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How to diagnose pathologic gambling in older patients

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How to diagnose pathologic gambling in older patients

Pathologic gambling among older patients causes more than financial losses; it also can lead to comorbid alcohol dependence, depression, anxiety disorders, and medical treatment nonadherence.1

Retirement, death of a spouse, “empty nest” syndrome, and other emotional, social, and financial stresses are common in later life. Some try to fill the gap with gambling, which can become pathologic. Early intervention and treatments addressing an older patient’s psychological and social needs can improve outcomes, however.

Screening for pathologic gambling

Late life pathologic gambling often goes undiagnosed but is thought to be on the rise. In a random sample of 843 older adults at scheduled primary-care appointments, 70% had gambled at least once in the past year and 11% were identified as at-risk gamblers.1

Diagnosing pathologic gambling requires a high degree of suspicion and inquiry. You must actively incorporate screening questions in the clinical interview to identify at-risk and pathologic gamblers in older patients.

Based on clinical experience and several DSM-IV-TR criteria,2 we developed a screening tool called PACE RULeS to identify pathologic gambling in this population (Box 1). A positive response to 5 or more of the 8 questions indicates a likely diagnosis of pathologic gambling. Lower scores may point to at-risk behavior and would require follow-up.

Box 1

8 questions to screen for pathologic gambling

Diagnose maladaptive or pathologic gambling if your patient answers yes to 5 or more of these “PACE RULeS” questions:

  • P—Are you often Preoccupied with thoughts of gambling?
  • A—Would you often gamble with increasing Amounts of money to achieve the same excitement?
  • C—Have you made repeated efforts to Control, cut back, or stop gambling?
  • E—Do you gamble to Escape daily problems and stresses?
  • R—After losing money, do you often Return another day to get even?
  • U—Have you ever committed Unlawful acts to finance gambling?
  • L—Have you Lost a significant relationship or job because of gambling?
  • S—Do you use your Savings to gamble?

Psychosocial intervention

After you make a diagnosis, manage your patient’s pathologic gambling with a comprehensive plan that includes family and community resources.3Box 2 shows interventions studied in the adult population that are appropriate for older patients.

Box 2

Interventions for older patients

  • Screen for active gambling
  • Intervene immediately if the patient is suicidal
  • Refer the patient to Gamblers Anonymous
  • Enlist family and friends to support treatment adherence and effectiveness. Be aware of confidentiality and ethical issues, however, especially during discussions with family members
  • Refer the patient to counseling
  • Actively participate in the treatment plan by assessing for relapses.

Medication

No psychotropics are FDA-approved for pathologic gambling, but adding medication to psychosocial interventions may help. Most medications studied in the general population are similarly efficacious in older adults. Slowly increase dosages, however, because of the greater risk of side effects in older patients.

Selective serotonin reuptake inhibitors help reduce gambling behavior, improve social and occupational functioning, and treat comorbid depression when used in relatively higher dosages. In anecdotal reports, the following medications have been found to be beneficial:

  • fluoxetine, 20 to 60 mg/d4
  • paroxetine, 20 to 60 mg/d5
  • fluvoxamine, 200 mg/d.6,7
Citalopram, 60 mg/d, also has shown efficacy in a single study of 15 adults ages 18 to 70.8 Similarly, clomipramine, 125 to 175 mg/d, has been effective in reducing gambling behavior. Naltrexone, 150 mg/d, appears to help individuals with intense urges to gamble, but liver function must be monitored.9 Anecdotal evidence also suggests that mood stabilizers including lithium, carbamazepine, and valproate may help treat impulsivity and comorbid bipolar disorder.

Although some medications treat pathologic gambling, others can cause it. Dopamine agonists such as pramipexole could cause reversible pathologic gambling in some older individuals who take it for Parkinson’s disease or restless legs syndrome.10

Drug brand names

  • Carbamazepine • Tegretol
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Fluvoxamine • Luvox
  • Lithium • Eskalith, Lithobid
  • Naltrexone • ReVia
  • Paroxetine • Paxil
  • Pramipexole • Mirapex
  • Valproate • Depakene, Depakote
References

1. Levens S, Dyer AM, Zubritsky C, et al. Gambling among older, primary-care patients: an important public health concern. Am J Geriatr Psychiatry 2005;13(1):69-76.

2. Diagnostic and statistical manual of mental disorders, 4th ed. text rev. Washington, DC: American Psychiatric Association; 2000.

3. Unwin B, Davis M, DeLeeuw J. Pathological gambling. Am Fam Physician 2000;61:741-9.

4. De la Gandara JJ. Fluoxetine: open-trial in pathological gambling. Paper presented at: Annual Meeting of the American Psychiatric Association; May 16-21, 1999; Washington, DC.

5. Kim SW, Grant JE, Adson DE, et al. A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling. J Clin Psychiatry 2002;63(6):501-7.

6. Hollander E, DeCaria CM, Mari E, et al. Short-term single-blind fluvoxamine treatment of pathological gambling. Am J Psychiatry 1998;155(12):1781-3.

7. Hollander E, DeCaria CM, Finkell JN, et al. A randomized double-blind fluvoxamine/placebo crossover trial in pathological gambling. Biol Psychiatry 2000;47(9):813-7.

8. Zimmerman M, Breen RB, Posternak MA. An open-label study of citalopram in the treatment of pathological gambling. J Clin Psychiatry 2002;63(1):44-8.

9. Kim SW, Grant JE. An open naltrexone treatment study of pathological gambling disorder. Int Clin Psychopharmacol 2001;16(5):285-9.

10. Dodd ML, Klos KJ, Bower JH, et al. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62(9):1377-81.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Padala is assistant professor, department of psychiatry, University of Nebraska Medical Center, Omaha, NE.

Dr. Sattar is assistant professor, department of psychiatry, Creighton University Medical Center, Omaha, NE.

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Pathologic gambling among older patients causes more than financial losses; it also can lead to comorbid alcohol dependence, depression, anxiety disorders, and medical treatment nonadherence.1

Retirement, death of a spouse, “empty nest” syndrome, and other emotional, social, and financial stresses are common in later life. Some try to fill the gap with gambling, which can become pathologic. Early intervention and treatments addressing an older patient’s psychological and social needs can improve outcomes, however.

Screening for pathologic gambling

Late life pathologic gambling often goes undiagnosed but is thought to be on the rise. In a random sample of 843 older adults at scheduled primary-care appointments, 70% had gambled at least once in the past year and 11% were identified as at-risk gamblers.1

Diagnosing pathologic gambling requires a high degree of suspicion and inquiry. You must actively incorporate screening questions in the clinical interview to identify at-risk and pathologic gamblers in older patients.

Based on clinical experience and several DSM-IV-TR criteria,2 we developed a screening tool called PACE RULeS to identify pathologic gambling in this population (Box 1). A positive response to 5 or more of the 8 questions indicates a likely diagnosis of pathologic gambling. Lower scores may point to at-risk behavior and would require follow-up.

Box 1

8 questions to screen for pathologic gambling

Diagnose maladaptive or pathologic gambling if your patient answers yes to 5 or more of these “PACE RULeS” questions:

  • P—Are you often Preoccupied with thoughts of gambling?
  • A—Would you often gamble with increasing Amounts of money to achieve the same excitement?
  • C—Have you made repeated efforts to Control, cut back, or stop gambling?
  • E—Do you gamble to Escape daily problems and stresses?
  • R—After losing money, do you often Return another day to get even?
  • U—Have you ever committed Unlawful acts to finance gambling?
  • L—Have you Lost a significant relationship or job because of gambling?
  • S—Do you use your Savings to gamble?

Psychosocial intervention

After you make a diagnosis, manage your patient’s pathologic gambling with a comprehensive plan that includes family and community resources.3Box 2 shows interventions studied in the adult population that are appropriate for older patients.

Box 2

Interventions for older patients

  • Screen for active gambling
  • Intervene immediately if the patient is suicidal
  • Refer the patient to Gamblers Anonymous
  • Enlist family and friends to support treatment adherence and effectiveness. Be aware of confidentiality and ethical issues, however, especially during discussions with family members
  • Refer the patient to counseling
  • Actively participate in the treatment plan by assessing for relapses.

Medication

No psychotropics are FDA-approved for pathologic gambling, but adding medication to psychosocial interventions may help. Most medications studied in the general population are similarly efficacious in older adults. Slowly increase dosages, however, because of the greater risk of side effects in older patients.

Selective serotonin reuptake inhibitors help reduce gambling behavior, improve social and occupational functioning, and treat comorbid depression when used in relatively higher dosages. In anecdotal reports, the following medications have been found to be beneficial:

  • fluoxetine, 20 to 60 mg/d4
  • paroxetine, 20 to 60 mg/d5
  • fluvoxamine, 200 mg/d.6,7
Citalopram, 60 mg/d, also has shown efficacy in a single study of 15 adults ages 18 to 70.8 Similarly, clomipramine, 125 to 175 mg/d, has been effective in reducing gambling behavior. Naltrexone, 150 mg/d, appears to help individuals with intense urges to gamble, but liver function must be monitored.9 Anecdotal evidence also suggests that mood stabilizers including lithium, carbamazepine, and valproate may help treat impulsivity and comorbid bipolar disorder.

Although some medications treat pathologic gambling, others can cause it. Dopamine agonists such as pramipexole could cause reversible pathologic gambling in some older individuals who take it for Parkinson’s disease or restless legs syndrome.10

Drug brand names

  • Carbamazepine • Tegretol
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Fluvoxamine • Luvox
  • Lithium • Eskalith, Lithobid
  • Naltrexone • ReVia
  • Paroxetine • Paxil
  • Pramipexole • Mirapex
  • Valproate • Depakene, Depakote

Pathologic gambling among older patients causes more than financial losses; it also can lead to comorbid alcohol dependence, depression, anxiety disorders, and medical treatment nonadherence.1

Retirement, death of a spouse, “empty nest” syndrome, and other emotional, social, and financial stresses are common in later life. Some try to fill the gap with gambling, which can become pathologic. Early intervention and treatments addressing an older patient’s psychological and social needs can improve outcomes, however.

Screening for pathologic gambling

Late life pathologic gambling often goes undiagnosed but is thought to be on the rise. In a random sample of 843 older adults at scheduled primary-care appointments, 70% had gambled at least once in the past year and 11% were identified as at-risk gamblers.1

Diagnosing pathologic gambling requires a high degree of suspicion and inquiry. You must actively incorporate screening questions in the clinical interview to identify at-risk and pathologic gamblers in older patients.

Based on clinical experience and several DSM-IV-TR criteria,2 we developed a screening tool called PACE RULeS to identify pathologic gambling in this population (Box 1). A positive response to 5 or more of the 8 questions indicates a likely diagnosis of pathologic gambling. Lower scores may point to at-risk behavior and would require follow-up.

Box 1

8 questions to screen for pathologic gambling

Diagnose maladaptive or pathologic gambling if your patient answers yes to 5 or more of these “PACE RULeS” questions:

  • P—Are you often Preoccupied with thoughts of gambling?
  • A—Would you often gamble with increasing Amounts of money to achieve the same excitement?
  • C—Have you made repeated efforts to Control, cut back, or stop gambling?
  • E—Do you gamble to Escape daily problems and stresses?
  • R—After losing money, do you often Return another day to get even?
  • U—Have you ever committed Unlawful acts to finance gambling?
  • L—Have you Lost a significant relationship or job because of gambling?
  • S—Do you use your Savings to gamble?

Psychosocial intervention

After you make a diagnosis, manage your patient’s pathologic gambling with a comprehensive plan that includes family and community resources.3Box 2 shows interventions studied in the adult population that are appropriate for older patients.

Box 2

Interventions for older patients

  • Screen for active gambling
  • Intervene immediately if the patient is suicidal
  • Refer the patient to Gamblers Anonymous
  • Enlist family and friends to support treatment adherence and effectiveness. Be aware of confidentiality and ethical issues, however, especially during discussions with family members
  • Refer the patient to counseling
  • Actively participate in the treatment plan by assessing for relapses.

Medication

No psychotropics are FDA-approved for pathologic gambling, but adding medication to psychosocial interventions may help. Most medications studied in the general population are similarly efficacious in older adults. Slowly increase dosages, however, because of the greater risk of side effects in older patients.

