Current Psychiatry

Since the first liver transplant (LT) was performed in 1963 by Starzl et al, there have been considerable advances in the field, with improvements in post-transplant survival.¹ There are multiple indications for LT, including acute liver failure and index complications of cirrhosis such as ascites, encephalopathy, and hepatopulmonary syndrome.² Once a patient develops one of these conditions, he/she is evaluated for LT, even as the complications of liver failure are being managed.

Although the number of LTs has risen, the demand for transplant continues to exceed availability. In 2015, chronic liver disease and cirrhosis was the 12th leading cause of death in the United States.³ In 2016, approximately 50% of waitlisted candidates received a transplant.⁴ There is also a donor shortage. In part, this shortage may be due to longer life spans and the subsequent increase in the age of the potential donor.⁵ In light of this shortage and increased demand, the pre-LT workup is comprehensive. The pre-transplant assessment typically consists of cardiology, surgery, hepatology, and psychosocial evaluations, and hence requires a team of experts to determine who is an ideal candidate for transplant.

Psychiatrists play a key role in the pre-transplant psychosocial evaluations. This article describes the elements of these evaluations, and what psychiatrists can do to help patients both before and after they undergo LT.

Elements of the pre-transplant evaluation

The psychosocial evaluation is a critical component of the pre-transplant assessment. As part of the evaluation, patients are screened for psychosocial limitations that may complicate transplantation, such as demonstrated noncompliance, ongoing alcohol or drug use, and lack of social support (Table 1² ). Other goals of the psychosocial evaluation are to identify in the pre-transplant period patients with possible risk factors, such as substance use or psychiatric disorders, and develop treatment plans to optimize transplant outcomes (Table 2⁶). There are relative contraindications to LT (Table 3⁷) but no absolute psychiatric contraindications, according to the 2013 American Association for the Study of Liver Diseases (AASLD) practice guideline for transplantation.²

Adherence. The 2013 AASLD practice guideline states that patients “should be evaluated for and meet reasonable expectations for adherence to medical directives and mental health stability as determined by the psychosocial evaluation.”² In the transplant setting, adherence is complex. It requires compliance with complicated medication regimens and laboratory testing, frequent follow-up appointments, and close, prompt communication of concerns to the health care team. Patient adherence to medication regimens plays an important role in transplant outcomes.⁸ In fact, in patients who have undergone renal transplant, nonadherence to therapy is considered the leading cause of avoidable graft failure.⁹

A retrospective study of adult LT recipients found that pre-transplant chart evidence of nonadherence, such as missed laboratory testing and clinic visits, was a significant predictor of post-transplant nonadherence with immunosuppressant therapy. Pre-transplant unemployment status and a history of substance abuse also were associated with nonadherence.⁹

Dobbels et al¹⁰ found that patients with a self-reported history of pre-transplant non-adherence had a higher risk of being nonadherent with their immunosuppressive therapy after transplant (odd ratio [OR]: 7.9). Their self-report adherence questionnaire included questions that addressed pre-transplant smoking status, alcohol use, and adherence with medication. In this prospective study, researchers also found that patients with a low “conscientiousness” score were at a higher risk for post-transplant medication nonadherence (OR: 0.8).

Continue to: Studies have also found...

Studies have also found that patients with higher education are more at risk for post-transplant medication nonadherence. Higher education may be associated with higher employment status resulting in a busier lifestyle, a known risk factor that may prevent patients from regular medication adherence.^11,12 Alternatively, it is possible that higher educated patients are “decisive” nonadherers who prefer independent decision-making regarding their disease and treatment.¹³

Substance use. The 2013 AASLD practice guideline lists “ongoing alcohol or illicit substance abuse” as one of the contraindications to LT.² In guidelines from the Austrian Society for Gastroenterology and Hepatology, Graziadei et al¹⁴ listed “alcohol addiction without motivation for alcohol abstinence and untreated/ongoing substance abuse” as absolute contraindications and “untreated alcohol abuse and other drug-related addiction” as relative contraindications. Hence, the pre-transplant evaluation should include a thorough substance use history, including duration, amount, previous attempts to quit, and motivation for abstinence.

Substance use history is especially important because alcoholic liver disease is the second most common indication for LT.² Most LT programs require 6 months of abstinence before a patient can be considered for transplant.¹⁵ The 6-month period was based on studies demonstrating that pre-transplant abstinence from alcohol for <6 months is a risk factor for relapse.¹⁵ However, this guideline remains controversial because the transplant referral and workup may be delayed as the patient’s liver disease worsens. Other risk factors for substance relapse should also be taken into consideration, such as depression, personality disorders, lack of social support, severity of alcohol use, and family history of alcoholism.¹⁶ Lee and Leggio¹⁶ developed the Sustained Alcohol Use Post-Liver Transplant (SALT) score to identify patients who were at risk for sustained alcohol use posttransplant. The 4 SALT criteria are:

• >10 drinks per day at initial hospitalization (+4 points)
• multiple prior rehabilitation attempts (+4 points)
• prior alcohol‐related legal issues (+2 points), and
• prior illicit substance abuse (+1 point).

A SALT score can range from 0 to 11. Lee et al¹⁷ found a SALT score ≥5 had a 25% positive predictive value (95% confidence interval [CI]: 10% to 47%) and a SALT score of <5 had a 95% negative predictive value (95% CI: 89% to 98%) for sustained alcohol use post‐LT. Thus, the 2013 AASLD guideline cautions against delaying evaluation based on the 6-month abstinence rule, and instead recommends early transplant referral for patients with alcoholic liver disease to encourage such patients to begin addiction treatment.²

As part of the substance use history, it is important to ask about the patient’s smoking history. Approximately 60% of LT candidates have a history of smoking cigarettes.¹⁸ Tobacco use history is associated with increased post-transplant vascular complications, such as hepatic artery thrombosis or stenosis, portal vein thrombosis, and deep vein thrombosis.¹⁹ The 2013 AASLD guideline recommends that tobacco use should be prohibited in LT candidates.² Pungpapong et al¹⁹ reported that smoking cessation for at least 2 years prior to transplant led to a significantly decreased risk of developing arterial complications, with an absolute risk reduction of approximately 16%.

Continue to: Liver cirrhosis due to...

Liver cirrhosis due to chronic hepatitis C virus (HCV) infection is one of the leading causes for LT. In the United States, HCV is commonly transmitted during injection drug use. According to the 2013 AASLD guideline, ongoing illicit substance use is a relative contraindication to LT.² It is important to note, however, that methadone maintenance therapy (MMT) is not a contraindication to LT. In fact, the 2013 AASLD guideline recommends that patients receiving MMT should not be required to reduce or stop therapy in order to be listed for transplant.² Studies have shown that in 80% of patients, tapering MMT leads to illicit opiate relapse.²⁰ Currently, there is no evidence that patients receiving MMT have poorer post-transplant outcomes compared with patients not receiving MMT.²¹

Whether cannabis use is a relative contraindication to LT remains controversial.²² Possible adverse effects of cannabis use in transplant patients include drug–drug interactions and infections. Hézode et al²³ reported that daily cannabis use is significantly associated with an increased fibrosis progression rate in patients with chronic HCV infection. Another recent study found that a history of cannabis use was not associated with worse outcomes among patients on the LT waitlist.²⁴ With the increased legalization of cannabis, more studies are needed to assess ongoing cannabis use in patients on the LT waitlist and post-LT outcomes.

Psychiatric history. When assessing a patient for possible LT, no psychiatric disorder is considered an absolute contraindication. Patients with a serious mental illness, such as schizophrenia, and those with intellectual disability can have successful, long-term outcomes with proper evaluation and preparation, including social support. However, empirical literature regarding transplant outcomes and predictive factors in patients with serious mental illness is scarce.²

Studies examining the predictive value of pre-transplant depression on post-transplant outcomes have had mixed results.²⁵ Depression may predict lower post-transplant quality of life. Pre-LT suicidal thoughts (as noted on the Beck Depression Inventory, for example) are associated with post-LT depression.²⁵ In contrast, available data show no significant effect of pre-transplant anxiety on post-LT outcomes. Similarly, pre-transplant cognitive performance appears not to predict survival or other post-transplant outcomes, but may predict poorer quality of life after transplant.²⁵

A few psychiatric factors are considered relative contraindications for LT. These include severe personality disorders, active substance use with no motivation for treatment or abstinence, active psychosis, severe neurocognitive disorders, suicidality, and factitious disorder.⁷

Continue to: Social support

Social support. Assessing a pre-LT patient’s level of social support is an essential part of the psychosocial evaluation. According to the 2013 AASLD guideline, patients should have “adequate” social support both during the waitlist and post-operative periods.² Lack of partnership is a significant predictor of poor post-transplant outcomes, such as late graft loss.¹⁰ Satapathy and Sanyal²⁶ reported that among patients who receive an LT for alcoholic liver disease, those with immediate family support were less likely to relapse to using alcohol after transplant. Poor social support was also a predictor of post-transplant medication nonadherence.¹⁰ Thus, the patient needs enough social support to engage in the pre-transplant health care requirements and to participate in post-transplant recommendations until he/she is functioning independently post-transplant.

Screening tools

Various screening tools may be useful in a pre-LT evaluation. Three standardized assessment tools available specifically for pre-transplant psychosocial assessments are the Stanford Integrated Psychosocial Assessment for Transplantation (Table 2⁶), the Psychosocial Assessment of Candidates for Transplantation,²⁷ and the Transplant Evaluation Rating Scale.²⁸ Instruments to aid in the assessment of depression, anxiety, and delirium,^29-31 a structured personality assessment,³² coping inventories,³³ neuropsychological batteries,³⁴ and others also have been used to evaluate patients before LT. The self-rated Beck Depression Inventory and the clinician-rated Hamilton Depression Rating Scale are commonly used.⁷ Other tools, such as the LEIPAD quality of life instrument and the Brief Symptom Inventory (BSI), have been used to assess for perceived quality of life and psychological distress, respectively.³⁵ These screening tools can be helpful as aids for the pre-LT evaluation; however, diagnoses and treatment plan recommendations require a psychiatric evaluation conducted by a trained clinician.

Treatment after liver transplant

Psychiatric issues. After LT, various psychiatric complications may arise, including (but not limited to) delirium⁷ and “paradoxical psychiatric syndrome” (PPS).³⁶ Delirium can be managed by administering low-dose antipsychotic medications, limiting the use of benzodiazepines and medications with anticholinergic effects, implementing behavioral interventions (frequent orientation, maintaining sleep/wake cycle, limiting noise, presence of a family member or a sitter at bedside),³⁷ and addressing the underlying etiology. Paradoxical psychiatric syndrome is defined as psychiatric symptoms that occur despite a successful LT. It develops within the first year of transplantation and is characterized by recipients having strong guilt feelings toward their donors.³⁸

Drug interactions. In the post-transplant period, antipsychotics are used for management of delirium and psychosis, antidepressants for anxiety and depression, and benzodiazepines for anxiety and sleep problems.⁷ Drug–drug interactions between psychotropic medications and the immunosuppressants required after LT must be closely monitored. First-generation antipsychotics should be avoided in post-transplant patients taking tacrolimus due to the increased risk of QTc prolongation. Tacrolimus can also increase the risk of nephrotoxicity when co-administered with lithium. Post-LT patients taking steroids and bupropion have an increased risk of seizure. Carbamazepine may decrease blood levels of cyclosporine due to the induction of hepatic metabolism.^39,40 The psychiatrist should review and update the patient’s complete medication list at each visit, checking for possible medication interactions.

Quality of life. In the first 6 months post-transplant, patients typically experience improved quality of life in both physical and psychological domains. However, this improvement vacillates as the patient adjusts to post-transplant life. A reduction in BSI score 1 year after transplant has been reported. The BSI evaluates psychopathological symptoms, which are early indicators of psychological discomfort. One study noted a reduction in the LEIPAD quality of life score, which measures overall quality of life, 2 years after transplant.³⁵ This decline may reflect the difficulties associated with the new challenges after transplant. Patients may endure both physical changes due to medical complications as well as psychological problems as they adjust to their new bodily integrity, their dependence on medications and medical staff, and other changes in function. Three to 5 years after transplant, patients reached a new psychological stability, with reported improvements in quality of life and decreased psychological distress.³⁵

Continue to: Special populations

Special populations

HCV infection. Recurrent HCV infection and liver disease after transplantation are associated with psychological distress. This is particularly evident in patients 6 months after transplantation. Depression and psychological distress have been reported in male patients with recurrent HCV infection within the first year after transplantation.³⁵

Acetaminophen overdose. Patients who receive a transplant for acetaminophen-induced acute liver failure (ALF) had a greater prevalence of psychiatric comorbidity as reflected by predefined diagnoses, medication, and previous suicide attempts.⁴¹ Despite this, outcomes for patients transplanted emergently for acetaminophen-induced ALF were comparable to those transplanted for non-acetaminophen-induced ALF and for chronic liver disease. Multidisciplinary approaches with long-term psychiatric follow-up may contribute to low post-transplant suicide rates and low rates of graft loss because of noncompliance.⁴¹

CASE REPORT

A complicated presentation

Ms. A, age 45, a married woman with history of chronic back pain and self-reported bipolar disorder, presented to our hospital with acute liver failure secondary to acetaminophen overdose. Her Model for End-Stage Liver Disease (MELD) score on presentation was 38 (range: 0 to 40 with higher scores indicating increased likelihood of mortality). Her urine drug screen was positive for benzodiazepines and opiates. On hospital Day 2, the primary team consulted psychiatry for a pre-transplant evaluation and consideration of suicidality. Hepatology, toxicology, and transplant surgery services also were consulted.

Because Ms. A was intubated for acute respiratory failure, the initial history was gathered from family, a review of the medical record, consultation with her pharmacy, and collateral from her outpatient physician. Ms. A had been taking diazepam and hydromorphone as prescribed by her primary care physician for several years for chronic back pain.

Four days before presenting with acute liver failure, Ms. A had visited another hospital for lethargy. Benzodiazepines and opiates were stopped abruptly, and she was discharged with the recommendation to take acetaminophen for her pain. Approximately 24 hours after returning home, Ms. A began having auditory and visual hallucinations, and she did not sleep for days. She continued to complain of pain and was taking acetaminophen as recommended by the outside hospital. Her husband notes that she was intermittently confused. He was unsure how much acetaminophen she was taking.

Continue to: Her family noted...

Her family noted Ms. A had been diagnosed with bipolar disorder “years ago” but was unable to describe any manic episodes, and Ms. A had been treated only with an antidepressant from her primary care physician. She had persistent low mood and increased sleep since developing chronic back pain that severely limited her functioning. Ms. A attempted suicide once years ago by cutting her wrists. She had 2 prior psychiatric hospitalizations for suicidal ideation and the suicide attempt; however, she had not recently voiced suicidal ideation to her husband or family. She was adherent to psychotropic medications and follow-up appointments. Ms. A is a current smoker. She had used marijuana in the past, but her family denies current use, as well as any alcohol use or illicit substance use.

Ms. A’s diagnosis was consistent with tobacco use disorder and major depressive disorder (MDD). She likely developed withdrawal after abrupt cessation of diazepam, which she had been taking as prescribed for years. There was no evidence at the time of her initial psychiatric evaluation that the acetaminophen overdose was a suicide attempt; however, because Ms. A was intubated and sedated at that time, the consultation team recommended direct observation until she could participate in a risk assessment.

For the pre-transplant psychiatric evaluation, our consultation-liaison team noted Ms. A’s history of MDD, with recent active symptoms, chronic pain, and a past suicide attempt. She was a current tobacco smoker, which increases the risk of post-transplant vascular problems. However, she had been adherent to medications and follow-up, had very close family support, and there was no clear evidence that this acetaminophen ingestion was a suicide attempt. We noted that outpatient psychiatric follow-up and better chronic pain management would be helpful post-transplant. We would have to re-evaluate Ms. A when she was medically stable enough to communicate before making any further recommendations. Due to medical complications that developed after our evaluation, the transplant team noted Ms. A was no longer a transplant candidate.

Fortunately, Ms. A recovered with medical management over the next 2 weeks. She denied any suicidal ideation throughout her hospitalization. She was restarted on an antidepressant and received supportive therapy until discharge. Outpatient psychiatry follow-up and pain management was set up before Ms. A was discharged. Inpatient psychiatric hospitalization was not recommended. Per available records, Ms. A followed up with all outpatient appointments, including with her psychiatrist, since discharge.

