen RLS

Ask patients about their intake of caffeine, nicotine, and alcohol. Use of these substances is common among psychiatric patients and can worsen RLS symptoms. Making a connection between these substances and RLS symptoms can help motivate patients to temper their use.

In addition to mimicking the subjective experience of RLS, many psychotropics, including antidepressants, neuroleptics, and antihistamines,^2-4 can worsen RLS symptoms in patients with a known RLS diagnosis.

The next step

RLS is a clinical diagnosis that’s usually made based on a patient’s medical history. Polysomnography is not necessary to make an RLS diagnosis but may be helpful if a patient is treatment-resistant or to monitor periodic leg movement disorders. Serum ferritin levels should be checked because normal hemoglobin levels do not rule out iron deficiency.

Disclosure

Dr. Baker 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

Combination therapies for major depressive disorder (MDD) may enhance antidepressant efficacy and long-term results by working synergistically to regulate monoamines availability. Low levels of serum and red blood cell folate are linked to severe symptoms of depression and some patients are less likely to respond to antidepressants.¹ Even in patients with normal serum or red blood cell folate levels, CNS folate levels may be suboptimal.¹

L-methylfolate is the centrally active derivative of folate that regulates synthesis of trimonoamines serotonin, dopamine, and norepinephrine and is a key regulator of the cofactor tetrahydrobiopterin (BH4). BH4 is required by tryptophan hydroxylase for serotonin synthesis and by tyrosine hydroxylase for dopamine and norepinephrine synthesis.²

Evidence suggests adding L-methylfolate to selective serotonin reuptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs) when starting pharmacotherapy leads to greater reduction of depressive symptoms in a shorter time compared with SSRI or SNRI monotherapy.¹ In a study of patients with MDD who partially responded or did not respond to SSRIs, adjunctive L-methylfolate, 15 mg/d, produced greater response rates compared with SSRIs plus placebo.³ L-methylfolate also was well tolerated in combination with SSRI or SNRI therapy. The rates of adverse effects were not significantly different in patients taking L-methylfolate plus an SSRI or SNRI compared with those taking SSRI or SNRI monotherapy.¹

MDD patients who may benefit from L-methylfolate include those with low levels of folate and its active metabolites—such as L-methylfolate—and inadequate response to antidepressants. Patients who have an alcohol use disorder, eating disorders, genetic C677-T polymorphism (present in half of the general population), or gastrointestinal disorders are at risk for low folate levels, as well as those who are pregnant.²

Folic acid needs to be converted to L-methylfolate to cross the blood-brain barrier, whereas L-methylfolate can be used directly by the brain.² Therefore, patients who take medications that can interfere with the conversion of folate to L-methylfolate might benefit from adjunctive L-methylfolate. These medications include lamotrigine, valproate, oral contraceptives, metformin, warfarin, fenofibrates, and certain retinoids.¹ Patients with C677-T polymorphism and patients from Hispanic or Mediterranean populations have shown impaired ability to convert folic acid to L-methylfolate.²

Disclosure

Dr. Fluitt 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

Combination therapies for major depressive disorder (MDD) may enhance antidepressant efficacy and long-term results by working synergistically to regulate monoamines availability. Low levels of serum and red blood cell folate are linked to severe symptoms of depression and some patients are less likely to respond to antidepressants.¹ Even in patients with normal serum or red blood cell folate levels, CNS folate levels may be suboptimal.¹

L-methylfolate is the centrally active derivative of folate that regulates synthesis of trimonoamines serotonin, dopamine, and norepinephrine and is a key regulator of the cofactor tetrahydrobiopterin (BH4). BH4 is required by tryptophan hydroxylase for serotonin synthesis and by tyrosine hydroxylase for dopamine and norepinephrine synthesis.²

Evidence suggests adding L-methylfolate to selective serotonin reuptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs) when starting pharmacotherapy leads to greater reduction of depressive symptoms in a shorter time compared with SSRI or SNRI monotherapy.¹ In a study of patients with MDD who partially responded or did not respond to SSRIs, adjunctive L-methylfolate, 15 mg/d, produced greater response rates compared with SSRIs plus placebo.³ L-methylfolate also was well tolerated in combination with SSRI or SNRI therapy. The rates of adverse effects were not significantly different in patients taking L-methylfolate plus an SSRI or SNRI compared with those taking SSRI or SNRI monotherapy.¹

MDD patients who may benefit from L-methylfolate include those with low levels of folate and its active metabolites—such as L-methylfolate—and inadequate response to antidepressants. Patients who have an alcohol use disorder, eating disorders, genetic C677-T polymorphism (present in half of the general population), or gastrointestinal disorders are at risk for low folate levels, as well as those who are pregnant.²

