Long utilized as a rapid anesthetic, ketamine has been increasingly used in sub-anesthetic doses for several psychiatric indications, including depression, suicidality, and chronic pain. Recently, an intranasal form of esketamine—the S-enantiomer of ketamine—was FDA-approved for treatment-resistant depression. Previously, researchers believed ketamine mediated its analgesic and psychotropic effects solely via N-methyl-D-aspartate (NMDA) receptor antagonism, but emerging research has described a seemingly more complex receptor profile.¹ One such ancillary pharmacologic mechanism is occupation of the serotonin receptor.^1,2 However, there is sparse literature describing the possible extent of ketamine’s involvement in serotonin syndrome.³ Here, we describe a case of serotonin syndrome that might have been induced by ketamine.

CASE REPORT

Ms. O, age 41, has a history of endometriosis, anticardiolipin antibody syndrome, major depressive disorder, and generalized anxiety disorder. She initially presented to an outside hospital and was admitted for chronic endometriosis pain. During that admission, her pain was treated with IV ketamine, 40 mg/hour, on hospital Days 1 through 4. While hospitalized, she continued to receive her home medications: fluoxetine, 40 mg/d, coumadin, 5 mg/d, and diphenhydramine, 25 mg/d. On Day 5, Ms. O experienced visual hallucinations and was diagnosed with ketamine-induced delirium. She was treated with haloperidol (dose unknown) with reportedly good effect. On Day 7, she was discharged home.

Upon returning home, she experienced persistent altered mental status. Her significant other brought her to our hospital for further workup. Ms. O’s body temperature was 37.6°C, and she was diaphoretic. Her blood pressure was 154/100 mm Hg, and her heart rate was 125 bpm. On physical examination, she had 4+ patellar and Achilles reflexes with left ankle clonus and crossed adductors. Her mental status exam showed increased latency of thought and speech, with bizarre affect as evidenced by illogical mannerisms and appearance. She said she was “not feeling myself” and would stare at walls for prolonged periods of time, appearing internally preoccupied and confused.

Ms. O was treated with IV lorazepam, 2 mg. Fourteen hours later, her temperature returned to normal, but she remained tachycardic, hypertensive, and altered. She received 2 additional doses of 2 mg and 1 mg. Seventeen hours after the initial dose of IV lorazepam was administered (and 3 hours after the second dose), Ms. O’s heart rate returned to normal. She was ultimately converted to oral lorazepam, 1 mg every 12 hours. Two hours later, Ms. O’s blood pressure returned to normal, and her physical exam showed normal reflexes.

Ms. O was given a presumptive diagnosis of ketamine-induced serotonin syndrome. She made a good recovery and was discharged home.

A suspected association

Serotonin syndrome is caused by increased levels of the neurotransmitter serotonin in the CNS. Clinical features of serotonin syndrome include agitation, restlessness, mydriasis, altered mental status or confusion, tachycardia, hypertension, muscle rigidity, diaphoresis, diarrhea, piloerection, headache, fasciculations, clonus, and shivering. Severe cases can be life-threatening and may present with high fever, seizures, arrhythmias, and loss of consciousness. Serotonin syndrome is a clinical diagnosis; the Hunter Serotonin Toxicity Criteria are often used to make the diagnosis. To meet these criteria, a patient must have received a serotonergic agent, and at least one of the following must be present⁴:

• spontaneous clonus
• inducible clonus and agitation or diaphoresis
• ocular clonus and agitation or diaphoresis
• tremor and hyperreflexia
• hypertonia, temperature >38°C, and ocular clonus or inducible clonus.

For Ms. O, we suspected that administration of ketamine in conjunction with fluoxetine, 40 mg/d, led to serotonin syndrome. Ms. O exhibited ocular clonus and diaphoresis, thus satisfying the Hunter Serotonin Toxicity Criteria, and she also had inducible clonus, altered mental status, hypertension, and tachycardia, which makes serotonin syndrome the most likely diagnosis. She improved after receiving lorazepam, which is often used to treat hypertonicity, decrease autonomic instability, and prevent seizures seen in serotonin syndrome.⁵

Continue to: There is sparse literature...

There is sparse literature describing serotonin syndrome related to ketamine use. Ketamine has been shown to increase levels of glutamate in the medial prefrontal cortex. Higher levels of glutamine in turn stimulate excitatory glutamatergic neurons that project to the dorsal raphe nucleus. When stimulated, the dorsal raphe nucleus releases serotonin.⁶ There is also evidence that ketamine inhibits uptake of serotonin in synapses.⁷ These mechanisms combine to create a net increase in CNS-wide serotonin.

Ketamine is being increasingly used to treat depression and other conditions. This case report underscores the importance of considering serotonin syndrome when treating patients receiving ketamine, especially when it is used in conjunction with selective serotonin reuptake inhibitors.

Long utilized as a rapid anesthetic, ketamine has been increasingly used in sub-anesthetic doses for several psychiatric indications, including depression, suicidality, and chronic pain. Recently, an intranasal form of esketamine—the S-enantiomer of ketamine—was FDA-approved for treatment-resistant depression. Previously, researchers believed ketamine mediated its analgesic and psychotropic effects solely via N-methyl-D-aspartate (NMDA) receptor antagonism, but emerging research has described a seemingly more complex receptor profile.¹ One such ancillary pharmacologic mechanism is occupation of the serotonin receptor.^1,2 However, there is sparse literature describing the possible extent of ketamine’s involvement in serotonin syndrome.³ Here, we describe a case of serotonin syndrome that might have been induced by ketamine.

CASE REPORT

Ms. O, age 41, has a history of endometriosis, anticardiolipin antibody syndrome, major depressive disorder, and generalized anxiety disorder. She initially presented to an outside hospital and was admitted for chronic endometriosis pain. During that admission, her pain was treated with IV ketamine, 40 mg/hour, on hospital Days 1 through 4. While hospitalized, she continued to receive her home medications: fluoxetine, 40 mg/d, coumadin, 5 mg/d, and diphenhydramine, 25 mg/d. On Day 5, Ms. O experienced visual hallucinations and was diagnosed with ketamine-induced delirium. She was treated with haloperidol (dose unknown) with reportedly good effect. On Day 7, she was discharged home.

Upon returning home, she experienced persistent altered mental status. Her significant other brought her to our hospital for further workup. Ms. O’s body temperature was 37.6°C, and she was diaphoretic. Her blood pressure was 154/100 mm Hg, and her heart rate was 125 bpm. On physical examination, she had 4+ patellar and Achilles reflexes with left ankle clonus and crossed adductors. Her mental status exam showed increased latency of thought and speech, with bizarre affect as evidenced by illogical mannerisms and appearance. She said she was “not feeling myself” and would stare at walls for prolonged periods of time, appearing internally preoccupied and confused.

Ms. O was treated with IV lorazepam, 2 mg. Fourteen hours later, her temperature returned to normal, but she remained tachycardic, hypertensive, and altered. She received 2 additional doses of 2 mg and 1 mg. Seventeen hours after the initial dose of IV lorazepam was administered (and 3 hours after the second dose), Ms. O’s heart rate returned to normal. She was ultimately converted to oral lorazepam, 1 mg every 12 hours. Two hours later, Ms. O’s blood pressure returned to normal, and her physical exam showed normal reflexes.

Ms. O was given a presumptive diagnosis of ketamine-induced serotonin syndrome. She made a good recovery and was discharged home.

A suspected association

Serotonin syndrome is caused by increased levels of the neurotransmitter serotonin in the CNS. Clinical features of serotonin syndrome include agitation, restlessness, mydriasis, altered mental status or confusion, tachycardia, hypertension, muscle rigidity, diaphoresis, diarrhea, piloerection, headache, fasciculations, clonus, and shivering. Severe cases can be life-threatening and may present with high fever, seizures, arrhythmias, and loss of consciousness. Serotonin syndrome is a clinical diagnosis; the Hunter Serotonin Toxicity Criteria are often used to make the diagnosis. To meet these criteria, a patient must have received a serotonergic agent, and at least one of the following must be present⁴:

• spontaneous clonus
• inducible clonus and agitation or diaphoresis
• ocular clonus and agitation or diaphoresis
• tremor and hyperreflexia
• hypertonia, temperature >38°C, and ocular clonus or inducible clonus.