Avoiding problems, maximizing outcomes

In addition to medical factors, psychosocial factors may affect the success of LT, although empirical data regarding which factors are most predictive of post-transplant outcomes is lacking, especially in patients with serious mental illness. The goals of a psychosocial pre-transplant evaluation are to promote fairness and equal access to care, maximize optimal outcomes, wisely use scarce resources, and ensure that the potential for benefits outweigh surgical risks to the patient. Identifying potential complicating factors (ie, substance abuse, nonadherence, serious psychopathology) can help guide the medical and psychiatric treatment plan and help minimize preventable problems both before and after transplant.⁴²

Continue to: In patients who have...

In patients who have a history of alcohol use and alcohol liver disease, relapse to alcohol is a significant problem. Relapse rates vary from 10% to 30%.⁷ The duration of abstinence before LT appears to be a poor predictor of abstinence after LT.⁴³ Polysubstance use also adversely affects outcomes in patients with alcohol liver disease. Approximately one-third of patients with polysubstance use who receive a LT relapse to substance use.⁴⁴ Coffman et al⁴⁵ showed that the presence of antisocial behavior and eating disorders may increase the risk of relapse after LT.

The psychiatrist’s role in the setting of LT spans from the pre-transplant assessment to post-transplant management and follow-up. Clarifying specific psychiatric diagnoses, psychosocial factors that need to be addressed before transplant, and substance use diagnoses and treatment recommendations can help the transplant team clearly identify modifiable factors that can affect transplant outcomes.

Bottom Line

Psychiatrists can help patients who are candidates for liver transplantation (LT) by performing a pre-transplant psychosocial assessment to identity factors that might complicate transplantation or recovery. After LT, patients require careful monitoring for psychiatric comorbidities, drug interactions, and other factors that can affect quality of life.

Related Resources

• Beresford TP, Lucey MR. Towards standardizing the alcoholism evaluation of potential liver transplant recipients. Alcohol Alcohol. 2018;53(2):135-144.
• Marcangelo MJ, Crone C. Tools, techniques to assess organ transplant candidates. Current Psychiatry. 2007;6(9):56-66.

Drug Brand Names

Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Cyclosporine • Gengraf, Neoral
Diazepam • Valium
Hydromorphone • Dilaudid
Lithium • Eskalith, Lithobid
Tacrolimus • Astagraf XL, Envarsus XR

Since the first liver transplant (LT) was performed in 1963 by Starzl et al, there have been considerable advances in the field, with improvements in post-transplant survival.¹ There are multiple indications for LT, including acute liver failure and index complications of cirrhosis such as ascites, encephalopathy, and hepatopulmonary syndrome.² Once a patient develops one of these conditions, he/she is evaluated for LT, even as the complications of liver failure are being managed.

Although the number of LTs has risen, the demand for transplant continues to exceed availability. In 2015, chronic liver disease and cirrhosis was the 12th leading cause of death in the United States.³ In 2016, approximately 50% of waitlisted candidates received a transplant.⁴ There is also a donor shortage. In part, this shortage may be due to longer life spans and the subsequent increase in the age of the potential donor.⁵ In light of this shortage and increased demand, the pre-LT workup is comprehensive. The pre-transplant assessment typically consists of cardiology, surgery, hepatology, and psychosocial evaluations, and hence requires a team of experts to determine who is an ideal candidate for transplant.

Psychiatrists play a key role in the pre-transplant psychosocial evaluations. This article describes the elements of these evaluations, and what psychiatrists can do to help patients both before and after they undergo LT.

Elements of the pre-transplant evaluation

The psychosocial evaluation is a critical component of the pre-transplant assessment. As part of the evaluation, patients are screened for psychosocial limitations that may complicate transplantation, such as demonstrated noncompliance, ongoing alcohol or drug use, and lack of social support (Table 1² ). Other goals of the psychosocial evaluation are to identify in the pre-transplant period patients with possible risk factors, such as substance use or psychiatric disorders, and develop treatment plans to optimize transplant outcomes (Table 2⁶). There are relative contraindications to LT (Table 3⁷) but no absolute psychiatric contraindications, according to the 2013 American Association for the Study of Liver Diseases (AASLD) practice guideline for transplantation.²

Adherence. The 2013 AASLD practice guideline states that patients “should be evaluated for and meet reasonable expectations for adherence to medical directives and mental health stability as determined by the psychosocial evaluation.”² In the transplant setting, adherence is complex. It requires compliance with complicated medication regimens and laboratory testing, frequent follow-up appointments, and close, prompt communication of concerns to the health care team. Patient adherence to medication regimens plays an important role in transplant outcomes.⁸ In fact, in patients who have undergone renal transplant, nonadherence to therapy is considered the leading cause of avoidable graft failure.⁹

A retrospective study of adult LT recipients found that pre-transplant chart evidence of nonadherence, such as missed laboratory testing and clinic visits, was a significant predictor of post-transplant nonadherence with immunosuppressant therapy. Pre-transplant unemployment status and a history of substance abuse also were associated with nonadherence.⁹

Dobbels et al¹⁰ found that patients with a self-reported history of pre-transplant non-adherence had a higher risk of being nonadherent with their immunosuppressive therapy after transplant (odd ratio [OR]: 7.9). Their self-report adherence questionnaire included questions that addressed pre-transplant smoking status, alcohol use, and adherence with medication. In this prospective study, researchers also found that patients with a low “conscientiousness” score were at a higher risk for post-transplant medication nonadherence (OR: 0.8).

Continue to: Studies have also found...

Studies have also found that patients with higher education are more at risk for post-transplant medication nonadherence. Higher education may be associated with higher employment status resulting in a busier lifestyle, a known risk factor that may prevent patients from regular medication adherence.^11,12 Alternatively, it is possible that higher educated patients are “decisive” nonadherers who prefer independent decision-making regarding their disease and treatment.¹³

Substance use. The 2013 AASLD practice guideline lists “ongoing alcohol or illicit substance abuse” as one of the contraindications to LT.² In guidelines from the Austrian Society for Gastroenterology and Hepatology, Graziadei et al¹⁴ listed “alcohol addiction without motivation for alcohol abstinence and untreated/ongoing substance abuse” as absolute contraindications and “untreated alcohol abuse and other drug-related addiction” as relative contraindications. Hence, the pre-transplant evaluation should include a thorough substance use history, including duration, amount, previous attempts to quit, and motivation for abstinence.

Substance use history is especially important because alcoholic liver disease is the second most common indication for LT.² Most LT programs require 6 months of abstinence before a patient can be considered for transplant.¹⁵ The 6-month period was based on studies demonstrating that pre-transplant abstinence from alcohol for <6 months is a risk factor for relapse.¹⁵ However, this guideline remains controversial because the transplant referral and workup may be delayed as the patient’s liver disease worsens. Other risk factors for substance relapse should also be taken into consideration, such as depression, personality disorders, lack of social support, severity of alcohol use, and family history of alcoholism.¹⁶ Lee and Leggio¹⁶ developed the Sustained Alcohol Use Post-Liver Transplant (SALT) score to identify patients who were at risk for sustained alcohol use posttransplant. The 4 SALT criteria are:

• >10 drinks per day at initial hospitalization (+4 points)
• multiple prior rehabilitation attempts (+4 points)
• prior alcohol‐related legal issues (+2 points), and
• prior illicit substance abuse (+1 point).

A SALT score can range from 0 to 11. Lee et al¹⁷ found a SALT score ≥5 had a 25% positive predictive value (95% confidence interval [CI]: 10% to 47%) and a SALT score of <5 had a 95% negative predictive value (95% CI: 89% to 98%) for sustained alcohol use post‐LT. Thus, the 2013 AASLD guideline cautions against delaying evaluation based on the 6-month abstinence rule, and instead recommends early transplant referral for patients with alcoholic liver disease to encourage such patients to begin addiction treatment.²

As part of the substance use history, it is important to ask about the patient’s smoking history. Approximately 60% of LT candidates have a history of smoking cigarettes.¹⁸ Tobacco use history is associated with increased post-transplant vascular complications, such as hepatic artery thrombosis or stenosis, portal vein thrombosis, and deep vein thrombosis.¹⁹ The 2013 AASLD guideline recommends that tobacco use should be prohibited in LT candidates.² Pungpapong et al¹⁹ reported that smoking cessation for at least 2 years prior to transplant led to a significantly decreased risk of developing arterial complications, with an absolute risk reduction of approximately 16%.

Continue to: Liver cirrhosis due to...

Liver cirrhosis due to chronic hepatitis C virus (HCV) infection is one of the leading causes for LT. In the United States, HCV is commonly transmitted during injection drug use. According to the 2013 AASLD guideline, ongoing illicit substance use is a relative contraindication to LT.² It is important to note, however, that methadone maintenance therapy (MMT) is not a contraindication to LT. In fact, the 2013 AASLD guideline recommends that patients receiving MMT should not be required to reduce or stop therapy in order to be listed for transplant.² Studies have shown that in 80% of patients, tapering MMT leads to illicit opiate relapse.²⁰ Currently, there is no evidence that patients receiving MMT have poorer post-transplant outcomes compared with patients not receiving MMT.²¹

Whether cannabis use is a relative contraindication to LT remains controversial.²² Possible adverse effects of cannabis use in transplant patients include drug–drug interactions and infections. Hézode et al²³ reported that daily cannabis use is significantly associated with an increased fibrosis progression rate in patients with chronic HCV infection. Another recent study found that a history of cannabis use was not associated with worse outcomes among patients on the LT waitlist.²⁴ With the increased legalization of cannabis, more studies are needed to assess ongoing cannabis use in patients on the LT waitlist and post-LT outcomes.

Psychiatric history. When assessing a patient for possible LT, no psychiatric disorder is considered an absolute contraindication. Patients with a serious mental illness, such as schizophrenia, and those with intellectual disability can have successful, long-term outcomes with proper evaluation and preparation, including social support. However, empirical literature regarding transplant outcomes and predictive factors in patients with serious mental illness is scarce.²

Studies examining the predictive value of pre-transplant depression on post-transplant outcomes have had mixed results.²⁵ Depression may predict lower post-transplant quality of life. Pre-LT suicidal thoughts (as noted on the Beck Depression Inventory, for example) are associated with post-LT depression.²⁵ In contrast, available data show no significant effect of pre-transplant anxiety on post-LT outcomes. Similarly, pre-transplant cognitive performance appears not to predict survival or other post-transplant outcomes, but may predict poorer quality of life after transplant.²⁵

A few psychiatric factors are considered relative contraindications for LT. These include severe personality disorders, active substance use with no motivation for treatment or abstinence, active psychosis, severe neurocognitive disorders, suicidality, and factitious disorder.⁷

Continue to: Social support

Social support. Assessing a pre-LT patient’s level of social support is an essential part of the psychosocial evaluation. According to the 2013 AASLD guideline, patients should have “adequate” social support both during the waitlist and post-operative periods.² Lack of partnership is a significant predictor of poor post-transplant outcomes, such as late graft loss.¹⁰ Satapathy and Sanyal²⁶ reported that among patients who receive an LT for alcoholic liver disease, those with immediate family support were less likely to relapse to using alcohol after transplant. Poor social support was also a predictor of post-transplant medication nonadherence.¹⁰ Thus, the patient needs enough social support to engage in the pre-transplant health care requirements and to participate in post-transplant recommendations until he/she is functioning independently post-transplant.

Screening tools

Various screening tools may be useful in a pre-LT evaluation. Three standardized assessment tools available specifically for pre-transplant psychosocial assessments are the Stanford Integrated Psychosocial Assessment for Transplantation (Table 2⁶), the Psychosocial Assessment of Candidates for Transplantation,²⁷ and the Transplant Evaluation Rating Scale.²⁸ Instruments to aid in the assessment of depression, anxiety, and delirium,^29-31 a structured personality assessment,³² coping inventories,³³ neuropsychological batteries,³⁴ and others also have been used to evaluate patients before LT. The self-rated Beck Depression Inventory and the clinician-rated Hamilton Depression Rating Scale are commonly used.⁷ Other tools, such as the LEIPAD quality of life instrument and the Brief Symptom Inventory (BSI), have been used to assess for perceived quality of life and psychological distress, respectively.³⁵ These screening tools can be helpful as aids for the pre-LT evaluation; however, diagnoses and treatment plan recommendations require a psychiatric evaluation conducted by a trained clinician.

Treatment after liver transplant

Psychiatric issues. After LT, various psychiatric complications may arise, including (but not limited to) delirium⁷ and “paradoxical psychiatric syndrome” (PPS).³⁶ Delirium can be managed by administering low-dose antipsychotic medications, limiting the use of benzodiazepines and medications with anticholinergic effects, implementing behavioral interventions (frequent orientation, maintaining sleep/wake cycle, limiting noise, presence of a family member or a sitter at bedside),³⁷ and addressing the underlying etiology. Paradoxical psychiatric syndrome is defined as psychiatric symptoms that occur despite a successful LT. It develops within the first year of transplantation and is characterized by recipients having strong guilt feelings toward their donors.³⁸

Drug interactions. In the post-transplant period, antipsychotics are used for management of delirium and psychosis, antidepressants for anxiety and depression, and benzodiazepines for anxiety and sleep problems.⁷ Drug–drug interactions between psychotropic medications and the immunosuppressants required after LT must be closely monitored. First-generation antipsychotics should be avoided in post-transplant patients taking tacrolimus due to the increased risk of QTc prolongation. Tacrolimus can also increase the risk of nephrotoxicity when co-administered with lithium. Post-LT patients taking steroids and bupropion have an increased risk of seizure. Carbamazepine may decrease blood levels of cyclosporine due to the induction of hepatic metabolism.^39,40 The psychiatrist should review and update the patient’s complete medication list at each visit, checking for possible medication interactions.

Quality of life. In the first 6 months post-transplant, patients typically experience improved quality of life in both physical and psychological domains. However, this improvement vacillates as the patient adjusts to post-transplant life. A reduction in BSI score 1 year after transplant has been reported. The BSI evaluates psychopathological symptoms, which are early indicators of psychological discomfort. One study noted a reduction in the LEIPAD quality of life score, which measures overall quality of life, 2 years after transplant.³⁵ This decline may reflect the difficulties associated with the new challenges after transplant. Patients may endure both physical changes due to medical complications as well as psychological problems as they adjust to their new bodily integrity, their dependence on medications and medical staff, and other changes in function. Three to 5 years after transplant, patients reached a new psychological stability, with reported improvements in quality of life and decreased psychological distress.³⁵

Continue to: Special populations

Special populations

HCV infection. Recurrent HCV infection and liver disease after transplantation are associated with psychological distress. This is particularly evident in patients 6 months after transplantation. Depression and psychological distress have been reported in male patients with recurrent HCV infection within the first year after transplantation.³⁵

Acetaminophen overdose. Patients who receive a transplant for acetaminophen-induced acute liver failure (ALF) had a greater prevalence of psychiatric comorbidity as reflected by predefined diagnoses, medication, and previous suicide attempts.⁴¹ Despite this, outcomes for patients transplanted emergently for acetaminophen-induced ALF were comparable to those transplanted for non-acetaminophen-induced ALF and for chronic liver disease. Multidisciplinary approaches with long-term psychiatric follow-up may contribute to low post-transplant suicide rates and low rates of graft loss because of noncompliance.⁴¹

CASE REPORT

A complicated presentation

Ms. A, age 45, a married woman with history of chronic back pain and self-reported bipolar disorder, presented to our hospital with acute liver failure secondary to acetaminophen overdose. Her Model for End-Stage Liver Disease (MELD) score on presentation was 38 (range: 0 to 40 with higher scores indicating increased likelihood of mortality). Her urine drug screen was positive for benzodiazepines and opiates. On hospital Day 2, the primary team consulted psychiatry for a pre-transplant evaluation and consideration of suicidality. Hepatology, toxicology, and transplant surgery services also were consulted.

Because Ms. A was intubated for acute respiratory failure, the initial history was gathered from family, a review of the medical record, consultation with her pharmacy, and collateral from her outpatient physician. Ms. A had been taking diazepam and hydromorphone as prescribed by her primary care physician for several years for chronic back pain.

