Pearls

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

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

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

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

Ms. B, age 29, has bipolar disorder that is stabilized by valproate, 1,250 mg/d. After 1 month of treatment, she shows scalp hair loss. She takes no other medications and is distressed because she had never experienced such copious hair loss. Ms. B’s blood valproate level is at a therapeutic level. She wants to know if the hair loss will be permanent and what she can do to stop it.

Up to 28% of patients who take valproate suffer temporary alopecia.^1,2 In most cases, hair loss is associated with long-term valproate pharmacotherapy. Hair loss appears to be dose-related² and may be more common in women than in men. Usually patients will report gradual but steady hair loss, commonly beginning 2 to 6 months after initiating treatment.³ Complete hair loss is rare and new hair growth typically begins approximately 2 to 3 months after alopecia onset.

Valproate can cause telogen effluvium, a non-scarring form of alopecia that occurs by precipitating the follicles into a premature rest phase. Other medications that may cause this type of hair loss include desipramine, imipramine, selective serotonin reuptake inhibitors, dopaminergics, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors, and cimetidine, as well as withdrawal from minoxidil, oral contraceptives, sulfasalazine, and antithyroid medicines.³

Advising patients

In addition to reducing a patient’s valproate dosage when clinically feasible, you can suggest pharmacologic and lifestyle changes to help patients minimize hair loss:

1. Recommend a biotin supplement. Valproate can cause biotin deficiency and may lead to low serum and liver tissue biotinidase enzyme⁴; a major clinical manifestation of biotin deficiency is alopecia.

2. Tell patients to avoid taking valproate during meals to prevent its chelating effect on food. The chelating effect of valproate makes metals that facilitate hair growth, such as zinc and selenium, unavailable for absorption.⁵

3. Recommend zinc and selenium supplements, which can help stop further hair loss and regenerate hair.⁵

4. Suggest practical advice for hair care, including using soft brushes and mild shampoos and avoiding dyes, heated curlers, and hair dryers.

5. Consider minoxidil therapy. However, this is an expensive option and there are no cases documenting its use for alopecia caused by mood stabilizers.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

As psychiatric care transitions to using electronic medical records, providers should be aware that patients—and their legal representation— have increasing access to their medical records. Use of patient-centered, nonjudgmental language will better preserve the physician/patient alliance.

Consider the type of language you would find acceptable in documents describing the care provided to you or a loved one. Whenever possible, describe behavior by using objective and phenomenological terms. Nothing is sacrificed by replacing words that carry a negative connotation with less charged words. However, it is acceptable— and can add to the evaluation—to quote the patient’s own words.

The Table below lists alternative terms and phrases for use in psychiatric documentation.

Table

Nonjudgmental language for psychiatric documentation

Disclosure

Dr. Nelson receives grant research/support from the Minnesota Medical Foundation.

Discuss this article at www.facebook.com/CurrentPsychiatry

As psychiatric care transitions to using electronic medical records, providers should be aware that patients—and their legal representation— have increasing access to their medical records. Use of patient-centered, nonjudgmental language will better preserve the physician/patient alliance.

Consider the type of language you would find acceptable in documents describing the care provided to you or a loved one. Whenever possible, describe behavior by using objective and phenomenological terms. Nothing is sacrificed by replacing words that carry a negative connotation with less charged words. However, it is acceptable— and can add to the evaluation—to quote the patient’s own words.

The Table below lists alternative terms and phrases for use in psychiatric documentation.

Table

Nonjudgmental language for psychiatric documentation

Disclosure

Dr. Nelson receives grant research/support from the Minnesota Medical Foundation.

Discuss this article at www.facebook.com/CurrentPsychiatry

As psychiatric care transitions to using electronic medical records, providers should be aware that patients—and their legal representation— have increasing access to their medical records. Use of patient-centered, nonjudgmental language will better preserve the physician/patient alliance.

Consider the type of language you would find acceptable in documents describing the care provided to you or a loved one. Whenever possible, describe behavior by using objective and phenomenological terms. Nothing is sacrificed by replacing words that carry a negative connotation with less charged words. However, it is acceptable— and can add to the evaluation—to quote the patient’s own words.

The Table below lists alternative terms and phrases for use in psychiatric documentation.

Table

Nonjudgmental language for psychiatric documentation

Disclosure

Dr. Nelson receives grant research/support from the Minnesota Medical Foundation.

Discuss this article at www.facebook.com/CurrentPsychiatry

Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.¹ Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.

Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.² By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.³ Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.⁴

Practical lifestyle changes

Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously⁵; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.

Pharmacologic treatments

Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,⁶ although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.⁷ The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.⁸ In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.⁹

Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.¹ Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.

Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.² By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.³ Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.⁴

Practical lifestyle changes

Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously⁵; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.

Pharmacologic treatments

Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,⁶ although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.⁷ The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.⁸ In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.⁹

Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Hypersalivation is a well-documented side effect of clozapine that may affect nearly 30% of patients who take this medication.¹ Because clozapine has anticholinergic properties that are expected to reduce secretions, hypersalivation is considered a paradoxical effect. This paradox can be explained by examining clozapine’s actions at the molecular level.

Clozapine has antagonistic activity at many types of receptors, including D1 to D5 dopaminergic, α1 and α2 adrenergic, serotonergic, histaminergic, and M1, M2, M3, and M5 cholinergic.² By contrast, clozapine’s activity at M4 cholinergic receptors is agonistic. The combination of clozapine’s antagonist activity at α2 adrenergic receptors and agonist activity at muscarinic M4 receptors results in hypersalivation.³ Clozapine also increases pooling of saliva in the mouth by diminishing esophageal motility, which gives the appearance of hypersalivation as a result of reduced saliva clearance through normal swallowing.⁴

Practical lifestyle changes

Excessive saliva secretion and pooling can be reduced by practical behavioral and/or pharmacologic interventions. Patients who chew gum during the day will increase their swallowing unconsciously⁵; recommend sugarless gum to help avoid tooth decay and gum disease. If hypersalivation is particularly bothersome at night, patients may find it useful to cover their pillows with an absorbent towel.

Pharmacologic treatments

Pharmacologic interventions rely on counteracting clozapine’s secretion-inducing effects by opposing M4 agonism, α2 antagonism, or both. Antimuscarinic medications such as benztropine, trihexyphenidyl, amitriptyline, or pirenzepine often are used to reduce hypersalivation,⁶ although 1 systematic review concluded further evidence is needed to support the effectiveness of this approach.⁷ The α2 antagonism can be opposed by using the α2 agonist clonidine, which can be administered as a weekly transdermal patch of 0.1 to 0.2 mg.⁸ In 1 retrospective study, the cholinergic and adrenergic mechanisms of hypersalivation were addressed by combining benztropine (2 mg/d in a divided dose) with the α1 antagonist terazosin (2 mg/d). This combination reduced hypersalivation significantly in all patients after 12 weeks, exceeding the efficacy of either benztropine or terazosin administered alone.⁹

Hypersalivation is an inconvenient, potentially embarrassing aspect of clozapine treatment that can cause avoidable distress. One or more of these suggestions may help control an adverse effect that could diminish patient satisfaction and undermine treatment compliance.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Because psychiatrists may be asked to determine if a hospitalized patient has the capacity to consent to or refuse treatment, capacity assessment is a fundamental skill. Every patient has a right to refuse or accept treatment and a psychiatric diagnosis by itself doesn’t make a person incapacitated. Each patient is assumed to have capacity until proven otherwise and the burden of proof lies on the physician who performs the assessment.^1,2 Consent obtained from an incapacitated patient is invalid and obtaining such consent can lead to legal proceedings.^1,2 This article highlights strategies for capacity assessment for psychiatrists.