For Ms. O, we suspected that administration of ketamine in conjunction with fluoxetine, 40 mg/d, led to serotonin syndrome. Ms. O exhibited ocular clonus and diaphoresis, thus satisfying the Hunter Serotonin Toxicity Criteria, and she also had inducible clonus, altered mental status, hypertension, and tachycardia, which makes serotonin syndrome the most likely diagnosis. She improved after receiving lorazepam, which is often used to treat hypertonicity, decrease autonomic instability, and prevent seizures seen in serotonin syndrome.⁵

Continue to: There is sparse literature...

There is sparse literature describing serotonin syndrome related to ketamine use. Ketamine has been shown to increase levels of glutamate in the medial prefrontal cortex. Higher levels of glutamine in turn stimulate excitatory glutamatergic neurons that project to the dorsal raphe nucleus. When stimulated, the dorsal raphe nucleus releases serotonin.⁶ There is also evidence that ketamine inhibits uptake of serotonin in synapses.⁷ These mechanisms combine to create a net increase in CNS-wide serotonin.

Ketamine is being increasingly used to treat depression and other conditions. This case report underscores the importance of considering serotonin syndrome when treating patients receiving ketamine, especially when it is used in conjunction with selective serotonin reuptake inhibitors.

Long utilized as a rapid anesthetic, ketamine has been increasingly used in sub-anesthetic doses for several psychiatric indications, including depression, suicidality, and chronic pain. Recently, an intranasal form of esketamine—the S-enantiomer of ketamine—was FDA-approved for treatment-resistant depression. Previously, researchers believed ketamine mediated its analgesic and psychotropic effects solely via N-methyl-D-aspartate (NMDA) receptor antagonism, but emerging research has described a seemingly more complex receptor profile.¹ One such ancillary pharmacologic mechanism is occupation of the serotonin receptor.^1,2 However, there is sparse literature describing the possible extent of ketamine’s involvement in serotonin syndrome.³ Here, we describe a case of serotonin syndrome that might have been induced by ketamine.

CASE REPORT

Ms. O, age 41, has a history of endometriosis, anticardiolipin antibody syndrome, major depressive disorder, and generalized anxiety disorder. She initially presented to an outside hospital and was admitted for chronic endometriosis pain. During that admission, her pain was treated with IV ketamine, 40 mg/hour, on hospital Days 1 through 4. While hospitalized, she continued to receive her home medications: fluoxetine, 40 mg/d, coumadin, 5 mg/d, and diphenhydramine, 25 mg/d. On Day 5, Ms. O experienced visual hallucinations and was diagnosed with ketamine-induced delirium. She was treated with haloperidol (dose unknown) with reportedly good effect. On Day 7, she was discharged home.

Upon returning home, she experienced persistent altered mental status. Her significant other brought her to our hospital for further workup. Ms. O’s body temperature was 37.6°C, and she was diaphoretic. Her blood pressure was 154/100 mm Hg, and her heart rate was 125 bpm. On physical examination, she had 4+ patellar and Achilles reflexes with left ankle clonus and crossed adductors. Her mental status exam showed increased latency of thought and speech, with bizarre affect as evidenced by illogical mannerisms and appearance. She said she was “not feeling myself” and would stare at walls for prolonged periods of time, appearing internally preoccupied and confused.

Ms. O was treated with IV lorazepam, 2 mg. Fourteen hours later, her temperature returned to normal, but she remained tachycardic, hypertensive, and altered. She received 2 additional doses of 2 mg and 1 mg. Seventeen hours after the initial dose of IV lorazepam was administered (and 3 hours after the second dose), Ms. O’s heart rate returned to normal. She was ultimately converted to oral lorazepam, 1 mg every 12 hours. Two hours later, Ms. O’s blood pressure returned to normal, and her physical exam showed normal reflexes.

Ms. O was given a presumptive diagnosis of ketamine-induced serotonin syndrome. She made a good recovery and was discharged home.

A suspected association

Serotonin syndrome is caused by increased levels of the neurotransmitter serotonin in the CNS. Clinical features of serotonin syndrome include agitation, restlessness, mydriasis, altered mental status or confusion, tachycardia, hypertension, muscle rigidity, diaphoresis, diarrhea, piloerection, headache, fasciculations, clonus, and shivering. Severe cases can be life-threatening and may present with high fever, seizures, arrhythmias, and loss of consciousness. Serotonin syndrome is a clinical diagnosis; the Hunter Serotonin Toxicity Criteria are often used to make the diagnosis. To meet these criteria, a patient must have received a serotonergic agent, and at least one of the following must be present⁴:

• spontaneous clonus
• inducible clonus and agitation or diaphoresis
• ocular clonus and agitation or diaphoresis
• tremor and hyperreflexia
• hypertonia, temperature >38°C, and ocular clonus or inducible clonus.

For Ms. O, we suspected that administration of ketamine in conjunction with fluoxetine, 40 mg/d, led to serotonin syndrome. Ms. O exhibited ocular clonus and diaphoresis, thus satisfying the Hunter Serotonin Toxicity Criteria, and she also had inducible clonus, altered mental status, hypertension, and tachycardia, which makes serotonin syndrome the most likely diagnosis. She improved after receiving lorazepam, which is often used to treat hypertonicity, decrease autonomic instability, and prevent seizures seen in serotonin syndrome.⁵

Continue to: There is sparse literature...

There is sparse literature describing serotonin syndrome related to ketamine use. Ketamine has been shown to increase levels of glutamate in the medial prefrontal cortex. Higher levels of glutamine in turn stimulate excitatory glutamatergic neurons that project to the dorsal raphe nucleus. When stimulated, the dorsal raphe nucleus releases serotonin.⁶ There is also evidence that ketamine inhibits uptake of serotonin in synapses.⁷ These mechanisms combine to create a net increase in CNS-wide serotonin.

Ketamine is being increasingly used to treat depression and other conditions. This case report underscores the importance of considering serotonin syndrome when treating patients receiving ketamine, especially when it is used in conjunction with selective serotonin reuptake inhibitors.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

CASE Suicidal behavior, severe headaches

Ms. A, age 60, presents to the emergency department (ED) with depression, suicidal behavior, and 3 days of severe headaches. Neurology is consulted and an MRI is ordered, which shows a 3.0-cm mass lesion in the left temporal lobe with associated vasogenic edema that is suspicious for metastatic disease (Figure).

Ms. A is admitted to the hospital for further workup of her brain lesion. She is started on IV dexamethasone, 10 mg every 6 hours, a glucocorticosteroid, for brain edema, and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

Upon admission, in addition to oncology and neurosurgery, psychiatry is also consulted to evaluate Ms. A for depression and suicidality.

EVALUATION Mood changes and poor judgment

Ms. A has a psychiatric history of depression and alcohol use disorder but says she has not consumed any alcohol in years. Her medical history includes hypertension, diabetes, and stage 4 non-small–cell lung cancer, for which she received surgery and adjuvant chemoradio­therapy 1 year ago.

On initial intake, Ms. A reports that in addition to the headaches, she has also been experiencing worsening depression and suicidal behavior. For the past 2 months, she has had a severely depressed mood, with notable anhedonia, poor appetite, insomnia, low energy, and decreased concentration. The changes in her mental health were triggered by her mother’s death. Three days prior to admission, the patient planned to overdose on anti­hypertensive pills, but her suicide attempt was interrupted when her family called. She denies any current suicidal ideation, intent, or plan.

According to her family, Ms. A has been increasingly irritable and her personality has changed in the past month. She also has been repeatedly sorting through her neighbors’ garbage.