Four days before presenting with acute liver failure, Ms. A had visited another hospital for lethargy. Benzodiazepines and opiates were stopped abruptly, and she was discharged with the recommendation to take acetaminophen for her pain. Approximately 24 hours after returning home, Ms. A began having auditory and visual hallucinations, and she did not sleep for days. She continued to complain of pain and was taking acetaminophen as recommended by the outside hospital. Her husband notes that she was intermittently confused. He was unsure how much acetaminophen she was taking.

Continue to: Her family noted...

Her family noted Ms. A had been diagnosed with bipolar disorder “years ago” but was unable to describe any manic episodes, and Ms. A had been treated only with an antidepressant from her primary care physician. She had persistent low mood and increased sleep since developing chronic back pain that severely limited her functioning. Ms. A attempted suicide once years ago by cutting her wrists. She had 2 prior psychiatric hospitalizations for suicidal ideation and the suicide attempt; however, she had not recently voiced suicidal ideation to her husband or family. She was adherent to psychotropic medications and follow-up appointments. Ms. A is a current smoker. She had used marijuana in the past, but her family denies current use, as well as any alcohol use or illicit substance use.

Ms. A’s diagnosis was consistent with tobacco use disorder and major depressive disorder (MDD). She likely developed withdrawal after abrupt cessation of diazepam, which she had been taking as prescribed for years. There was no evidence at the time of her initial psychiatric evaluation that the acetaminophen overdose was a suicide attempt; however, because Ms. A was intubated and sedated at that time, the consultation team recommended direct observation until she could participate in a risk assessment.

For the pre-transplant psychiatric evaluation, our consultation-liaison team noted Ms. A’s history of MDD, with recent active symptoms, chronic pain, and a past suicide attempt. She was a current tobacco smoker, which increases the risk of post-transplant vascular problems. However, she had been adherent to medications and follow-up, had very close family support, and there was no clear evidence that this acetaminophen ingestion was a suicide attempt. We noted that outpatient psychiatric follow-up and better chronic pain management would be helpful post-transplant. We would have to re-evaluate Ms. A when she was medically stable enough to communicate before making any further recommendations. Due to medical complications that developed after our evaluation, the transplant team noted Ms. A was no longer a transplant candidate.

Fortunately, Ms. A recovered with medical management over the next 2 weeks. She denied any suicidal ideation throughout her hospitalization. She was restarted on an antidepressant and received supportive therapy until discharge. Outpatient psychiatry follow-up and pain management was set up before Ms. A was discharged. Inpatient psychiatric hospitalization was not recommended. Per available records, Ms. A followed up with all outpatient appointments, including with her psychiatrist, since discharge.

Avoiding problems, maximizing outcomes

In addition to medical factors, psychosocial factors may affect the success of LT, although empirical data regarding which factors are most predictive of post-transplant outcomes is lacking, especially in patients with serious mental illness. The goals of a psychosocial pre-transplant evaluation are to promote fairness and equal access to care, maximize optimal outcomes, wisely use scarce resources, and ensure that the potential for benefits outweigh surgical risks to the patient. Identifying potential complicating factors (ie, substance abuse, nonadherence, serious psychopathology) can help guide the medical and psychiatric treatment plan and help minimize preventable problems both before and after transplant.⁴²

Continue to: In patients who have...

In patients who have a history of alcohol use and alcohol liver disease, relapse to alcohol is a significant problem. Relapse rates vary from 10% to 30%.⁷ The duration of abstinence before LT appears to be a poor predictor of abstinence after LT.⁴³ Polysubstance use also adversely affects outcomes in patients with alcohol liver disease. Approximately one-third of patients with polysubstance use who receive a LT relapse to substance use.⁴⁴ Coffman et al⁴⁵ showed that the presence of antisocial behavior and eating disorders may increase the risk of relapse after LT.

The psychiatrist’s role in the setting of LT spans from the pre-transplant assessment to post-transplant management and follow-up. Clarifying specific psychiatric diagnoses, psychosocial factors that need to be addressed before transplant, and substance use diagnoses and treatment recommendations can help the transplant team clearly identify modifiable factors that can affect transplant outcomes.

Bottom Line

Psychiatrists can help patients who are candidates for liver transplantation (LT) by performing a pre-transplant psychosocial assessment to identity factors that might complicate transplantation or recovery. After LT, patients require careful monitoring for psychiatric comorbidities, drug interactions, and other factors that can affect quality of life.

Related Resources

• Beresford TP, Lucey MR. Towards standardizing the alcoholism evaluation of potential liver transplant recipients. Alcohol Alcohol. 2018;53(2):135-144.
• Marcangelo MJ, Crone C. Tools, techniques to assess organ transplant candidates. Current Psychiatry. 2007;6(9):56-66.

Drug Brand Names

Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Cyclosporine • Gengraf, Neoral
Diazepam • Valium
Hydromorphone • Dilaudid
Lithium • Eskalith, Lithobid
Tacrolimus • Astagraf XL, Envarsus XR

Since the first liver transplant (LT) was performed in 1963 by Starzl et al, there have been considerable advances in the field, with improvements in post-transplant survival.¹ There are multiple indications for LT, including acute liver failure and index complications of cirrhosis such as ascites, encephalopathy, and hepatopulmonary syndrome.² Once a patient develops one of these conditions, he/she is evaluated for LT, even as the complications of liver failure are being managed.

Although the number of LTs has risen, the demand for transplant continues to exceed availability. In 2015, chronic liver disease and cirrhosis was the 12th leading cause of death in the United States.³ In 2016, approximately 50% of waitlisted candidates received a transplant.⁴ There is also a donor shortage. In part, this shortage may be due to longer life spans and the subsequent increase in the age of the potential donor.⁵ In light of this shortage and increased demand, the pre-LT workup is comprehensive. The pre-transplant assessment typically consists of cardiology, surgery, hepatology, and psychosocial evaluations, and hence requires a team of experts to determine who is an ideal candidate for transplant.

Psychiatrists play a key role in the pre-transplant psychosocial evaluations. This article describes the elements of these evaluations, and what psychiatrists can do to help patients both before and after they undergo LT.

Elements of the pre-transplant evaluation

The psychosocial evaluation is a critical component of the pre-transplant assessment. As part of the evaluation, patients are screened for psychosocial limitations that may complicate transplantation, such as demonstrated noncompliance, ongoing alcohol or drug use, and lack of social support (Table 1² ). Other goals of the psychosocial evaluation are to identify in the pre-transplant period patients with possible risk factors, such as substance use or psychiatric disorders, and develop treatment plans to optimize transplant outcomes (Table 2⁶). There are relative contraindications to LT (Table 3⁷) but no absolute psychiatric contraindications, according to the 2013 American Association for the Study of Liver Diseases (AASLD) practice guideline for transplantation.²

Adherence. The 2013 AASLD practice guideline states that patients “should be evaluated for and meet reasonable expectations for adherence to medical directives and mental health stability as determined by the psychosocial evaluation.”² In the transplant setting, adherence is complex. It requires compliance with complicated medication regimens and laboratory testing, frequent follow-up appointments, and close, prompt communication of concerns to the health care team. Patient adherence to medication regimens plays an important role in transplant outcomes.⁸ In fact, in patients who have undergone renal transplant, nonadherence to therapy is considered the leading cause of avoidable graft failure.⁹

A retrospective study of adult LT recipients found that pre-transplant chart evidence of nonadherence, such as missed laboratory testing and clinic visits, was a significant predictor of post-transplant nonadherence with immunosuppressant therapy. Pre-transplant unemployment status and a history of substance abuse also were associated with nonadherence.⁹

Dobbels et al¹⁰ found that patients with a self-reported history of pre-transplant non-adherence had a higher risk of being nonadherent with their immunosuppressive therapy after transplant (odd ratio [OR]: 7.9). Their self-report adherence questionnaire included questions that addressed pre-transplant smoking status, alcohol use, and adherence with medication. In this prospective study, researchers also found that patients with a low “conscientiousness” score were at a higher risk for post-transplant medication nonadherence (OR: 0.8).

Continue to: Studies have also found...

Studies have also found that patients with higher education are more at risk for post-transplant medication nonadherence. Higher education may be associated with higher employment status resulting in a busier lifestyle, a known risk factor that may prevent patients from regular medication adherence.^11,12 Alternatively, it is possible that higher educated patients are “decisive” nonadherers who prefer independent decision-making regarding their disease and treatment.¹³

Substance use. The 2013 AASLD practice guideline lists “ongoing alcohol or illicit substance abuse” as one of the contraindications to LT.² In guidelines from the Austrian Society for Gastroenterology and Hepatology, Graziadei et al¹⁴ listed “alcohol addiction without motivation for alcohol abstinence and untreated/ongoing substance abuse” as absolute contraindications and “untreated alcohol abuse and other drug-related addiction” as relative contraindications. Hence, the pre-transplant evaluation should include a thorough substance use history, including duration, amount, previous attempts to quit, and motivation for abstinence.

Substance use history is especially important because alcoholic liver disease is the second most common indication for LT.² Most LT programs require 6 months of abstinence before a patient can be considered for transplant.¹⁵ The 6-month period was based on studies demonstrating that pre-transplant abstinence from alcohol for <6 months is a risk factor for relapse.¹⁵ However, this guideline remains controversial because the transplant referral and workup may be delayed as the patient’s liver disease worsens. Other risk factors for substance relapse should also be taken into consideration, such as depression, personality disorders, lack of social support, severity of alcohol use, and family history of alcoholism.¹⁶ Lee and Leggio¹⁶ developed the Sustained Alcohol Use Post-Liver Transplant (SALT) score to identify patients who were at risk for sustained alcohol use posttransplant. The 4 SALT criteria are:

• >10 drinks per day at initial hospitalization (+4 points)
• multiple prior rehabilitation attempts (+4 points)
• prior alcohol‐related legal issues (+2 points), and
• prior illicit substance abuse (+1 point).

A SALT score can range from 0 to 11. Lee et al¹⁷ found a SALT score ≥5 had a 25% positive predictive value (95% confidence interval [CI]: 10% to 47%) and a SALT score of <5 had a 95% negative predictive value (95% CI: 89% to 98%) for sustained alcohol use post‐LT. Thus, the 2013 AASLD guideline cautions against delaying evaluation based on the 6-month abstinence rule, and instead recommends early transplant referral for patients with alcoholic liver disease to encourage such patients to begin addiction treatment.²

As part of the substance use history, it is important to ask about the patient’s smoking history. Approximately 60% of LT candidates have a history of smoking cigarettes.¹⁸ Tobacco use history is associated with increased post-transplant vascular complications, such as hepatic artery thrombosis or stenosis, portal vein thrombosis, and deep vein thrombosis.¹⁹ The 2013 AASLD guideline recommends that tobacco use should be prohibited in LT candidates.² Pungpapong et al¹⁹ reported that smoking cessation for at least 2 years prior to transplant led to a significantly decreased risk of developing arterial complications, with an absolute risk reduction of approximately 16%.

Continue to: Liver cirrhosis due to...

Liver cirrhosis due to chronic hepatitis C virus (HCV) infection is one of the leading causes for LT. In the United States, HCV is commonly transmitted during injection drug use. According to the 2013 AASLD guideline, ongoing illicit substance use is a relative contraindication to LT.² It is important to note, however, that methadone maintenance therapy (MMT) is not a contraindication to LT. In fact, the 2013 AASLD guideline recommends that patients receiving MMT should not be required to reduce or stop therapy in order to be listed for transplant.² Studies have shown that in 80% of patients, tapering MMT leads to illicit opiate relapse.²⁰ Currently, there is no evidence that patients receiving MMT have poorer post-transplant outcomes compared with patients not receiving MMT.²¹

Whether cannabis use is a relative contraindication to LT remains controversial.²² Possible adverse effects of cannabis use in transplant patients include drug–drug interactions and infections. Hézode et al²³ reported that daily cannabis use is significantly associated with an increased fibrosis progression rate in patients with chronic HCV infection. Another recent study found that a history of cannabis use was not associated with worse outcomes among patients on the LT waitlist.²⁴ With the increased legalization of cannabis, more studies are needed to assess ongoing cannabis use in patients on the LT waitlist and post-LT outcomes.

Psychiatric history. When assessing a patient for possible LT, no psychiatric disorder is considered an absolute contraindication. Patients with a serious mental illness, such as schizophrenia, and those with intellectual disability can have successful, long-term outcomes with proper evaluation and preparation, including social support. However, empirical literature regarding transplant outcomes and predictive factors in patients with serious mental illness is scarce.²

Studies examining the predictive value of pre-transplant depression on post-transplant outcomes have had mixed results.²⁵ Depression may predict lower post-transplant quality of life. Pre-LT suicidal thoughts (as noted on the Beck Depression Inventory, for example) are associated with post-LT depression.²⁵ In contrast, available data show no significant effect of pre-transplant anxiety on post-LT outcomes. Similarly, pre-transplant cognitive performance appears not to predict survival or other post-transplant outcomes, but may predict poorer quality of life after transplant.²⁵

A few psychiatric factors are considered relative contraindications for LT. These include severe personality disorders, active substance use with no motivation for treatment or abstinence, active psychosis, severe neurocognitive disorders, suicidality, and factitious disorder.⁷

Continue to: Social support

Social support. Assessing a pre-LT patient’s level of social support is an essential part of the psychosocial evaluation. According to the 2013 AASLD guideline, patients should have “adequate” social support both during the waitlist and post-operative periods.² Lack of partnership is a significant predictor of poor post-transplant outcomes, such as late graft loss.¹⁰ Satapathy and Sanyal²⁶ reported that among patients who receive an LT for alcoholic liver disease, those with immediate family support were less likely to relapse to using alcohol after transplant. Poor social support was also a predictor of post-transplant medication nonadherence.¹⁰ Thus, the patient needs enough social support to engage in the pre-transplant health care requirements and to participate in post-transplant recommendations until he/she is functioning independently post-transplant.

Screening tools

Various screening tools may be useful in a pre-LT evaluation. Three standardized assessment tools available specifically for pre-transplant psychosocial assessments are the Stanford Integrated Psychosocial Assessment for Transplantation (Table 2⁶), the Psychosocial Assessment of Candidates for Transplantation,²⁷ and the Transplant Evaluation Rating Scale.²⁸ Instruments to aid in the assessment of depression, anxiety, and delirium,^29-31 a structured personality assessment,³² coping inventories,³³ neuropsychological batteries,³⁴ and others also have been used to evaluate patients before LT. The self-rated Beck Depression Inventory and the clinician-rated Hamilton Depression Rating Scale are commonly used.⁷ Other tools, such as the LEIPAD quality of life instrument and the Brief Symptom Inventory (BSI), have been used to assess for perceived quality of life and psychological distress, respectively.³⁵ These screening tools can be helpful as aids for the pre-LT evaluation; however, diagnoses and treatment plan recommendations require a psychiatric evaluation conducted by a trained clinician.

Treatment after liver transplant

Psychiatric issues. After LT, various psychiatric complications may arise, including (but not limited to) delirium⁷ and “paradoxical psychiatric syndrome” (PPS).³⁶ Delirium can be managed by administering low-dose antipsychotic medications, limiting the use of benzodiazepines and medications with anticholinergic effects, implementing behavioral interventions (frequent orientation, maintaining sleep/wake cycle, limiting noise, presence of a family member or a sitter at bedside),³⁷ and addressing the underlying etiology. Paradoxical psychiatric syndrome is defined as psychiatric symptoms that occur despite a successful LT. It develops within the first year of transplantation and is characterized by recipients having strong guilt feelings toward their donors.³⁸

Drug interactions. In the post-transplant period, antipsychotics are used for management of delirium and psychosis, antidepressants for anxiety and depression, and benzodiazepines for anxiety and sleep problems.⁷ Drug–drug interactions between psychotropic medications and the immunosuppressants required after LT must be closely monitored. First-generation antipsychotics should be avoided in post-transplant patients taking tacrolimus due to the increased risk of QTc prolongation. Tacrolimus can also increase the risk of nephrotoxicity when co-administered with lithium. Post-LT patients taking steroids and bupropion have an increased risk of seizure. Carbamazepine may decrease blood levels of cyclosporine due to the induction of hepatic metabolism.^39,40 The psychiatrist should review and update the patient’s complete medication list at each visit, checking for possible medication interactions.