Selective serotonin reuptake inhibitors help reduce gambling behavior, improve social and occupational functioning, and treat comorbid depression when used in relatively higher dosages. In anecdotal reports, the following medications have been found to be beneficial:

  • fluoxetine, 20 to 60 mg/d4
  • paroxetine, 20 to 60 mg/d5
  • fluvoxamine, 200 mg/d.6,7
Citalopram, 60 mg/d, also has shown efficacy in a single study of 15 adults ages 18 to 70.8 Similarly, clomipramine, 125 to 175 mg/d, has been effective in reducing gambling behavior. Naltrexone, 150 mg/d, appears to help individuals with intense urges to gamble, but liver function must be monitored.9 Anecdotal evidence also suggests that mood stabilizers including lithium, carbamazepine, and valproate may help treat impulsivity and comorbid bipolar disorder.

Although some medications treat pathologic gambling, others can cause it. Dopamine agonists such as pramipexole could cause reversible pathologic gambling in some older individuals who take it for Parkinson’s disease or restless legs syndrome.10

Drug brand names

  • Carbamazepine • Tegretol
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Fluvoxamine • Luvox
  • Lithium • Eskalith, Lithobid
  • Naltrexone • ReVia
  • Paroxetine • Paxil
  • Pramipexole • Mirapex
  • Valproate • Depakene, Depakote
References

1. Levens S, Dyer AM, Zubritsky C, et al. Gambling among older, primary-care patients: an important public health concern. Am J Geriatr Psychiatry 2005;13(1):69-76.

2. Diagnostic and statistical manual of mental disorders, 4th ed. text rev. Washington, DC: American Psychiatric Association; 2000.

3. Unwin B, Davis M, DeLeeuw J. Pathological gambling. Am Fam Physician 2000;61:741-9.

4. De la Gandara JJ. Fluoxetine: open-trial in pathological gambling. Paper presented at: Annual Meeting of the American Psychiatric Association; May 16-21, 1999; Washington, DC.

5. Kim SW, Grant JE, Adson DE, et al. A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling. J Clin Psychiatry 2002;63(6):501-7.

6. Hollander E, DeCaria CM, Mari E, et al. Short-term single-blind fluvoxamine treatment of pathological gambling. Am J Psychiatry 1998;155(12):1781-3.

7. Hollander E, DeCaria CM, Finkell JN, et al. A randomized double-blind fluvoxamine/placebo crossover trial in pathological gambling. Biol Psychiatry 2000;47(9):813-7.

8. Zimmerman M, Breen RB, Posternak MA. An open-label study of citalopram in the treatment of pathological gambling. J Clin Psychiatry 2002;63(1):44-8.

9. Kim SW, Grant JE. An open naltrexone treatment study of pathological gambling disorder. Int Clin Psychopharmacol 2001;16(5):285-9.

10. Dodd ML, Klos KJ, Bower JH, et al. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62(9):1377-81.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Padala is assistant professor, department of psychiatry, University of Nebraska Medical Center, Omaha, NE.

Dr. Sattar is assistant professor, department of psychiatry, Creighton University Medical Center, Omaha, NE.

References

1. Levens S, Dyer AM, Zubritsky C, et al. Gambling among older, primary-care patients: an important public health concern. Am J Geriatr Psychiatry 2005;13(1):69-76.

2. Diagnostic and statistical manual of mental disorders, 4th ed. text rev. Washington, DC: American Psychiatric Association; 2000.

3. Unwin B, Davis M, DeLeeuw J. Pathological gambling. Am Fam Physician 2000;61:741-9.

4. De la Gandara JJ. Fluoxetine: open-trial in pathological gambling. Paper presented at: Annual Meeting of the American Psychiatric Association; May 16-21, 1999; Washington, DC.

5. Kim SW, Grant JE, Adson DE, et al. A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling. J Clin Psychiatry 2002;63(6):501-7.

6. Hollander E, DeCaria CM, Mari E, et al. Short-term single-blind fluvoxamine treatment of pathological gambling. Am J Psychiatry 1998;155(12):1781-3.

7. Hollander E, DeCaria CM, Finkell JN, et al. A randomized double-blind fluvoxamine/placebo crossover trial in pathological gambling. Biol Psychiatry 2000;47(9):813-7.

8. Zimmerman M, Breen RB, Posternak MA. An open-label study of citalopram in the treatment of pathological gambling. J Clin Psychiatry 2002;63(1):44-8.

9. Kim SW, Grant JE. An open naltrexone treatment study of pathological gambling disorder. Int Clin Psychopharmacol 2001;16(5):285-9.

10. Dodd ML, Klos KJ, Bower JH, et al. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62(9):1377-81.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Padala is assistant professor, department of psychiatry, University of Nebraska Medical Center, Omaha, NE.

Dr. Sattar is assistant professor, department of psychiatry, Creighton University Medical Center, Omaha, NE.

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PDA prescription program pros and cons

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Personal digital assistant (PDA)-based drug reference software can help you make informed point-of-care prescription decisions, but accuracy, usability, and comprehensiveness vary greatly among programs.

This article looks at the benefits and drawbacks of popular PDA drug reference programs and offers advice on choosing the right one for your practice.

PDA Program benefits

Equipping your PDA with drug reference software makes prescription information portable and accessible. PDA-based drug guides also:

 

  • are easy to update. Most PDA-based systems automatically update as part of routine synchronization procedures between the device and its host computer, keeping the information up-to-date. This is an important feature as some drug databases are updated daily.
  • list potential side effects. Most programs list all potential medication side effects and distinguish between common and uncommon adverse events.
  • list possible drug-drug interactions. This feature gives PDA-based drug guides a clear advantage over print textbooks. Users enter two or more medications, and the program searches for potential interactions between them.
  • list interactions with alternative medications. Many databases include herbal supplements and other nontraditional pharmaceuticals.
  • offer additional tools, such as medical calculators, treatment algorithms, and other handy features.

Drawbacks

Because PDA screens are so small, PDA-based drug guides must compromise between level of detail and ease of use. Unlike standard drug reference books, for example, PDA programs rarely list rates of side effects or comparisons with placebo.

PDA-based drug guides usually do not display references or analyses of the data behind the lists. For example, many programs provide dosing suggestions for special populations—such as the elderly, medically ill, and children—but the basis for these dose adjustments often is unclear or does not jibe with other programs. Most PDA drug software excludes other specific information, such as the evidence behind drug indications.

Researchers’ ratings

Some PDA-based drug databases, such as mobilePDR, evolved from written pharmacy databases. Others, such as ePharmacopoeia or Epocrates, were developed from more-general reference tools aimed at students and physicians. Overall, the former type of drug guide is more comprehensive and the latter is easier to use, although all PDA drug software offers some degree of comprehensiveness and usability.

PDA-based programs differ greatly, however, and the following researchers have explored the differences.

 

  • Enders et al1 in 2001 rated Lexi-Drugs Platinum the most comprehensive and accurate among nine programs.
  • Galt and colleagues,2 placing more weight on safety concerns than ease of use, in 2005 also rated Lexi-Drugs Platinum number one among 11 programs.
  • Clauson et al3 in 2004 rated Lexi-Drugs number one among 10 programs, but noted that other products were catching up.
  • Knollmann et al4 in 2004 rated 11 PDA-based drug databases on ease of use, comprehensiveness, and accuracy. They entered three pairs of drug names into each program; one pair included an herbal supplement.
  • Perkins et al5 in 2004 entered 37 pairs of drug names into eight programs to test their ability to detect drug-drug interactions. They found that Epocrates offered the best combination of sensitivity (identifying all potential interactions) and specificity (reporting only important interactions). Lexi-Drugs had perfect sensitivity but comparatively poor specificity.

Which program should you choose?

No PDA-based drug reference will provide everything you need, so be clear on what you desire most when choosing a program:

 

  • If drug safety is your primary concern, Lexi-Drugs might be best, although it tends to report clinically insignificant interactions.
  • If you want only clinically significant interactions, consider Epocrates or Epocrates RX Pro.
  • If a comprehensive database is critical, Clinical Pharmacology OnHand has the most extensive drug database.
  • If you’re looking for the best combination of accuracy, comprehensiveness, and physician-friendly features, Lexi-Drugs and PEPID PDC might be most effective, though Epocrates is also a reasonable performer.
  • If you wish to understand the evidence behind each recommendation, books and online pharmaceutical references remain better options.

Cost is another factor. This might explain why Epocrates—which offers a free version for physicians and medical students—is more popular than Lexi-Drugs, which is one of the most expensive programs at $70 for the basic version and $285 for the comprehensive suite. Most programs have two options: a less expensive—or even free—drug database that costs up to $75 and a suite of features such as treatment algorithms or diagnosis databases that range from $60 to almost $300.

Personal experience is the best way to determine which product is best. Most manufacturers let you try their programs before buying.

Related resources

Chan CH, Luo JS, Kennedy RS. Concise Guide to Computers in Clinical Psychiatry. Washington DC: American Psychiatric Press; 2002

American Association for Technology in Psychiatry. www.techpsych.org

References

1. Enders SJ, Enders JM, Holstad SG. Drug-information software for Palm operating system personal digital assistants: breadth, clinical dependability, and ease of use. Pharmacotherapy 2002;22:1036-40.

2. Galt KA, Rule AM, Houghton B, et al. Personal digital assistant-based drug information sources: potential to improve medication safety. J Med Librar Assoc. 2005;93:229-36.

3. Clauson KA, Seamon MJ, Clauson AS, et al. Evaluation of drug information databases for personal digital assistants. Am J Health Syst Pharm 2004;61:1015-24.

4. Knollmann BC, Smyth BJ, Garnett CE, et al. Personal digital assistant-based drug reference software as tools to improve rational prescribing: benchmark criteria and performance. Clin Pharmacol Ther 2005;78:7-18.

5. Perkins NA, Murphy JE, Malone DC, Armstrong EP. Performance of drug-drug interaction software for personal digital assistants. Ann Pharmacother 2006;40:850-5.

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Personal digital assistant (PDA)-based drug reference software can help you make informed point-of-care prescription decisions, but accuracy, usability, and comprehensiveness vary greatly among programs.

This article looks at the benefits and drawbacks of popular PDA drug reference programs and offers advice on choosing the right one for your practice.

PDA Program benefits

Equipping your PDA with drug reference software makes prescription information portable and accessible. PDA-based drug guides also:

 

  • are easy to update. Most PDA-based systems automatically update as part of routine synchronization procedures between the device and its host computer, keeping the information up-to-date. This is an important feature as some drug databases are updated daily.
  • list potential side effects. Most programs list all potential medication side effects and distinguish between common and uncommon adverse events.
  • list possible drug-drug interactions. This feature gives PDA-based drug guides a clear advantage over print textbooks. Users enter two or more medications, and the program searches for potential interactions between them.
  • list interactions with alternative medications. Many databases include herbal supplements and other nontraditional pharmaceuticals.
  • offer additional tools, such as medical calculators, treatment algorithms, and other handy features.

Drawbacks

Because PDA screens are so small, PDA-based drug guides must compromise between level of detail and ease of use. Unlike standard drug reference books, for example, PDA programs rarely list rates of side effects or comparisons with placebo.

PDA-based drug guides usually do not display references or analyses of the data behind the lists. For example, many programs provide dosing suggestions for special populations—such as the elderly, medically ill, and children—but the basis for these dose adjustments often is unclear or does not jibe with other programs. Most PDA drug software excludes other specific information, such as the evidence behind drug indications.

Researchers’ ratings

Some PDA-based drug databases, such as mobilePDR, evolved from written pharmacy databases. Others, such as ePharmacopoeia or Epocrates, were developed from more-general reference tools aimed at students and physicians. Overall, the former type of drug guide is more comprehensive and the latter is easier to use, although all PDA drug software offers some degree of comprehensiveness and usability.

PDA-based programs differ greatly, however, and the following researchers have explored the differences.

 

  • Enders et al1 in 2001 rated Lexi-Drugs Platinum the most comprehensive and accurate among nine programs.
  • Galt and colleagues,2 placing more weight on safety concerns than ease of use, in 2005 also rated Lexi-Drugs Platinum number one among 11 programs.
  • Clauson et al3 in 2004 rated Lexi-Drugs number one among 10 programs, but noted that other products were catching up.
  • Knollmann et al4 in 2004 rated 11 PDA-based drug databases on ease of use, comprehensiveness, and accuracy. They entered three pairs of drug names into each program; one pair included an herbal supplement.
  • Perkins et al5 in 2004 entered 37 pairs of drug names into eight programs to test their ability to detect drug-drug interactions. They found that Epocrates offered the best combination of sensitivity (identifying all potential interactions) and specificity (reporting only important interactions). Lexi-Drugs had perfect sensitivity but comparatively poor specificity.