Ms. A’s current psychiatric medications are duloxetine, 30 mg/d; quetiapine, 50 mg every night at bedtime; and buspirone, 10 mg/d. However, it is unclear if she is consistently taking these medications.

Continue to: On mental status examination...

On mental status examination, Ms. A is calm and she has no abnormal movements. She says she is depressed. Her affect is reactive and labile. She is alert and oriented to person, place, and time. Her attention, registration, and recall are intact. Her executive function is not tested. However, Ms. A’s insight and judgment seem poor.

To address Ms. A’s worsening depression, the psychiatry team increases her duloxetine from 30 to 60 mg/d, and she continues quetiapine, 50 mg every night at bedtime, for mood lability. Buspirone is not continued because she was not taking a therapeutic dosage in the community.

Within 4 days, Ms. A shows improvement in sleep, appetite, and mood. She has no further suicidal ideation.

[polldaddy:10511743]

The authors’ observations

Ms. A had a recurrence of what was presumed to be major depressive disorder (MDD) in the context of her mother’s death. However, she also exhibited irritability, mood lability, and impulsivity, all of which could be part of her depression, or a separate problem related to her brain tumor. Because Ms. A had never displayed bizarre behavior before the past few weeks, it is likely that her CNS lesion was directly affecting her personality and possibly underlying her planned suicide attempt.

Fifty to 80% of patients with CNS tumors, either primary or metastatic, present with psychiatric symptoms.¹ Table 1^1-3 lists common psychiatric symptoms of brain tumors. Unfortunately, there is little reliable evidence that directly correlates tumor location with specific psychiatric symptoms. A 2010 meta-analysis found a statistically significant link between anorexia nervosa and hypothalamic tumors.¹ However, for other brain regions, there is only an increased likelihood that any given tumor location will produce psychiatric symptoms.^1,4 For instance, compared to patients with tumors in other locations, those with temporal lobe tumors are more likely to present with mood disorders, personality changes, and memory problems.¹ In contrast, patients with frontal lobe tumors have an increased likelihood of psychosis, mood disorders, and personality changes.¹ Patients with tumors in the pituitary region often present with anxiety.¹

Continue to: When considering treatment options...

When considering treatment options for Ms. A, alcohol withdrawal was unlikely given the remote history of alcohol use, low alcohol blood level, and lack of evidence of unstable vital signs or tremor. Although she might have benefited from inpatient psychiatric treatment, this needed to wait until there was a definitive treatment plan for her brain tumor. Finally, although a paraneoplastic syndrome, such as limbic encephalitis, could be causing her psychiatric symptoms, this scenario is less likely with non-small–cell lung cancer.

Although uncommon, CNS tumors can present with psychiatric symptoms as the only manifestation. This is more likely when a patient exhibits new-onset or atypical symptoms, or fails to respond to standard psychiatric treatment.⁴ Case reports have described patients with brain tumors being misdiagnosed as having a primary psychiatric condition, which delays treatment of their CNS cancer.² Additionally, frontal and limbic tumors are more likely to present with psychiatric manifestations; up to 90% of patients exhibit altered mental status or personality changes, as did Ms. A.^1,4 Clearly, it is easier to identify patients with psychiatric symptoms resulting from a brain tumor when they also present with focal neurologic deficits or systemic symptoms, such as headache or nausea and vomiting. Ms. A presented with severe headaches, which is what led to her early imaging and prompt diagnosis.

Numerous proposed mechanisms might account for the psychiatric symptoms that occur during the course of a brain tumor, including direct injury to neuronal cells, secretion of hormones or other tumor-derived substances, and peri-ictal phenomena.³

TREATMENT Tumor is removed, but memory is impaired

Ms. A is scheduled for craniotomy and surgical resection of the frontal mass. Prior to surgery, Ms. A shows interest in improving her health, cooperates with staff, and seeks her daughter’s input on treatment. One week after admission, Ms. A has her mass resected, which is confirmed on biopsy to be a lung metastasis. Post-surgery, Ms. A receives codeine, 30 mg every 6 hours as needed, for pain; she continues dexamethasone, 4 mg IV every 6 hours, for brain edema and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

On Day 2 after surgery, Ms. A attempts to elope. When she is approached by a psychiatrist on the treatment team, she does not recognize him. Although her long-term memory seems intact, she is unable to remember the details of recent events, including her medical and surgical treatments.

[polldaddy:10511745]

Continue to: The authors' observations

 

 

The authors’ observations

Ms. A’s memory impairment may be secondary to a surgically acquired neurocognitive deficit. In the United States, brain metastases represent a significant public health issue, affecting >100,000 patients per year.⁵ Metastatic lesions are the most common brain tumors. Lung cancer, breast cancer, and melanoma are the leading solid tumors to spread to the CNS.⁵ In cases of single brain metastasis, similar to Ms. A’s solitary left temporal lobe lesion, surgical resection plays a critical role in treatment. It provides histological confirmation of metastatic disease and can relieve mass effect if present. Studies have shown that combined surgical resection with radiation improves survival relative to patients who undergo radiation therapy alone.^6,7

However, the benefits of surgical resection need to be balanced with preservation of neurologic function. Emerging evidence suggests that a majority of patients have surgically-acquired cognitive deficits due to damage of normal surrounding tissues, and these deficits are associated with reduced quality of life.^8,9 Further, a study examining glioma surgical resections found that patients with left temporal lobe tumors exhibit more frequent and severe neurocognitive decline than patients with right temporal lobe tumors, especially in domains such as verbal memory.⁸ Ms. A’s memory impairment was persistent during her postoperative course, which suggests that it was not just an immediate post-surgical phenomenon, but a longer-lasting cognitive change directly related to the resection.

It is also possible that Ms. A had a prior neurocognitive disorder that manifested to a greater degree as a result of the CNS tumor. Ms. A might have had early-onset Alzheimer’s disease, although her intact memory before surgery makes this less likely. Alternatively, she could have had vascular dementia, especially given her long-standing hypertension and diabetes. This might have been missed in the initial evaluation because executive function was not tested. However, the relatively abrupt onset of memory problems after surgery suggests that she had no underlying neurocognitive disorder.

Ms. A’s presumed episode of MDD might also explain her memory changes. Major depressive disorder is increasingly common among geriatric patients, affecting approximately 5% of community-dwelling older adults.¹⁰ Its incidence increases with medical comorbidities, as suggested by depression rates of 5% to 10% in the primary care setting vs 37% in patients after critical-care hospitalizations.¹⁰ Late-life depression (LLD) occurs in adults age ≥60. Unlike depression in younger patients, LLD is more likely to be associated with cognitive impairment, specifically impairment of executive function and memory.¹¹ The incidence of cognitive impairment in LLD is higher in patients with a history of depression, such as Ms. A.^11,12 However, in general, patients who are depressed have memory complaints out of proportion to the clinical findings, and they show poor effort on cognitive testing. Ms. A exhibited neither of these, which makes it less likely that LLD was the exclusive cause of her memory loss.¹³ Table 2¹⁴ outlines the management of cognitive deficits in a patient with a brain tumor.

EVALUATION Increasingly agitated and paranoid

After the tumor resection, Ms. A becomes increasingly irritable, uncooperative, and agitated. She repeatedly demands to be discharged. She insists she is fine and refuses medications and further laboratory workup. She becomes paranoid about the nursing staff and believes they are trying to kill her.

Continue to: On psychiatric re-evaluation...

On psychiatric re-evaluation, Ms. A demonstrates pressured speech, perseveration about going home, paranoid delusions, and anger at her family and physicians.