Quality of life. In the first 6 months post-transplant, patients typically experience improved quality of life in both physical and psychological domains. However, this improvement vacillates as the patient adjusts to post-transplant life. A reduction in BSI score 1 year after transplant has been reported. The BSI evaluates psychopathological symptoms, which are early indicators of psychological discomfort. One study noted a reduction in the LEIPAD quality of life score, which measures overall quality of life, 2 years after transplant.³⁵ This decline may reflect the difficulties associated with the new challenges after transplant. Patients may endure both physical changes due to medical complications as well as psychological problems as they adjust to their new bodily integrity, their dependence on medications and medical staff, and other changes in function. Three to 5 years after transplant, patients reached a new psychological stability, with reported improvements in quality of life and decreased psychological distress.³⁵

Continue to: Special populations

Special populations

HCV infection. Recurrent HCV infection and liver disease after transplantation are associated with psychological distress. This is particularly evident in patients 6 months after transplantation. Depression and psychological distress have been reported in male patients with recurrent HCV infection within the first year after transplantation.³⁵

Acetaminophen overdose. Patients who receive a transplant for acetaminophen-induced acute liver failure (ALF) had a greater prevalence of psychiatric comorbidity as reflected by predefined diagnoses, medication, and previous suicide attempts.⁴¹ Despite this, outcomes for patients transplanted emergently for acetaminophen-induced ALF were comparable to those transplanted for non-acetaminophen-induced ALF and for chronic liver disease. Multidisciplinary approaches with long-term psychiatric follow-up may contribute to low post-transplant suicide rates and low rates of graft loss because of noncompliance.⁴¹

CASE REPORT

A complicated presentation

Ms. A, age 45, a married woman with history of chronic back pain and self-reported bipolar disorder, presented to our hospital with acute liver failure secondary to acetaminophen overdose. Her Model for End-Stage Liver Disease (MELD) score on presentation was 38 (range: 0 to 40 with higher scores indicating increased likelihood of mortality). Her urine drug screen was positive for benzodiazepines and opiates. On hospital Day 2, the primary team consulted psychiatry for a pre-transplant evaluation and consideration of suicidality. Hepatology, toxicology, and transplant surgery services also were consulted.

Because Ms. A was intubated for acute respiratory failure, the initial history was gathered from family, a review of the medical record, consultation with her pharmacy, and collateral from her outpatient physician. Ms. A had been taking diazepam and hydromorphone as prescribed by her primary care physician for several years for chronic back pain.

Four days before presenting with acute liver failure, Ms. A had visited another hospital for lethargy. Benzodiazepines and opiates were stopped abruptly, and she was discharged with the recommendation to take acetaminophen for her pain. Approximately 24 hours after returning home, Ms. A began having auditory and visual hallucinations, and she did not sleep for days. She continued to complain of pain and was taking acetaminophen as recommended by the outside hospital. Her husband notes that she was intermittently confused. He was unsure how much acetaminophen she was taking.

Continue to: Her family noted...

Her family noted Ms. A had been diagnosed with bipolar disorder “years ago” but was unable to describe any manic episodes, and Ms. A had been treated only with an antidepressant from her primary care physician. She had persistent low mood and increased sleep since developing chronic back pain that severely limited her functioning. Ms. A attempted suicide once years ago by cutting her wrists. She had 2 prior psychiatric hospitalizations for suicidal ideation and the suicide attempt; however, she had not recently voiced suicidal ideation to her husband or family. She was adherent to psychotropic medications and follow-up appointments. Ms. A is a current smoker. She had used marijuana in the past, but her family denies current use, as well as any alcohol use or illicit substance use.

Ms. A’s diagnosis was consistent with tobacco use disorder and major depressive disorder (MDD). She likely developed withdrawal after abrupt cessation of diazepam, which she had been taking as prescribed for years. There was no evidence at the time of her initial psychiatric evaluation that the acetaminophen overdose was a suicide attempt; however, because Ms. A was intubated and sedated at that time, the consultation team recommended direct observation until she could participate in a risk assessment.

For the pre-transplant psychiatric evaluation, our consultation-liaison team noted Ms. A’s history of MDD, with recent active symptoms, chronic pain, and a past suicide attempt. She was a current tobacco smoker, which increases the risk of post-transplant vascular problems. However, she had been adherent to medications and follow-up, had very close family support, and there was no clear evidence that this acetaminophen ingestion was a suicide attempt. We noted that outpatient psychiatric follow-up and better chronic pain management would be helpful post-transplant. We would have to re-evaluate Ms. A when she was medically stable enough to communicate before making any further recommendations. Due to medical complications that developed after our evaluation, the transplant team noted Ms. A was no longer a transplant candidate.

Fortunately, Ms. A recovered with medical management over the next 2 weeks. She denied any suicidal ideation throughout her hospitalization. She was restarted on an antidepressant and received supportive therapy until discharge. Outpatient psychiatry follow-up and pain management was set up before Ms. A was discharged. Inpatient psychiatric hospitalization was not recommended. Per available records, Ms. A followed up with all outpatient appointments, including with her psychiatrist, since discharge.

Avoiding problems, maximizing outcomes

In addition to medical factors, psychosocial factors may affect the success of LT, although empirical data regarding which factors are most predictive of post-transplant outcomes is lacking, especially in patients with serious mental illness. The goals of a psychosocial pre-transplant evaluation are to promote fairness and equal access to care, maximize optimal outcomes, wisely use scarce resources, and ensure that the potential for benefits outweigh surgical risks to the patient. Identifying potential complicating factors (ie, substance abuse, nonadherence, serious psychopathology) can help guide the medical and psychiatric treatment plan and help minimize preventable problems both before and after transplant.⁴²

Continue to: In patients who have...

In patients who have a history of alcohol use and alcohol liver disease, relapse to alcohol is a significant problem. Relapse rates vary from 10% to 30%.⁷ The duration of abstinence before LT appears to be a poor predictor of abstinence after LT.⁴³ Polysubstance use also adversely affects outcomes in patients with alcohol liver disease. Approximately one-third of patients with polysubstance use who receive a LT relapse to substance use.⁴⁴ Coffman et al⁴⁵ showed that the presence of antisocial behavior and eating disorders may increase the risk of relapse after LT.

The psychiatrist’s role in the setting of LT spans from the pre-transplant assessment to post-transplant management and follow-up. Clarifying specific psychiatric diagnoses, psychosocial factors that need to be addressed before transplant, and substance use diagnoses and treatment recommendations can help the transplant team clearly identify modifiable factors that can affect transplant outcomes.

Bottom Line

Psychiatrists can help patients who are candidates for liver transplantation (LT) by performing a pre-transplant psychosocial assessment to identity factors that might complicate transplantation or recovery. After LT, patients require careful monitoring for psychiatric comorbidities, drug interactions, and other factors that can affect quality of life.

Related Resources

• Beresford TP, Lucey MR. Towards standardizing the alcoholism evaluation of potential liver transplant recipients. Alcohol Alcohol. 2018;53(2):135-144.
• Marcangelo MJ, Crone C. Tools, techniques to assess organ transplant candidates. Current Psychiatry. 2007;6(9):56-66.

Drug Brand Names

Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Cyclosporine • Gengraf, Neoral
Diazepam • Valium
Hydromorphone • Dilaudid
Lithium • Eskalith, Lithobid
Tacrolimus • Astagraf XL, Envarsus XR

Aparna Atluru, MD
Stanford Medicine

Anjan Bhattacharyya, MD
Saint Louis University

Caroline Bonham, MD
The University of New Mexico

Catherine Crone, MD
Inova Health System

Sheila Dowd, PhD
Rush Medical College

Ahmed Z. Elmaadawi, MD
Indiana University School of Medicine

Donald Gilbert, MD, MS
Cincinnati Children’s Hospital Medical Center

Mark Gold, MD
Washington University in St. Louis

Elana Harris, MD, PhD
Cincinnati Children’s Hospital

Susan Hatters-Friedman, MD
Case Western Reserve University

Faisal Islam, MD, MBA
Greenvale, New York

Kaustubh G. Joshi, MD
University of South Carolina School of Medicine

Rita Khoury, MD
Saint George Hospital University Medical Center

Suneeta Kumari, MD, MPH
Howard University Hospital

Michelle Magid, MD
Austin PsychCare PA

Michael Maksimowski, MD
Wayne State University

Jose Maldonado, MD
Stanford University

Thomas W. Meeks, MD
Portland VA Medical Center

John Miller, MD
University of South Florida

Armando Morera-Fumero, MD, PhD
Universidad de La Laguna

Mary K. Morreale, MD
Wayne State University

Philip Muskin, MD
Columbia University College of Physicians and Surgeons

Katharine Nelson, MD
University of Minnesota

Carol North, MD
University of Texas Southwestern Medical Center at Dallas

Douglas Opler, MD
Rutgers University School of Medicine

Joseph Pierre, MD
University of California, Los Angeles

Jerrold Pollak, PhD, ABN, ABPP
Seacoast Mental Health Center

Edwin Raffi, MD, MPH
Massachusetts General Hospital Center for Women’s Mental Health

Y. Pritham Raj, MD
Oregon Health and Science University

Jeffrey Rakofsky, MD
Emory University School of Medicine

Laura Ramsey, PhD
Cincinnati Children’s Hospital Medical Center

Erica Rapp, MD
University of Colorado School of Medicine

Abhishek Reddy, MD
The University of Alabama at Birmingham

Eduardo Rueda Vasquez, MD
Williamsport, Pennsylvania

Stephen Saklad, PharmD, BCPP
The University of Texas at Austin

Lauren Schwarz, PhD, ABPP-CN
Saint Louis University School of Medicine

Andreas Sidiropoulos, MD
University of Michigan

Shirshendu Sinha, MD
Mayo Clinic Health System and Mayo Clinic

Cornel Stanciu, MD
Dartmouth’s Geisel School of Medicine

Jeffrey Sung, MD
University of Washington

Thida Thant, MD
University of Colorado at Denver

Adele Viguera, MD
Cleveland Clinic Lerner College of Medicine

Aparna Atluru, MD
Stanford Medicine

Anjan Bhattacharyya, MD
Saint Louis University

Caroline Bonham, MD
The University of New Mexico

Catherine Crone, MD
Inova Health System

Sheila Dowd, PhD
Rush Medical College

Ahmed Z. Elmaadawi, MD
Indiana University School of Medicine

Donald Gilbert, MD, MS
Cincinnati Children’s Hospital Medical Center

Mark Gold, MD
Washington University in St. Louis

Elana Harris, MD, PhD
Cincinnati Children’s Hospital

Susan Hatters-Friedman, MD
Case Western Reserve University

Faisal Islam, MD, MBA
Greenvale, New York

Kaustubh G. Joshi, MD
University of South Carolina School of Medicine

Rita Khoury, MD
Saint George Hospital University Medical Center

Suneeta Kumari, MD, MPH
Howard University Hospital

Michelle Magid, MD
Austin PsychCare PA

Michael Maksimowski, MD
Wayne State University

Jose Maldonado, MD
Stanford University

Thomas W. Meeks, MD
Portland VA Medical Center

John Miller, MD
University of South Florida

Armando Morera-Fumero, MD, PhD
Universidad de La Laguna

Mary K. Morreale, MD
Wayne State University

Philip Muskin, MD
Columbia University College of Physicians and Surgeons

Katharine Nelson, MD
University of Minnesota

Carol North, MD
University of Texas Southwestern Medical Center at Dallas

Douglas Opler, MD
Rutgers University School of Medicine

Joseph Pierre, MD
University of California, Los Angeles

Jerrold Pollak, PhD, ABN, ABPP
Seacoast Mental Health Center

Edwin Raffi, MD, MPH
Massachusetts General Hospital Center for Women’s Mental Health

Y. Pritham Raj, MD
Oregon Health and Science University

Jeffrey Rakofsky, MD
Emory University School of Medicine

Laura Ramsey, PhD
Cincinnati Children’s Hospital Medical Center

Erica Rapp, MD
University of Colorado School of Medicine

Abhishek Reddy, MD
The University of Alabama at Birmingham

Eduardo Rueda Vasquez, MD
Williamsport, Pennsylvania

Stephen Saklad, PharmD, BCPP
The University of Texas at Austin

Lauren Schwarz, PhD, ABPP-CN
Saint Louis University School of Medicine

Andreas Sidiropoulos, MD
University of Michigan

Shirshendu Sinha, MD
Mayo Clinic Health System and Mayo Clinic

Cornel Stanciu, MD
Dartmouth’s Geisel School of Medicine

Jeffrey Sung, MD
University of Washington

Thida Thant, MD
University of Colorado at Denver

Adele Viguera, MD
Cleveland Clinic Lerner College of Medicine

Aparna Atluru, MD
Stanford Medicine

Anjan Bhattacharyya, MD
Saint Louis University

Caroline Bonham, MD
The University of New Mexico

Catherine Crone, MD
Inova Health System

Sheila Dowd, PhD
Rush Medical College

Ahmed Z. Elmaadawi, MD
Indiana University School of Medicine

Donald Gilbert, MD, MS
Cincinnati Children’s Hospital Medical Center

Mark Gold, MD
Washington University in St. Louis

Elana Harris, MD, PhD
Cincinnati Children’s Hospital

Susan Hatters-Friedman, MD
Case Western Reserve University

Faisal Islam, MD, MBA
Greenvale, New York

Kaustubh G. Joshi, MD
University of South Carolina School of Medicine

Rita Khoury, MD
Saint George Hospital University Medical Center

Suneeta Kumari, MD, MPH
Howard University Hospital

Michelle Magid, MD
Austin PsychCare PA

Michael Maksimowski, MD
Wayne State University

Jose Maldonado, MD
Stanford University

Thomas W. Meeks, MD
Portland VA Medical Center

John Miller, MD
University of South Florida

Armando Morera-Fumero, MD, PhD
Universidad de La Laguna

Mary K. Morreale, MD
Wayne State University

Philip Muskin, MD
Columbia University College of Physicians and Surgeons

Katharine Nelson, MD
University of Minnesota

Carol North, MD
University of Texas Southwestern Medical Center at Dallas

Douglas Opler, MD
Rutgers University School of Medicine

Joseph Pierre, MD
University of California, Los Angeles

Jerrold Pollak, PhD, ABN, ABPP
Seacoast Mental Health Center

Edwin Raffi, MD, MPH
Massachusetts General Hospital Center for Women’s Mental Health

Y. Pritham Raj, MD
Oregon Health and Science University

Jeffrey Rakofsky, MD
Emory University School of Medicine

Laura Ramsey, PhD
Cincinnati Children’s Hospital Medical Center

Erica Rapp, MD
University of Colorado School of Medicine

Abhishek Reddy, MD
The University of Alabama at Birmingham

Eduardo Rueda Vasquez, MD
Williamsport, Pennsylvania

Stephen Saklad, PharmD, BCPP
The University of Texas at Austin

Lauren Schwarz, PhD, ABPP-CN
Saint Louis University School of Medicine

Andreas Sidiropoulos, MD
University of Michigan

Shirshendu Sinha, MD
Mayo Clinic Health System and Mayo Clinic

Cornel Stanciu, MD
Dartmouth’s Geisel School of Medicine

Jeffrey Sung, MD
University of Washington

Thida Thant, MD
University of Colorado at Denver

Adele Viguera, MD
Cleveland Clinic Lerner College of Medicine

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Recent advances in neuroscience and genetics are providing a new view of brain function in health and disease.¹ As discussed in Drs. Hripsime Kalanderian and Henry Nasrallah’s article “Artificial intelligence in psychiatry” (Evidence-Based Reviews, Current Psychiatry. August 2019, p. 33-38), machine learning technologies are capable of analyzing vast amounts of personal and biologic data for diagnosing and treating mental disorders.

In a 2016 article, Dr. Arshya Vahabzadeh² wrote, “In the near term, humans will continue to make the majority of psychiatric diagnoses and provide treatment.” He predicted that data science—specifically machine learning—will help revolutionize how we diagnose, treat, and monitor depression. He foresees a future where AI machines or learning machines will more accurately diagnose and treat depression.