Which program should you choose?

No PDA-based drug reference will provide everything you need, so be clear on what you desire most when choosing a program:

 

  • If drug safety is your primary concern, Lexi-Drugs might be best, although it tends to report clinically insignificant interactions.
  • If you want only clinically significant interactions, consider Epocrates or Epocrates RX Pro.
  • If a comprehensive database is critical, Clinical Pharmacology OnHand has the most extensive drug database.
  • If you’re looking for the best combination of accuracy, comprehensiveness, and physician-friendly features, Lexi-Drugs and PEPID PDC might be most effective, though Epocrates is also a reasonable performer.
  • If you wish to understand the evidence behind each recommendation, books and online pharmaceutical references remain better options.

Cost is another factor. This might explain why Epocrates—which offers a free version for physicians and medical students—is more popular than Lexi-Drugs, which is one of the most expensive programs at $70 for the basic version and $285 for the comprehensive suite. Most programs have two options: a less expensive—or even free—drug database that costs up to $75 and a suite of features such as treatment algorithms or diagnosis databases that range from $60 to almost $300.

Personal experience is the best way to determine which product is best. Most manufacturers let you try their programs before buying.

Related resources

Chan CH, Luo JS, Kennedy RS. Concise Guide to Computers in Clinical Psychiatry. Washington DC: American Psychiatric Press; 2002

American Association for Technology in Psychiatry. www.techpsych.org

Personal digital assistant (PDA)-based drug reference software can help you make informed point-of-care prescription decisions, but accuracy, usability, and comprehensiveness vary greatly among programs.

This article looks at the benefits and drawbacks of popular PDA drug reference programs and offers advice on choosing the right one for your practice.

PDA Program benefits

Equipping your PDA with drug reference software makes prescription information portable and accessible. PDA-based drug guides also:

 

  • are easy to update. Most PDA-based systems automatically update as part of routine synchronization procedures between the device and its host computer, keeping the information up-to-date. This is an important feature as some drug databases are updated daily.
  • list potential side effects. Most programs list all potential medication side effects and distinguish between common and uncommon adverse events.
  • list possible drug-drug interactions. This feature gives PDA-based drug guides a clear advantage over print textbooks. Users enter two or more medications, and the program searches for potential interactions between them.
  • list interactions with alternative medications. Many databases include herbal supplements and other nontraditional pharmaceuticals.
  • offer additional tools, such as medical calculators, treatment algorithms, and other handy features.

Drawbacks

Because PDA screens are so small, PDA-based drug guides must compromise between level of detail and ease of use. Unlike standard drug reference books, for example, PDA programs rarely list rates of side effects or comparisons with placebo.

PDA-based drug guides usually do not display references or analyses of the data behind the lists. For example, many programs provide dosing suggestions for special populations—such as the elderly, medically ill, and children—but the basis for these dose adjustments often is unclear or does not jibe with other programs. Most PDA drug software excludes other specific information, such as the evidence behind drug indications.

Researchers’ ratings

Some PDA-based drug databases, such as mobilePDR, evolved from written pharmacy databases. Others, such as ePharmacopoeia or Epocrates, were developed from more-general reference tools aimed at students and physicians. Overall, the former type of drug guide is more comprehensive and the latter is easier to use, although all PDA drug software offers some degree of comprehensiveness and usability.

PDA-based programs differ greatly, however, and the following researchers have explored the differences.

 

  • Enders et al1 in 2001 rated Lexi-Drugs Platinum the most comprehensive and accurate among nine programs.
  • Galt and colleagues,2 placing more weight on safety concerns than ease of use, in 2005 also rated Lexi-Drugs Platinum number one among 11 programs.
  • Clauson et al3 in 2004 rated Lexi-Drugs number one among 10 programs, but noted that other products were catching up.
  • Knollmann et al4 in 2004 rated 11 PDA-based drug databases on ease of use, comprehensiveness, and accuracy. They entered three pairs of drug names into each program; one pair included an herbal supplement.
  • Perkins et al5 in 2004 entered 37 pairs of drug names into eight programs to test their ability to detect drug-drug interactions. They found that Epocrates offered the best combination of sensitivity (identifying all potential interactions) and specificity (reporting only important interactions). Lexi-Drugs had perfect sensitivity but comparatively poor specificity.

Which program should you choose?

No PDA-based drug reference will provide everything you need, so be clear on what you desire most when choosing a program:

 

  • If drug safety is your primary concern, Lexi-Drugs might be best, although it tends to report clinically insignificant interactions.
  • If you want only clinically significant interactions, consider Epocrates or Epocrates RX Pro.
  • If a comprehensive database is critical, Clinical Pharmacology OnHand has the most extensive drug database.
  • If you’re looking for the best combination of accuracy, comprehensiveness, and physician-friendly features, Lexi-Drugs and PEPID PDC might be most effective, though Epocrates is also a reasonable performer.
  • If you wish to understand the evidence behind each recommendation, books and online pharmaceutical references remain better options.

Cost is another factor. This might explain why Epocrates—which offers a free version for physicians and medical students—is more popular than Lexi-Drugs, which is one of the most expensive programs at $70 for the basic version and $285 for the comprehensive suite. Most programs have two options: a less expensive—or even free—drug database that costs up to $75 and a suite of features such as treatment algorithms or diagnosis databases that range from $60 to almost $300.

Personal experience is the best way to determine which product is best. Most manufacturers let you try their programs before buying.

Related resources

Chan CH, Luo JS, Kennedy RS. Concise Guide to Computers in Clinical Psychiatry. Washington DC: American Psychiatric Press; 2002

American Association for Technology in Psychiatry. www.techpsych.org

References

1. Enders SJ, Enders JM, Holstad SG. Drug-information software for Palm operating system personal digital assistants: breadth, clinical dependability, and ease of use. Pharmacotherapy 2002;22:1036-40.

2. Galt KA, Rule AM, Houghton B, et al. Personal digital assistant-based drug information sources: potential to improve medication safety. J Med Librar Assoc. 2005;93:229-36.

3. Clauson KA, Seamon MJ, Clauson AS, et al. Evaluation of drug information databases for personal digital assistants. Am J Health Syst Pharm 2004;61:1015-24.

4. Knollmann BC, Smyth BJ, Garnett CE, et al. Personal digital assistant-based drug reference software as tools to improve rational prescribing: benchmark criteria and performance. Clin Pharmacol Ther 2005;78:7-18.

5. Perkins NA, Murphy JE, Malone DC, Armstrong EP. Performance of drug-drug interaction software for personal digital assistants. Ann Pharmacother 2006;40:850-5.

References

1. Enders SJ, Enders JM, Holstad SG. Drug-information software for Palm operating system personal digital assistants: breadth, clinical dependability, and ease of use. Pharmacotherapy 2002;22:1036-40.

2. Galt KA, Rule AM, Houghton B, et al. Personal digital assistant-based drug information sources: potential to improve medication safety. J Med Librar Assoc. 2005;93:229-36.

3. Clauson KA, Seamon MJ, Clauson AS, et al. Evaluation of drug information databases for personal digital assistants. Am J Health Syst Pharm 2004;61:1015-24.

4. Knollmann BC, Smyth BJ, Garnett CE, et al. Personal digital assistant-based drug reference software as tools to improve rational prescribing: benchmark criteria and performance. Clin Pharmacol Ther 2005;78:7-18.

5. Perkins NA, Murphy JE, Malone DC, Armstrong EP. Performance of drug-drug interaction software for personal digital assistants. Ann Pharmacother 2006;40:850-5.

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Medicare, private HMOs, and Veterans Affairs medical centers justify drug formularies by claiming lower co-payments and insurance premiums and cost-effective health care without diminishing quality. But some physicians believe having to prescribe from a list interferes in medical practice and reduces clinical autonomy.

You may view having to request a consult as a hassle when you wish to prescribe a nonformulary drug. A thoroughly researched nonformulary request can expedite the process, however.

5 strategies for nonformulary requests

  1. Reference evidence-based information to support your request.
  2. Document your patient’s drug trials, dosages, clinical response failure, and adverse effects to expedite review of nonformulary requests.
  3. Ask the patient about family history of response to a medication. Such pharmacogenetic data may predict response in first-degree relatives and support a nonformulary request.
  4. Document pharmacokinetic or pharmacodynamic interactions between the formulary drug and other medications the patient is taking.
  5. List known interactions with foods and diseases.

5 tips for practicing within a formulary

Physicians are not alone in being leery of drug formularies. Patients encouraged by direct-to-consumer advertising ask for the newest—and often most expensive medications—may share that wariness.1 To help us work within the restrictions of a drug formulary system and provide appropriate patient care, we suggest the following helpful strategies:

  1. Understand that formularies are well intentioned and highly calculated. Lists are updated frequently to represent physicians’ and other experts’ clinical judgment on the use of safe, appropriate, and cost-effective medications, therapies, and health products that best serve patients.2
  2. Address patient concerns to help them accept and adhere to prescribed formulary drugs. Emphasize that a medication’s cost does not determine its efficacy.
  3. Remember that your duty to provide proper treatment supersedes cost considerations.
  4. Ask for a physician review when your request for a nonformulary drug is denied.
  5. Use nonpharmacologic treatments such as sleep hygiene, cognitive-behavioral therapy, or relaxation techniques when possible. This approach reduces polypharmacy and keeps costs low.
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Medicare, private HMOs, and Veterans Affairs medical centers justify drug formularies by claiming lower co-payments and insurance premiums and cost-effective health care without diminishing quality. But some physicians believe having to prescribe from a list interferes in medical practice and reduces clinical autonomy.

You may view having to request a consult as a hassle when you wish to prescribe a nonformulary drug. A thoroughly researched nonformulary request can expedite the process, however.

5 strategies for nonformulary requests

  1. Reference evidence-based information to support your request.
  2. Document your patient’s drug trials, dosages, clinical response failure, and adverse effects to expedite review of nonformulary requests.
  3. Ask the patient about family history of response to a medication. Such pharmacogenetic data may predict response in first-degree relatives and support a nonformulary request.
  4. Document pharmacokinetic or pharmacodynamic interactions between the formulary drug and other medications the patient is taking.
  5. List known interactions with foods and diseases.

5 tips for practicing within a formulary

Physicians are not alone in being leery of drug formularies. Patients encouraged by direct-to-consumer advertising ask for the newest—and often most expensive medications—may share that wariness.1 To help us work within the restrictions of a drug formulary system and provide appropriate patient care, we suggest the following helpful strategies:

  1. Understand that formularies are well intentioned and highly calculated. Lists are updated frequently to represent physicians’ and other experts’ clinical judgment on the use of safe, appropriate, and cost-effective medications, therapies, and health products that best serve patients.2
  2. Address patient concerns to help them accept and adhere to prescribed formulary drugs. Emphasize that a medication’s cost does not determine its efficacy.
  3. Remember that your duty to provide proper treatment supersedes cost considerations.
  4. Ask for a physician review when your request for a nonformulary drug is denied.
  5. Use nonpharmacologic treatments such as sleep hygiene, cognitive-behavioral therapy, or relaxation techniques when possible. This approach reduces polypharmacy and keeps costs low.

Medicare, private HMOs, and Veterans Affairs medical centers justify drug formularies by claiming lower co-payments and insurance premiums and cost-effective health care without diminishing quality. But some physicians believe having to prescribe from a list interferes in medical practice and reduces clinical autonomy.

You may view having to request a consult as a hassle when you wish to prescribe a nonformulary drug. A thoroughly researched nonformulary request can expedite the process, however.

5 strategies for nonformulary requests

  1. Reference evidence-based information to support your request.
  2. Document your patient’s drug trials, dosages, clinical response failure, and adverse effects to expedite review of nonformulary requests.
  3. Ask the patient about family history of response to a medication. Such pharmacogenetic data may predict response in first-degree relatives and support a nonformulary request.
  4. Document pharmacokinetic or pharmacodynamic interactions between the formulary drug and other medications the patient is taking.
  5. List known interactions with foods and diseases.