[polldaddy:10511747]

The authors’ observations

Ms. A’s refusal of medications and agitation may be explained by postoperative delirium, a surgical complication that is increasingly common among geriatric patients and is associated with poor clinical outcomes. Delirium is characterized by an acute onset and fluctuating course of symptoms that include inattention, motoric hypo- or hyperactivity, inappropriate behavior, emotional lability, cognitive dysfunction, and psychotic symptoms.¹⁵ Risk factors that contribute to postoperative delirium include older age, alcohol use, and poor baseline functional and cognitive status.¹⁶ The pathophysiology of delirium is not fully understood, but accumulating evidence suggests that different sets of interacting biologic factors (ie, neuro­transmitters and inflammation) contribute to a disruption of large-scale neuronal networks in the brain, resulting in cognitive dysfunction.¹⁵ Patients who develop postoperative delirium are more likely to develop long-term cognitive dysfunction and have an increased risk of dementia.¹⁶

Another potential source of Ms. A’s agitation is steroid use. Ms. A received IV dexamethasone, 8 to 16 mg/d, around the time of her surgery. Steroids are commonly used to treat brain tumors, particularly when there is vasogenic edema. Steroid psychosis is a term loosely used to describe a wide range of psychiatric symptoms induced by corticosteroids that includes, but is not limited to, depression, mania, psychosis, delirium, and cognitive impairment.¹⁷ Steroid-induced psychiatric adverse effects occur in 5% to 18% of patients receiving corticosteroids and often happen early in treatment, although they can occur at any point.¹⁸ Corticosteroids influence brain activity via glucocorticoid and mineralocorticoid receptors. These receptors are widely distributed throughout the brain and affect neurotransmitter systems, such as the serotonergic system, that are associated with changes in mood, behavior, and cognition.¹⁷ While the adverse psychiatric manifestations of steroid use vary, higher dosages are associated with an increased risk of psychiatric complications; mania is more prevalent early in the course of treatment, and depression is more common with long-term use.^17,19 Table 3^17,18 outlines the evidence-based treatment of corticosteroid-induced adverse psychiatric effects.

Although there are no clinical guidelines or FDA-approved medications for treating steroid-induced psychiatric adverse events, these are best managed by tapering and discontinuing steroids when possible and simultaneously using psychotropic medications to treat psychiatric symptoms. Case reports and limited evidence-based literature have demonstrated that steroid-induced mania responds to mood stabilizers or antipsychotics, while depression can be managed with antidepressants or lithium.¹⁷

Additionally, patients with CNS tumors are at risk for seizures and often are prescribed antiepileptics. Because it is easy to administer and does not need to be titrated, levetiracetam is a commonly used agent. However, levetiracetam can cause psychiatric adverse effects, including behavior changes and frank psychosis.²⁰

Continue to: Finally, Ms. A's altered mental status...

Finally, Ms. A’s altered mental status could have been related to opioid intoxication. Opioids are used to manage post­surgical pain, and studies have shown these medications can be a precipitating factor for delirium in geriatric patients.²¹

TREATMENT Medication adjustments

At the request of the psychiatry team, levetiracetam is discontinued due to its potential for psychiatric adverse effects. The neurosurgery team replaces it with valproic acid, 500 mg every 12 hours. Ms. A is also tapered off steroids fairly rapidly because of the potential for steroid-induced psychiatric adverse effects. Her quetiapine is titrated from 50 to 150 mg every night at bedtime, and duloxetine is discontinued.

OUTCOME Agitation improves dramatically

Ms. A’s new medication regimen dramatically improves her agitation, which allows Ms. A, her family, and the medical team to work together to establish treatment goals. Ms. A ultimately returns home with the assistance of her family. She continues to have memory issues, but with improved emotion regulation. Several months later, Ms. A is readmitted to the hospital because her cancer has progressed despite treatment.

Bottom Line

Brain tumors may present with various psychiatric manifestations that can change during the course of the patient’s treatment. A comprehensive psychiatric evaluation should parse out the interplay between direct effects of the tumor and any adverse effects that are the result of medical and/or surgical interventions to determine the cause of psychiatric symptoms and their appropriate management.

Related Resource

Madhusoodanan S, Ting MB, Farah T, et al. Psychiatric aspects of brain tumors: a review. World J Psychiatry. 2015;5(3):273-285.

Drug Brand Names

Aripiprazole • Abilify
Buspirone • Buspar
Chlorpromazine • Thorazine
Codeine • Codeine systemic
Dexamethasone • Decadron
Duloxetine • Cymbalta
Haloperidol • Haldol
Levetiracetam • Keppra
Lorazepam • Ativan
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Quetiapine • Seroquel
Risperidone • Risperdal
Sertraline • Zoloft
Valproic acid • Depakene

CASE Suicidal behavior, severe headaches

Ms. A, age 60, presents to the emergency department (ED) with depression, suicidal behavior, and 3 days of severe headaches. Neurology is consulted and an MRI is ordered, which shows a 3.0-cm mass lesion in the left temporal lobe with associated vasogenic edema that is suspicious for metastatic disease (Figure).

Ms. A is admitted to the hospital for further workup of her brain lesion. She is started on IV dexamethasone, 10 mg every 6 hours, a glucocorticosteroid, for brain edema, and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

Upon admission, in addition to oncology and neurosurgery, psychiatry is also consulted to evaluate Ms. A for depression and suicidality.

EVALUATION Mood changes and poor judgment

Ms. A has a psychiatric history of depression and alcohol use disorder but says she has not consumed any alcohol in years. Her medical history includes hypertension, diabetes, and stage 4 non-small–cell lung cancer, for which she received surgery and adjuvant chemoradio­therapy 1 year ago.

On initial intake, Ms. A reports that in addition to the headaches, she has also been experiencing worsening depression and suicidal behavior. For the past 2 months, she has had a severely depressed mood, with notable anhedonia, poor appetite, insomnia, low energy, and decreased concentration. The changes in her mental health were triggered by her mother’s death. Three days prior to admission, the patient planned to overdose on anti­hypertensive pills, but her suicide attempt was interrupted when her family called. She denies any current suicidal ideation, intent, or plan.

According to her family, Ms. A has been increasingly irritable and her personality has changed in the past month. She also has been repeatedly sorting through her neighbors’ garbage.

Ms. A’s current psychiatric medications are duloxetine, 30 mg/d; quetiapine, 50 mg every night at bedtime; and buspirone, 10 mg/d. However, it is unclear if she is consistently taking these medications.

Continue to: On mental status examination...

On mental status examination, Ms. A is calm and she has no abnormal movements. She says she is depressed. Her affect is reactive and labile. She is alert and oriented to person, place, and time. Her attention, registration, and recall are intact. Her executive function is not tested. However, Ms. A’s insight and judgment seem poor.

To address Ms. A’s worsening depression, the psychiatry team increases her duloxetine from 30 to 60 mg/d, and she continues quetiapine, 50 mg every night at bedtime, for mood lability. Buspirone is not continued because she was not taking a therapeutic dosage in the community.

Within 4 days, Ms. A shows improvement in sleep, appetite, and mood. She has no further suicidal ideation.

[polldaddy:10511743]

The authors’ observations

Ms. A had a recurrence of what was presumed to be major depressive disorder (MDD) in the context of her mother’s death. However, she also exhibited irritability, mood lability, and impulsivity, all of which could be part of her depression, or a separate problem related to her brain tumor. Because Ms. A had never displayed bizarre behavior before the past few weeks, it is likely that her CNS lesion was directly affecting her personality and possibly underlying her planned suicide attempt.

Fifty to 80% of patients with CNS tumors, either primary or metastatic, present with psychiatric symptoms.¹ Table 1^1-3 lists common psychiatric symptoms of brain tumors. Unfortunately, there is little reliable evidence that directly correlates tumor location with specific psychiatric symptoms. A 2010 meta-analysis found a statistically significant link between anorexia nervosa and hypothalamic tumors.¹ However, for other brain regions, there is only an increased likelihood that any given tumor location will produce psychiatric symptoms.^1,4 For instance, compared to patients with tumors in other locations, those with temporal lobe tumors are more likely to present with mood disorders, personality changes, and memory problems.¹ In contrast, patients with frontal lobe tumors have an increased likelihood of psychosis, mood disorders, and personality changes.¹ Patients with tumors in the pituitary region often present with anxiety.¹

Continue to: When considering treatment options...