These predictions remind us of the promises made with the introduction of psychoactive drugs to the practice of psychiatry. In the 1970s, the increased emphasis on neurotransmitters led to new biologic models of mental illness and the expansion of the Diagnostic and Statistical Manual of Mental Disorders. The increased use of psychoactive medications relegated the practice of psychotherapy to other mental health professionals. Psychiatry became a “drug-intensive” specialty, and psychiatrists saw themselves as psychopharmacologists.³ During this time, psychiatry became progressively dominated by the pharmaceutical industry. The deregulation of the markets and the for-profit ideology of the pharmaceutical industry resulted in an economically and mutually beneficial alliance between pharmaceutical companies, academic faculty, and individual psychiatrists.

Using the same for-profit ideology and ethics of the pharmaceutical industry, technology-based corporations are making massive investments in the application of these technologies in neuroscience research and clinical practice. The “promise” that AI will diagnose and treat depression more accurately than clinicians will again radically change the psychiatrist’s role. Most of a psychiatrist’s clinical work eventually will be replicated by machine learning and technicians. The human-to-human encounter that is at core of the profession will be replaced by the machine-to-human encounter.⁴

From the social economic perspective, the American health care system is designed to increase profit and maximize the earnings of the industries.⁵ Unless social policy changes, expensive new technologies will increase the cost and limit accessibility to health care, benefiting the few at the expense of the majority of people. These technologies will produce a robust return on investment, but the wealth they create will benefit fewer and fewer people.

Several writers have called attention to the social, economic, and ethical consequences of these advances and recommended that the academics and technologists who support AI and machine learning in medicine must “receive sufficient training in ethics” and gain exposure to social and economic issues.⁶ Darcy et al⁷ warns of the risks of introducing these advanced technologies in medicine: “As machine learning enters the state-of-the-art clinical practice, medicine thus has the immense obligation to ensure that this technology is harnessed for societal and individual good, fulfilling the ethical basis of the profession.… Ethical design thinking is essential at every stage of development and application of machine learning in advancing health. Toward this aim, physicians with integrity and sophistication should partner closely with computer and data scientists to reimagine clinical medicine and to anticipate its ethical implications. It is important to systematically validate data from mobile health and consumer-facing technologies, particularly for cases in which dynamic intervention is provided.”

Marco T. Carpio, MD
Psychiatrist, Private Practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m², and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).¹ BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.² The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.² The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.³

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 1⁴.

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al⁵ found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 2^1,6).

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

[polldaddy:10446187]

Continue to: TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

• abstinence from binge eating
• sustainable weight loss and metabolic health
• reduction in symptoms associated with comorbid conditions
• improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.⁷ The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.⁷

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

• National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
• Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m², and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).¹ BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.² The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.² The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.³

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 1⁴.

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al⁵ found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 2^1,6).

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

[polldaddy:10446187]

Continue to: TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

• abstinence from binge eating
• sustainable weight loss and metabolic health
• reduction in symptoms associated with comorbid conditions
• improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.⁷ The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.⁷

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

• National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
• Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

CASE Uncontrollable eating and weight gain

Ms. C, age 33, presents to an outpatient clinic with complaints of weight gain and “uncontrollable eating.” Ms. C says she’s gained >50 lb over the last year. She describes progressively frequent episodes of overeating during which she feels that she has no control over the amount of food she consumes. She reports eating as often as 10 times a day, and overeating to the point of physical discomfort during most meals. She gives an example of having recently consumed a large pizza, several portions of Chinese food, approximately 20 chicken wings, and half a chocolate cake for dinner. Ms. C admits that on several occasions she has vomited after meals due to feeling extremely full; however, she denies having done so intentionally. She also denies restricting her food intake, misusing laxatives or diuretics, or exercising excessively.

Ms. C expresses frustration and embarrassment with her eating and resulting weight gain. She says she has poor self-esteem, low energy and motivation, and poor concentration. She feels that her condition has significantly impacted her social life, romantic relationships, and family life. She admits she’s been avoiding dating and seeing friends due to her weight gain, and has been irritable with her teenage daughter.

During her initial evaluation, Ms. C is alert and oriented, with a linear and goal-directed thought process. She is somewhat irritable and guarded, wearing large sunglasses that cover most of her face, but is not overtly paranoid. Although she appears frustrated when discussing her condition, she denies feeling hopeless or helpless.

HISTORY Thyroid cancer and mood swings

Ms. C, who is single and unemployed, lives in an apartment with her teenage daughter, with whom she describes having a good relationship. She has been receiving disability benefits for the past 2 years after a motor vehicle accident resulted in multiple fractures of her arm and elbow, and subsequent chronic pain. Ms. C reports a distant history of “problems with alcohol,” but denies drinking any alcohol since being charged with driving under the influence several years ago. She has a 10 pack-year history of smoking and denies any history of illicit drug use.

Two years ago, Ms. C was diagnosed with thyroid carcinoma, and treated with surgical resection and a course of radiation. She has regular visits with her endocrinologist and has been prescribed oral levothyroxine, 150 mcg/d.

Ms. C reports a history of “mood swings” characterized by “snapping at people” and becoming irritable in response to stressful situations, but denies any past symptoms consistent with a manic or hypomanic episode. Ms. C has not been admitted to a psychiatric hospital, nor has she received any prior psychiatric treatment. She reluctantly discloses that approximately 3 years ago she had a less severe episode of uncontrollable eating and weight gain (20 to 30 lb). At that time, she was able to regain her desired physical appearance by going on the “Subway diet” and undergoing liposuction and plastic surgery.

At her current outpatient clinic visit, Ms. C expresses an interest in exploring bariatric surgery as a potential solution to her weight gain.

[polldaddy:10446186]

Continue to: EVALUATION Obese; stable thyroid function

We refer Ms. C for a physical examination and routine blood analysis to rule out any medical contributors to her condition. Her physical examination is reported as normal, with no signs of skin changes, goiter, or exophthalmos. Ms. C is noted to be obese, with a body mass index of 37.2 kg/m², and an abdominal circumference of 38.5 in.

A blood analysis shows that Ms. C has elevated triglyceride levels (202 mg/dL) and elevated cholesterol levels (210 mg/dL). Her thyroid function tests are within normal limits based on the dose of levothyroxine she’s been receiving. A pregnancy test is negative.

Ms. C gives the team at the clinic permission to contact her endocrinologist, who reports that he does not suspect that Ms. C’s drastic weight gain and abnormal eating patterns are attributable to her history of thyroid carcinoma because her thyroid function tests have been stable on her current regimen.

The authors’ observations

Based on Ms. C’s initial presentation, we strongly suspected a diagnosis of binge eating disorder (BED). Several differential diagnoses were considered and carefully ruled out; Ms. C’s medical workup did not suggest that her weight gain was due to an active medical condition, and she did not meet DSM-5 criteria for a mood or psychotic disorder or anorexia nervosa or bulimia nervosa.

With an estimated lifetime prevalence in the United States of 2.6%, BED is the most prevalent eating disorder (compared with 0.6% for anorexia nervosa and 1% for bulimia nervosa).¹ BED is more prevalent in women than in men, and the mean age of onset is mid-20s.

Continue to: BED may be difficult...

BED may be difficult to detect because patients may feel ashamed or guilty and are often hesitant to disclose and discuss their symptoms. Furthermore, they are frequently frustrated by the subjective loss of control over their behaviors. Patients with BED often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics.

Screening for eating disorders

Several screening instruments have been developed to help clinicians identify patients who may need further evaluation for possible diagnosis of an eating disorder, including anorexia nervosa, bulimia nervosa, and BED.² The SCOFF questionnaire is composed of 5 brief clinician-administered questions to screen for eating disorders.² The 7-item Binge Eating Disorder Screener (BED-7) is a screening instrument specific for BED that examines a patient’s eating patterns and behaviors during the past 3 months.³

In general, suspect BED in patients who have significant weight dissatisfaction, fluctuation in weight, and depressive symptoms. The DSM-5 criteria for binge eating disorder are shown in Table 1⁴.

BED and comorbid psychiatric disorders

Patients with BED are more likely than the general population to have comorbid psychiatric disorders, including mood and anxiety disorders, attention-deficit/hyperactivity disorder, posttraumatic stress disorder, and substance use disorders. Swanson et al⁵ found that 83.5% of adolescents who met criteria for BED also met criteria for at least 1 other psychiatric disorder, and 37% endorsed >3 concurrent psychiatric conditions. Once BED is confirmed, it is important to screen for other psychiatric and medical comorbidities that are often present in individuals with BED (Table 2^1,6).

The rates of diagnosis and treatment of BED remain low. This is likely due to patient factors such as shame and fear of stigma and clinician factors such as lack of awareness, ineffective communication, hesitation to discuss the sensitive topic, or insufficient knowledge about treatment options once BED is diagnosed.

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Continue to: TREATMENT Combination therapy

Ms. C is ambivalent about her BED diagnosis, and becomes angry about it when the proposed treatments do not involve bariatric surgery or cosmetic procedures. Ms. C is enrolled in weekly individual psychotherapy, where she receives a combination of CBT and psychodynamic therapy; however, her attendance is inconsistent. Ms. C is offered a trial of fluoxetine, but adamantly refuses, citing a relative who experienced adverse effects while receiving this type of antidepressant. Ms. C also refuses a trial of topiramate due to concerns of feeling sedated. Finally, she is offered a trial of lisdexamfetamine, 30 mg/d, which was FDA-approved in 2015 to treat moderate to severe BED. We discuss the risks, benefits, and adverse effects of lisdexamfetamine with Ms. C; however, she is hesitant to start this medication and expresses increasing interest in obtaining a consultation for bariatric surgery. Ms. C is provided with extensive education about the risks and dangers of surgery before addressing her eating patterns, and the clinician provides validation, verbal support, and counseling. Ms. C eventually agrees to a trial of lisdexamfetamine, but her insurance denies coverage of this medication.

The authors’ observations

When developing an individualized treatment plan for a patient with BED, the patient’s psychiatric and medical comorbidities should be considered. Treatment goals for patients with BED include:

• abstinence from binge eating
• sustainable weight loss and metabolic health
• reduction in symptoms associated with comorbid conditions
• improvement in self-esteem and overall quality of life.

A 2015 comparative effectiveness review of management and outcomes for patients with BED evaluated pharmacologic, psychologic, behavioral, and combined approaches for treating patients with BED.⁷ The results suggested that second-generation antidepressants, topiramate, and lisdexamfetamine were superior to placebo in reducing binge-eating episodes and achieving abstinence from binge-eating. Weight reduction was also achieved with topiramate and lisdexamfetamine, and antidepressants helped relieve symptoms of comorbid depression.

Various formats of CBT, including therapist-led and guided self-help, were also superior to placebo in reducing the frequency of binge-eating and promoting abstinence; however, they were generally not effective in treating depression or reducing patients’ weight.⁷

OUTCOME Fixated on surgery

We appeal the decision of Ms. C’s insurance company; however, during the appeals process, Ms. C becomes increasingly irritable and informs us that she has changed her mind and, with the reported support of her medical doctors, wishes to undergo bariatric surgery. Although we made multiple attempts to engage Ms. C in further treatment, she is lost to follow-up.

Continue to: Bottom Line

Diagnosing and managing patients with binge eating disorder (BED) can be challenging because patients may hesitate to seek help, and/or have psychiatric and medical comorbidities. They often present to medical facilities seeking weight loss solutions rather than to psychiatric clinics. Once BED is confirmed, screen for other psychiatric and medical comorbidities. A combination of pharmacologic and psychotherapeutic interventions can benefit some patients with BED, but treatment should be individualized.

Related Resources

• National Eating Disorders Association. NEDA. www.nationaleatingdisorders.org/.
• Safer D, Telch C, Chen EY. Dialectical behavior therapy for binge eating and bulimia. New York, NY: Guilford Press; 2017.

Drug Brand Names

Fluoxetine • Prozac
Levothyroxine • Synthroid
Lisdexamfetamine • Vyvanse
Topiramate • Topamax

Ms. L, age 53, presents to an inpatient psychiatric unit with depression, difficulty concentrating, fatigue, cognitive blunting, loss of appetite, increased alcohol intake, and recent suicidal ideation. Her symptoms began 3 months ago and gradually worsened. Her medical and psychiatric history is significant for hypertension, fibromyalgia, and chronic pain (back and neck), major depressive disorder (MDD; recurrent, severe), and generalized anxiety disorder (GAD). Ms. L’s current medication regimen includes lisinopril, 40 mg daily; fluoxetine, 60 mg daily; mirtazapine, 30 mg at bedtime; gabapentin, 300 mg twice daily; alprazolam, 0.5 mg twice daily as needed for anxiety; and oral docusate, 100 mg twice daily as needed. Her blood pressure is 124/85 mm Hg, heart rate is 66 beats per minute, and an electrocardiogram is normal. Laboratory workup reveals a potassium level of 4.4 mEq/L, blood urea nitrogen level of 20 mg/dL, serum creatinine level of 0.8 mg/dL, estimated creatinine clearance of 89.6 mL/min, free triiodothyronine (T3) levels of 2.7 pg/mL, thyroid-stimulating hormone (TSH) level of 7.68 mIU/L, free thyroxine (T4) level of 1.3 ng/dL, and blood ethanol level <10 mg/dL. In addition to the symptoms Ms. L initially described, a review of systems reveals word-finding difficulty, cold intolerance, constipation, hair loss, brittle nails, and dry skin.

To target Ms. L’s MDD, GAD, fibromyalgia, and chronic pain, fluoxetine, 60 mg daily is cross titrated beginning on Day 1 to duloxetine, 60 mg twice daily, over 4 days. Mirtazapine is decreased on Day 3 to 7.5 mg at bedtime to target Ms. L’s sleep and appetite. Due to the presence of several symptoms associated with hypothyroidism and a slightly elevated TSH level, on Day 6 we initiate adjunctive levothyroxine, 50 mcg daily each morning to target symptomatic subclinical hypothyroidism, and to potentially augment the other medications prescribed to address Ms. L’s MDD.

Thyroid hormone function is a complex physiological process controlled through the hypothalamic-pituitary-thyroid (HPT) axis. Psychotropic medications can impact thyroid hormone function and contribute to aberrations in thyroid physiology.¹ Because patients with mental illness may require multiple psychotropic medications, it is imperative to understand the potential effects of these agents.

Antidepressants can induce hypothyroidism along multiple points of hormonal synthesis and iodine utilization. Tricyclic antidepressants have been implicated in the development of drug-iodide complexes, thus reducing biologically active iodine.² Tricyclic antidepressants also can bind thyroid peroxidase, an enzyme necessary in the production of T4 and T3, altering hormonal production, resulting in a hypothyroid state.¹ Non-tricyclic antidepressants (ie, selective serotonin reuptake inhibitors [SSRIs] and non-SSRIs [including serotonin-norepinephrine reuptake inhibitors and mirtazapine]) have also been implicated in thyroid dysfunction. Selective serotonin reuptake inhibitors have the propensity to induce hypothyroidism through inhibition of thyroid hormones T4 and T3.^1,3 This inhibition is not always seen with concurrent reductions in TSH levels. Conversely, non-SSRIs can influence thyroid hormone levels with great variation, leading to thyroid hormone levels that are increased, decreased, or unchanged.¹ Patients with a history of thyroid dysfunction should receive close thyroid function monitoring, especially while taking antidepressants.

Antipsychotics have a proclivity to induce hypothyroidism by means similar to antidepressants via hormonal manipulation and immunogenicity. Phenothiazines impact thyroid function through hormonal activation and degradation, and induction of autoimmunity.¹ Autoimmunity may develop by means of antibody production or antigen immunization through the major histocompatibility complex.² Other first-generation antipsychotics (FGAs) (eg, haloperidol and loxapine) are known to antagonize dopamine receptors in the tuberoinfundibular pathway, resulting in increased prolactin levels. Hyperprolactinemia may result in increased TSH levels through HPT axis activation.¹ Additionally, FGAs can induce an immunogenic effect through production of antithyroid antibodies.¹ Similar to FGAs, second-generation antipsychotics (SGAs) can increase TSH levels through hyper­prolactinemia. Further research focused on SGAs is needed to determine how profound this effect may be.

The Table¹ outlines considerations for modifying psychotropic therapy based on the presence of concurrent thyroid dysfunction. Thyroid function should be routinely assessed in patients treated with antipsychotics.