5 tips for practicing within a formulary

Physicians are not alone in being leery of drug formularies. Patients encouraged by direct-to-consumer advertising ask for the newest—and often most expensive medications—may share that wariness.1 To help us work within the restrictions of a drug formulary system and provide appropriate patient care, we suggest the following helpful strategies:

  1. Understand that formularies are well intentioned and highly calculated. Lists are updated frequently to represent physicians’ and other experts’ clinical judgment on the use of safe, appropriate, and cost-effective medications, therapies, and health products that best serve patients.2
  2. Address patient concerns to help them accept and adhere to prescribed formulary drugs. Emphasize that a medication’s cost does not determine its efficacy.
  3. Remember that your duty to provide proper treatment supersedes cost considerations.
  4. Ask for a physician review when your request for a nonformulary drug is denied.
  5. Use nonpharmacologic treatments such as sleep hygiene, cognitive-behavioral therapy, or relaxation techniques when possible. This approach reduces polypharmacy and keeps costs low.
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6 safety rules for tapering antidepressants

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Side effects to discontinuing serotonin reuptake inhibitor (SRI) treatment are common and may be severe.1 Patients who are not prepared for these reactions may attribute symptoms to other causes such as a medical illness. Educate your patient about potential side effects to mitigate problems such as relapse or patient distress.

1 Warn your patient

Alert patients to potential discontinuation reactions when prescribing any antidepressant, particularly SRIs because they seem to cause more discontinuation problems than other classes of drugs. Although reactions appear to be more common and severe with short-acting drugs such as venlafaxine and paroxetine, they can occur with longer half-life agents such as fluoxetine and sertraline.

Warn patients about discontinuation effects when starting treatment and before the planned drug taper. In particular, caution them against missing doses or stopping a drug without informing you.

2 Know the symptoms

Common discontinuation symptoms can be grouped into six areas:

  • Neurosensory—vertigo, paresthesias, shock-like reactions, myalgia
  • Neuromotor—tremor, myoclonus, ataxia, visual changes, piloerection
  • Gastrointestinal—nausea, vomiting, diarrhea
  • Psychiatric—anxiety, depressed mood, suicidal ideation, irritability
  • Vasomotor—flushing, diaphoresis
  • Other neuropsychiatric—anorexia, insomnia, vivid dreams, asthenia, chills.2
Typical onset is rapid, and symptoms usually resolve in 2 to 3 weeks or if treatment is restarted.

3 Distinguish discontinuation reactions from relapse

Although depressed mood and anxiety may occur during taper, these symptoms tend to be transient in most patients. Severe or persistent symptoms—including emerging suicidal ideation—may indicate a relapse.

4 Reduce medication slowly

Tapering is recommended for all antidepressants but should be particularly slow for certain drugs—including venlafaxine, paroxetine, and clomipramine—which can cause significant discontinuation effects. For example, venlafaxine at 225 mg/d could be reduced by 75 mg/d every 1 to 2 weeks, with a final step at 37.5 mg/d for at least 1 week.

If discontinuation reactions are a problem, ultimate discontinuation may require substituting a longer-acting medication such as fluoxetine during the tapering period. For example, add fluoxetine, 10 to 20 mg/d, for 1 week, then stop both antidepressants or discontinue the first medication and continue fluoxetine for 2 to 3 weeks until the risk of reactions passes.

Clinicians often are concerned about serotonin syndrome caused by combining SRIs. Isolated cases have been reported, but the small, finite chance of serotonin syndrome is much lower than the risk of severe discontinuation reactions.

5 Titrate up and taper down

When switching to another SRI, titrate the second drug upward while tapering off the first. Remember that changing to a drug that does not act on serotonin, such as bupropion, can protect against discontinuation effects.

6 Allow for pregnancy

Infants born to mothers taking antidepressants can exhibit discontinuation symptoms,2 particularly with shorter-acting drugs such as paroxetine or venlafaxine. Consider tapering the antidepressant early in the patient’s third trimester, then re-institute treatment after delivery. If an antidepressant is required during pregnancy, try using one with a longer half-life such as fluoxetine.

Drug brand names

  • Bupropion • Wellbutrin
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Paroxetine • Paxil
  • Sertraline • Zoloft
  • Venlafaxine • Effexor
References

1. Schatzberg AF, Blier P, Delgado PL, et al. Antidepressant discontinuation syndrome: consensus panel recommendations for clinical management and additional research. J Clin Psychiatry 2006;67 (suppl 4):27-30.

2. Shelton RC. The nature of the discontinuation syndrome associated with antidepressant drugs. J Clin Psychiatry 2006;67(suppl 4):3-7.

Dr. Shelton is the James G. Blakemore Research Professor and vice-chair for research, department of psychiatry, and professor of pharmacology, Vanderbilt University, Nashville, TN.

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Side effects to discontinuing serotonin reuptake inhibitor (SRI) treatment are common and may be severe.1 Patients who are not prepared for these reactions may attribute symptoms to other causes such as a medical illness. Educate your patient about potential side effects to mitigate problems such as relapse or patient distress.

1 Warn your patient

Alert patients to potential discontinuation reactions when prescribing any antidepressant, particularly SRIs because they seem to cause more discontinuation problems than other classes of drugs. Although reactions appear to be more common and severe with short-acting drugs such as venlafaxine and paroxetine, they can occur with longer half-life agents such as fluoxetine and sertraline.

Warn patients about discontinuation effects when starting treatment and before the planned drug taper. In particular, caution them against missing doses or stopping a drug without informing you.

2 Know the symptoms

Common discontinuation symptoms can be grouped into six areas:

  • Neurosensory—vertigo, paresthesias, shock-like reactions, myalgia
  • Neuromotor—tremor, myoclonus, ataxia, visual changes, piloerection
  • Gastrointestinal—nausea, vomiting, diarrhea
  • Psychiatric—anxiety, depressed mood, suicidal ideation, irritability
  • Vasomotor—flushing, diaphoresis
  • Other neuropsychiatric—anorexia, insomnia, vivid dreams, asthenia, chills.2
Typical onset is rapid, and symptoms usually resolve in 2 to 3 weeks or if treatment is restarted.

3 Distinguish discontinuation reactions from relapse

Although depressed mood and anxiety may occur during taper, these symptoms tend to be transient in most patients. Severe or persistent symptoms—including emerging suicidal ideation—may indicate a relapse.

4 Reduce medication slowly

Tapering is recommended for all antidepressants but should be particularly slow for certain drugs—including venlafaxine, paroxetine, and clomipramine—which can cause significant discontinuation effects. For example, venlafaxine at 225 mg/d could be reduced by 75 mg/d every 1 to 2 weeks, with a final step at 37.5 mg/d for at least 1 week.

If discontinuation reactions are a problem, ultimate discontinuation may require substituting a longer-acting medication such as fluoxetine during the tapering period. For example, add fluoxetine, 10 to 20 mg/d, for 1 week, then stop both antidepressants or discontinue the first medication and continue fluoxetine for 2 to 3 weeks until the risk of reactions passes.

Clinicians often are concerned about serotonin syndrome caused by combining SRIs. Isolated cases have been reported, but the small, finite chance of serotonin syndrome is much lower than the risk of severe discontinuation reactions.

5 Titrate up and taper down

When switching to another SRI, titrate the second drug upward while tapering off the first. Remember that changing to a drug that does not act on serotonin, such as bupropion, can protect against discontinuation effects.

6 Allow for pregnancy

Infants born to mothers taking antidepressants can exhibit discontinuation symptoms,2 particularly with shorter-acting drugs such as paroxetine or venlafaxine. Consider tapering the antidepressant early in the patient’s third trimester, then re-institute treatment after delivery. If an antidepressant is required during pregnancy, try using one with a longer half-life such as fluoxetine.

Drug brand names

  • Bupropion • Wellbutrin
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Paroxetine • Paxil
  • Sertraline • Zoloft
  • Venlafaxine • Effexor

Side effects to discontinuing serotonin reuptake inhibitor (SRI) treatment are common and may be severe.1 Patients who are not prepared for these reactions may attribute symptoms to other causes such as a medical illness. Educate your patient about potential side effects to mitigate problems such as relapse or patient distress.

1 Warn your patient

Alert patients to potential discontinuation reactions when prescribing any antidepressant, particularly SRIs because they seem to cause more discontinuation problems than other classes of drugs. Although reactions appear to be more common and severe with short-acting drugs such as venlafaxine and paroxetine, they can occur with longer half-life agents such as fluoxetine and sertraline.

Warn patients about discontinuation effects when starting treatment and before the planned drug taper. In particular, caution them against missing doses or stopping a drug without informing you.

2 Know the symptoms

Common discontinuation symptoms can be grouped into six areas:

  • Neurosensory—vertigo, paresthesias, shock-like reactions, myalgia
  • Neuromotor—tremor, myoclonus, ataxia, visual changes, piloerection
  • Gastrointestinal—nausea, vomiting, diarrhea
  • Psychiatric—anxiety, depressed mood, suicidal ideation, irritability
  • Vasomotor—flushing, diaphoresis
  • Other neuropsychiatric—anorexia, insomnia, vivid dreams, asthenia, chills.2
Typical onset is rapid, and symptoms usually resolve in 2 to 3 weeks or if treatment is restarted.

3 Distinguish discontinuation reactions from relapse

Although depressed mood and anxiety may occur during taper, these symptoms tend to be transient in most patients. Severe or persistent symptoms—including emerging suicidal ideation—may indicate a relapse.

4 Reduce medication slowly

Tapering is recommended for all antidepressants but should be particularly slow for certain drugs—including venlafaxine, paroxetine, and clomipramine—which can cause significant discontinuation effects. For example, venlafaxine at 225 mg/d could be reduced by 75 mg/d every 1 to 2 weeks, with a final step at 37.5 mg/d for at least 1 week.

If discontinuation reactions are a problem, ultimate discontinuation may require substituting a longer-acting medication such as fluoxetine during the tapering period. For example, add fluoxetine, 10 to 20 mg/d, for 1 week, then stop both antidepressants or discontinue the first medication and continue fluoxetine for 2 to 3 weeks until the risk of reactions passes.

Clinicians often are concerned about serotonin syndrome caused by combining SRIs. Isolated cases have been reported, but the small, finite chance of serotonin syndrome is much lower than the risk of severe discontinuation reactions.

5 Titrate up and taper down

When switching to another SRI, titrate the second drug upward while tapering off the first. Remember that changing to a drug that does not act on serotonin, such as bupropion, can protect against discontinuation effects.

6 Allow for pregnancy

Infants born to mothers taking antidepressants can exhibit discontinuation symptoms,2 particularly with shorter-acting drugs such as paroxetine or venlafaxine. Consider tapering the antidepressant early in the patient’s third trimester, then re-institute treatment after delivery. If an antidepressant is required during pregnancy, try using one with a longer half-life such as fluoxetine.

Drug brand names

  • Bupropion • Wellbutrin
  • Clomipramine • Anafranil
  • Fluoxetine • Prozac
  • Paroxetine • Paxil
  • Sertraline • Zoloft
  • Venlafaxine • Effexor
References

1. Schatzberg AF, Blier P, Delgado PL, et al. Antidepressant discontinuation syndrome: consensus panel recommendations for clinical management and additional research. J Clin Psychiatry 2006;67 (suppl 4):27-30.

2. Shelton RC. The nature of the discontinuation syndrome associated with antidepressant drugs. J Clin Psychiatry 2006;67(suppl 4):3-7.

Dr. Shelton is the James G. Blakemore Research Professor and vice-chair for research, department of psychiatry, and professor of pharmacology, Vanderbilt University, Nashville, TN.

References

1. Schatzberg AF, Blier P, Delgado PL, et al. Antidepressant discontinuation syndrome: consensus panel recommendations for clinical management and additional research. J Clin Psychiatry 2006;67 (suppl 4):27-30.

2. Shelton RC. The nature of the discontinuation syndrome associated with antidepressant drugs. J Clin Psychiatry 2006;67(suppl 4):3-7.

Dr. Shelton is the James G. Blakemore Research Professor and vice-chair for research, department of psychiatry, and professor of pharmacology, Vanderbilt University, Nashville, TN.

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Drink to your health? Beware energy drinks’ risks

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Energy drinks’ popularity has soared among consumers who crave an energy boost from the highly caffeinated herbal concoctions. Clinicians should ask patients about energy drink consumption because:

  • caffeine abuse can exacerbate mood and anxiety disorders and disrupt sleep patterns
  • herbal additives can cause physical and/or psychiatric side effects
  • some ingredients interact with prescription or OTC medications
  • effects of energy drinks may contribute to a patient’s presenting complaint.