A patient may need a capacity assessment if he or she refuses a procedure, treatment, placement, or food; wants to leave against medical advice; or is a candidate for organ transplantation.³ Physicians might consult psychiatry for a capacity assessment because they fear medico-legal consequences, do not understand patients’ right to refuse treatment, lack the skills necessary to perform a capacity assessment, have a poor relationship with a patient, or are not comfortable performing such assessments on a patient with a psychiatric diagnosis.³

Physicians should advocate for patients and take measures to protect them from harm while respecting their autonomy. This can be challenging if there are doubts about the patient’s cognitive abilities. Collateral information from family and other allied health care professionals can help in distinguishing what patients say from the facts.

Assessing capacity: Key questions

Various instruments are available for capacity assessment, including the MacArthur Competence Assessment Tool for Treatment, a structured interview that takes approximately 20 minutes to administer and score. A Mini-Mental State Examination (MMSE) can be a starting point for evaluating capacity, especially in geriatric patients.^1,2 An MMSE score <19 is likely to be associated with a lack of capacity.¹ However, there is no substitute for clinical judgment.

Asking a few key questions can help determine if a patient meets 4 criteria in relation to a specific treatment decision:¹

Ability to understand relevant information. Ask patients to explain to you what’s wrong with their health, what’s being done, and the recommended treatment plan.

Ability to retain information. Question patients to see if they can recall details of previous discussions.

Ability to use or weigh information. Ask patients if they understand the risks and benefits of treatment options, including the recommended plan and alternatives. Also ask about the consequences of not getting treatment.

Ability to communicate a decision. Ask patients to indicate whether they agree or disagree with the physician’s recommendation.

A patient can be considered competent to make a treatment decision if he or she can understand and retain information about his or her condition, appreciate the consequences of his or her choices, and weigh the relative risks and benefits of the options.¹

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Because psychiatrists may be asked to determine if a hospitalized patient has the capacity to consent to or refuse treatment, capacity assessment is a fundamental skill. Every patient has a right to refuse or accept treatment and a psychiatric diagnosis by itself doesn’t make a person incapacitated. Each patient is assumed to have capacity until proven otherwise and the burden of proof lies on the physician who performs the assessment.^1,2 Consent obtained from an incapacitated patient is invalid and obtaining such consent can lead to legal proceedings.^1,2 This article highlights strategies for capacity assessment for psychiatrists.

A patient may need a capacity assessment if he or she refuses a procedure, treatment, placement, or food; wants to leave against medical advice; or is a candidate for organ transplantation.³ Physicians might consult psychiatry for a capacity assessment because they fear medico-legal consequences, do not understand patients’ right to refuse treatment, lack the skills necessary to perform a capacity assessment, have a poor relationship with a patient, or are not comfortable performing such assessments on a patient with a psychiatric diagnosis.³

Physicians should advocate for patients and take measures to protect them from harm while respecting their autonomy. This can be challenging if there are doubts about the patient’s cognitive abilities. Collateral information from family and other allied health care professionals can help in distinguishing what patients say from the facts.

Assessing capacity: Key questions

Various instruments are available for capacity assessment, including the MacArthur Competence Assessment Tool for Treatment, a structured interview that takes approximately 20 minutes to administer and score. A Mini-Mental State Examination (MMSE) can be a starting point for evaluating capacity, especially in geriatric patients.^1,2 An MMSE score <19 is likely to be associated with a lack of capacity.¹ However, there is no substitute for clinical judgment.

Asking a few key questions can help determine if a patient meets 4 criteria in relation to a specific treatment decision:¹

Ability to understand relevant information. Ask patients to explain to you what’s wrong with their health, what’s being done, and the recommended treatment plan.

Ability to retain information. Question patients to see if they can recall details of previous discussions.

Ability to use or weigh information. Ask patients if they understand the risks and benefits of treatment options, including the recommended plan and alternatives. Also ask about the consequences of not getting treatment.

Ability to communicate a decision. Ask patients to indicate whether they agree or disagree with the physician’s recommendation.

A patient can be considered competent to make a treatment decision if he or she can understand and retain information about his or her condition, appreciate the consequences of his or her choices, and weigh the relative risks and benefits of the options.¹

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Because psychiatrists may be asked to determine if a hospitalized patient has the capacity to consent to or refuse treatment, capacity assessment is a fundamental skill. Every patient has a right to refuse or accept treatment and a psychiatric diagnosis by itself doesn’t make a person incapacitated. Each patient is assumed to have capacity until proven otherwise and the burden of proof lies on the physician who performs the assessment.^1,2 Consent obtained from an incapacitated patient is invalid and obtaining such consent can lead to legal proceedings.^1,2 This article highlights strategies for capacity assessment for psychiatrists.

A patient may need a capacity assessment if he or she refuses a procedure, treatment, placement, or food; wants to leave against medical advice; or is a candidate for organ transplantation.³ Physicians might consult psychiatry for a capacity assessment because they fear medico-legal consequences, do not understand patients’ right to refuse treatment, lack the skills necessary to perform a capacity assessment, have a poor relationship with a patient, or are not comfortable performing such assessments on a patient with a psychiatric diagnosis.³

Physicians should advocate for patients and take measures to protect them from harm while respecting their autonomy. This can be challenging if there are doubts about the patient’s cognitive abilities. Collateral information from family and other allied health care professionals can help in distinguishing what patients say from the facts.

Assessing capacity: Key questions

Various instruments are available for capacity assessment, including the MacArthur Competence Assessment Tool for Treatment, a structured interview that takes approximately 20 minutes to administer and score. A Mini-Mental State Examination (MMSE) can be a starting point for evaluating capacity, especially in geriatric patients.^1,2 An MMSE score <19 is likely to be associated with a lack of capacity.¹ However, there is no substitute for clinical judgment.

Asking a few key questions can help determine if a patient meets 4 criteria in relation to a specific treatment decision:¹

Ability to understand relevant information. Ask patients to explain to you what’s wrong with their health, what’s being done, and the recommended treatment plan.

Ability to retain information. Question patients to see if they can recall details of previous discussions.

Ability to use or weigh information. Ask patients if they understand the risks and benefits of treatment options, including the recommended plan and alternatives. Also ask about the consequences of not getting treatment.

Ability to communicate a decision. Ask patients to indicate whether they agree or disagree with the physician’s recommendation.

A patient can be considered competent to make a treatment decision if he or she can understand and retain information about his or her condition, appreciate the consequences of his or her choices, and weigh the relative risks and benefits of the options.¹

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists often are asked to help medical colleagues deal with difficult patients. A typical situation involves a patient with a psychiatric diagnosis who refuses medical treatment. Asking 4 questions—adapted from the 4-quadrant model proffered by Jonsen et al^1,2 for ethical decision making in medicine—will help you make pragmatic and helpful treatment recommendations.