Mood stabilizers are capable of altering thyroid function and inducing a hypothyroid state. Lithium has been implicated in both hypothyroidism and hyperthyroidism due to its inhibition of hormonal secretion, and toxicity to thyroid cells with chronic use, respectively.^1,4 Hypothyroidism can develop shortly after initiating lithium; women tend to have a greater predilection for thyroid dysfunction than men.¹ Carbamazepine (CBZ) can reduce thyroid hormone levels without having a direct effect on TSH or thyroid dysfunction.¹ As with lithium, women tend to be more susceptible to this effect. Valproic acid (VPA) has been shown to either increase, decrease, or have no impact on thyroid hormone levels, with little effect on TSH.¹ When VPA is given in combination with CBZ, significant reductions in thyroid levels with a concurrent increase in TSH can occur.¹ In patients with preexisting thyroid dysfunction, the combination of VPA and CBZ should be used with caution.

Continue to: CASE

By Day 8, Ms. L reports less fatigue, clearer thinking, improved concentration, and less pain. She also no longer reports suicidal ideation, and demonstrates improved appetite and mood. She is discharged on Day 9 of her hospitalization.

The treatment team refers Ms. L for outpatient follow-up in 4 weeks, with a goal TSH level <3.0. Unfortunately, the effects of levothyroxine on Ms. L’s TSH level could not be determined during her hospital stay, and she has not returned to the facility since the initial presentation.

Thyroid function and mood

Ms. L’s case illustrates how thyroid function, pain, cognition, and mood may be interconnected. It is important to address all potential underlying comorbidities and establish appropriate outpatient care and follow-up so that patients may experience a more robust recovery. Further, this case highlights the importance of ruling out other potential medical causes of MDD during the initial diagnosis, and during times of recurrence or relapse, especially when a recent stressor, medication changes, or medication nonadherence cannot be identified as potential contributors.

Related Resources

• Cojić M, Cvejanov-Kezunović L. Subclinical hypothyroidism – whether and when to start treatment? Open Access Maced J Med Sci. 2017;5(7):1042-1046.
• Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200-1235.
• Iosifescu DV. ‘Supercharge’ antidepressants by adding thyroid hormones. Current Psychiatry. 2006;5(7):15-20,25.

Drug Brand Names

Alprazolam • Xanax
Aripiprazole • Abilify
Bupropion • Wellbutrin
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Clozapine • Clozaril
Duloxetine • Cymbalta
Fluoxetine • Prozac
Fluphenazine • Prolixin
Gabapentin • Neurontin
Haloperidol • Haldol
Levothyroxine • Synthroid
Lisinopril • Prinivil, Zestril
Lithium • Eskalith, Lithobid
Loxapine • Loxitane
Mirtazapine • Remeron
Quetiapine • Seroquel
Risperidone • Risperdal
Thioridazine • Mellaril
Valproic acid • Depakote

Ms. L, age 53, presents to an inpatient psychiatric unit with depression, difficulty concentrating, fatigue, cognitive blunting, loss of appetite, increased alcohol intake, and recent suicidal ideation. Her symptoms began 3 months ago and gradually worsened. Her medical and psychiatric history is significant for hypertension, fibromyalgia, and chronic pain (back and neck), major depressive disorder (MDD; recurrent, severe), and generalized anxiety disorder (GAD). Ms. L’s current medication regimen includes lisinopril, 40 mg daily; fluoxetine, 60 mg daily; mirtazapine, 30 mg at bedtime; gabapentin, 300 mg twice daily; alprazolam, 0.5 mg twice daily as needed for anxiety; and oral docusate, 100 mg twice daily as needed. Her blood pressure is 124/85 mm Hg, heart rate is 66 beats per minute, and an electrocardiogram is normal. Laboratory workup reveals a potassium level of 4.4 mEq/L, blood urea nitrogen level of 20 mg/dL, serum creatinine level of 0.8 mg/dL, estimated creatinine clearance of 89.6 mL/min, free triiodothyronine (T3) levels of 2.7 pg/mL, thyroid-stimulating hormone (TSH) level of 7.68 mIU/L, free thyroxine (T4) level of 1.3 ng/dL, and blood ethanol level <10 mg/dL. In addition to the symptoms Ms. L initially described, a review of systems reveals word-finding difficulty, cold intolerance, constipation, hair loss, brittle nails, and dry skin.

To target Ms. L’s MDD, GAD, fibromyalgia, and chronic pain, fluoxetine, 60 mg daily is cross titrated beginning on Day 1 to duloxetine, 60 mg twice daily, over 4 days. Mirtazapine is decreased on Day 3 to 7.5 mg at bedtime to target Ms. L’s sleep and appetite. Due to the presence of several symptoms associated with hypothyroidism and a slightly elevated TSH level, on Day 6 we initiate adjunctive levothyroxine, 50 mcg daily each morning to target symptomatic subclinical hypothyroidism, and to potentially augment the other medications prescribed to address Ms. L’s MDD.

Thyroid hormone function is a complex physiological process controlled through the hypothalamic-pituitary-thyroid (HPT) axis. Psychotropic medications can impact thyroid hormone function and contribute to aberrations in thyroid physiology.¹ Because patients with mental illness may require multiple psychotropic medications, it is imperative to understand the potential effects of these agents.

Antidepressants can induce hypothyroidism along multiple points of hormonal synthesis and iodine utilization. Tricyclic antidepressants have been implicated in the development of drug-iodide complexes, thus reducing biologically active iodine.² Tricyclic antidepressants also can bind thyroid peroxidase, an enzyme necessary in the production of T4 and T3, altering hormonal production, resulting in a hypothyroid state.¹ Non-tricyclic antidepressants (ie, selective serotonin reuptake inhibitors [SSRIs] and non-SSRIs [including serotonin-norepinephrine reuptake inhibitors and mirtazapine]) have also been implicated in thyroid dysfunction. Selective serotonin reuptake inhibitors have the propensity to induce hypothyroidism through inhibition of thyroid hormones T4 and T3.^1,3 This inhibition is not always seen with concurrent reductions in TSH levels. Conversely, non-SSRIs can influence thyroid hormone levels with great variation, leading to thyroid hormone levels that are increased, decreased, or unchanged.¹ Patients with a history of thyroid dysfunction should receive close thyroid function monitoring, especially while taking antidepressants.

Antipsychotics have a proclivity to induce hypothyroidism by means similar to antidepressants via hormonal manipulation and immunogenicity. Phenothiazines impact thyroid function through hormonal activation and degradation, and induction of autoimmunity.¹ Autoimmunity may develop by means of antibody production or antigen immunization through the major histocompatibility complex.² Other first-generation antipsychotics (FGAs) (eg, haloperidol and loxapine) are known to antagonize dopamine receptors in the tuberoinfundibular pathway, resulting in increased prolactin levels. Hyperprolactinemia may result in increased TSH levels through HPT axis activation.¹ Additionally, FGAs can induce an immunogenic effect through production of antithyroid antibodies.¹ Similar to FGAs, second-generation antipsychotics (SGAs) can increase TSH levels through hyper­prolactinemia. Further research focused on SGAs is needed to determine how profound this effect may be.

The Table¹ outlines considerations for modifying psychotropic therapy based on the presence of concurrent thyroid dysfunction. Thyroid function should be routinely assessed in patients treated with antipsychotics.

Mood stabilizers are capable of altering thyroid function and inducing a hypothyroid state. Lithium has been implicated in both hypothyroidism and hyperthyroidism due to its inhibition of hormonal secretion, and toxicity to thyroid cells with chronic use, respectively.^1,4 Hypothyroidism can develop shortly after initiating lithium; women tend to have a greater predilection for thyroid dysfunction than men.¹ Carbamazepine (CBZ) can reduce thyroid hormone levels without having a direct effect on TSH or thyroid dysfunction.¹ As with lithium, women tend to be more susceptible to this effect. Valproic acid (VPA) has been shown to either increase, decrease, or have no impact on thyroid hormone levels, with little effect on TSH.¹ When VPA is given in combination with CBZ, significant reductions in thyroid levels with a concurrent increase in TSH can occur.¹ In patients with preexisting thyroid dysfunction, the combination of VPA and CBZ should be used with caution.

Continue to: CASE

By Day 8, Ms. L reports less fatigue, clearer thinking, improved concentration, and less pain. She also no longer reports suicidal ideation, and demonstrates improved appetite and mood. She is discharged on Day 9 of her hospitalization.

The treatment team refers Ms. L for outpatient follow-up in 4 weeks, with a goal TSH level <3.0. Unfortunately, the effects of levothyroxine on Ms. L’s TSH level could not be determined during her hospital stay, and she has not returned to the facility since the initial presentation.

Thyroid function and mood

Ms. L’s case illustrates how thyroid function, pain, cognition, and mood may be interconnected. It is important to address all potential underlying comorbidities and establish appropriate outpatient care and follow-up so that patients may experience a more robust recovery. Further, this case highlights the importance of ruling out other potential medical causes of MDD during the initial diagnosis, and during times of recurrence or relapse, especially when a recent stressor, medication changes, or medication nonadherence cannot be identified as potential contributors.

Related Resources

• Cojić M, Cvejanov-Kezunović L. Subclinical hypothyroidism – whether and when to start treatment? Open Access Maced J Med Sci. 2017;5(7):1042-1046.
• Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200-1235.
• Iosifescu DV. ‘Supercharge’ antidepressants by adding thyroid hormones. Current Psychiatry. 2006;5(7):15-20,25.

Drug Brand Names

Alprazolam • Xanax
Aripiprazole • Abilify
Bupropion • Wellbutrin
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Clozapine • Clozaril
Duloxetine • Cymbalta
Fluoxetine • Prozac
Fluphenazine • Prolixin
Gabapentin • Neurontin
Haloperidol • Haldol
Levothyroxine • Synthroid
Lisinopril • Prinivil, Zestril
Lithium • Eskalith, Lithobid
Loxapine • Loxitane
Mirtazapine • Remeron
Quetiapine • Seroquel
Risperidone • Risperdal
Thioridazine • Mellaril
Valproic acid • Depakote

Ms. L, age 53, presents to an inpatient psychiatric unit with depression, difficulty concentrating, fatigue, cognitive blunting, loss of appetite, increased alcohol intake, and recent suicidal ideation. Her symptoms began 3 months ago and gradually worsened. Her medical and psychiatric history is significant for hypertension, fibromyalgia, and chronic pain (back and neck), major depressive disorder (MDD; recurrent, severe), and generalized anxiety disorder (GAD). Ms. L’s current medication regimen includes lisinopril, 40 mg daily; fluoxetine, 60 mg daily; mirtazapine, 30 mg at bedtime; gabapentin, 300 mg twice daily; alprazolam, 0.5 mg twice daily as needed for anxiety; and oral docusate, 100 mg twice daily as needed. Her blood pressure is 124/85 mm Hg, heart rate is 66 beats per minute, and an electrocardiogram is normal. Laboratory workup reveals a potassium level of 4.4 mEq/L, blood urea nitrogen level of 20 mg/dL, serum creatinine level of 0.8 mg/dL, estimated creatinine clearance of 89.6 mL/min, free triiodothyronine (T3) levels of 2.7 pg/mL, thyroid-stimulating hormone (TSH) level of 7.68 mIU/L, free thyroxine (T4) level of 1.3 ng/dL, and blood ethanol level <10 mg/dL. In addition to the symptoms Ms. L initially described, a review of systems reveals word-finding difficulty, cold intolerance, constipation, hair loss, brittle nails, and dry skin.

To target Ms. L’s MDD, GAD, fibromyalgia, and chronic pain, fluoxetine, 60 mg daily is cross titrated beginning on Day 1 to duloxetine, 60 mg twice daily, over 4 days. Mirtazapine is decreased on Day 3 to 7.5 mg at bedtime to target Ms. L’s sleep and appetite. Due to the presence of several symptoms associated with hypothyroidism and a slightly elevated TSH level, on Day 6 we initiate adjunctive levothyroxine, 50 mcg daily each morning to target symptomatic subclinical hypothyroidism, and to potentially augment the other medications prescribed to address Ms. L’s MDD.

Thyroid hormone function is a complex physiological process controlled through the hypothalamic-pituitary-thyroid (HPT) axis. Psychotropic medications can impact thyroid hormone function and contribute to aberrations in thyroid physiology.¹ Because patients with mental illness may require multiple psychotropic medications, it is imperative to understand the potential effects of these agents.

Antidepressants can induce hypothyroidism along multiple points of hormonal synthesis and iodine utilization. Tricyclic antidepressants have been implicated in the development of drug-iodide complexes, thus reducing biologically active iodine.² Tricyclic antidepressants also can bind thyroid peroxidase, an enzyme necessary in the production of T4 and T3, altering hormonal production, resulting in a hypothyroid state.¹ Non-tricyclic antidepressants (ie, selective serotonin reuptake inhibitors [SSRIs] and non-SSRIs [including serotonin-norepinephrine reuptake inhibitors and mirtazapine]) have also been implicated in thyroid dysfunction. Selective serotonin reuptake inhibitors have the propensity to induce hypothyroidism through inhibition of thyroid hormones T4 and T3.^1,3 This inhibition is not always seen with concurrent reductions in TSH levels. Conversely, non-SSRIs can influence thyroid hormone levels with great variation, leading to thyroid hormone levels that are increased, decreased, or unchanged.¹ Patients with a history of thyroid dysfunction should receive close thyroid function monitoring, especially while taking antidepressants.

Antipsychotics have a proclivity to induce hypothyroidism by means similar to antidepressants via hormonal manipulation and immunogenicity. Phenothiazines impact thyroid function through hormonal activation and degradation, and induction of autoimmunity.¹ Autoimmunity may develop by means of antibody production or antigen immunization through the major histocompatibility complex.² Other first-generation antipsychotics (FGAs) (eg, haloperidol and loxapine) are known to antagonize dopamine receptors in the tuberoinfundibular pathway, resulting in increased prolactin levels. Hyperprolactinemia may result in increased TSH levels through HPT axis activation.¹ Additionally, FGAs can induce an immunogenic effect through production of antithyroid antibodies.¹ Similar to FGAs, second-generation antipsychotics (SGAs) can increase TSH levels through hyper­prolactinemia. Further research focused on SGAs is needed to determine how profound this effect may be.

The Table¹ outlines considerations for modifying psychotropic therapy based on the presence of concurrent thyroid dysfunction. Thyroid function should be routinely assessed in patients treated with antipsychotics.

Mood stabilizers are capable of altering thyroid function and inducing a hypothyroid state. Lithium has been implicated in both hypothyroidism and hyperthyroidism due to its inhibition of hormonal secretion, and toxicity to thyroid cells with chronic use, respectively.^1,4 Hypothyroidism can develop shortly after initiating lithium; women tend to have a greater predilection for thyroid dysfunction than men.¹ Carbamazepine (CBZ) can reduce thyroid hormone levels without having a direct effect on TSH or thyroid dysfunction.¹ As with lithium, women tend to be more susceptible to this effect. Valproic acid (VPA) has been shown to either increase, decrease, or have no impact on thyroid hormone levels, with little effect on TSH.¹ When VPA is given in combination with CBZ, significant reductions in thyroid levels with a concurrent increase in TSH can occur.¹ In patients with preexisting thyroid dysfunction, the combination of VPA and CBZ should be used with caution.

Continue to: CASE

By Day 8, Ms. L reports less fatigue, clearer thinking, improved concentration, and less pain. She also no longer reports suicidal ideation, and demonstrates improved appetite and mood. She is discharged on Day 9 of her hospitalization.

The treatment team refers Ms. L for outpatient follow-up in 4 weeks, with a goal TSH level <3.0. Unfortunately, the effects of levothyroxine on Ms. L’s TSH level could not be determined during her hospital stay, and she has not returned to the facility since the initial presentation.

Thyroid function and mood

Ms. L’s case illustrates how thyroid function, pain, cognition, and mood may be interconnected. It is important to address all potential underlying comorbidities and establish appropriate outpatient care and follow-up so that patients may experience a more robust recovery. Further, this case highlights the importance of ruling out other potential medical causes of MDD during the initial diagnosis, and during times of recurrence or relapse, especially when a recent stressor, medication changes, or medication nonadherence cannot be identified as potential contributors.