When considering treatment options for Ms. A, alcohol withdrawal was unlikely given the remote history of alcohol use, low alcohol blood level, and lack of evidence of unstable vital signs or tremor. Although she might have benefited from inpatient psychiatric treatment, this needed to wait until there was a definitive treatment plan for her brain tumor. Finally, although a paraneoplastic syndrome, such as limbic encephalitis, could be causing her psychiatric symptoms, this scenario is less likely with non-small–cell lung cancer.

Although uncommon, CNS tumors can present with psychiatric symptoms as the only manifestation. This is more likely when a patient exhibits new-onset or atypical symptoms, or fails to respond to standard psychiatric treatment.⁴ Case reports have described patients with brain tumors being misdiagnosed as having a primary psychiatric condition, which delays treatment of their CNS cancer.² Additionally, frontal and limbic tumors are more likely to present with psychiatric manifestations; up to 90% of patients exhibit altered mental status or personality changes, as did Ms. A.^1,4 Clearly, it is easier to identify patients with psychiatric symptoms resulting from a brain tumor when they also present with focal neurologic deficits or systemic symptoms, such as headache or nausea and vomiting. Ms. A presented with severe headaches, which is what led to her early imaging and prompt diagnosis.

Numerous proposed mechanisms might account for the psychiatric symptoms that occur during the course of a brain tumor, including direct injury to neuronal cells, secretion of hormones or other tumor-derived substances, and peri-ictal phenomena.³

TREATMENT Tumor is removed, but memory is impaired

Ms. A is scheduled for craniotomy and surgical resection of the frontal mass. Prior to surgery, Ms. A shows interest in improving her health, cooperates with staff, and seeks her daughter’s input on treatment. One week after admission, Ms. A has her mass resected, which is confirmed on biopsy to be a lung metastasis. Post-surgery, Ms. A receives codeine, 30 mg every 6 hours as needed, for pain; she continues dexamethasone, 4 mg IV every 6 hours, for brain edema and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

On Day 2 after surgery, Ms. A attempts to elope. When she is approached by a psychiatrist on the treatment team, she does not recognize him. Although her long-term memory seems intact, she is unable to remember the details of recent events, including her medical and surgical treatments.

[polldaddy:10511745]

Continue to: The authors' observations

 

 

The authors’ observations

Ms. A’s memory impairment may be secondary to a surgically acquired neurocognitive deficit. In the United States, brain metastases represent a significant public health issue, affecting >100,000 patients per year.⁵ Metastatic lesions are the most common brain tumors. Lung cancer, breast cancer, and melanoma are the leading solid tumors to spread to the CNS.⁵ In cases of single brain metastasis, similar to Ms. A’s solitary left temporal lobe lesion, surgical resection plays a critical role in treatment. It provides histological confirmation of metastatic disease and can relieve mass effect if present. Studies have shown that combined surgical resection with radiation improves survival relative to patients who undergo radiation therapy alone.^6,7

However, the benefits of surgical resection need to be balanced with preservation of neurologic function. Emerging evidence suggests that a majority of patients have surgically-acquired cognitive deficits due to damage of normal surrounding tissues, and these deficits are associated with reduced quality of life.^8,9 Further, a study examining glioma surgical resections found that patients with left temporal lobe tumors exhibit more frequent and severe neurocognitive decline than patients with right temporal lobe tumors, especially in domains such as verbal memory.⁸ Ms. A’s memory impairment was persistent during her postoperative course, which suggests that it was not just an immediate post-surgical phenomenon, but a longer-lasting cognitive change directly related to the resection.

It is also possible that Ms. A had a prior neurocognitive disorder that manifested to a greater degree as a result of the CNS tumor. Ms. A might have had early-onset Alzheimer’s disease, although her intact memory before surgery makes this less likely. Alternatively, she could have had vascular dementia, especially given her long-standing hypertension and diabetes. This might have been missed in the initial evaluation because executive function was not tested. However, the relatively abrupt onset of memory problems after surgery suggests that she had no underlying neurocognitive disorder.

Ms. A’s presumed episode of MDD might also explain her memory changes. Major depressive disorder is increasingly common among geriatric patients, affecting approximately 5% of community-dwelling older adults.¹⁰ Its incidence increases with medical comorbidities, as suggested by depression rates of 5% to 10% in the primary care setting vs 37% in patients after critical-care hospitalizations.¹⁰ Late-life depression (LLD) occurs in adults age ≥60. Unlike depression in younger patients, LLD is more likely to be associated with cognitive impairment, specifically impairment of executive function and memory.¹¹ The incidence of cognitive impairment in LLD is higher in patients with a history of depression, such as Ms. A.^11,12 However, in general, patients who are depressed have memory complaints out of proportion to the clinical findings, and they show poor effort on cognitive testing. Ms. A exhibited neither of these, which makes it less likely that LLD was the exclusive cause of her memory loss.¹³ Table 2¹⁴ outlines the management of cognitive deficits in a patient with a brain tumor.

EVALUATION Increasingly agitated and paranoid

After the tumor resection, Ms. A becomes increasingly irritable, uncooperative, and agitated. She repeatedly demands to be discharged. She insists she is fine and refuses medications and further laboratory workup. She becomes paranoid about the nursing staff and believes they are trying to kill her.

Continue to: On psychiatric re-evaluation...

On psychiatric re-evaluation, Ms. A demonstrates pressured speech, perseveration about going home, paranoid delusions, and anger at her family and physicians.

[polldaddy:10511747]

The authors’ observations

Ms. A’s refusal of medications and agitation may be explained by postoperative delirium, a surgical complication that is increasingly common among geriatric patients and is associated with poor clinical outcomes. Delirium is characterized by an acute onset and fluctuating course of symptoms that include inattention, motoric hypo- or hyperactivity, inappropriate behavior, emotional lability, cognitive dysfunction, and psychotic symptoms.¹⁵ Risk factors that contribute to postoperative delirium include older age, alcohol use, and poor baseline functional and cognitive status.¹⁶ The pathophysiology of delirium is not fully understood, but accumulating evidence suggests that different sets of interacting biologic factors (ie, neuro­transmitters and inflammation) contribute to a disruption of large-scale neuronal networks in the brain, resulting in cognitive dysfunction.¹⁵ Patients who develop postoperative delirium are more likely to develop long-term cognitive dysfunction and have an increased risk of dementia.¹⁶

Another potential source of Ms. A’s agitation is steroid use. Ms. A received IV dexamethasone, 8 to 16 mg/d, around the time of her surgery. Steroids are commonly used to treat brain tumors, particularly when there is vasogenic edema. Steroid psychosis is a term loosely used to describe a wide range of psychiatric symptoms induced by corticosteroids that includes, but is not limited to, depression, mania, psychosis, delirium, and cognitive impairment.¹⁷ Steroid-induced psychiatric adverse effects occur in 5% to 18% of patients receiving corticosteroids and often happen early in treatment, although they can occur at any point.¹⁸ Corticosteroids influence brain activity via glucocorticoid and mineralocorticoid receptors. These receptors are widely distributed throughout the brain and affect neurotransmitter systems, such as the serotonergic system, that are associated with changes in mood, behavior, and cognition.¹⁷ While the adverse psychiatric manifestations of steroid use vary, higher dosages are associated with an increased risk of psychiatric complications; mania is more prevalent early in the course of treatment, and depression is more common with long-term use.^17,19 Table 3^17,18 outlines the evidence-based treatment of corticosteroid-induced adverse psychiatric effects.

Although there are no clinical guidelines or FDA-approved medications for treating steroid-induced psychiatric adverse events, these are best managed by tapering and discontinuing steroids when possible and simultaneously using psychotropic medications to treat psychiatric symptoms. Case reports and limited evidence-based literature have demonstrated that steroid-induced mania responds to mood stabilizers or antipsychotics, while depression can be managed with antidepressants or lithium.¹⁷

Additionally, patients with CNS tumors are at risk for seizures and often are prescribed antiepileptics. Because it is easy to administer and does not need to be titrated, levetiracetam is a commonly used agent. However, levetiracetam can cause psychiatric adverse effects, including behavior changes and frank psychosis.²⁰

Continue to: Finally, Ms. A's altered mental status...