1. What does psychiatry have to offer? Consider all the psychiatric facts:

• Are you treating a well-established psychiatric syndrome or mere symptoms?
• What are all your treatment options?
• Which psychiatric treatment would be optimal?
• What is the prognosis for each psychiatric intervention, including no treatment?

2. What does the patient want? Patient-centered medicine tries to work out a competent patient’s preferred course of action. Even for patients deemed incompetent and under court-ordered guardianship, find out what might be acceptable to avoid confrontations. For example, obtaining a guardian for a patient with dementia who refuses hemodialysis is pointless unless everyone involved is willing to restrain and sedate the patient 3 times weekly for the procedure.

3. What kind of life does the patient both hope for and fear? Quality of life features prominently in patients’ minds. Make sure you know how each of the proposed psychiatric interventions might affect the patient’s quality of life. Make explicit what the patient fears. For example, do not assume a patient with human immunodeficiency virus/acquired immune deficiency syndrome who wants to continue to live necessarily wants or is willing to take antiretroviral medications.

4. Who and what else matters? Clinical decision making does not occur in a vacuum. Many stakeholders (people and “systems”) will have legitimate concerns: family members will not take a patient back; hospital policies do not allow use of a particular drug; state laws must be obeyed. In addition, physicians have their own biases regarding what should or should not be done based on their worldview.

Asking these 4 questions in a structured way will not necessarily lead to “the solution.” It will, however, ensure that important areas to consider are all made explicit, and all stakeholders and their concerns were heard.

Disclosures

Dr. Freudenreich receives grant/research support from Pfizer Inc. He is a consultant to Transcept Pharmaceuticals, Inc. and Beacon Health Strategies, LLC and is a CME developer and speaker for Reed Medical Education.

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

Psychiatric decision making: Applying the 4 key questions

Mr. A is a 55-year-old homeless man with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) who displays prominent disinhibition and witzelsucht—brain dysfunction marked by telling inappropriate or irrelevant jokes. He rarely misses clinic appointments and when acutely ill, seeks medical attention and cooperates with inpatient treatment. But he has a long pattern of poor adherence to HIV medications—in part as a result of being homeless—and mostly rejects outreach efforts (eg, visiting nurses to help with adherence); no arrangement has lasted more than a few months. Psychopharmacologic interventions have made no appreciable difference in Mr. A’s frontal impairment. He declines further treatment with psychotropic medications but agrees to take antiretroviral agents.

After Mr. A is diagnosed with thyroid cancer, the medical team recommends a total thyroidectomy; a partial thyroidectomy with close follow-up and a potential second surgery is discussed as a reasonable alternative. Mr. A opts for total thyroid removal.

Mr. A’s medical team asks you if he should be admitted to a psychiatric hospital to treat his disinhibition with the goal of improving his ability to adhere to a lifelong thyroid-replacement medication regimen.

Using the 4-Quadrant Method

1. What does psychiatry have to offer?

From the psychiatric viewpoint, the most critical feature is Mr. A’s “frontal lobe syndrome” with elements of disinhibition, executive dysfunction, and impairments in persistence and long-term planning, likely secondary to severe past alcohol and drug use and long-standing, poorly controlled HIV infection. This neurocognitive dysfunction has been stable for many years, which argues against a progressive process that could be interrupted. Although further trials of psychotropics could be proposed, it is uncertain if any intervention could improve Mr. A’s medication adherence. Even assuming a judge would authorize an involuntary admission and compulsory treatment—which would be required in Mr. A’s case because he has refused further psychiatric treatment—no psychiatric treatment would reverse his executive dysfunction in a reliable and timely manner. Better adherence to HIV medications might offer the best chance for improvement, but Mr. A would need to be in a supervised setting indefinitely, assuming such a setting exists and he agrees to be essentially immobilized.

One could argue Mr. A might be incapable of making some treatment decisions, but simply recommending and pursuing guardianship is not the purpose of this quadrant.

2. What does the patient want?

Mr. A’s preference is not to take psychotropic medications because none helped in the past. His medical choice is clear: to have a total thyroidectomy. He is afraid of dying, explaining, “I don’t want them to leave any cancer in there.”

3. What kind of life does the patient both hope for and fear?

Although Mr. A generally rejects excessive intrusion into his life by the medical profession, he nevertheless takes HIV medications (albeit intermittently), wants surgery, and says he will take thyroid replacement medications. He is willing to tackle the issues he fears. He readily agrees to curative surgery for his thyroid cancer because he fears nothing more than dying of cancer.

4. Who and what else matters?

Besides the patient, the 2 people who matter most are the primary care doctor and the endocrinologist, who are concerned about Mr. A’s ability to take thyroid replacement therapy reliably. Their shared concern is based on the patient’s history of intermittent adherence to antiretroviral medications. Family does not figure in to Mr. A’s situation, as it usually does in cases such as this when family members are available to help the patient negotiate medical decisions.

Recommendation

The crux of the analysis is recognizing that a psychiatric intervention in the form of medication trials—even if a first-line treatment were clear—would be of uncertain benefit and involuntary psychiatric hospitalization would not accomplish the long-term goal of remediating Mr. A’s executive dysfunction. In the final analysis, the patient’s medical team accepted Mr. A’s wish for optimal medical treatment now, while accepting the uncertainty of his ability to follow through later.

Clinical outcome

Mr. A underwent a successful total thyroidectomy and is believed to be cancer-free. He continues to work with his infectious diseases doctor and endocrinologist; as expected, his adherence to thyroid replacement has been suboptimal. However, through occasional “loading doses,” Mr. A has managed to remain only mildly hypothyroid with no clinical sequelae.

Current Psychiatry ©2011 Quadrant HealthCom Inc.

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists often are asked to help medical colleagues deal with difficult patients. A typical situation involves a patient with a psychiatric diagnosis who refuses medical treatment. Asking 4 questions—adapted from the 4-quadrant model proffered by Jonsen et al^1,2 for ethical decision making in medicine—will help you make pragmatic and helpful treatment recommendations.

1. What does psychiatry have to offer? Consider all the psychiatric facts:

• Are you treating a well-established psychiatric syndrome or mere symptoms?
• What are all your treatment options?
• Which psychiatric treatment would be optimal?
• What is the prognosis for each psychiatric intervention, including no treatment?

2. What does the patient want? Patient-centered medicine tries to work out a competent patient’s preferred course of action. Even for patients deemed incompetent and under court-ordered guardianship, find out what might be acceptable to avoid confrontations. For example, obtaining a guardian for a patient with dementia who refuses hemodialysis is pointless unless everyone involved is willing to restrain and sedate the patient 3 times weekly for the procedure.

3. What kind of life does the patient both hope for and fear? Quality of life features prominently in patients’ minds. Make sure you know how each of the proposed psychiatric interventions might affect the patient’s quality of life. Make explicit what the patient fears. For example, do not assume a patient with human immunodeficiency virus/acquired immune deficiency syndrome who wants to continue to live necessarily wants or is willing to take antiretroviral medications.

4. Who and what else matters? Clinical decision making does not occur in a vacuum. Many stakeholders (people and “systems”) will have legitimate concerns: family members will not take a patient back; hospital policies do not allow use of a particular drug; state laws must be obeyed. In addition, physicians have their own biases regarding what should or should not be done based on their worldview.