Folic acid needs to be converted to L-methylfolate to cross the blood-brain barrier, whereas L-methylfolate can be used directly by the brain.² Therefore, patients who take medications that can interfere with the conversion of folate to L-methylfolate might benefit from adjunctive L-methylfolate. These medications include lamotrigine, valproate, oral contraceptives, metformin, warfarin, fenofibrates, and certain retinoids.¹ Patients with C677-T polymorphism and patients from Hispanic or Mediterranean populations have shown impaired ability to convert folic acid to L-methylfolate.²

Disclosure

Dr. Fluitt 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

Combination therapies for major depressive disorder (MDD) may enhance antidepressant efficacy and long-term results by working synergistically to regulate monoamines availability. Low levels of serum and red blood cell folate are linked to severe symptoms of depression and some patients are less likely to respond to antidepressants.¹ Even in patients with normal serum or red blood cell folate levels, CNS folate levels may be suboptimal.¹

L-methylfolate is the centrally active derivative of folate that regulates synthesis of trimonoamines serotonin, dopamine, and norepinephrine and is a key regulator of the cofactor tetrahydrobiopterin (BH4). BH4 is required by tryptophan hydroxylase for serotonin synthesis and by tyrosine hydroxylase for dopamine and norepinephrine synthesis.²

Evidence suggests adding L-methylfolate to selective serotonin reuptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs) when starting pharmacotherapy leads to greater reduction of depressive symptoms in a shorter time compared with SSRI or SNRI monotherapy.¹ In a study of patients with MDD who partially responded or did not respond to SSRIs, adjunctive L-methylfolate, 15 mg/d, produced greater response rates compared with SSRIs plus placebo.³ L-methylfolate also was well tolerated in combination with SSRI or SNRI therapy. The rates of adverse effects were not significantly different in patients taking L-methylfolate plus an SSRI or SNRI compared with those taking SSRI or SNRI monotherapy.¹

MDD patients who may benefit from L-methylfolate include those with low levels of folate and its active metabolites—such as L-methylfolate—and inadequate response to antidepressants. Patients who have an alcohol use disorder, eating disorders, genetic C677-T polymorphism (present in half of the general population), or gastrointestinal disorders are at risk for low folate levels, as well as those who are pregnant.²

Folic acid needs to be converted to L-methylfolate to cross the blood-brain barrier, whereas L-methylfolate can be used directly by the brain.² Therefore, patients who take medications that can interfere with the conversion of folate to L-methylfolate might benefit from adjunctive L-methylfolate. These medications include lamotrigine, valproate, oral contraceptives, metformin, warfarin, fenofibrates, and certain retinoids.¹ Patients with C677-T polymorphism and patients from Hispanic or Mediterranean populations have shown impaired ability to convert folic acid to L-methylfolate.²

Disclosure

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

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

Caffeine belongs to the xanthine chemical group and its stimulant effects are the result of its competitive antagonism on adenosine receptors A1 and A2A in the CNS. Caffeine also slows the rate of dopamine reuptake and increases glutamate release, which theoretically could cause neuropsychiatric symptoms.1,2 Toxicity ranges have been recorded at 150 to 200 mg/kg. Increased psychotic features in schizophrenia patients have been reported at doses as low as 10 mg/kg.1 Earlier studies of caffeine use in patients with psychotic disorders reveal induction in thought disorders, social withdrawal, and euphoric activation3; however, these results have been variable.1

The American Association of Poison Control Centers reported 4,600 caffeine-related calls in 2005; one-half of which involved patients age <19.⁴ For a list of the caffeine content of 20 popular drinks, see the Table.

TABLE

Caffeine content of 20 popular drinks^a

Caffeine-induced psychosis?

My team recently treated a woman with prodromal psychotic symptoms for whom ingesting a high dose of caffeine precipitated a psychotic break.

Ms. P, age 19, presented to our Naval outpatient psychiatry clinic reporting a decline in her ability to organize her thoughts over the past 6 months. She said at times she experienced visual hallucinations and feeling that she was being followed but no one was there. Ms. P also stated she felt other people were talking about her and described ideas of reference. She described her prodrome as an unrelenting and existential interest in the number 33.

The patient drank 4 cups of coffee each day, plus an additional 3 to 4 cups of coffee and 2 to 3 Monster energy drinks on days she was on duty. Ms. P was ingesting approximately 21 to 22 mg/kg/d of caffeine. Basic lab and radiographic work were unremarkable. We asked her to reduce or discontinue her use of caffeinated beverages and return for follow-up in 1 to 2 weeks.

When Ms. P returned 2 weeks later, she said she had reduced her caffeine intake to a periodic cup of coffee or Monster drink. She reported improved sleep quality and quantity; moreover, she experienced a substantial decline in thought disruptions and paranoid thought patterns. However, over the next 4 weeks Ms. P’s reality testing gradually deteriorated, so we prescribed ziprasidone, 20 mg/d, which dissipated her perceptual disturbances. Ms. P tolerated the low-dose antipsychotic and medically retired from military service.

Disclosure

Dr. Whiting reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. The views expressed in this article are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.