Finally, Ms. A’s altered mental status could have been related to opioid intoxication. Opioids are used to manage post­surgical pain, and studies have shown these medications can be a precipitating factor for delirium in geriatric patients.²¹

TREATMENT Medication adjustments

At the request of the psychiatry team, levetiracetam is discontinued due to its potential for psychiatric adverse effects. The neurosurgery team replaces it with valproic acid, 500 mg every 12 hours. Ms. A is also tapered off steroids fairly rapidly because of the potential for steroid-induced psychiatric adverse effects. Her quetiapine is titrated from 50 to 150 mg every night at bedtime, and duloxetine is discontinued.

OUTCOME Agitation improves dramatically

Ms. A’s new medication regimen dramatically improves her agitation, which allows Ms. A, her family, and the medical team to work together to establish treatment goals. Ms. A ultimately returns home with the assistance of her family. She continues to have memory issues, but with improved emotion regulation. Several months later, Ms. A is readmitted to the hospital because her cancer has progressed despite treatment.

Bottom Line

Brain tumors may present with various psychiatric manifestations that can change during the course of the patient’s treatment. A comprehensive psychiatric evaluation should parse out the interplay between direct effects of the tumor and any adverse effects that are the result of medical and/or surgical interventions to determine the cause of psychiatric symptoms and their appropriate management.

Related Resource

Madhusoodanan S, Ting MB, Farah T, et al. Psychiatric aspects of brain tumors: a review. World J Psychiatry. 2015;5(3):273-285.

Drug Brand Names

Aripiprazole • Abilify
Buspirone • Buspar
Chlorpromazine • Thorazine
Codeine • Codeine systemic
Dexamethasone • Decadron
Duloxetine • Cymbalta
Haloperidol • Haldol
Levetiracetam • Keppra
Lorazepam • Ativan
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Quetiapine • Seroquel
Risperidone • Risperdal
Sertraline • Zoloft
Valproic acid • Depakene

CASE Suicidal behavior, severe headaches

Ms. A, age 60, presents to the emergency department (ED) with depression, suicidal behavior, and 3 days of severe headaches. Neurology is consulted and an MRI is ordered, which shows a 3.0-cm mass lesion in the left temporal lobe with associated vasogenic edema that is suspicious for metastatic disease (Figure).

Ms. A is admitted to the hospital for further workup of her brain lesion. She is started on IV dexamethasone, 10 mg every 6 hours, a glucocorticosteroid, for brain edema, and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

Upon admission, in addition to oncology and neurosurgery, psychiatry is also consulted to evaluate Ms. A for depression and suicidality.

EVALUATION Mood changes and poor judgment

Ms. A has a psychiatric history of depression and alcohol use disorder but says she has not consumed any alcohol in years. Her medical history includes hypertension, diabetes, and stage 4 non-small–cell lung cancer, for which she received surgery and adjuvant chemoradio­therapy 1 year ago.

On initial intake, Ms. A reports that in addition to the headaches, she has also been experiencing worsening depression and suicidal behavior. For the past 2 months, she has had a severely depressed mood, with notable anhedonia, poor appetite, insomnia, low energy, and decreased concentration. The changes in her mental health were triggered by her mother’s death. Three days prior to admission, the patient planned to overdose on anti­hypertensive pills, but her suicide attempt was interrupted when her family called. She denies any current suicidal ideation, intent, or plan.

According to her family, Ms. A has been increasingly irritable and her personality has changed in the past month. She also has been repeatedly sorting through her neighbors’ garbage.

Ms. A’s current psychiatric medications are duloxetine, 30 mg/d; quetiapine, 50 mg every night at bedtime; and buspirone, 10 mg/d. However, it is unclear if she is consistently taking these medications.

Continue to: On mental status examination...

On mental status examination, Ms. A is calm and she has no abnormal movements. She says she is depressed. Her affect is reactive and labile. She is alert and oriented to person, place, and time. Her attention, registration, and recall are intact. Her executive function is not tested. However, Ms. A’s insight and judgment seem poor.

To address Ms. A’s worsening depression, the psychiatry team increases her duloxetine from 30 to 60 mg/d, and she continues quetiapine, 50 mg every night at bedtime, for mood lability. Buspirone is not continued because she was not taking a therapeutic dosage in the community.

Within 4 days, Ms. A shows improvement in sleep, appetite, and mood. She has no further suicidal ideation.

[polldaddy:10511743]

The authors’ observations

Ms. A had a recurrence of what was presumed to be major depressive disorder (MDD) in the context of her mother’s death. However, she also exhibited irritability, mood lability, and impulsivity, all of which could be part of her depression, or a separate problem related to her brain tumor. Because Ms. A had never displayed bizarre behavior before the past few weeks, it is likely that her CNS lesion was directly affecting her personality and possibly underlying her planned suicide attempt.

Fifty to 80% of patients with CNS tumors, either primary or metastatic, present with psychiatric symptoms.¹ Table 1^1-3 lists common psychiatric symptoms of brain tumors. Unfortunately, there is little reliable evidence that directly correlates tumor location with specific psychiatric symptoms. A 2010 meta-analysis found a statistically significant link between anorexia nervosa and hypothalamic tumors.¹ However, for other brain regions, there is only an increased likelihood that any given tumor location will produce psychiatric symptoms.^1,4 For instance, compared to patients with tumors in other locations, those with temporal lobe tumors are more likely to present with mood disorders, personality changes, and memory problems.¹ In contrast, patients with frontal lobe tumors have an increased likelihood of psychosis, mood disorders, and personality changes.¹ Patients with tumors in the pituitary region often present with anxiety.¹

Continue to: When considering treatment options...

When considering treatment options for Ms. A, alcohol withdrawal was unlikely given the remote history of alcohol use, low alcohol blood level, and lack of evidence of unstable vital signs or tremor. Although she might have benefited from inpatient psychiatric treatment, this needed to wait until there was a definitive treatment plan for her brain tumor. Finally, although a paraneoplastic syndrome, such as limbic encephalitis, could be causing her psychiatric symptoms, this scenario is less likely with non-small–cell lung cancer.

Although uncommon, CNS tumors can present with psychiatric symptoms as the only manifestation. This is more likely when a patient exhibits new-onset or atypical symptoms, or fails to respond to standard psychiatric treatment.⁴ Case reports have described patients with brain tumors being misdiagnosed as having a primary psychiatric condition, which delays treatment of their CNS cancer.² Additionally, frontal and limbic tumors are more likely to present with psychiatric manifestations; up to 90% of patients exhibit altered mental status or personality changes, as did Ms. A.^1,4 Clearly, it is easier to identify patients with psychiatric symptoms resulting from a brain tumor when they also present with focal neurologic deficits or systemic symptoms, such as headache or nausea and vomiting. Ms. A presented with severe headaches, which is what led to her early imaging and prompt diagnosis.

Numerous proposed mechanisms might account for the psychiatric symptoms that occur during the course of a brain tumor, including direct injury to neuronal cells, secretion of hormones or other tumor-derived substances, and peri-ictal phenomena.³

TREATMENT Tumor is removed, but memory is impaired

Ms. A is scheduled for craniotomy and surgical resection of the frontal mass. Prior to surgery, Ms. A shows interest in improving her health, cooperates with staff, and seeks her daughter’s input on treatment. One week after admission, Ms. A has her mass resected, which is confirmed on biopsy to be a lung metastasis. Post-surgery, Ms. A receives codeine, 30 mg every 6 hours as needed, for pain; she continues dexamethasone, 4 mg IV every 6 hours, for brain edema and levetiracetam, 500 mg twice a day, for seizure prophylaxis.