Asking these 4 questions in a structured way will not necessarily lead to “the solution.” It will, however, ensure that important areas to consider are all made explicit, and all stakeholders and their concerns were heard.

Disclosures

Dr. Freudenreich receives grant/research support from Pfizer Inc. He is a consultant to Transcept Pharmaceuticals, Inc. and Beacon Health Strategies, LLC and is a CME developer and speaker for Reed Medical Education.

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

Psychiatric decision making: Applying the 4 key questions

Mr. A is a 55-year-old homeless man with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) who displays prominent disinhibition and witzelsucht—brain dysfunction marked by telling inappropriate or irrelevant jokes. He rarely misses clinic appointments and when acutely ill, seeks medical attention and cooperates with inpatient treatment. But he has a long pattern of poor adherence to HIV medications—in part as a result of being homeless—and mostly rejects outreach efforts (eg, visiting nurses to help with adherence); no arrangement has lasted more than a few months. Psychopharmacologic interventions have made no appreciable difference in Mr. A’s frontal impairment. He declines further treatment with psychotropic medications but agrees to take antiretroviral agents.

After Mr. A is diagnosed with thyroid cancer, the medical team recommends a total thyroidectomy; a partial thyroidectomy with close follow-up and a potential second surgery is discussed as a reasonable alternative. Mr. A opts for total thyroid removal.

Mr. A’s medical team asks you if he should be admitted to a psychiatric hospital to treat his disinhibition with the goal of improving his ability to adhere to a lifelong thyroid-replacement medication regimen.

Using the 4-Quadrant Method

1. What does psychiatry have to offer?

From the psychiatric viewpoint, the most critical feature is Mr. A’s “frontal lobe syndrome” with elements of disinhibition, executive dysfunction, and impairments in persistence and long-term planning, likely secondary to severe past alcohol and drug use and long-standing, poorly controlled HIV infection. This neurocognitive dysfunction has been stable for many years, which argues against a progressive process that could be interrupted. Although further trials of psychotropics could be proposed, it is uncertain if any intervention could improve Mr. A’s medication adherence. Even assuming a judge would authorize an involuntary admission and compulsory treatment—which would be required in Mr. A’s case because he has refused further psychiatric treatment—no psychiatric treatment would reverse his executive dysfunction in a reliable and timely manner. Better adherence to HIV medications might offer the best chance for improvement, but Mr. A would need to be in a supervised setting indefinitely, assuming such a setting exists and he agrees to be essentially immobilized.

One could argue Mr. A might be incapable of making some treatment decisions, but simply recommending and pursuing guardianship is not the purpose of this quadrant.

2. What does the patient want?

Mr. A’s preference is not to take psychotropic medications because none helped in the past. His medical choice is clear: to have a total thyroidectomy. He is afraid of dying, explaining, “I don’t want them to leave any cancer in there.”

3. What kind of life does the patient both hope for and fear?

Although Mr. A generally rejects excessive intrusion into his life by the medical profession, he nevertheless takes HIV medications (albeit intermittently), wants surgery, and says he will take thyroid replacement medications. He is willing to tackle the issues he fears. He readily agrees to curative surgery for his thyroid cancer because he fears nothing more than dying of cancer.

4. Who and what else matters?

Besides the patient, the 2 people who matter most are the primary care doctor and the endocrinologist, who are concerned about Mr. A’s ability to take thyroid replacement therapy reliably. Their shared concern is based on the patient’s history of intermittent adherence to antiretroviral medications. Family does not figure in to Mr. A’s situation, as it usually does in cases such as this when family members are available to help the patient negotiate medical decisions.

Recommendation

The crux of the analysis is recognizing that a psychiatric intervention in the form of medication trials—even if a first-line treatment were clear—would be of uncertain benefit and involuntary psychiatric hospitalization would not accomplish the long-term goal of remediating Mr. A’s executive dysfunction. In the final analysis, the patient’s medical team accepted Mr. A’s wish for optimal medical treatment now, while accepting the uncertainty of his ability to follow through later.

Clinical outcome

Mr. A underwent a successful total thyroidectomy and is believed to be cancer-free. He continues to work with his infectious diseases doctor and endocrinologist; as expected, his adherence to thyroid replacement has been suboptimal. However, through occasional “loading doses,” Mr. A has managed to remain only mildly hypothyroid with no clinical sequelae.

Current Psychiatry ©2011 Quadrant HealthCom Inc.

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists often are asked to help medical colleagues deal with difficult patients. A typical situation involves a patient with a psychiatric diagnosis who refuses medical treatment. Asking 4 questions—adapted from the 4-quadrant model proffered by Jonsen et al^1,2 for ethical decision making in medicine—will help you make pragmatic and helpful treatment recommendations.

1. What does psychiatry have to offer? Consider all the psychiatric facts:

• Are you treating a well-established psychiatric syndrome or mere symptoms?
• What are all your treatment options?
• Which psychiatric treatment would be optimal?
• What is the prognosis for each psychiatric intervention, including no treatment?

2. What does the patient want? Patient-centered medicine tries to work out a competent patient’s preferred course of action. Even for patients deemed incompetent and under court-ordered guardianship, find out what might be acceptable to avoid confrontations. For example, obtaining a guardian for a patient with dementia who refuses hemodialysis is pointless unless everyone involved is willing to restrain and sedate the patient 3 times weekly for the procedure.

3. What kind of life does the patient both hope for and fear? Quality of life features prominently in patients’ minds. Make sure you know how each of the proposed psychiatric interventions might affect the patient’s quality of life. Make explicit what the patient fears. For example, do not assume a patient with human immunodeficiency virus/acquired immune deficiency syndrome who wants to continue to live necessarily wants or is willing to take antiretroviral medications.

4. Who and what else matters? Clinical decision making does not occur in a vacuum. Many stakeholders (people and “systems”) will have legitimate concerns: family members will not take a patient back; hospital policies do not allow use of a particular drug; state laws must be obeyed. In addition, physicians have their own biases regarding what should or should not be done based on their worldview.

Asking these 4 questions in a structured way will not necessarily lead to “the solution.” It will, however, ensure that important areas to consider are all made explicit, and all stakeholders and their concerns were heard.

Disclosures

Dr. Freudenreich receives grant/research support from Pfizer Inc. He is a consultant to Transcept Pharmaceuticals, Inc. and Beacon Health Strategies, LLC and is a CME developer and speaker for Reed Medical Education.

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

Psychiatric decision making: Applying the 4 key questions

Mr. A is a 55-year-old homeless man with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) who displays prominent disinhibition and witzelsucht—brain dysfunction marked by telling inappropriate or irrelevant jokes. He rarely misses clinic appointments and when acutely ill, seeks medical attention and cooperates with inpatient treatment. But he has a long pattern of poor adherence to HIV medications—in part as a result of being homeless—and mostly rejects outreach efforts (eg, visiting nurses to help with adherence); no arrangement has lasted more than a few months. Psychopharmacologic interventions have made no appreciable difference in Mr. A’s frontal impairment. He declines further treatment with psychotropic medications but agrees to take antiretroviral agents.

After Mr. A is diagnosed with thyroid cancer, the medical team recommends a total thyroidectomy; a partial thyroidectomy with close follow-up and a potential second surgery is discussed as a reasonable alternative. Mr. A opts for total thyroid removal.