Approximately 70% of patients1 do not report energy drink use because they believe these products are natural and safe. Ask patients if they consume energy drinks so you can alert them to the health risks.

A Stimulating recipe

Two main ingredients in most energy drinks are caffeine and carbohydrates in the form of glucose, sucrose, fructose, galactose, and maltodextrins (Table).

Table

Caffeine and carbohydrate content of popular energy drinks

Drink nameCaffeine contentCarbohydrate content
Red Bull (8.5 oz)80 mg28 g
Full Throttle (16 oz)144 mg57 g
SoBe No Fear (16 oz)158 mg66 g
Source: American Beverage Association, SoBe Beverages, Red Bull
Carbohydrates. Four popular brands of energy drinks contain 28 to 66 grams of carbohydrates—a slice of whole wheat bread has 20 grams of carbohydrates. Urge patients taking antipsychotics that could cause weight gain to avoid these drinks.

Caffeine. Energy drinks contain 75 to 158 mg of caffeine per can—8 ounces of coffee has 150 mg of caffeine. Also, some products include the South American plant extracts guarana or yerba mate, which contain an unknown amount of caffeine.

High caffeine intake—≥300 mg/d—might exacerbate bipolar disorder’s manic symptoms. Also find out about additional caffeine intake from coffee, tea, soda, and some OTC medications, such as Excedrin.

Herbal ingredients. Ginseng or ginkgo biloba can cause patients to feel jittery or anxious. When taken in large amounts—the FDA has no guidelines on safe dosages—these ingredients can aggravate manic or psychotic symptoms.

Significant energy drink consumption—3 or more 8-oz drinks per day—can bring about physical side effects such as tachycardia and insomnia. Advise patients to limit their intake to 2 drinks per day, and suggest safer ways to increase energy levels such as moderate exercise and adequate sleep.

References

1. Ciocon JO, Ciocon DG, Galindo DJ. Dietary supplements in primary care: botanicals can affect surgical outcomes and follow-up. Geriatrics 2004;59(9):20-4.

Dr. Berigan is a contracting psychiatrist at Behavioral Health Services, Fort Huachuca, AZ.

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Energy drinks’ popularity has soared among consumers who crave an energy boost from the highly caffeinated herbal concoctions. Clinicians should ask patients about energy drink consumption because:

  • caffeine abuse can exacerbate mood and anxiety disorders and disrupt sleep patterns
  • herbal additives can cause physical and/or psychiatric side effects
  • some ingredients interact with prescription or OTC medications
  • effects of energy drinks may contribute to a patient’s presenting complaint.

Approximately 70% of patients1 do not report energy drink use because they believe these products are natural and safe. Ask patients if they consume energy drinks so you can alert them to the health risks.

A Stimulating recipe

Two main ingredients in most energy drinks are caffeine and carbohydrates in the form of glucose, sucrose, fructose, galactose, and maltodextrins (Table).

Table

Caffeine and carbohydrate content of popular energy drinks

Drink nameCaffeine contentCarbohydrate content
Red Bull (8.5 oz)80 mg28 g
Full Throttle (16 oz)144 mg57 g
SoBe No Fear (16 oz)158 mg66 g
Source: American Beverage Association, SoBe Beverages, Red Bull
Carbohydrates. Four popular brands of energy drinks contain 28 to 66 grams of carbohydrates—a slice of whole wheat bread has 20 grams of carbohydrates. Urge patients taking antipsychotics that could cause weight gain to avoid these drinks.

Caffeine. Energy drinks contain 75 to 158 mg of caffeine per can—8 ounces of coffee has 150 mg of caffeine. Also, some products include the South American plant extracts guarana or yerba mate, which contain an unknown amount of caffeine.

High caffeine intake—≥300 mg/d—might exacerbate bipolar disorder’s manic symptoms. Also find out about additional caffeine intake from coffee, tea, soda, and some OTC medications, such as Excedrin.

Herbal ingredients. Ginseng or ginkgo biloba can cause patients to feel jittery or anxious. When taken in large amounts—the FDA has no guidelines on safe dosages—these ingredients can aggravate manic or psychotic symptoms.

Significant energy drink consumption—3 or more 8-oz drinks per day—can bring about physical side effects such as tachycardia and insomnia. Advise patients to limit their intake to 2 drinks per day, and suggest safer ways to increase energy levels such as moderate exercise and adequate sleep.

Energy drinks’ popularity has soared among consumers who crave an energy boost from the highly caffeinated herbal concoctions. Clinicians should ask patients about energy drink consumption because:

  • caffeine abuse can exacerbate mood and anxiety disorders and disrupt sleep patterns
  • herbal additives can cause physical and/or psychiatric side effects
  • some ingredients interact with prescription or OTC medications
  • effects of energy drinks may contribute to a patient’s presenting complaint.

Approximately 70% of patients1 do not report energy drink use because they believe these products are natural and safe. Ask patients if they consume energy drinks so you can alert them to the health risks.

A Stimulating recipe

Two main ingredients in most energy drinks are caffeine and carbohydrates in the form of glucose, sucrose, fructose, galactose, and maltodextrins (Table).

Table

Caffeine and carbohydrate content of popular energy drinks

Drink nameCaffeine contentCarbohydrate content
Red Bull (8.5 oz)80 mg28 g
Full Throttle (16 oz)144 mg57 g
SoBe No Fear (16 oz)158 mg66 g
Source: American Beverage Association, SoBe Beverages, Red Bull
Carbohydrates. Four popular brands of energy drinks contain 28 to 66 grams of carbohydrates—a slice of whole wheat bread has 20 grams of carbohydrates. Urge patients taking antipsychotics that could cause weight gain to avoid these drinks.

Caffeine. Energy drinks contain 75 to 158 mg of caffeine per can—8 ounces of coffee has 150 mg of caffeine. Also, some products include the South American plant extracts guarana or yerba mate, which contain an unknown amount of caffeine.

High caffeine intake—≥300 mg/d—might exacerbate bipolar disorder’s manic symptoms. Also find out about additional caffeine intake from coffee, tea, soda, and some OTC medications, such as Excedrin.

Herbal ingredients. Ginseng or ginkgo biloba can cause patients to feel jittery or anxious. When taken in large amounts—the FDA has no guidelines on safe dosages—these ingredients can aggravate manic or psychotic symptoms.

Significant energy drink consumption—3 or more 8-oz drinks per day—can bring about physical side effects such as tachycardia and insomnia. Advise patients to limit their intake to 2 drinks per day, and suggest safer ways to increase energy levels such as moderate exercise and adequate sleep.

References

1. Ciocon JO, Ciocon DG, Galindo DJ. Dietary supplements in primary care: botanicals can affect surgical outcomes and follow-up. Geriatrics 2004;59(9):20-4.

Dr. Berigan is a contracting psychiatrist at Behavioral Health Services, Fort Huachuca, AZ.

References

1. Ciocon JO, Ciocon DG, Galindo DJ. Dietary supplements in primary care: botanicals can affect surgical outcomes and follow-up. Geriatrics 2004;59(9):20-4.

Dr. Berigan is a contracting psychiatrist at Behavioral Health Services, Fort Huachuca, AZ.

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A consultation-liaison psychiatrist is called in to help manage “schizophrenia” in a middle-aged attorney who is recovering from a complicated cardiac bypass procedure. This patient is not mentally ill, the psychiatrist realizes, but has delirium with rapid-onset neuropsychiatric symptoms noted by fluctuations in arousal and associated changes in sleep, mood, personality, and cognition. This example illustrates 1 of 10 myths about delirium:

1. My patient is paranoid, therefore he or she must be schizophrenic

Patients with delirium may present with perceptual disturbances such as hallucinations, delusions, or paranoia. An otherwise highly functioning individual with symptom onset while in a medical setting likely has delirium, not a chronic mental disorder such as schizophrenia.

2. Delirium is rare

Delirium is found frequently in medically ill populations. In some groups, such as stem-cell transplant patients, rates may approach 50%. Risk factors include medical severity and advanced patient age.1

3. Delirium is not serious

Delirium is associated with increased morbidity and mortality. It is a marker for “cerebral insufficiency”—reversible impairment in brain function—and requires prompt treatment.2-4

4. Sleep deprivation causes delirium

Disrupted sleep in hospitalized patients—otherwise known as “ICU psychosis”—is more likely the result of delirium than the cause. Patients’ delirium and sleep both improve when they move from the ICU to a general medical floor, a reflection of their improved medical condition.5

5. Delirium goes away rapidly

Delirium usually lasts for days or weeks. Many patients—although superficially improved—still have subtle cognitive deficits and difficulty with daily activities.

6. The patient’s medical problem has been treated, so the delirium should resolve

A patient’s CNS often needs time to recover, and delirium may persist after the underlying medical cause has been treated. Delirium can be caused by factors other than medical illness, such as sedating, analgesic, or antiemetic medications.

7. My delirious patient cannot make medical decisions

Many patients with delirium can make decisions during more lucid periods. As their delirium improves, they should be able to participate in decision-making.

8. My patient cannot be delirious because he or she is oriented to time and place

Simple orientation questions can miss subtle signs of delirium. Watch for an inability to function cognitively at the individual’s baseline level. For example, a software engineer who is unable to draw a clock could be delirious.

9. My patient has depression, not delirium, because he or she is not getting out of bed

Delirium can present with changes of mood, energy, and personality that mimic depression. Even severely depressed individuals can function at a basic cognitive level and maintain daytime wakefulness, whereas patients with delirium may not.

10. Delirium cannot be treated

Manage delirium by evaluating and treating underlying medical precipitants such as metabolic derangement, infection, dehydration, hypoxia, pain, or medication effects. Also consider CNS injuries including stroke, head injury, or neoplasm. Research suggests antipsychotic medications at low dosages6,7 can safely treat delirium. Improving orientation and comfort by reassuring the patient, assessing for anxiety, and reducing excessive noise and stimulation also help.

References

1. Fann JR, Roth-Roemer S, Burington BE, et al. Delirium in patients undergoing hematopoietic stem cell transplantation. Cancer 2002;95(9):1971-81.

2. Engel GL, Romano J. Delirium, a syndrome of cerebral insufficiency. 1959. J Neuropsychiatry Clin Neurosci 2004;16(4):526-38.

3. Thomason JW, Shintani A, Peterson JF, et al. Intensive care unit delirium is an independent predictor of longer hospital stay: a prospective analysis of 261 non-ventilated patients. Crit Care. [serial online]. 2005;9(4):R375-81.

4. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA 2004;291(14):1753-62.

5. Justic M. Does “ICU psychosis” really exist? Crit Care Nurse 2000;20(3):28-37.

6. Schwartz TL, Masand PS. The role of atypical antipsychotics in the treatment of delirium. Psychosomatics 2002;43(3):171-4.

7. Hassaballa HA, Balk RA. Torsade de pointes associated with the administration of intravenous haloperidol: a review of the literature and practical guidelines for use. Expert Opin Drug Saf 2003;2(6):543-7.

Dr. Levy is assistant professor in psychiatry, University of Washington, Seattle.

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A consultation-liaison psychiatrist is called in to help manage “schizophrenia” in a middle-aged attorney who is recovering from a complicated cardiac bypass procedure. This patient is not mentally ill, the psychiatrist realizes, but has delirium with rapid-onset neuropsychiatric symptoms noted by fluctuations in arousal and associated changes in sleep, mood, personality, and cognition. This example illustrates 1 of 10 myths about delirium:

1. My patient is paranoid, therefore he or she must be schizophrenic

Patients with delirium may present with perceptual disturbances such as hallucinations, delusions, or paranoia. An otherwise highly functioning individual with symptom onset while in a medical setting likely has delirium, not a chronic mental disorder such as schizophrenia.

2. Delirium is rare

Delirium is found frequently in medically ill populations. In some groups, such as stem-cell transplant patients, rates may approach 50%. Risk factors include medical severity and advanced patient age.1

3. Delirium is not serious

Delirium is associated with increased morbidity and mortality. It is a marker for “cerebral insufficiency”—reversible impairment in brain function—and requires prompt treatment.2-4

4. Sleep deprivation causes delirium

Disrupted sleep in hospitalized patients—otherwise known as “ICU psychosis”—is more likely the result of delirium than the cause. Patients’ delirium and sleep both improve when they move from the ICU to a general medical floor, a reflection of their improved medical condition.5

5. Delirium goes away rapidly

Delirium usually lasts for days or weeks. Many patients—although superficially improved—still have subtle cognitive deficits and difficulty with daily activities.