Related Resources

• Cojić M, Cvejanov-Kezunović L. Subclinical hypothyroidism – whether and when to start treatment? Open Access Maced J Med Sci. 2017;5(7):1042-1046.
• Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22(12):1200-1235.
• Iosifescu DV. ‘Supercharge’ antidepressants by adding thyroid hormones. Current Psychiatry. 2006;5(7):15-20,25.

Drug Brand Names

Alprazolam • Xanax
Aripiprazole • Abilify
Bupropion • Wellbutrin
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Clozapine • Clozaril
Duloxetine • Cymbalta
Fluoxetine • Prozac
Fluphenazine • Prolixin
Gabapentin • Neurontin
Haloperidol • Haldol
Levothyroxine • Synthroid
Lisinopril • Prinivil, Zestril
Lithium • Eskalith, Lithobid
Loxapine • Loxitane
Mirtazapine • Remeron
Quetiapine • Seroquel
Risperidone • Risperdal
Thioridazine • Mellaril
Valproic acid • Depakote

Emergent medication use is indicated in numerous clinical scenarios, including psychotic agitation, physical aggression, or withdrawal from substances. While there is plenty of literature to help clinicians with medical record documentation in various other settings,^1-3 there is minimal guidance on how to document your rationale for using psychiatric medications in emergency situations.

I have designed a template for structuring progress notes that has helped me to quickly explain my decision-making for using psychiatric medications during an emergency. When writing a progress note to justify your clinical actions in these situations, ask yourself the following questions:

• What symptoms/behaviors needed to be emergently treated? (Use direct quotes from the patient.)
• Which nonpharmacologic interventions were attempted prior to using a medication?
• Does the patient have any medication allergies? (Document if you were unable to assess for allergies.)
• Why did you select this specific route for medication administration?
• What was your rationale for using the specific medication(s)?
• What was the rationale for the selected dose?
• Who was present during medication administration?
• Which (if any) concurrent interventions did you order during or after medication administration?
• Were any safety follow-up checks ordered after medication administration?

A sample progress note

To help illustrate how these questions could guide a clinician’s writing, the following is a progress note I created using this template:

“Patient woke up at 3:15 am, ran out of his room, and demanded to be discharged: ‘Get me out of here now!’ He started cursing and threatened to attack staff. Multiple members of the nursing staff and I initially tried to calm him down by talking with him and asking him to return to his room. He refused. Patient has no known medication allergies. I ordered oral risperidone, 2 mg, but he refused to take any oral medication to treat his agitation. Because of his continued safety threats toward staff, I decided to administer a 5-mg IM injection of olanzapine to treat his agitation. I selected olanzapine per contemporary agitation treatment guidelines. Because patient is unknown to our psychiatric emergency room and had admitted to frequent alcohol use, I did not select the higher 10-mg dose to avoid oversedation and respiratory depression. Multiple nursing staff, sheriff deputies, and I were present when IM olanzapine was administered. Patient was physically held/restrained by nursing staff and deputies to administer IM olanzapine. After olanzapine was given, patient was moved to a seclusion room by nursing staff and deputies, and I started a locked seclusion order for safety concerns. I instructed a nurse to document any adverse effects and check vital signs 45 minutes after olanzapine was administered.”

Emergent medication use is indicated in numerous clinical scenarios, including psychotic agitation, physical aggression, or withdrawal from substances. While there is plenty of literature to help clinicians with medical record documentation in various other settings,^1-3 there is minimal guidance on how to document your rationale for using psychiatric medications in emergency situations.

I have designed a template for structuring progress notes that has helped me to quickly explain my decision-making for using psychiatric medications during an emergency. When writing a progress note to justify your clinical actions in these situations, ask yourself the following questions:

• What symptoms/behaviors needed to be emergently treated? (Use direct quotes from the patient.)
• Which nonpharmacologic interventions were attempted prior to using a medication?
• Does the patient have any medication allergies? (Document if you were unable to assess for allergies.)
• Why did you select this specific route for medication administration?
• What was your rationale for using the specific medication(s)?
• What was the rationale for the selected dose?
• Who was present during medication administration?
• Which (if any) concurrent interventions did you order during or after medication administration?
• Were any safety follow-up checks ordered after medication administration?

A sample progress note

To help illustrate how these questions could guide a clinician’s writing, the following is a progress note I created using this template:

“Patient woke up at 3:15 am, ran out of his room, and demanded to be discharged: ‘Get me out of here now!’ He started cursing and threatened to attack staff. Multiple members of the nursing staff and I initially tried to calm him down by talking with him and asking him to return to his room. He refused. Patient has no known medication allergies. I ordered oral risperidone, 2 mg, but he refused to take any oral medication to treat his agitation. Because of his continued safety threats toward staff, I decided to administer a 5-mg IM injection of olanzapine to treat his agitation. I selected olanzapine per contemporary agitation treatment guidelines. Because patient is unknown to our psychiatric emergency room and had admitted to frequent alcohol use, I did not select the higher 10-mg dose to avoid oversedation and respiratory depression. Multiple nursing staff, sheriff deputies, and I were present when IM olanzapine was administered. Patient was physically held/restrained by nursing staff and deputies to administer IM olanzapine. After olanzapine was given, patient was moved to a seclusion room by nursing staff and deputies, and I started a locked seclusion order for safety concerns. I instructed a nurse to document any adverse effects and check vital signs 45 minutes after olanzapine was administered.”

Emergent medication use is indicated in numerous clinical scenarios, including psychotic agitation, physical aggression, or withdrawal from substances. While there is plenty of literature to help clinicians with medical record documentation in various other settings,^1-3 there is minimal guidance on how to document your rationale for using psychiatric medications in emergency situations.

I have designed a template for structuring progress notes that has helped me to quickly explain my decision-making for using psychiatric medications during an emergency. When writing a progress note to justify your clinical actions in these situations, ask yourself the following questions:

• What symptoms/behaviors needed to be emergently treated? (Use direct quotes from the patient.)
• Which nonpharmacologic interventions were attempted prior to using a medication?
• Does the patient have any medication allergies? (Document if you were unable to assess for allergies.)
• Why did you select this specific route for medication administration?
• What was your rationale for using the specific medication(s)?
• What was the rationale for the selected dose?
• Who was present during medication administration?
• Which (if any) concurrent interventions did you order during or after medication administration?
• Were any safety follow-up checks ordered after medication administration?

A sample progress note

To help illustrate how these questions could guide a clinician’s writing, the following is a progress note I created using this template:

“Patient woke up at 3:15 am, ran out of his room, and demanded to be discharged: ‘Get me out of here now!’ He started cursing and threatened to attack staff. Multiple members of the nursing staff and I initially tried to calm him down by talking with him and asking him to return to his room. He refused. Patient has no known medication allergies. I ordered oral risperidone, 2 mg, but he refused to take any oral medication to treat his agitation. Because of his continued safety threats toward staff, I decided to administer a 5-mg IM injection of olanzapine to treat his agitation. I selected olanzapine per contemporary agitation treatment guidelines. Because patient is unknown to our psychiatric emergency room and had admitted to frequent alcohol use, I did not select the higher 10-mg dose to avoid oversedation and respiratory depression. Multiple nursing staff, sheriff deputies, and I were present when IM olanzapine was administered. Patient was physically held/restrained by nursing staff and deputies to administer IM olanzapine. After olanzapine was given, patient was moved to a seclusion room by nursing staff and deputies, and I started a locked seclusion order for safety concerns. I instructed a nurse to document any adverse effects and check vital signs 45 minutes after olanzapine was administered.”

Patients who fabricate or exaggerate psychiatric symptoms for primary or secondary gain may elicit negative responses from health care professionals. As clinicians, we may believe that such patients are wasting our time and taking resources away from other patients who are genuinely struggling with mental illness and are more deserving of assistance. However, patients who are fabricating or exaggerating their symptoms have legitimate clinical needs that we should strive to understand. If we view them as having reasons for their actions without becoming complicit in their deception, we may find it easier to work with them.

Managing patients who are fabricating or exaggerating

Caring for patients who attempt to mislead us is a challenging proposition. The relevant research is scarce, and there are few recommended interventions for managing patients who fabricate or exaggerate symptoms.¹ Direct confrontation and accusation are often unproductive and should be used sparingly. Indirect approaches tend to be more effective.

It is important to manage our countertransference at the outset while establishing and maintaining rapport. Although we may become frustrated, we should avoid using sarcasm or overt skepticism; instead, we should validate these patients’ emotions because their emotional turmoil could be driving their fabrication or exaggeration. We should attempt to explore their specific motivations by focusing our questions on detecting the underlying stressors or conditions.²

To assess our patients’ motives, consider asking the following:

• What kind of problems have these symptoms caused you in your day-to-day life?
• What would make life better for you?
• What are you hoping I can do for you today?

We should ask open-ended questions as well as interview patients over a long period of time and on multiple occasions to observe the consistency of their reported symptoms. In addition, we should take good notes and document our observations to compare what our patients tell us during their appointments.

Addressing inconsistencies

While exploring our patients’ motives, when it is appropriate, we can gently confront discrepancies in their report by asking:

• I am confused about your symptoms. Help me understand what is happening. Can you tell me more? (Then ask specific follow-up questions based on their answer.)
• What do you mean when you say you are experiencing this symptom?
• I am not sure if I understand what you said correctly. These symptoms do not typically occur in the way that you described. Could you tell me more?
• The symptoms you described are unusual to me. Is there something else going on that I am not aware of?
• Do you think these symptoms have been coming up because you are under stress?
• Is it possible that you want to (avoid work, avoid jail, be prescribed a specific medication, etc.) and that this is the only way you could think of to get what you need?
• Is it possible that you are describing what you are experiencing so that you can convince others that you are having problems?

Despite our best efforts, some patients may not drop their guard and will continue to fabricate or exaggerate their symptoms. However, establishing and maintaining rapport, exploring our patients’ potential motives to mislead, and gently confronting discrepancies in their report may maximize the chances of successfully engaging them and developing appropriate treatment plans.

Patients who fabricate or exaggerate psychiatric symptoms for primary or secondary gain may elicit negative responses from health care professionals. As clinicians, we may believe that such patients are wasting our time and taking resources away from other patients who are genuinely struggling with mental illness and are more deserving of assistance. However, patients who are fabricating or exaggerating their symptoms have legitimate clinical needs that we should strive to understand. If we view them as having reasons for their actions without becoming complicit in their deception, we may find it easier to work with them.

Managing patients who are fabricating or exaggerating

Caring for patients who attempt to mislead us is a challenging proposition. The relevant research is scarce, and there are few recommended interventions for managing patients who fabricate or exaggerate symptoms.¹ Direct confrontation and accusation are often unproductive and should be used sparingly. Indirect approaches tend to be more effective.

It is important to manage our countertransference at the outset while establishing and maintaining rapport. Although we may become frustrated, we should avoid using sarcasm or overt skepticism; instead, we should validate these patients’ emotions because their emotional turmoil could be driving their fabrication or exaggeration. We should attempt to explore their specific motivations by focusing our questions on detecting the underlying stressors or conditions.²

To assess our patients’ motives, consider asking the following:

• What kind of problems have these symptoms caused you in your day-to-day life?
• What would make life better for you?
• What are you hoping I can do for you today?

We should ask open-ended questions as well as interview patients over a long period of time and on multiple occasions to observe the consistency of their reported symptoms. In addition, we should take good notes and document our observations to compare what our patients tell us during their appointments.

Addressing inconsistencies

While exploring our patients’ motives, when it is appropriate, we can gently confront discrepancies in their report by asking:

• I am confused about your symptoms. Help me understand what is happening. Can you tell me more? (Then ask specific follow-up questions based on their answer.)
• What do you mean when you say you are experiencing this symptom?
• I am not sure if I understand what you said correctly. These symptoms do not typically occur in the way that you described. Could you tell me more?
• The symptoms you described are unusual to me. Is there something else going on that I am not aware of?
• Do you think these symptoms have been coming up because you are under stress?
• Is it possible that you want to (avoid work, avoid jail, be prescribed a specific medication, etc.) and that this is the only way you could think of to get what you need?
• Is it possible that you are describing what you are experiencing so that you can convince others that you are having problems?

Despite our best efforts, some patients may not drop their guard and will continue to fabricate or exaggerate their symptoms. However, establishing and maintaining rapport, exploring our patients’ potential motives to mislead, and gently confronting discrepancies in their report may maximize the chances of successfully engaging them and developing appropriate treatment plans.

Patients who fabricate or exaggerate psychiatric symptoms for primary or secondary gain may elicit negative responses from health care professionals. As clinicians, we may believe that such patients are wasting our time and taking resources away from other patients who are genuinely struggling with mental illness and are more deserving of assistance. However, patients who are fabricating or exaggerating their symptoms have legitimate clinical needs that we should strive to understand. If we view them as having reasons for their actions without becoming complicit in their deception, we may find it easier to work with them.

Managing patients who are fabricating or exaggerating

Caring for patients who attempt to mislead us is a challenging proposition. The relevant research is scarce, and there are few recommended interventions for managing patients who fabricate or exaggerate symptoms.¹ Direct confrontation and accusation are often unproductive and should be used sparingly. Indirect approaches tend to be more effective.

It is important to manage our countertransference at the outset while establishing and maintaining rapport. Although we may become frustrated, we should avoid using sarcasm or overt skepticism; instead, we should validate these patients’ emotions because their emotional turmoil could be driving their fabrication or exaggeration. We should attempt to explore their specific motivations by focusing our questions on detecting the underlying stressors or conditions.²

To assess our patients’ motives, consider asking the following:

• What kind of problems have these symptoms caused you in your day-to-day life?
• What would make life better for you?
• What are you hoping I can do for you today?

We should ask open-ended questions as well as interview patients over a long period of time and on multiple occasions to observe the consistency of their reported symptoms. In addition, we should take good notes and document our observations to compare what our patients tell us during their appointments.

Addressing inconsistencies

While exploring our patients’ motives, when it is appropriate, we can gently confront discrepancies in their report by asking:

• I am confused about your symptoms. Help me understand what is happening. Can you tell me more? (Then ask specific follow-up questions based on their answer.)
• What do you mean when you say you are experiencing this symptom?
• I am not sure if I understand what you said correctly. These symptoms do not typically occur in the way that you described. Could you tell me more?
• The symptoms you described are unusual to me. Is there something else going on that I am not aware of?
• Do you think these symptoms have been coming up because you are under stress?
• Is it possible that you want to (avoid work, avoid jail, be prescribed a specific medication, etc.) and that this is the only way you could think of to get what you need?
• Is it possible that you are describing what you are experiencing so that you can convince others that you are having problems?

Despite our best efforts, some patients may not drop their guard and will continue to fabricate or exaggerate their symptoms. However, establishing and maintaining rapport, exploring our patients’ potential motives to mislead, and gently confronting discrepancies in their report may maximize the chances of successfully engaging them and developing appropriate treatment plans.

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at [email protected] in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at [email protected] in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

The quarterly report of the State Medical Board can be a sobering read. In addition to the usual updates about new regulations or requirements for licensed physicians, there is always the disciplinary actions “blacklist” of dozens of medical practitioners in all specialties whose licenses were revoked or suspended due to a shocking array of serious violations.

Those infractions range from Medicare billing fraud to prescribing narcotics to fictitious patients to engaging in sex with a patient to walking into the operating room drunk. It is truly disheartening to see dozens of physicians destroy their careers by committing a panoply of odious, repugnant, or illegal actions.

The term “anathema” comes to mind when I read about those miscreants. This Greek term is occasionally used in scholarly or religious publications, but rarely in everyday conversations or articles. Anathema refers to something detested, shunned, or denounced. When used by the clergy, it connotes something to condemn, such as a sinful or evil act.

Like all other medical specialists, we psychiatrists have a noble mission of treating and relieving the suffering of those afflicted with brain disorders that manifest as mood, thought, perceptual, behavioral, or cognitive abnormalities. Our main goal is to restore health, wellness, and quality of life to the millions of individuals who buckle under the weight of genetic redispersion, adverse environmental events, or both. So psychiatrists do a lot of “good,” which benefits all those who live with mental illness. However, psychiatric practice may have some pitfalls that occasionally lead to anathemas, no matter how diligently a practitioner tries to avoid them. The code of psychiatric ethics is a shield that can preempt anathemas from contaminating clinical practice, but human error will occur when the ethical compass fails.