Mr. A’s medical team asks you if he should be admitted to a psychiatric hospital to treat his disinhibition with the goal of improving his ability to adhere to a lifelong thyroid-replacement medication regimen.

Using the 4-Quadrant Method

1. What does psychiatry have to offer?

From the psychiatric viewpoint, the most critical feature is Mr. A’s “frontal lobe syndrome” with elements of disinhibition, executive dysfunction, and impairments in persistence and long-term planning, likely secondary to severe past alcohol and drug use and long-standing, poorly controlled HIV infection. This neurocognitive dysfunction has been stable for many years, which argues against a progressive process that could be interrupted. Although further trials of psychotropics could be proposed, it is uncertain if any intervention could improve Mr. A’s medication adherence. Even assuming a judge would authorize an involuntary admission and compulsory treatment—which would be required in Mr. A’s case because he has refused further psychiatric treatment—no psychiatric treatment would reverse his executive dysfunction in a reliable and timely manner. Better adherence to HIV medications might offer the best chance for improvement, but Mr. A would need to be in a supervised setting indefinitely, assuming such a setting exists and he agrees to be essentially immobilized.

One could argue Mr. A might be incapable of making some treatment decisions, but simply recommending and pursuing guardianship is not the purpose of this quadrant.

2. What does the patient want?

Mr. A’s preference is not to take psychotropic medications because none helped in the past. His medical choice is clear: to have a total thyroidectomy. He is afraid of dying, explaining, “I don’t want them to leave any cancer in there.”

3. What kind of life does the patient both hope for and fear?

Although Mr. A generally rejects excessive intrusion into his life by the medical profession, he nevertheless takes HIV medications (albeit intermittently), wants surgery, and says he will take thyroid replacement medications. He is willing to tackle the issues he fears. He readily agrees to curative surgery for his thyroid cancer because he fears nothing more than dying of cancer.

4. Who and what else matters?

Besides the patient, the 2 people who matter most are the primary care doctor and the endocrinologist, who are concerned about Mr. A’s ability to take thyroid replacement therapy reliably. Their shared concern is based on the patient’s history of intermittent adherence to antiretroviral medications. Family does not figure in to Mr. A’s situation, as it usually does in cases such as this when family members are available to help the patient negotiate medical decisions.

Recommendation

The crux of the analysis is recognizing that a psychiatric intervention in the form of medication trials—even if a first-line treatment were clear—would be of uncertain benefit and involuntary psychiatric hospitalization would not accomplish the long-term goal of remediating Mr. A’s executive dysfunction. In the final analysis, the patient’s medical team accepted Mr. A’s wish for optimal medical treatment now, while accepting the uncertainty of his ability to follow through later.

Clinical outcome

Mr. A underwent a successful total thyroidectomy and is believed to be cancer-free. He continues to work with his infectious diseases doctor and endocrinologist; as expected, his adherence to thyroid replacement has been suboptimal. However, through occasional “loading doses,” Mr. A has managed to remain only mildly hypothyroid with no clinical sequelae.

Current Psychiatry ©2011 Quadrant HealthCom Inc.

Discuss this article at www.facebook.com/CurrentPsychiatry

Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.¹ Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.

Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.²

I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.

Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.

Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,² a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.³ In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.⁴ In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.⁵

CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.⁶ Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.

Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.⁷

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.¹ Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.

Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.²

I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.

Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.

Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,² a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.³ In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.⁴ In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.⁵

CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.⁶ Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.

Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.⁷

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.¹ Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.

Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.²

I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.

Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.

Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,² a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.³ In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.⁴ In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.⁵

CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.⁶ Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.

Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.⁷

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists—especially residents—often prefer to reside close to the hospitals in which they train and work. Training programs in urban settings may offer their residents housing either attached to the hospital or immediately adjacent to it.

Psychiatry residents often discover their most ill patients also prefer to live close to the hospital. They become acquainted with their neighbors on the streets and in the emergency room. As a consequence, new residents must learn how to maintain appropriate boundaries in these situations.

Patients as neighbors

Chronic psychiatric patients are likely to utilize the services of the closest hospital. Individuals with severe mental illness seem especially prone to move to and live in areas near a hospital. For example, a study of VA patients with schizophrenia, bipolar disorder, and depression found those with schizophrenia and bipolar disorder were more likely to move closer to their health care providers.¹ Also, many hospitals and training programs are located in inner-city areas, where individuals with severe mental illness are known to cluster.^2-4

Managing boundaries

When encountering their chronically mentally ill patients on the street, psychiatric residents could have a host of reactions—ranging from becoming over-involved in their patients’ lives to completely avoiding them—that could cause them and their patients significant distress. The literature on boundary management in these situations is immense, and conclusions often are nebulous. Most authors suggest if a psychiatrist encounters a patient outside of the office, he or she should follow the patient’s lead while trying to avoid discussing the patient’s problems in public.⁵

It is important for residency training programs to educate residents on how to manage these professional boundaries. Residents should seek out support from their training department when they encounter these difficult situations.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists—especially residents—often prefer to reside close to the hospitals in which they train and work. Training programs in urban settings may offer their residents housing either attached to the hospital or immediately adjacent to it.

Psychiatry residents often discover their most ill patients also prefer to live close to the hospital. They become acquainted with their neighbors on the streets and in the emergency room. As a consequence, new residents must learn how to maintain appropriate boundaries in these situations.

Patients as neighbors

Chronic psychiatric patients are likely to utilize the services of the closest hospital. Individuals with severe mental illness seem especially prone to move to and live in areas near a hospital. For example, a study of VA patients with schizophrenia, bipolar disorder, and depression found those with schizophrenia and bipolar disorder were more likely to move closer to their health care providers.¹ Also, many hospitals and training programs are located in inner-city areas, where individuals with severe mental illness are known to cluster.^2-4

Managing boundaries

When encountering their chronically mentally ill patients on the street, psychiatric residents could have a host of reactions—ranging from becoming over-involved in their patients’ lives to completely avoiding them—that could cause them and their patients significant distress. The literature on boundary management in these situations is immense, and conclusions often are nebulous. Most authors suggest if a psychiatrist encounters a patient outside of the office, he or she should follow the patient’s lead while trying to avoid discussing the patient’s problems in public.⁵

It is important for residency training programs to educate residents on how to manage these professional boundaries. Residents should seek out support from their training department when they encounter these difficult situations.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Psychiatrists—especially residents—often prefer to reside close to the hospitals in which they train and work. Training programs in urban settings may offer their residents housing either attached to the hospital or immediately adjacent to it.

Psychiatry residents often discover their most ill patients also prefer to live close to the hospital. They become acquainted with their neighbors on the streets and in the emergency room. As a consequence, new residents must learn how to maintain appropriate boundaries in these situations.