6. The patient’s medical problem has been treated, so the delirium should resolve

A patient’s CNS often needs time to recover, and delirium may persist after the underlying medical cause has been treated. Delirium can be caused by factors other than medical illness, such as sedating, analgesic, or antiemetic medications.

7. My delirious patient cannot make medical decisions

Many patients with delirium can make decisions during more lucid periods. As their delirium improves, they should be able to participate in decision-making.

8. My patient cannot be delirious because he or she is oriented to time and place

Simple orientation questions can miss subtle signs of delirium. Watch for an inability to function cognitively at the individual’s baseline level. For example, a software engineer who is unable to draw a clock could be delirious.

9. My patient has depression, not delirium, because he or she is not getting out of bed

Delirium can present with changes of mood, energy, and personality that mimic depression. Even severely depressed individuals can function at a basic cognitive level and maintain daytime wakefulness, whereas patients with delirium may not.

10. Delirium cannot be treated

Manage delirium by evaluating and treating underlying medical precipitants such as metabolic derangement, infection, dehydration, hypoxia, pain, or medication effects. Also consider CNS injuries including stroke, head injury, or neoplasm. Research suggests antipsychotic medications at low dosages6,7 can safely treat delirium. Improving orientation and comfort by reassuring the patient, assessing for anxiety, and reducing excessive noise and stimulation also help.

A consultation-liaison psychiatrist is called in to help manage “schizophrenia” in a middle-aged attorney who is recovering from a complicated cardiac bypass procedure. This patient is not mentally ill, the psychiatrist realizes, but has delirium with rapid-onset neuropsychiatric symptoms noted by fluctuations in arousal and associated changes in sleep, mood, personality, and cognition. This example illustrates 1 of 10 myths about delirium:

1. My patient is paranoid, therefore he or she must be schizophrenic

Patients with delirium may present with perceptual disturbances such as hallucinations, delusions, or paranoia. An otherwise highly functioning individual with symptom onset while in a medical setting likely has delirium, not a chronic mental disorder such as schizophrenia.

2. Delirium is rare

Delirium is found frequently in medically ill populations. In some groups, such as stem-cell transplant patients, rates may approach 50%. Risk factors include medical severity and advanced patient age.1

3. Delirium is not serious

Delirium is associated with increased morbidity and mortality. It is a marker for “cerebral insufficiency”—reversible impairment in brain function—and requires prompt treatment.2-4

4. Sleep deprivation causes delirium

Disrupted sleep in hospitalized patients—otherwise known as “ICU psychosis”—is more likely the result of delirium than the cause. Patients’ delirium and sleep both improve when they move from the ICU to a general medical floor, a reflection of their improved medical condition.5

5. Delirium goes away rapidly

Delirium usually lasts for days or weeks. Many patients—although superficially improved—still have subtle cognitive deficits and difficulty with daily activities.

6. The patient’s medical problem has been treated, so the delirium should resolve

A patient’s CNS often needs time to recover, and delirium may persist after the underlying medical cause has been treated. Delirium can be caused by factors other than medical illness, such as sedating, analgesic, or antiemetic medications.

7. My delirious patient cannot make medical decisions

Many patients with delirium can make decisions during more lucid periods. As their delirium improves, they should be able to participate in decision-making.

8. My patient cannot be delirious because he or she is oriented to time and place

Simple orientation questions can miss subtle signs of delirium. Watch for an inability to function cognitively at the individual’s baseline level. For example, a software engineer who is unable to draw a clock could be delirious.

9. My patient has depression, not delirium, because he or she is not getting out of bed

Delirium can present with changes of mood, energy, and personality that mimic depression. Even severely depressed individuals can function at a basic cognitive level and maintain daytime wakefulness, whereas patients with delirium may not.

10. Delirium cannot be treated

Manage delirium by evaluating and treating underlying medical precipitants such as metabolic derangement, infection, dehydration, hypoxia, pain, or medication effects. Also consider CNS injuries including stroke, head injury, or neoplasm. Research suggests antipsychotic medications at low dosages6,7 can safely treat delirium. Improving orientation and comfort by reassuring the patient, assessing for anxiety, and reducing excessive noise and stimulation also help.

References

1. Fann JR, Roth-Roemer S, Burington BE, et al. Delirium in patients undergoing hematopoietic stem cell transplantation. Cancer 2002;95(9):1971-81.

2. Engel GL, Romano J. Delirium, a syndrome of cerebral insufficiency. 1959. J Neuropsychiatry Clin Neurosci 2004;16(4):526-38.

3. Thomason JW, Shintani A, Peterson JF, et al. Intensive care unit delirium is an independent predictor of longer hospital stay: a prospective analysis of 261 non-ventilated patients. Crit Care. [serial online]. 2005;9(4):R375-81.

4. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA 2004;291(14):1753-62.

5. Justic M. Does “ICU psychosis” really exist? Crit Care Nurse 2000;20(3):28-37.

6. Schwartz TL, Masand PS. The role of atypical antipsychotics in the treatment of delirium. Psychosomatics 2002;43(3):171-4.

7. Hassaballa HA, Balk RA. Torsade de pointes associated with the administration of intravenous haloperidol: a review of the literature and practical guidelines for use. Expert Opin Drug Saf 2003;2(6):543-7.

Dr. Levy is assistant professor in psychiatry, University of Washington, Seattle.

References

1. Fann JR, Roth-Roemer S, Burington BE, et al. Delirium in patients undergoing hematopoietic stem cell transplantation. Cancer 2002;95(9):1971-81.

2. Engel GL, Romano J. Delirium, a syndrome of cerebral insufficiency. 1959. J Neuropsychiatry Clin Neurosci 2004;16(4):526-38.

3. Thomason JW, Shintani A, Peterson JF, et al. Intensive care unit delirium is an independent predictor of longer hospital stay: a prospective analysis of 261 non-ventilated patients. Crit Care. [serial online]. 2005;9(4):R375-81.

4. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit. JAMA 2004;291(14):1753-62.

5. Justic M. Does “ICU psychosis” really exist? Crit Care Nurse 2000;20(3):28-37.

6. Schwartz TL, Masand PS. The role of atypical antipsychotics in the treatment of delirium. Psychosomatics 2002;43(3):171-4.

7. Hassaballa HA, Balk RA. Torsade de pointes associated with the administration of intravenous haloperidol: a review of the literature and practical guidelines for use. Expert Opin Drug Saf 2003;2(6):543-7.

Dr. Levy is assistant professor in psychiatry, University of Washington, Seattle.

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With today’s practice environment, most patient visits are limited to 15 minutes. Make the most of that time with the patient by following these guidelines organized by the mnemonic MEDCHECK. Try to cover all eight guidelines during each appointment, even if briefly.

Medication. Begin with an open-ended question to elicit the patient’s thoughts on his or her treatment, such as, “How’s the medication working for you?” Also ask what he or she expects to accomplish during the session. With the patient’s permission, get the family’s perspective on how the patient is doing.

Environmental changes. Learn about events in your patient’s life and how he or she is coping with them. Try to uncover information about stressors—such as a new job—or positive changes such as an old friend returning to the area. Finding a topic that the patient likes to talk about—a favorite activity or television show, for example—can help monitor improvement over time.

Diagnoses. Continually reassess the primary diagnosis and look for evidence of a medical illness, medication side effects, or secondary psychiatric conditions—especially alcohol or drug abuse.

Coordination of care. Update the patient’s file on dealings with therapists, case managers, and other physicians.

Handouts. Provide handouts and/or Web sites describing a medication’s therapeutic and side effects. Get handouts from numerous sources or develop information sheets and adapt them to your patient population. Include generic and brand names of medications to avoid confusion.

Empathy. Conveying empathy for the patient’s problems or pleasures is crucial to a strong therapeutic alliance and effective treatment.

Costs. Don’t ignore medication costs. Being up-to-date on formulary options helps patients get needed prescriptions.

Knowledge. End the session by asking the patient to summarize the medication plan to ensure that he or she knows what to do.

The MEDCHECK guidelines do not take into account necessary tasks outside of the session:

  • Schedule time before your appointments to review charts and recall information from a patient’s last visit. If you cannot update the chart during the visit, reserve a few minutes later for documentation.
  • Take periodic breaks to return phone calls or e-mails or take a short walk.
  • Read up on relevant treatment guidelines to ensure you are providing evidence-based care.
  • Finally, reserve time to be an advocate for your patient by addressing any administrative short-comings or removing obstacles to therapeutic recommendations.

Of course, short visits are not appropriate for all patients. Give more time to patients in crisis or to complicated cases such as children, pregnant women, or those needing interpreters.

References

Dr. Moffic is professor of psychiatry and behavioral medicine, Medical College of Wisconsin, Milwaukee.

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With today’s practice environment, most patient visits are limited to 15 minutes. Make the most of that time with the patient by following these guidelines organized by the mnemonic MEDCHECK. Try to cover all eight guidelines during each appointment, even if briefly.

Medication. Begin with an open-ended question to elicit the patient’s thoughts on his or her treatment, such as, “How’s the medication working for you?” Also ask what he or she expects to accomplish during the session. With the patient’s permission, get the family’s perspective on how the patient is doing.

Environmental changes. Learn about events in your patient’s life and how he or she is coping with them. Try to uncover information about stressors—such as a new job—or positive changes such as an old friend returning to the area. Finding a topic that the patient likes to talk about—a favorite activity or television show, for example—can help monitor improvement over time.

Diagnoses. Continually reassess the primary diagnosis and look for evidence of a medical illness, medication side effects, or secondary psychiatric conditions—especially alcohol or drug abuse.

Coordination of care. Update the patient’s file on dealings with therapists, case managers, and other physicians.

Handouts. Provide handouts and/or Web sites describing a medication’s therapeutic and side effects. Get handouts from numerous sources or develop information sheets and adapt them to your patient population. Include generic and brand names of medications to avoid confusion.

Empathy. Conveying empathy for the patient’s problems or pleasures is crucial to a strong therapeutic alliance and effective treatment.

Costs. Don’t ignore medication costs. Being up-to-date on formulary options helps patients get needed prescriptions.

Knowledge. End the session by asking the patient to summarize the medication plan to ensure that he or she knows what to do.

The MEDCHECK guidelines do not take into account necessary tasks outside of the session:

  • Schedule time before your appointments to review charts and recall information from a patient’s last visit. If you cannot update the chart during the visit, reserve a few minutes later for documentation.
  • Take periodic breaks to return phone calls or e-mails or take a short walk.
  • Read up on relevant treatment guidelines to ensure you are providing evidence-based care.
  • Finally, reserve time to be an advocate for your patient by addressing any administrative short-comings or removing obstacles to therapeutic recommendations.

Of course, short visits are not appropriate for all patients. Give more time to patients in crisis or to complicated cases such as children, pregnant women, or those needing interpreters.

With today’s practice environment, most patient visits are limited to 15 minutes. Make the most of that time with the patient by following these guidelines organized by the mnemonic MEDCHECK. Try to cover all eight guidelines during each appointment, even if briefly.

Medication. Begin with an open-ended question to elicit the patient’s thoughts on his or her treatment, such as, “How’s the medication working for you?” Also ask what he or she expects to accomplish during the session. With the patient’s permission, get the family’s perspective on how the patient is doing.

Environmental changes. Learn about events in your patient’s life and how he or she is coping with them. Try to uncover information about stressors—such as a new job—or positive changes such as an old friend returning to the area. Finding a topic that the patient likes to talk about—a favorite activity or television show, for example—can help monitor improvement over time.

Diagnoses. Continually reassess the primary diagnosis and look for evidence of a medical illness, medication side effects, or secondary psychiatric conditions—especially alcohol or drug abuse.

Coordination of care. Update the patient’s file on dealings with therapists, case managers, and other physicians.

Handouts. Provide handouts and/or Web sites describing a medication’s therapeutic and side effects. Get handouts from numerous sources or develop information sheets and adapt them to your patient population. Include generic and brand names of medications to avoid confusion.

Empathy. Conveying empathy for the patient’s problems or pleasures is crucial to a strong therapeutic alliance and effective treatment.

Costs. Don’t ignore medication costs. Being up-to-date on formulary options helps patients get needed prescriptions.