Here are some examples of anathemas that may rear their ugly heads if a practitioner is not constantly on the alert. It is likely you, the readers of Current Psychiatry, may think of additional anathemas not listed below. If so, I encourage you to send them to me at [email protected] in the form of a brief Letter to the Editor, which may be considered for publication.

• Sexual contact with a patient. This major anathema must not occur under any circumstance. It will have grave professional consequences for the practitioner and serious emotional repercussions for the patient.
• Breach of confidentiality. This is a sacred rule in psychiatric practice that must not be broken under any circumstance. Breaching confidentiality will rupture the therapeutic bond and trust that a patient has with a psychiatrist (or psychiatric nurse practitioner).
• Causing physical or emotional harm. This anathema can have serious legal implications in addition to being an unacceptable professional violation.
• Failure to assess patients for suicidal or homicidal risk. The life of the patient, and others, may be at stake if this critical component is missing in the evaluation of psychiatric patients, even if they appear “stable.”
• Irrational and hazardous polypharmacy. This type of harm must never occur during medical management of psychiatric patients, and may have legal consequences.
• Not seeking collateral information. This may seem like a “minor” anathema, but it can have major repercussions if a gap of clinically important data about the patient leads to erroneous diagnosis or inappropriate treatment. Regrettably, informants are sometimes unavailable.
• Assessing patients from the neck up only. Psychiatrists are, first and foremost, physicians who must evaluate the entire medical status of the patient, not just his/her mind. There are numerous bidirectional effects between the body and the brain that can influence diagnosis, holistic treatment, medical outcomes, and prognosis.
• Treating patients with medication only, without any concomitant psychotherapy. Such a suboptimal practice is an anathema that is not excusable due to a “lack of time.” Every psychiatric patient deserves a biopsychosocial treatment approach.
• Not inquiring about adherence at every visit. It is impossible to assess the effectiveness of treatment if adherence is partial or poor. Patients must be constantly reminded that while their psychiatrists are committed to their care, full adherence is a vital responsibility for them to fulfill to ensure optimal outcome.
• Ignoring the patient’s cues, both verbal and nonverbal. Being rushed by a large workload, a full schedule, or the demands of electronic medical records that distract a psychiatrist from fully attending to what the patient’s words, facial expressions, or body language convey can lead to a failure to meet the patient’s needs. Even worse, it may lead to missing a serious message a patient is consciously or unconsciously trying to relay.
• Lowering expectations. Nothing is more devastating for patients than to feel that the psychiatrist does not believe he/she will ever achieve wellness, or that they are beyond help and will never improve, recover, or overcome disabling psychiatric illness. This will generate profound hopelessness in vulnerable patients, who crave having a normal life free from illness or disability.
• Using the same medication for all patients. This is an anathema because one size does not fit all, and patients deserve to have their psychiatrists customize their pharmacotherapy to match their medical status and tolerability. For example, the 11 FDA-approved second-generation antipsychotics are not all the same, and a psychiatrist must select the member of that class that is most likely to be a good match for each patient based on that patient’s medical history and the safety/tolerability profile of each antipsychotic.
• Not continuously upgrading one’s practice to incorporate new evidence-based findings of more effective therapeutic strategies. It is an anathema to continue practicing what was learned in residency 25 to 30 years ago when there’s new knowledge and many advances permeating psychiatric practice today.
• Using alcohol or recreational drugs during a shift in the clinic or the hospital. No explanation is needed for this anathema!
• Prescribing for patients without a full evaluation. That’s poor clinical practice, and also is illegal.
• Billing for patients who were never examined. That’s fraudulent, and stupid!

In an editorial I wrote last year intended for graduates of psychiatry residency training programs about the “DNA of psychiatric practice,” I described what comprises good psychiatric practice.¹ Anathemas can be regarded as “mutations” within the DNA of psychiatric practice. It is always my hope that none of the freshly minted psychiatrists going into practice will ever commit an anathema, and end up on the “list of shame” in their State Medical Board’s quarterly report….

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon

In our experience, most psychiatrists are uncomfortable with prescribing a medication when they feel that doing so would be outside their scope of practice. But there are many situations when prescribing a nonpsychotropic medication would be the correct choice. In this article, we discuss the scope of psychiatric practice, and present 4 case studies that illustrate situations in which psychiatrists should feel comfortable prescribing nonpsychotropic medications.

Defining the scope of practice

What is the scope of a psychiatrist’s practice? Scope of practice usually describes activities that a health care practitioner is allowed to undertake as defined by the terms of his/her license. A license to practice medicine does not include any stipulation restricting practice to a specific medical specialty. However, a local entity may delineate scope of practice within its organization. For instance, local practice standards held by the Detroit Wayne Mental Health Authority (DWMHA) state “Psychiatrists…shall not exceed their scope of practice as per DWMHA credentialing and privileging. For example, a Psychiatrist…who [has] not been appropriately privileged to deliver services to children shall not treat children, excepting crisis situations.”¹

Like physicians in other specialties, psychiatrists are not limited to prescribing only a subset of medications commonly associated with their specialty. But for many psychiatrists, prescribing nonpsychotropic medications is complicated by individual and local factors. On one hand, some psychiatrists do not feel it is their role to prescribe nonpsychotropic medications,² or even some psychotropic medications that may be more complex to prescribe, such as lithium, clozapine, or monoamine oxidase inhibitors.^3-5 However, many feel comfortable prescribing complex combinations of psychotropic medications, or prescribing in a way that does not necessarily make sense (eg, prescribing benztropine as prophylaxis for dystonia when starting an antipsychotic).

Reviewing an average day at one urban psychiatric clinic, these questions seem to come up in half of the patient population, especially in patients with chronic mental illness, multiple medical comorbidities, and limited access to health care. When a young patient walks in without an appointment with an acute dystonic reaction secondary to the initiation of antipsychotics a couple of days ago, there is no hesitation to swiftly and appropriately prescribe an IM anticholinergic medication. But why are psychiatrists often hesitant to prescribe nonpsychotropic medications to treat other adverse effects of medications? Lack of knowledge? Lack of training?

Psychiatrists who practice in hospital systems often have immediate access to consultants, and this availability may encourage them to defer to the consultant for treatment of certain adverse effects. We have seen psychiatrists consult Neurology regarding the prescription of donepezil for mild neurocognitive disorder due to Alzheimer’s disease, or Endocrinology regarding prescription of levothyroxine for lithium-induced hypothyroidism.

However, there are numerous scenarios in which psychiatrists should feel comfortable prescribing nonpsychotropic medications or managing medication adverse effects, regardless of whether they consider it to be within or outside their scope of practice. The following case examples illustrate several such situations.

CASE 1

Ms. W, age 30, has been diagnosed with schizophrenia. She requests a refill of quetiapine, 800 mg/d. This medication has been clearly beneficial in alleviating her psychotic symptoms. However, since her last visit 3 months ago, her face appears more round, and she has gained 9 kg. Further evaluation indicates that she has developed metabolic syndrome and pre-diabetes.

Continue to: Metabolic adverse effects

Metabolic adverse effects, such as metabolic syndrome, diabetic ketoacidosis, and cardiovascular disease, are well-known risks of prescribing second-generation antipsychotics.⁶ In such situations, psychiatrists often advise patients to modify their diet, increase physical activity, and follow up with their primary care physician to determine if other medications are needed. However, getting a patient with a serious mental illness to exercise and modify her/his diet is difficult, and many of these patients do not have a primary care physician.

For patients such as Ms. W, a psychiatrist should consider prescribing metformin. Wu et al⁷ found that in addition to lifestyle modifications, metformin had the greatest effect on antipsychotic-induced weight gain. In this study, metformin alone had more impact on reversing weight gain and increasing insulin sensitivity than lifestyle modifications alone.⁷ This is crucial because these patients are especially vulnerable to cardiac disease.⁸ Metformin is well tolerated and has a low risk of causing hypoglycemia. Concerns regarding lactic acidosis have abated to the extent that the estimated glomerular filtration rate (eGFR) limits for using metformin have been lowered significantly. After reviewing the contraindications, the only knowledge needed to prescribe metformin is the patient’s kidney function and a brief understanding of the titration needed to minimize gastrointestinal adverse effects.⁹ Thus, prescribing metformin would be a fairly logical and easy first step for managing metabolic syndrome, especially in a patient whose motivation for increasing physical activity and modifying his/her diet is doubtful.

CASE 2

Mr. B, age 45, has major depressive disorder that has been well-controlled on paroxetine, 40 mg/d, for the past 2 years. He has no history of physical illness. On his most recent visit, he appears uncomfortable and nervous. After a long discussion, he discloses that his sex life isn’t what it used to be since starting paroxetine. He is bothered by erectile problems and asks whether he can “get some Viagra.”

Sexual adverse effects, such as erectile dysfunction, are frequently associated with the use of selective serotonin reuptake inhibitors.¹⁰ Although managing these adverse effects requires careful evaluation, in most cases, psychiatrists should be able to treat them.¹⁰ The logical choice in this case would be to prescribe one of the 4 FDA-approved phosphodiesterase-5 inhibitors (sildenafil [Viagra], tadalafil [Cialis], vardenafil [Levitra], and avanafil [Stendra]. However, Balon et al¹¹ found that few psychiatrists prescribe phosphodiesterase-5 inhibitors, although they believed that they should be prescribing to treat their patients’ sexual dysfunction. Managing these adverse effects is important not only for the patient’s quality of life and relationship with his/her partner, but also for the therapeutic alliance. In a systematic review of 23 trials, Taylor et al¹² examined >1,800 patients who were prescribed a medication to address sexual dysfunction secondary to antidepressants. They found that for men, adding a phosphodiesterase-5 inhibitor was appropriate and effective, and for women, adding bupropion at high doses should be considered.¹² Like many other adverse effects, sexual adverse effects surely play a role in medication compliance. Dording et al¹³ found that the addition of sildenafil, 50 to 100 mg as needed, resulted in increased treatment satisfaction and overall contentment in 102 patients who complained of sexual dysfunction in the follow-up phase of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) antidepressant trials. In most cases, with proper psychoeducation, prescription of phosphodiesterase-5 inhibitors is fairly straightforward.

CASE 3

Ms. G, age 22, was recently discharged from an inpatient psychiatric unit after an episode of mania. She was prescribed carbamazepine, 600 mg/d, and ziprasidone, 40 mg twice a day, and appears to be doing well on this regimen. When asked about what led to her admission, she recalls having an elevated mood, increased energy, hypersexuality, impulsivity, and poor judgment. She reveals that she had several sexual partners during her manic episode, and worries that if such behavior occurs again, she may get pregnant. Yet Ms. G was not prescribed birth control upon discharge.

Continue to: Contraception

Contraception. We believe that psychiatrists have an obligation to protect patients from consequences of mental illness. Much the same way that psychiatrists hope to prevent suicide in a patient who has depression, patients should be protected from risks encountered in the manic phase of bipolar disorder. Another reason to prescribe contraceptives in such patients is the teratogenic effects of mood stabilizers. Pagano et al¹⁴ reviewed 6 studies that examined common forms of hormonal birth control to determine their safety in patients with depression or bipolar disorder. They found that overall, use of hormonal contraception was not associated with a worse clinical course of disease.

Many available forms of birth control are available. When prescribing in an outpatient setting, a daily oral medication or a monthly depot injection are convenient options.

CASE 4

Mr. P, age 65, has bipolar I disorder and is stable on risperidone long-acting injection, 37.7 mg bimonthly, and lithium, 1,200 mg/d. He reports that he is doing well but has noticed a recent decrease in energy and weight gain without any change in mood. Laboratory testing conducted prior to this visit revealed a thyroid-stimulating hormone (TSH) level of 4 mU/L (normal range: 0.4 to 4.0 mU/L). Six months ago, Mr. P’s TSH level was 2.8 mU/L. The resident supervisor suggests discussing the case with an endocrinologist.

Thyroid function. The impact of lithium on the thyroid gland is well established; however, psychiatrists’ response to such changes are not.¹⁵ Gitlin¹⁶ reviewed the many adverse effects of lithium and presented various management strategies to address findings such as Mr. P’s. Two important points are that lithium should not be discontinued in light of hypothyroidism, and synthetic thyroxine (levothyroxine) can be initiated and titrated to return TSH levels to a normal range.¹⁶ Levothyroxine can be started at low doses (eg, 25 to 50 mcg/d) and increased every 6 weeks until a normal TSH level is achieved.¹⁷ Managing lithium-induced clinical or subclinical hypothyroidism can prevent further pathology and possible relapse to depression.

Incorporating integrated care

In all these cases, the prescription of a medication with which some psychiatrists are not comfortable prescribing would have been the logical, easiest, and preferable choice. Of course, when initiating any medication, boxed warnings, contraindications, and drug–drug interactions should be reviewed. Initial dosages and titration schedules can be found in every medication’s FDA-approved prescribing information document (package insert), as well as in numerous reference books and articles.

Continue to: We acknowledge...

We acknowledge that prescribing a nonpsychotropic medication is not always a psychiatrist’s best choice, and that in patients with multiple medical comorbidities and drug–drug interactions that are not clearly defined, referring to or consulting a specialist is appropriate. We in no way support reckless prescribing, but instead present an opportunity to expand the perception of what should be considered within a psychiatrist’s scope of practice, and call for further education of psychiatrists so that they are more comfortable managing these adverse effects and/or prescribing at least some nonpsychotropic medications. For example, metabolic syndrome, uncomplicated hypertension, and hypothyroidism (not necessarily lithium-induced) could be managed by psychiatrists practicing integrated care (Table).

We exhort integrated medical care during this time of a physician shortage; however, we do not practice this way. Interestingly, physicians in primary care, such as those in family medicine or obstetrics and gynecology, frequently attempt to treat patients with psychiatric conditions in an attempt to provide integrated care. Numerous articles have discussed these efforts.^18-20 However, this type of integrated care seems less frequent in psychiatry, even though the practice of modern psychiatry in the United States shows substantial overlap with the practice of physicians in primary care specialties.²¹ There are few articles or practical guidelines for psychiatrists who wish to treat patients’ physical illnesses, particularly patients with severe mental illness (see Related Resources, page 56). If we practice in an integrated manner to treat one of the simple conditions we described above, we can eliminate the need for a patient to visit a second physician, pay another co-pay, pay another bus fare, and take another day off work. This can be particularly helpful for patients who at times have to decide between paying for groceries or for medications. Having one clinician manage a patient’s medications also can decrease the risk of polypharmacy.

In addition to the case scenarios described in this article, there are more clinical situations and nonpsychotropic medications that psychiatrists could manage. Considering them outside the scope of psychiatric practice and being uncomfortable or ambivalent about them is not an excuse. We hope that psychiatrists can increase their expertise in this area, and can start to practice as the primary care physicians they claim they are, and should be.

Bottom Line

Many psychiatrists are uncomfortable prescribing nonpsychotropic medications, but there are numerous clinical scenarios in which the practice would make sense. This could include cases of metabolic syndrome, sexual dysfunction secondary to antidepressant use, or other adverse effects of commonly prescribed psychotropic medications.

Related Resources

• McCarron RM, Xiong GL, Keenan CR, et al. Preventive medical care in psychiatry. A practical guide for clinicians. Arlington, VA: American Psychiatric Association Publishing; 2015.
• McCarron RM, Xiong GL, Keenan CR, et al. Study guide to preventive medical care in psychiatry. Arlington, VA: American Psychiatric Association Publishing; 2017.
• Goldberg JF, Ernst CL. Managing the side effects of psychotropic medications. Washington, DC: American Psychiatric Association Publishing; 2019.

Drug Brand Names

Avanafil • Stendra
Benztropine • Cogentin
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Clozapine • Clozaril
Donepezil • Aricept
Levothyroxine • Levoxyl, Synthroid
Lithium • Eskalith, Lithobid
Metformin • Fortamet, Glucophage
Paroxetine • Paxil
Quetiapine • Seroquel
Risperidone long-acting injection • Risperdal Consta
Sildenafil • Viagra
Tadalafil • Cialis
Vardenafil • Levitra
Ziprasidone • Geodon