Patients as neighbors

Chronic psychiatric patients are likely to utilize the services of the closest hospital. Individuals with severe mental illness seem especially prone to move to and live in areas near a hospital. For example, a study of VA patients with schizophrenia, bipolar disorder, and depression found those with schizophrenia and bipolar disorder were more likely to move closer to their health care providers.¹ Also, many hospitals and training programs are located in inner-city areas, where individuals with severe mental illness are known to cluster.^2-4

Managing boundaries

When encountering their chronically mentally ill patients on the street, psychiatric residents could have a host of reactions—ranging from becoming over-involved in their patients’ lives to completely avoiding them—that could cause them and their patients significant distress. The literature on boundary management in these situations is immense, and conclusions often are nebulous. Most authors suggest if a psychiatrist encounters a patient outside of the office, he or she should follow the patient’s lead while trying to avoid discussing the patient’s problems in public.⁵

It is important for residency training programs to educate residents on how to manage these professional boundaries. Residents should seek out support from their training department when they encounter these difficult situations.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Partial responsiveness to antidepressant monotherapy is a struggle for many depressed patients. The literature supports the effectiveness of augmenting tricyclic antidepressants (TCAs) with triiodothyronine (T3) in unipolar depression. One meta-analysis suggests that T3 may accelerate antidepressant response in patients with treatment-resistant depression.¹ Likewise, T3 augmentation can improve depressive symptoms in patients without subclinical hypothyroidism whose depression did not fully respond to selective serotonin reuptake inhibitors (SSRIs).² In the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, patients received lithium or T3 augmentation after they failed 2 antidepressant trials.³ Patients receiving lithium or T3 augmentation showed similar remission rates, but the latter was associated with lower discontinuation rates because of its more favorable side effect profile.

Despite its reported effectiveness, T3 may be underutilized or misunderstood by prescribers.⁴ Familiarity and use of liothyronine (the exogenous levorotatory form of T3) augmentation may improve response rates for depressed patients taking antidepressants.

Thyroid workup

Untreated thyroid conditions may reduce a depressed patient’s response to antidepressants.¹ Check thyroid-stimulating hormone (TSH) levels as part of a medical workup for depressed mood before initiating T3. If TSH is elevated, a free thyroxine (T4) level should be ordered to detect clinical hypothyroidism. T4 as a sole initial screening test will not reveal subclinical hypothyroidism. Likewise, unbound T3 levels may be normal in patients with hypothyroidism, which could demonstrate endogenous adaptations in deiodination. Consult with an endocrinologist if you suspect Hashimoto’s thyroiditis or if a patient has other abnormal laboratory values.

Patient selection

Preliminary data suggest that women respond better to T3 augmentation than men,¹ possibly because of women’s greater susceptibility to clinical and subclinical hypothyroidism. Patients also should demonstrate partial response to a TCA or SSRI at an adequate dose and duration. Reconsider augmentation if you are concerned that a patient might divert or abuse T3, such as patients with eating disorders.

Safety considerations

In general, most patients tolerate T3. However, risks of T3 supplementation include hyperthyroidism. Severely depressed TSH levels (<0.1 mIU/mL) may predispose patients to atrial arrhythmias or osteoporosis, which compromise the benefits of thyroid augmentation. Low serum TSH increases the risk of atrial fibrillation, and higher free T4 levels are associated with a graded risk of atrial fibrillation.⁵ Thyroid hormone may cause bone resorption. Although 1 study did not demonstrate accelerated bone loss with exogenous levothyroxine,⁶ caution is warranted in vulnerable populations, such as postmenopausal women.

T3 is a FDA pregnancy category A medication, making it a viable augmentation agent for pregnant women when lithium use may not be possible. However, we do not recommend T3 use in pregnant women without obstetric consultation.

Drug interactions

Cholestyramine decreases T3’s clinical effect, as can antacids and iron and calcium supplements.⁷ Similarly, carbamazepine will decrease T3 effectiveness by inducing hepatic metabolism. T3 may enhance warfarin’s anticoagulant effect and increase insulin requirements among diabetic individuals.

Augmentation dosing

Liothyronine should be started at 25 mcg/d taken on an empty stomach in the morning at least 30 minutes before eating. Signs of hyperthyroidism, such as sweating, anxiety, loose stools, heat intolerance, irritability, and tachycardia, suggest that the patient may not tolerate further increases. In geriatric patients or those with elevated cardiovascular risk, consider starting T3 at 12.5 mcg/d.

After 1 to 2 weeks, increase to 37.5 or 50 mcg/d. Evidence is limited for doses >50 mcg/d, the maximum dose used in the STAR*D study. Be aware that depressed patients may be tempted to increase their T3 dose, especially if they experience increased energy or weight loss. Doses >75 mcg/d are associated with an increased mortality rate.⁸

Monitor TSH levels after the first month of augmentation or when adding medications that change absorption or metabolism of thyroid hormones. If the T3 dose is stable, annual TSH measurements are adequate. Using standard hypothyroidism guidelines, maintain serum TSH between 0.4 and 2.0 mU/L.⁹ T3 levels do not need monitoring.

Response monitoring

As highlighted by STAR*D, the goal of depression treatment is remission, and symptom severity should be tracked. The self-reported 9-item Patient Health Questionnaire can complement clinical impressions as a quick and easy outcome measure when administered every 2 weeks. In STAR*D, the mean response time and time to remission for patients receiving T3 augmentation was 6 weeks and 6.6 weeks, respectively. However, 28% of patients did not achieve remission until week 14,³ which highlights the need for an adequate trial of T3.

Disclosures

Dr. Casher is a speaker for AstraZeneca, Pfizer Inc, and Sunovion Pharmaceuticals.

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Partial responsiveness to antidepressant monotherapy is a struggle for many depressed patients. The literature supports the effectiveness of augmenting tricyclic antidepressants (TCAs) with triiodothyronine (T3) in unipolar depression. One meta-analysis suggests that T3 may accelerate antidepressant response in patients with treatment-resistant depression.¹ Likewise, T3 augmentation can improve depressive symptoms in patients without subclinical hypothyroidism whose depression did not fully respond to selective serotonin reuptake inhibitors (SSRIs).² In the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, patients received lithium or T3 augmentation after they failed 2 antidepressant trials.³ Patients receiving lithium or T3 augmentation showed similar remission rates, but the latter was associated with lower discontinuation rates because of its more favorable side effect profile.

Despite its reported effectiveness, T3 may be underutilized or misunderstood by prescribers.⁴ Familiarity and use of liothyronine (the exogenous levorotatory form of T3) augmentation may improve response rates for depressed patients taking antidepressants.

Thyroid workup

Untreated thyroid conditions may reduce a depressed patient’s response to antidepressants.¹ Check thyroid-stimulating hormone (TSH) levels as part of a medical workup for depressed mood before initiating T3. If TSH is elevated, a free thyroxine (T4) level should be ordered to detect clinical hypothyroidism. T4 as a sole initial screening test will not reveal subclinical hypothyroidism. Likewise, unbound T3 levels may be normal in patients with hypothyroidism, which could demonstrate endogenous adaptations in deiodination. Consult with an endocrinologist if you suspect Hashimoto’s thyroiditis or if a patient has other abnormal laboratory values.

Patient selection

Preliminary data suggest that women respond better to T3 augmentation than men,¹ possibly because of women’s greater susceptibility to clinical and subclinical hypothyroidism. Patients also should demonstrate partial response to a TCA or SSRI at an adequate dose and duration. Reconsider augmentation if you are concerned that a patient might divert or abuse T3, such as patients with eating disorders.