Knowledge. End the session by asking the patient to summarize the medication plan to ensure that he or she knows what to do.

The MEDCHECK guidelines do not take into account necessary tasks outside of the session:

  • Schedule time before your appointments to review charts and recall information from a patient’s last visit. If you cannot update the chart during the visit, reserve a few minutes later for documentation.
  • Take periodic breaks to return phone calls or e-mails or take a short walk.
  • Read up on relevant treatment guidelines to ensure you are providing evidence-based care.
  • Finally, reserve time to be an advocate for your patient by addressing any administrative short-comings or removing obstacles to therapeutic recommendations.

Of course, short visits are not appropriate for all patients. Give more time to patients in crisis or to complicated cases such as children, pregnant women, or those needing interpreters.

References

Dr. Moffic is professor of psychiatry and behavioral medicine, Medical College of Wisconsin, Milwaukee.

References

Dr. Moffic is professor of psychiatry and behavioral medicine, Medical College of Wisconsin, Milwaukee.

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Keeping track of outpatients with psychosis can be challenging when multiple clinicians provide care and social services are disjointed. To ensure continuity of care and achieve optimal functional outcome, answer these five questions periodically during long-term treatment.

1. Are you acquainted with the patient’s primary care physician? If not, introduce yourself by e-mail, letter, or telephone.

For some patients, you are the primary physician by default, so know some medical monitoring guidelines such as the Mount Sinai Consensus Conference Recommendations for Physical Health Monitoring in Schizophrenia.1 Also encourage the patient to exercise, stop smoking, and lose weight, if necessary.2

2. When did you last request a written consultation from a specialist? Documenting consultations helps other clinicians follow the steps you took to care for the patient. Requesting and preparing the written consultation also forces you and the consultant to think about the exact nature of the patient’s problem.

3. How strong is the patient’s social network? To identify who can help with the patient’s care, draw a schematic of his or her family tree. Determine who lives with the patient or lives nearby and regularly sees him or her. Repeat this exercise every year because family networks change.

4. Do you have data regarding the patient’s complaints? Get as much information as possible to determine a cause. For example, if the patient has:

  • Insomnia—Have the patient or caregiver complete a sleep log and count the number of caffeinated drinks and cigarettes the patient consumes daily.
  • Overweight/obesity—Weigh the patient at each visit and suggest that the patient or caregiver keep a food diary.
  • Worsening psychosis—Use a psychopathology rating scale such as the Brief Psychiatric Rating Scale. Count pills, and order antipsychotic blood levels and urine drug screens if necessary to test for medication non-adherence or unrecognized drug use.
  • Possible cognitive problems—Order neuropsychological tests, particularly to assess memory, attention, and executive function.

5. How much progress can you expect in 1 year? To help you set feasible rehabilitation goals, make a schedule of a typical week in the patient’s life. This schedule will suggest how to engage the patient in work, family, and the community. Have the patient bring in a resume or work history as a starting point for discussion. Repeat this exercise annually.

References

Reference

1. Marder SR, Essock SM, Miller AL, et al. Physical health monitoring of patients with schizophrenia. Am J Psychiatry 2004;16:1334-49.

2. Goff DC, Cather C, Evins AE, et al. Medical morbidity and mortality in schizophrenia; guidelines for psychiatrists. J Clin Psychiatry 2005;66:183-94.

Dr. Freudenreich is director, first episode and early psychosis program, Massachusetts General Hospital, Boston, MA.

Dr. Querques is an assistant in psychiatry, Massachusetts General Hospital.

Dr. Kontos is associate director consultationliaison psychiatry, Cambridge Health Alliance, Cambridge, MA.

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Keeping track of outpatients with psychosis can be challenging when multiple clinicians provide care and social services are disjointed. To ensure continuity of care and achieve optimal functional outcome, answer these five questions periodically during long-term treatment.

1. Are you acquainted with the patient’s primary care physician? If not, introduce yourself by e-mail, letter, or telephone.

For some patients, you are the primary physician by default, so know some medical monitoring guidelines such as the Mount Sinai Consensus Conference Recommendations for Physical Health Monitoring in Schizophrenia.1 Also encourage the patient to exercise, stop smoking, and lose weight, if necessary.2

2. When did you last request a written consultation from a specialist? Documenting consultations helps other clinicians follow the steps you took to care for the patient. Requesting and preparing the written consultation also forces you and the consultant to think about the exact nature of the patient’s problem.

3. How strong is the patient’s social network? To identify who can help with the patient’s care, draw a schematic of his or her family tree. Determine who lives with the patient or lives nearby and regularly sees him or her. Repeat this exercise every year because family networks change.

4. Do you have data regarding the patient’s complaints? Get as much information as possible to determine a cause. For example, if the patient has:

  • Insomnia—Have the patient or caregiver complete a sleep log and count the number of caffeinated drinks and cigarettes the patient consumes daily.
  • Overweight/obesity—Weigh the patient at each visit and suggest that the patient or caregiver keep a food diary.
  • Worsening psychosis—Use a psychopathology rating scale such as the Brief Psychiatric Rating Scale. Count pills, and order antipsychotic blood levels and urine drug screens if necessary to test for medication non-adherence or unrecognized drug use.
  • Possible cognitive problems—Order neuropsychological tests, particularly to assess memory, attention, and executive function.

5. How much progress can you expect in 1 year? To help you set feasible rehabilitation goals, make a schedule of a typical week in the patient’s life. This schedule will suggest how to engage the patient in work, family, and the community. Have the patient bring in a resume or work history as a starting point for discussion. Repeat this exercise annually.

Keeping track of outpatients with psychosis can be challenging when multiple clinicians provide care and social services are disjointed. To ensure continuity of care and achieve optimal functional outcome, answer these five questions periodically during long-term treatment.

1. Are you acquainted with the patient’s primary care physician? If not, introduce yourself by e-mail, letter, or telephone.

For some patients, you are the primary physician by default, so know some medical monitoring guidelines such as the Mount Sinai Consensus Conference Recommendations for Physical Health Monitoring in Schizophrenia.1 Also encourage the patient to exercise, stop smoking, and lose weight, if necessary.2

2. When did you last request a written consultation from a specialist? Documenting consultations helps other clinicians follow the steps you took to care for the patient. Requesting and preparing the written consultation also forces you and the consultant to think about the exact nature of the patient’s problem.

3. How strong is the patient’s social network? To identify who can help with the patient’s care, draw a schematic of his or her family tree. Determine who lives with the patient or lives nearby and regularly sees him or her. Repeat this exercise every year because family networks change.

4. Do you have data regarding the patient’s complaints? Get as much information as possible to determine a cause. For example, if the patient has:

  • Insomnia—Have the patient or caregiver complete a sleep log and count the number of caffeinated drinks and cigarettes the patient consumes daily.
  • Overweight/obesity—Weigh the patient at each visit and suggest that the patient or caregiver keep a food diary.
  • Worsening psychosis—Use a psychopathology rating scale such as the Brief Psychiatric Rating Scale. Count pills, and order antipsychotic blood levels and urine drug screens if necessary to test for medication non-adherence or unrecognized drug use.
  • Possible cognitive problems—Order neuropsychological tests, particularly to assess memory, attention, and executive function.

5. How much progress can you expect in 1 year? To help you set feasible rehabilitation goals, make a schedule of a typical week in the patient’s life. This schedule will suggest how to engage the patient in work, family, and the community. Have the patient bring in a resume or work history as a starting point for discussion. Repeat this exercise annually.

References

Reference

1. Marder SR, Essock SM, Miller AL, et al. Physical health monitoring of patients with schizophrenia. Am J Psychiatry 2004;16:1334-49.

2. Goff DC, Cather C, Evins AE, et al. Medical morbidity and mortality in schizophrenia; guidelines for psychiatrists. J Clin Psychiatry 2005;66:183-94.

Dr. Freudenreich is director, first episode and early psychosis program, Massachusetts General Hospital, Boston, MA.

Dr. Querques is an assistant in psychiatry, Massachusetts General Hospital.

Dr. Kontos is associate director consultationliaison psychiatry, Cambridge Health Alliance, Cambridge, MA.

References

Reference

1. Marder SR, Essock SM, Miller AL, et al. Physical health monitoring of patients with schizophrenia. Am J Psychiatry 2004;16:1334-49.

2. Goff DC, Cather C, Evins AE, et al. Medical morbidity and mortality in schizophrenia; guidelines for psychiatrists. J Clin Psychiatry 2005;66:183-94.

Dr. Freudenreich is director, first episode and early psychosis program, Massachusetts General Hospital, Boston, MA.

Dr. Querques is an assistant in psychiatry, Massachusetts General Hospital.

Dr. Kontos is associate director consultationliaison psychiatry, Cambridge Health Alliance, Cambridge, MA.

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‘WEED’ out false-positive urine drug screens

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Numerous medications and other substances can appear in a urine drug screen (UDS) as an illicit narcotic (Table). These false positives can:

  • lead to incorrect diagnosis and inappropriate intervention, particularly if the result determines treatment
  • endanger the therapeutic alliance by making the patient uncomfortable and defensive.

Table

Substances that may trigger a false urinary drug screen result

Prescription drugsNonprescription drugsCould appear in urinary drug screen as
AmphetaminesNasal decongestantsAmphetamines
MethamphetaminesMDMA 
BupropionPseudoephedrine 
Fluoxetine  
Ranitidine  
Trazodone  
Nefazodone  
DiazepamNoneAlcohol
SertralineNoneBenzodiazepines
Oxaprozin  
AmoxicillinNSAIDsCocaine
Most antibiotics  
MS Contin (false negative)Poppy seedsHeroin (morphine)
Quinolones  
Rifampin (6-Acetylmorphine)
Codeine  
Oxycodone (false negative)  
DronabinolVisine eye drops (false negative)Marijuana
PantoprazoleHemp seeds (false negative) 
Diazepam (false negative)NyquilMethadone
 DextromethorphanPCP
Source: References 1,4-6

Why Drug Screens Are Sometimes Wrong

A UDS for recreational drug use is commonly performed when the patient presents to the ER with acute changes in mental or behavioral status.

Ms. A, age 57, presents to the ER with fluctuating consciousness. The cause is unknown.

Surgical removal of a pituitary tumor 39 years earlier caused hormone deficiencies, seizures, and excessive sleepiness. Symptoms of panhypopituitarism have been managed with medication, and her current regimen includes thyroxine, phenytoin, the proton pump inhibitor pantoprazole, and prednisone. Recently, comorbid depression caused her to skip doses.

ER physicians order a UDS because of Ms. A’s mental status changes. The enzyme-linked immunosorbent (ELISA) toxicology test for alcohol, amphetamines, barbiturates, benzodiazepines, cocaine, opiates, marijuana, and phencyclidine (PCP) is positive for marijuana. When the attending psychiatrist informs Ms. A of the result, she is shocked. She tells the psychiatrist she is active in church and opposes recreational use of narcotics. She adamantly denies using marijuana or other street drugs, alcohol, nicotine, or caffeine.

Eventually, physicians attributed Ms. A’s mental status changes to several underlying medical issues, including Addison’s disease. A thorough review of the case revealed that the proton pump inhibitor pantoprazole caused the false-positive UDS.

UDS tests are sensitive but not highly specific. A medication or other substance with a chemical structure similar to that of the suspected drug can cause a false positive.1-3

The “WEED” mnemonic spells out steps for critically evaluating UDS test results to ensure appropriate care:

  • Write out a list of the patient’s medications. This list may explain the symptoms or help interpret UDS results. If a narcotic dose was recently increased, for example, a UDS might not be needed to confirm what caused the change in mental status.
  • Examine the patient carefully. Evaluate physical signs, take a thorough medical history, and consider the potential for drug use. Although not impossible, for example, PCP intoxication is not a likely cause of psychosis in nursing home patients.
  • Equate UDS results with presenting complaints and symptoms. For example, if a patient with sudden syncope tests positive for marijuana, the syncopal symptoms demand further investigation because marijuana is not the likely cause.
  • Duplicate the UDS screen with confirmatory tests if the result will determine treatment. When UDS results are ambiguous, use highly specific tests such as gas chromatography with mass spectrometry and high-performance liquid chromatography. Although expensive and time consuming, these tests confirm the presence or absence of substances with few false results.
If you’re still unsure about the UDS results, ask a medical review officer or addiction psychiatrist to evaluate the results. A specialist can determine if the patient is in denial about his or her drug use and provide appropriate counseling.
References

1. Casavant MJ. Urine drug screening in adolescents. Pediatr Clin North Am 2002;49(2):317-27.

2. Baden LR, Horowitz G, Jacoby H, Eliopoulos GM. Quinolones and false-positive urine screening for opiates by immunoassay technology. JAMA 2001;286:3115-9.