On Day 2 after surgery, Ms. A attempts to elope. When she is approached by a psychiatrist on the treatment team, she does not recognize him. Although her long-term memory seems intact, she is unable to remember the details of recent events, including her medical and surgical treatments.

[polldaddy:10511745]

Continue to: The authors' observations

 

 

The authors’ observations

Ms. A’s memory impairment may be secondary to a surgically acquired neurocognitive deficit. In the United States, brain metastases represent a significant public health issue, affecting >100,000 patients per year.⁵ Metastatic lesions are the most common brain tumors. Lung cancer, breast cancer, and melanoma are the leading solid tumors to spread to the CNS.⁵ In cases of single brain metastasis, similar to Ms. A’s solitary left temporal lobe lesion, surgical resection plays a critical role in treatment. It provides histological confirmation of metastatic disease and can relieve mass effect if present. Studies have shown that combined surgical resection with radiation improves survival relative to patients who undergo radiation therapy alone.^6,7

However, the benefits of surgical resection need to be balanced with preservation of neurologic function. Emerging evidence suggests that a majority of patients have surgically-acquired cognitive deficits due to damage of normal surrounding tissues, and these deficits are associated with reduced quality of life.^8,9 Further, a study examining glioma surgical resections found that patients with left temporal lobe tumors exhibit more frequent and severe neurocognitive decline than patients with right temporal lobe tumors, especially in domains such as verbal memory.⁸ Ms. A’s memory impairment was persistent during her postoperative course, which suggests that it was not just an immediate post-surgical phenomenon, but a longer-lasting cognitive change directly related to the resection.

It is also possible that Ms. A had a prior neurocognitive disorder that manifested to a greater degree as a result of the CNS tumor. Ms. A might have had early-onset Alzheimer’s disease, although her intact memory before surgery makes this less likely. Alternatively, she could have had vascular dementia, especially given her long-standing hypertension and diabetes. This might have been missed in the initial evaluation because executive function was not tested. However, the relatively abrupt onset of memory problems after surgery suggests that she had no underlying neurocognitive disorder.

Ms. A’s presumed episode of MDD might also explain her memory changes. Major depressive disorder is increasingly common among geriatric patients, affecting approximately 5% of community-dwelling older adults.¹⁰ Its incidence increases with medical comorbidities, as suggested by depression rates of 5% to 10% in the primary care setting vs 37% in patients after critical-care hospitalizations.¹⁰ Late-life depression (LLD) occurs in adults age ≥60. Unlike depression in younger patients, LLD is more likely to be associated with cognitive impairment, specifically impairment of executive function and memory.¹¹ The incidence of cognitive impairment in LLD is higher in patients with a history of depression, such as Ms. A.^11,12 However, in general, patients who are depressed have memory complaints out of proportion to the clinical findings, and they show poor effort on cognitive testing. Ms. A exhibited neither of these, which makes it less likely that LLD was the exclusive cause of her memory loss.¹³ Table 2¹⁴ outlines the management of cognitive deficits in a patient with a brain tumor.

EVALUATION Increasingly agitated and paranoid

After the tumor resection, Ms. A becomes increasingly irritable, uncooperative, and agitated. She repeatedly demands to be discharged. She insists she is fine and refuses medications and further laboratory workup. She becomes paranoid about the nursing staff and believes they are trying to kill her.

Continue to: On psychiatric re-evaluation...

On psychiatric re-evaluation, Ms. A demonstrates pressured speech, perseveration about going home, paranoid delusions, and anger at her family and physicians.

[polldaddy:10511747]

The authors’ observations

Ms. A’s refusal of medications and agitation may be explained by postoperative delirium, a surgical complication that is increasingly common among geriatric patients and is associated with poor clinical outcomes. Delirium is characterized by an acute onset and fluctuating course of symptoms that include inattention, motoric hypo- or hyperactivity, inappropriate behavior, emotional lability, cognitive dysfunction, and psychotic symptoms.¹⁵ Risk factors that contribute to postoperative delirium include older age, alcohol use, and poor baseline functional and cognitive status.¹⁶ The pathophysiology of delirium is not fully understood, but accumulating evidence suggests that different sets of interacting biologic factors (ie, neuro­transmitters and inflammation) contribute to a disruption of large-scale neuronal networks in the brain, resulting in cognitive dysfunction.¹⁵ Patients who develop postoperative delirium are more likely to develop long-term cognitive dysfunction and have an increased risk of dementia.¹⁶

Another potential source of Ms. A’s agitation is steroid use. Ms. A received IV dexamethasone, 8 to 16 mg/d, around the time of her surgery. Steroids are commonly used to treat brain tumors, particularly when there is vasogenic edema. Steroid psychosis is a term loosely used to describe a wide range of psychiatric symptoms induced by corticosteroids that includes, but is not limited to, depression, mania, psychosis, delirium, and cognitive impairment.¹⁷ Steroid-induced psychiatric adverse effects occur in 5% to 18% of patients receiving corticosteroids and often happen early in treatment, although they can occur at any point.¹⁸ Corticosteroids influence brain activity via glucocorticoid and mineralocorticoid receptors. These receptors are widely distributed throughout the brain and affect neurotransmitter systems, such as the serotonergic system, that are associated with changes in mood, behavior, and cognition.¹⁷ While the adverse psychiatric manifestations of steroid use vary, higher dosages are associated with an increased risk of psychiatric complications; mania is more prevalent early in the course of treatment, and depression is more common with long-term use.^17,19 Table 3^17,18 outlines the evidence-based treatment of corticosteroid-induced adverse psychiatric effects.

Although there are no clinical guidelines or FDA-approved medications for treating steroid-induced psychiatric adverse events, these are best managed by tapering and discontinuing steroids when possible and simultaneously using psychotropic medications to treat psychiatric symptoms. Case reports and limited evidence-based literature have demonstrated that steroid-induced mania responds to mood stabilizers or antipsychotics, while depression can be managed with antidepressants or lithium.¹⁷

Additionally, patients with CNS tumors are at risk for seizures and often are prescribed antiepileptics. Because it is easy to administer and does not need to be titrated, levetiracetam is a commonly used agent. However, levetiracetam can cause psychiatric adverse effects, including behavior changes and frank psychosis.²⁰

Continue to: Finally, Ms. A's altered mental status...

Finally, Ms. A’s altered mental status could have been related to opioid intoxication. Opioids are used to manage post­surgical pain, and studies have shown these medications can be a precipitating factor for delirium in geriatric patients.²¹

TREATMENT Medication adjustments

At the request of the psychiatry team, levetiracetam is discontinued due to its potential for psychiatric adverse effects. The neurosurgery team replaces it with valproic acid, 500 mg every 12 hours. Ms. A is also tapered off steroids fairly rapidly because of the potential for steroid-induced psychiatric adverse effects. Her quetiapine is titrated from 50 to 150 mg every night at bedtime, and duloxetine is discontinued.

OUTCOME Agitation improves dramatically

Ms. A’s new medication regimen dramatically improves her agitation, which allows Ms. A, her family, and the medical team to work together to establish treatment goals. Ms. A ultimately returns home with the assistance of her family. She continues to have memory issues, but with improved emotion regulation. Several months later, Ms. A is readmitted to the hospital because her cancer has progressed despite treatment.

Bottom Line

Brain tumors may present with various psychiatric manifestations that can change during the course of the patient’s treatment. A comprehensive psychiatric evaluation should parse out the interplay between direct effects of the tumor and any adverse effects that are the result of medical and/or surgical interventions to determine the cause of psychiatric symptoms and their appropriate management.

Related Resource

Madhusoodanan S, Ting MB, Farah T, et al. Psychiatric aspects of brain tumors: a review. World J Psychiatry. 2015;5(3):273-285.