Safety considerations

In general, most patients tolerate T3. However, risks of T3 supplementation include hyperthyroidism. Severely depressed TSH levels (<0.1 mIU/mL) may predispose patients to atrial arrhythmias or osteoporosis, which compromise the benefits of thyroid augmentation. Low serum TSH increases the risk of atrial fibrillation, and higher free T4 levels are associated with a graded risk of atrial fibrillation.⁵ Thyroid hormone may cause bone resorption. Although 1 study did not demonstrate accelerated bone loss with exogenous levothyroxine,⁶ caution is warranted in vulnerable populations, such as postmenopausal women.

T3 is a FDA pregnancy category A medication, making it a viable augmentation agent for pregnant women when lithium use may not be possible. However, we do not recommend T3 use in pregnant women without obstetric consultation.

Drug interactions

Cholestyramine decreases T3’s clinical effect, as can antacids and iron and calcium supplements.⁷ Similarly, carbamazepine will decrease T3 effectiveness by inducing hepatic metabolism. T3 may enhance warfarin’s anticoagulant effect and increase insulin requirements among diabetic individuals.

Augmentation dosing

Liothyronine should be started at 25 mcg/d taken on an empty stomach in the morning at least 30 minutes before eating. Signs of hyperthyroidism, such as sweating, anxiety, loose stools, heat intolerance, irritability, and tachycardia, suggest that the patient may not tolerate further increases. In geriatric patients or those with elevated cardiovascular risk, consider starting T3 at 12.5 mcg/d.

After 1 to 2 weeks, increase to 37.5 or 50 mcg/d. Evidence is limited for doses >50 mcg/d, the maximum dose used in the STAR*D study. Be aware that depressed patients may be tempted to increase their T3 dose, especially if they experience increased energy or weight loss. Doses >75 mcg/d are associated with an increased mortality rate.⁸

Monitor TSH levels after the first month of augmentation or when adding medications that change absorption or metabolism of thyroid hormones. If the T3 dose is stable, annual TSH measurements are adequate. Using standard hypothyroidism guidelines, maintain serum TSH between 0.4 and 2.0 mU/L.⁹ T3 levels do not need monitoring.

Response monitoring

As highlighted by STAR*D, the goal of depression treatment is remission, and symptom severity should be tracked. The self-reported 9-item Patient Health Questionnaire can complement clinical impressions as a quick and easy outcome measure when administered every 2 weeks. In STAR*D, the mean response time and time to remission for patients receiving T3 augmentation was 6 weeks and 6.6 weeks, respectively. However, 28% of patients did not achieve remission until week 14,³ which highlights the need for an adequate trial of T3.

Disclosures

Dr. Casher is a speaker for AstraZeneca, Pfizer Inc, and Sunovion Pharmaceuticals.

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

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Partial responsiveness to antidepressant monotherapy is a struggle for many depressed patients. The literature supports the effectiveness of augmenting tricyclic antidepressants (TCAs) with triiodothyronine (T3) in unipolar depression. One meta-analysis suggests that T3 may accelerate antidepressant response in patients with treatment-resistant depression.¹ Likewise, T3 augmentation can improve depressive symptoms in patients without subclinical hypothyroidism whose depression did not fully respond to selective serotonin reuptake inhibitors (SSRIs).² In the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, patients received lithium or T3 augmentation after they failed 2 antidepressant trials.³ Patients receiving lithium or T3 augmentation showed similar remission rates, but the latter was associated with lower discontinuation rates because of its more favorable side effect profile.

Despite its reported effectiveness, T3 may be underutilized or misunderstood by prescribers.⁴ Familiarity and use of liothyronine (the exogenous levorotatory form of T3) augmentation may improve response rates for depressed patients taking antidepressants.

Thyroid workup

Untreated thyroid conditions may reduce a depressed patient’s response to antidepressants.¹ Check thyroid-stimulating hormone (TSH) levels as part of a medical workup for depressed mood before initiating T3. If TSH is elevated, a free thyroxine (T4) level should be ordered to detect clinical hypothyroidism. T4 as a sole initial screening test will not reveal subclinical hypothyroidism. Likewise, unbound T3 levels may be normal in patients with hypothyroidism, which could demonstrate endogenous adaptations in deiodination. Consult with an endocrinologist if you suspect Hashimoto’s thyroiditis or if a patient has other abnormal laboratory values.

Patient selection

Preliminary data suggest that women respond better to T3 augmentation than men,¹ possibly because of women’s greater susceptibility to clinical and subclinical hypothyroidism. Patients also should demonstrate partial response to a TCA or SSRI at an adequate dose and duration. Reconsider augmentation if you are concerned that a patient might divert or abuse T3, such as patients with eating disorders.

Safety considerations

In general, most patients tolerate T3. However, risks of T3 supplementation include hyperthyroidism. Severely depressed TSH levels (<0.1 mIU/mL) may predispose patients to atrial arrhythmias or osteoporosis, which compromise the benefits of thyroid augmentation. Low serum TSH increases the risk of atrial fibrillation, and higher free T4 levels are associated with a graded risk of atrial fibrillation.⁵ Thyroid hormone may cause bone resorption. Although 1 study did not demonstrate accelerated bone loss with exogenous levothyroxine,⁶ caution is warranted in vulnerable populations, such as postmenopausal women.

T3 is a FDA pregnancy category A medication, making it a viable augmentation agent for pregnant women when lithium use may not be possible. However, we do not recommend T3 use in pregnant women without obstetric consultation.

Drug interactions

Cholestyramine decreases T3’s clinical effect, as can antacids and iron and calcium supplements.⁷ Similarly, carbamazepine will decrease T3 effectiveness by inducing hepatic metabolism. T3 may enhance warfarin’s anticoagulant effect and increase insulin requirements among diabetic individuals.

Augmentation dosing

Liothyronine should be started at 25 mcg/d taken on an empty stomach in the morning at least 30 minutes before eating. Signs of hyperthyroidism, such as sweating, anxiety, loose stools, heat intolerance, irritability, and tachycardia, suggest that the patient may not tolerate further increases. In geriatric patients or those with elevated cardiovascular risk, consider starting T3 at 12.5 mcg/d.

After 1 to 2 weeks, increase to 37.5 or 50 mcg/d. Evidence is limited for doses >50 mcg/d, the maximum dose used in the STAR*D study. Be aware that depressed patients may be tempted to increase their T3 dose, especially if they experience increased energy or weight loss. Doses >75 mcg/d are associated with an increased mortality rate.⁸

Monitor TSH levels after the first month of augmentation or when adding medications that change absorption or metabolism of thyroid hormones. If the T3 dose is stable, annual TSH measurements are adequate. Using standard hypothyroidism guidelines, maintain serum TSH between 0.4 and 2.0 mU/L.⁹ T3 levels do not need monitoring.

Response monitoring

As highlighted by STAR*D, the goal of depression treatment is remission, and symptom severity should be tracked. The self-reported 9-item Patient Health Questionnaire can complement clinical impressions as a quick and easy outcome measure when administered every 2 weeks. In STAR*D, the mean response time and time to remission for patients receiving T3 augmentation was 6 weeks and 6.6 weeks, respectively. However, 28% of patients did not achieve remission until week 14,³ which highlights the need for an adequate trial of T3.

Disclosures

Dr. Casher is a speaker for AstraZeneca, Pfizer Inc, and Sunovion Pharmaceuticals.