3. Fraser AD, Howell P. Oxaprozin cross-reactivity in three commercial immunoassays for benzodiazepines in urine. J Anal Toxicol 1998;22:50-4.

4. Pearson SD, Ash KO, Urry FM. Mechanism of false-negative urine cannabinoid immunoassay screens by Visine eyedrops. Clin Chem 1989;35:636-8.

5. The Merck Index: An encyclopedia of chemicals, drugs, and biologicals. Whitehouse Station, NJ: Merck Research Laboratories; 2001.

6. Baselt RC. Disposition of toxic drugs and chemicals in man. Foster City, CA: Chemical Toxicology Institute; 2000.

Dr. Rapuri is a family practice resident, Memorial Medical Center, Johnstown, PA, and clinical attache, VA Medical Center, Omaha, NE.

Dr. Ramaswamy is an instructor, Creighton University, and staff psychiatrist, VA Medical Center, Omaha, NE.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Rasimas is chief resident, department of psychiatry and psychology, Mayo Clinic, Rochester, MN.

Dr. Krahn is deputy editor, Current Psychiatry, and chair, psychiatry department, Mayo Clinic, Scottsdale, AZ

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Numerous medications and other substances can appear in a urine drug screen (UDS) as an illicit narcotic (Table). These false positives can:

  • lead to incorrect diagnosis and inappropriate intervention, particularly if the result determines treatment
  • endanger the therapeutic alliance by making the patient uncomfortable and defensive.

Table

Substances that may trigger a false urinary drug screen result

Prescription drugsNonprescription drugsCould appear in urinary drug screen as
AmphetaminesNasal decongestantsAmphetamines
MethamphetaminesMDMA 
BupropionPseudoephedrine 
Fluoxetine  
Ranitidine  
Trazodone  
Nefazodone  
DiazepamNoneAlcohol
SertralineNoneBenzodiazepines
Oxaprozin  
AmoxicillinNSAIDsCocaine
Most antibiotics  
MS Contin (false negative)Poppy seedsHeroin (morphine)
Quinolones  
Rifampin (6-Acetylmorphine)
Codeine  
Oxycodone (false negative)  
DronabinolVisine eye drops (false negative)Marijuana
PantoprazoleHemp seeds (false negative) 
Diazepam (false negative)NyquilMethadone
 DextromethorphanPCP
Source: References 1,4-6

Why Drug Screens Are Sometimes Wrong

A UDS for recreational drug use is commonly performed when the patient presents to the ER with acute changes in mental or behavioral status.

Ms. A, age 57, presents to the ER with fluctuating consciousness. The cause is unknown.

Surgical removal of a pituitary tumor 39 years earlier caused hormone deficiencies, seizures, and excessive sleepiness. Symptoms of panhypopituitarism have been managed with medication, and her current regimen includes thyroxine, phenytoin, the proton pump inhibitor pantoprazole, and prednisone. Recently, comorbid depression caused her to skip doses.

ER physicians order a UDS because of Ms. A’s mental status changes. The enzyme-linked immunosorbent (ELISA) toxicology test for alcohol, amphetamines, barbiturates, benzodiazepines, cocaine, opiates, marijuana, and phencyclidine (PCP) is positive for marijuana. When the attending psychiatrist informs Ms. A of the result, she is shocked. She tells the psychiatrist she is active in church and opposes recreational use of narcotics. She adamantly denies using marijuana or other street drugs, alcohol, nicotine, or caffeine.

Eventually, physicians attributed Ms. A’s mental status changes to several underlying medical issues, including Addison’s disease. A thorough review of the case revealed that the proton pump inhibitor pantoprazole caused the false-positive UDS.

UDS tests are sensitive but not highly specific. A medication or other substance with a chemical structure similar to that of the suspected drug can cause a false positive.1-3

The “WEED” mnemonic spells out steps for critically evaluating UDS test results to ensure appropriate care:

  • Write out a list of the patient’s medications. This list may explain the symptoms or help interpret UDS results. If a narcotic dose was recently increased, for example, a UDS might not be needed to confirm what caused the change in mental status.
  • Examine the patient carefully. Evaluate physical signs, take a thorough medical history, and consider the potential for drug use. Although not impossible, for example, PCP intoxication is not a likely cause of psychosis in nursing home patients.
  • Equate UDS results with presenting complaints and symptoms. For example, if a patient with sudden syncope tests positive for marijuana, the syncopal symptoms demand further investigation because marijuana is not the likely cause.
  • Duplicate the UDS screen with confirmatory tests if the result will determine treatment. When UDS results are ambiguous, use highly specific tests such as gas chromatography with mass spectrometry and high-performance liquid chromatography. Although expensive and time consuming, these tests confirm the presence or absence of substances with few false results.
If you’re still unsure about the UDS results, ask a medical review officer or addiction psychiatrist to evaluate the results. A specialist can determine if the patient is in denial about his or her drug use and provide appropriate counseling.

Numerous medications and other substances can appear in a urine drug screen (UDS) as an illicit narcotic (Table). These false positives can:

  • lead to incorrect diagnosis and inappropriate intervention, particularly if the result determines treatment
  • endanger the therapeutic alliance by making the patient uncomfortable and defensive.

Table

Substances that may trigger a false urinary drug screen result

Prescription drugsNonprescription drugsCould appear in urinary drug screen as
AmphetaminesNasal decongestantsAmphetamines
MethamphetaminesMDMA 
BupropionPseudoephedrine 
Fluoxetine  
Ranitidine  
Trazodone  
Nefazodone  
DiazepamNoneAlcohol
SertralineNoneBenzodiazepines
Oxaprozin  
AmoxicillinNSAIDsCocaine
Most antibiotics  
MS Contin (false negative)Poppy seedsHeroin (morphine)
Quinolones  
Rifampin (6-Acetylmorphine)
Codeine  
Oxycodone (false negative)  
DronabinolVisine eye drops (false negative)Marijuana
PantoprazoleHemp seeds (false negative) 
Diazepam (false negative)NyquilMethadone
 DextromethorphanPCP
Source: References 1,4-6

Why Drug Screens Are Sometimes Wrong

A UDS for recreational drug use is commonly performed when the patient presents to the ER with acute changes in mental or behavioral status.

Ms. A, age 57, presents to the ER with fluctuating consciousness. The cause is unknown.

Surgical removal of a pituitary tumor 39 years earlier caused hormone deficiencies, seizures, and excessive sleepiness. Symptoms of panhypopituitarism have been managed with medication, and her current regimen includes thyroxine, phenytoin, the proton pump inhibitor pantoprazole, and prednisone. Recently, comorbid depression caused her to skip doses.

ER physicians order a UDS because of Ms. A’s mental status changes. The enzyme-linked immunosorbent (ELISA) toxicology test for alcohol, amphetamines, barbiturates, benzodiazepines, cocaine, opiates, marijuana, and phencyclidine (PCP) is positive for marijuana. When the attending psychiatrist informs Ms. A of the result, she is shocked. She tells the psychiatrist she is active in church and opposes recreational use of narcotics. She adamantly denies using marijuana or other street drugs, alcohol, nicotine, or caffeine.

Eventually, physicians attributed Ms. A’s mental status changes to several underlying medical issues, including Addison’s disease. A thorough review of the case revealed that the proton pump inhibitor pantoprazole caused the false-positive UDS.

UDS tests are sensitive but not highly specific. A medication or other substance with a chemical structure similar to that of the suspected drug can cause a false positive.1-3

The “WEED” mnemonic spells out steps for critically evaluating UDS test results to ensure appropriate care:

  • Write out a list of the patient’s medications. This list may explain the symptoms or help interpret UDS results. If a narcotic dose was recently increased, for example, a UDS might not be needed to confirm what caused the change in mental status.
  • Examine the patient carefully. Evaluate physical signs, take a thorough medical history, and consider the potential for drug use. Although not impossible, for example, PCP intoxication is not a likely cause of psychosis in nursing home patients.
  • Equate UDS results with presenting complaints and symptoms. For example, if a patient with sudden syncope tests positive for marijuana, the syncopal symptoms demand further investigation because marijuana is not the likely cause.
  • Duplicate the UDS screen with confirmatory tests if the result will determine treatment. When UDS results are ambiguous, use highly specific tests such as gas chromatography with mass spectrometry and high-performance liquid chromatography. Although expensive and time consuming, these tests confirm the presence or absence of substances with few false results.
If you’re still unsure about the UDS results, ask a medical review officer or addiction psychiatrist to evaluate the results. A specialist can determine if the patient is in denial about his or her drug use and provide appropriate counseling.
References

1. Casavant MJ. Urine drug screening in adolescents. Pediatr Clin North Am 2002;49(2):317-27.

2. Baden LR, Horowitz G, Jacoby H, Eliopoulos GM. Quinolones and false-positive urine screening for opiates by immunoassay technology. JAMA 2001;286:3115-9.

3. Fraser AD, Howell P. Oxaprozin cross-reactivity in three commercial immunoassays for benzodiazepines in urine. J Anal Toxicol 1998;22:50-4.

4. Pearson SD, Ash KO, Urry FM. Mechanism of false-negative urine cannabinoid immunoassay screens by Visine eyedrops. Clin Chem 1989;35:636-8.

5. The Merck Index: An encyclopedia of chemicals, drugs, and biologicals. Whitehouse Station, NJ: Merck Research Laboratories; 2001.

6. Baselt RC. Disposition of toxic drugs and chemicals in man. Foster City, CA: Chemical Toxicology Institute; 2000.

Dr. Rapuri is a family practice resident, Memorial Medical Center, Johnstown, PA, and clinical attache, VA Medical Center, Omaha, NE.

Dr. Ramaswamy is an instructor, Creighton University, and staff psychiatrist, VA Medical Center, Omaha, NE.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Rasimas is chief resident, department of psychiatry and psychology, Mayo Clinic, Rochester, MN.

Dr. Krahn is deputy editor, Current Psychiatry, and chair, psychiatry department, Mayo Clinic, Scottsdale, AZ

References

1. Casavant MJ. Urine drug screening in adolescents. Pediatr Clin North Am 2002;49(2):317-27.

2. Baden LR, Horowitz G, Jacoby H, Eliopoulos GM. Quinolones and false-positive urine screening for opiates by immunoassay technology. JAMA 2001;286:3115-9.

3. Fraser AD, Howell P. Oxaprozin cross-reactivity in three commercial immunoassays for benzodiazepines in urine. J Anal Toxicol 1998;22:50-4.

4. Pearson SD, Ash KO, Urry FM. Mechanism of false-negative urine cannabinoid immunoassay screens by Visine eyedrops. Clin Chem 1989;35:636-8.

5. The Merck Index: An encyclopedia of chemicals, drugs, and biologicals. Whitehouse Station, NJ: Merck Research Laboratories; 2001.

6. Baselt RC. Disposition of toxic drugs and chemicals in man. Foster City, CA: Chemical Toxicology Institute; 2000.

Dr. Rapuri is a family practice resident, Memorial Medical Center, Johnstown, PA, and clinical attache, VA Medical Center, Omaha, NE.

Dr. Ramaswamy is an instructor, Creighton University, and staff psychiatrist, VA Medical Center, Omaha, NE.

Dr. Madaan is a fellow in child and adolescent psychiatry, Creighton University, Omaha, NE.

Dr. Rasimas is chief resident, department of psychiatry and psychology, Mayo Clinic, Rochester, MN.

Dr. Krahn is deputy editor, Current Psychiatry, and chair, psychiatry department, Mayo Clinic, Scottsdale, AZ

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‘Prescribing’ behavioral and lifestyle changes

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Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

References

Dr. Christensen is associate professor of psychiatry, University of Florida College of Medicine, Jacksonville, and director of the university’s community psychiatry program.

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Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

References

Dr. Christensen is associate professor of psychiatry, University of Florida College of Medicine, Jacksonville, and director of the university’s community psychiatry program.

References

Dr. Christensen is associate professor of psychiatry, University of Florida College of Medicine, Jacksonville, and director of the university’s community psychiatry program.

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