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

Post hoc ergo propter hoc—”after this, therefore because of this”—suggests that 2 distinct events linked temporally are related causally. Clinicians often apply this dictum when monitoring effects of psychotropics. Because of stigma associated with psychiatric medications, and the readiness with which many practitioners blame them for unexpected results, it is important to develop a rational approach to evaluating outcomes—particularly adverse ones—after administering psychotropic agents.

Consider a geriatric patient admitted to the hospital for a urinary tract infection. He becomes verbally aggressive and is given IV haloperidol. Five minutes later he strikes a nurse and receives lorazepam. Twenty minutes later, he is lying calmly in his bed. The nursing staff and primary team conclude that the patient’s agitation worsened because of the antipsychotic and responded to the benzodiazepine; the physician documents in the patient’s chart that he had an adverse reaction to haloperidol.

In light of what we know about psychotropic medications’ mechanism of action, a more plausible explanation is that whatever caused the patient to become agitated (delirium) resulted in physical aggression. Haloperidol simply did not have enough time to exert its effect before the patient hit the nurse. It also would be wrong to automatically conclude that the last intervention (a benzodiazepine) produced the beneficial outcome. Was it the lorazepam, the haloperidol finally “kicking in,” or a combination of both? Perhaps it was none of the above but rather a worsening infection or irregular waxing and waning of delirium that was the culprit.

To avoid incorrectly attributing negative outcomes to medications, we suggest asking yourself 3 questions:

1. Is the negative outcome a potential consequence of the underlying condition?

Consider the possibility that the medication did not cause the adverse event but merely failed to adequately treat the underlying problem. A teenager who attempts suicide 2 weeks after starting an antidepressant may be exhibiting symptoms related to depression rather than behavior caused by the medication.

2. Are other medical conditions or medications responsible for the negative outcome?

Weigh the relative likelihood that these factors are contributing to your patient’s presentation. In a surgical patient who is overly somnolent after receiving an anxiolytic, consider the possibility that a narcotic or worsening hypoxia are contributing to her somnolence.

3. Is the negative outcome likely to have occurred spontaneously?

Consider the possibility of coincidence. Lithium might not be causing declining renal function in an older patient. A dosing adjustment based on the patient’s current renal function may be a better harm-reduction strategy than discontinuing a potentially useful medication.

Careful evaluation of these potential confounding factors will greatly reduce the likelihood of falsely identifying psychotropic medications as responsible for negative outcomes. After this, but not always because of this.

Disclosure

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

Post hoc ergo propter hoc—”after this, therefore because of this”—suggests that 2 distinct events linked temporally are related causally. Clinicians often apply this dictum when monitoring effects of psychotropics. Because of stigma associated with psychiatric medications, and the readiness with which many practitioners blame them for unexpected results, it is important to develop a rational approach to evaluating outcomes—particularly adverse ones—after administering psychotropic agents.

Consider a geriatric patient admitted to the hospital for a urinary tract infection. He becomes verbally aggressive and is given IV haloperidol. Five minutes later he strikes a nurse and receives lorazepam. Twenty minutes later, he is lying calmly in his bed. The nursing staff and primary team conclude that the patient’s agitation worsened because of the antipsychotic and responded to the benzodiazepine; the physician documents in the patient’s chart that he had an adverse reaction to haloperidol.

In light of what we know about psychotropic medications’ mechanism of action, a more plausible explanation is that whatever caused the patient to become agitated (delirium) resulted in physical aggression. Haloperidol simply did not have enough time to exert its effect before the patient hit the nurse. It also would be wrong to automatically conclude that the last intervention (a benzodiazepine) produced the beneficial outcome. Was it the lorazepam, the haloperidol finally “kicking in,” or a combination of both? Perhaps it was none of the above but rather a worsening infection or irregular waxing and waning of delirium that was the culprit.

To avoid incorrectly attributing negative outcomes to medications, we suggest asking yourself 3 questions:

1. Is the negative outcome a potential consequence of the underlying condition?

Consider the possibility that the medication did not cause the adverse event but merely failed to adequately treat the underlying problem. A teenager who attempts suicide 2 weeks after starting an antidepressant may be exhibiting symptoms related to depression rather than behavior caused by the medication.

2. Are other medical conditions or medications responsible for the negative outcome?

Weigh the relative likelihood that these factors are contributing to your patient’s presentation. In a surgical patient who is overly somnolent after receiving an anxiolytic, consider the possibility that a narcotic or worsening hypoxia are contributing to her somnolence.

3. Is the negative outcome likely to have occurred spontaneously?

Consider the possibility of coincidence. Lithium might not be causing declining renal function in an older patient. A dosing adjustment based on the patient’s current renal function may be a better harm-reduction strategy than discontinuing a potentially useful medication.

Careful evaluation of these potential confounding factors will greatly reduce the likelihood of falsely identifying psychotropic medications as responsible for negative outcomes. After this, but not always because of this.

Disclosure

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

Post hoc ergo propter hoc—”after this, therefore because of this”—suggests that 2 distinct events linked temporally are related causally. Clinicians often apply this dictum when monitoring effects of psychotropics. Because of stigma associated with psychiatric medications, and the readiness with which many practitioners blame them for unexpected results, it is important to develop a rational approach to evaluating outcomes—particularly adverse ones—after administering psychotropic agents.

Consider a geriatric patient admitted to the hospital for a urinary tract infection. He becomes verbally aggressive and is given IV haloperidol. Five minutes later he strikes a nurse and receives lorazepam. Twenty minutes later, he is lying calmly in his bed. The nursing staff and primary team conclude that the patient’s agitation worsened because of the antipsychotic and responded to the benzodiazepine; the physician documents in the patient’s chart that he had an adverse reaction to haloperidol.

In light of what we know about psychotropic medications’ mechanism of action, a more plausible explanation is that whatever caused the patient to become agitated (delirium) resulted in physical aggression. Haloperidol simply did not have enough time to exert its effect before the patient hit the nurse. It also would be wrong to automatically conclude that the last intervention (a benzodiazepine) produced the beneficial outcome. Was it the lorazepam, the haloperidol finally “kicking in,” or a combination of both? Perhaps it was none of the above but rather a worsening infection or irregular waxing and waning of delirium that was the culprit.

To avoid incorrectly attributing negative outcomes to medications, we suggest asking yourself 3 questions:

1. Is the negative outcome a potential consequence of the underlying condition?

Consider the possibility that the medication did not cause the adverse event but merely failed to adequately treat the underlying problem. A teenager who attempts suicide 2 weeks after starting an antidepressant may be exhibiting symptoms related to depression rather than behavior caused by the medication.

2. Are other medical conditions or medications responsible for the negative outcome?

Weigh the relative likelihood that these factors are contributing to your patient’s presentation. In a surgical patient who is overly somnolent after receiving an anxiolytic, consider the possibility that a narcotic or worsening hypoxia are contributing to her somnolence.

3. Is the negative outcome likely to have occurred spontaneously?

Consider the possibility of coincidence. Lithium might not be causing declining renal function in an older patient. A dosing adjustment based on the patient’s current renal function may be a better harm-reduction strategy than discontinuing a potentially useful medication.

Careful evaluation of these potential confounding factors will greatly reduce the likelihood of falsely identifying psychotropic medications as responsible for negative outcomes. After this, but not always because of this.

Disclosure

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