Drug Brand Names

Aripiprazole • Abilify
Buspirone • Buspar
Chlorpromazine • Thorazine
Codeine • Codeine systemic
Dexamethasone • Decadron
Duloxetine • Cymbalta
Haloperidol • Haldol
Levetiracetam • Keppra
Lorazepam • Ativan
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Quetiapine • Seroquel
Risperidone • Risperdal
Sertraline • Zoloft
Valproic acid • Depakene

Nearly 3.5 million adherents to the religion of Islam (Muslims) live in the United States, and this number is projected to more than double to 8.1 million by 2050.¹ As of 2017, an estimated 58% of American Muslims were immigrants, but nearly 25% were born in the United States to parents who also were US-born, including many African American Muslims.¹ American Muslims face a rise of Islamophobia, hate crimes, and discrimination at school, work, and the communities in which they live.² This population may experience feelings of anger as well as rejection and abandonment by the country they call home. They may also wrestle with conforming to American social norms while maintaining their Muslim identity.

When providing psychiatric care to American Muslim patients, clinicians need to understand these patients’ specific stressors. American Muslim patients may experience a variety of mental health conditions, including posttraumatic stress disorder, major depressive disorder, generalized anxiety disorder, panic attacks, adjustment disorder, and somatization.² Unfortunately, American Muslims may be less likely to seek psychiatric help because the stigma of mental illness remains a barrier to care in this community.³ In addition, entrenched cultural beliefs about mental illness may discourage many from seeking treatment. Because of a paucity of data on the psychiatric care of American Muslim patients, there is a great need to understand how to treat this vulnerable, often marginalized population.

Suggestions for improving care

Based on my clinical experience, I recommend the following practices for clinicians to consider when caring for American Muslim patients:

• Ensure that your assessment accounts for religious and cultural factors to help understand your patient’s perception of his/her illness.⁴ Consider using the DSM-IV Outline for Culture Formulation,⁵ DSM-5 Cultural Formulation Interview,⁶ or the American Academy of Child and Adolescent Psychiatry Practice Parameter for Cultural Competence in Child and Adolescent Psychiatric Practice.⁷
• Be sensitive to your patient’s family hierarchy and history. Often, extended family members will accompany an American Muslim patient for input and support during a clinical visit.
• Provide appropriate psychoeducation, because some patients may shun medication, especially those who think that medication should be reserved for severe illness that requires long-term inpatient stays.
• Listen for somatic symptoms that may mask distress.⁸
• Be mindful of your patient’s preferences regarding gender roles. For example, a female patient may prefer to receive care from a female clinician.
• Align therapy with your patient’s religious and cultural beliefs. Some research shows that for Muslim patients, modified short-term psychodynamic therapy fares better than classic long-term psychoanalysis.⁹ Therapy should focus on family dynamics, conflicts, and relationships.⁹
• Consider employing cognitive-behavioral therapy, solution-focused therapy, modeling, and behavioral techniques such as behavioral modification, systemic desensitization, and flooding because these may be effective for Muslim patients.^9,10
• Suggest guided imagery and relaxation techniques because some Muslim patients may find that these could be a natural extension of prayer and meditation.⁹
• Work with local Imams (Muslim spiritual leaders) to recognize mental illness, overcome stigma in the community, dispel misinformation, and refer patients.¹¹
• If the patient has a “traditional healer,” such as a Sheikh or Imam, understand the extent of this individual’s involvement. Some healers may tell patients that mental illness is a problem of faith or being possessed by a spirit (ie, “jinn” or Satan-like spirits).
• Use an interpreter if English is not the patient’s primary language.
• Respect the patient’s religious practices. When possible, offer alternative treatments to medication formulations that include pork (most gelatins). Also, patients may want to adjust their medication schedule during Ramadan, when many Muslims fast from dawn to dusk.

Future goals: Increasing access, reducing stigma

More research on the mental health needs of American Muslim patients is needed, especially as discrimination and hate crimes against this population continue to rise. Clinicians should tailor their assessments and recommended treatments to these patients’ preferences, and address how religious and cultural connectedness may impact their patient’s mental health. Increasing access to services and reducing stigma associated with mental health care are critical for improving outcomes among Muslim patients.

Nearly 3.5 million adherents to the religion of Islam (Muslims) live in the United States, and this number is projected to more than double to 8.1 million by 2050.¹ As of 2017, an estimated 58% of American Muslims were immigrants, but nearly 25% were born in the United States to parents who also were US-born, including many African American Muslims.¹ American Muslims face a rise of Islamophobia, hate crimes, and discrimination at school, work, and the communities in which they live.² This population may experience feelings of anger as well as rejection and abandonment by the country they call home. They may also wrestle with conforming to American social norms while maintaining their Muslim identity.

When providing psychiatric care to American Muslim patients, clinicians need to understand these patients’ specific stressors. American Muslim patients may experience a variety of mental health conditions, including posttraumatic stress disorder, major depressive disorder, generalized anxiety disorder, panic attacks, adjustment disorder, and somatization.² Unfortunately, American Muslims may be less likely to seek psychiatric help because the stigma of mental illness remains a barrier to care in this community.³ In addition, entrenched cultural beliefs about mental illness may discourage many from seeking treatment. Because of a paucity of data on the psychiatric care of American Muslim patients, there is a great need to understand how to treat this vulnerable, often marginalized population.

Suggestions for improving care

Based on my clinical experience, I recommend the following practices for clinicians to consider when caring for American Muslim patients:

• Ensure that your assessment accounts for religious and cultural factors to help understand your patient’s perception of his/her illness.⁴ Consider using the DSM-IV Outline for Culture Formulation,⁵ DSM-5 Cultural Formulation Interview,⁶ or the American Academy of Child and Adolescent Psychiatry Practice Parameter for Cultural Competence in Child and Adolescent Psychiatric Practice.⁷
• Be sensitive to your patient’s family hierarchy and history. Often, extended family members will accompany an American Muslim patient for input and support during a clinical visit.
• Provide appropriate psychoeducation, because some patients may shun medication, especially those who think that medication should be reserved for severe illness that requires long-term inpatient stays.
• Listen for somatic symptoms that may mask distress.⁸
• Be mindful of your patient’s preferences regarding gender roles. For example, a female patient may prefer to receive care from a female clinician.
• Align therapy with your patient’s religious and cultural beliefs. Some research shows that for Muslim patients, modified short-term psychodynamic therapy fares better than classic long-term psychoanalysis.⁹ Therapy should focus on family dynamics, conflicts, and relationships.⁹
• Consider employing cognitive-behavioral therapy, solution-focused therapy, modeling, and behavioral techniques such as behavioral modification, systemic desensitization, and flooding because these may be effective for Muslim patients.^9,10
• Suggest guided imagery and relaxation techniques because some Muslim patients may find that these could be a natural extension of prayer and meditation.⁹
• Work with local Imams (Muslim spiritual leaders) to recognize mental illness, overcome stigma in the community, dispel misinformation, and refer patients.¹¹
• If the patient has a “traditional healer,” such as a Sheikh or Imam, understand the extent of this individual’s involvement. Some healers may tell patients that mental illness is a problem of faith or being possessed by a spirit (ie, “jinn” or Satan-like spirits).
• Use an interpreter if English is not the patient’s primary language.
• Respect the patient’s religious practices. When possible, offer alternative treatments to medication formulations that include pork (most gelatins). Also, patients may want to adjust their medication schedule during Ramadan, when many Muslims fast from dawn to dusk.

Future goals: Increasing access, reducing stigma

More research on the mental health needs of American Muslim patients is needed, especially as discrimination and hate crimes against this population continue to rise. Clinicians should tailor their assessments and recommended treatments to these patients’ preferences, and address how religious and cultural connectedness may impact their patient’s mental health. Increasing access to services and reducing stigma associated with mental health care are critical for improving outcomes among Muslim patients.

Nearly 3.5 million adherents to the religion of Islam (Muslims) live in the United States, and this number is projected to more than double to 8.1 million by 2050.¹ As of 2017, an estimated 58% of American Muslims were immigrants, but nearly 25% were born in the United States to parents who also were US-born, including many African American Muslims.¹ American Muslims face a rise of Islamophobia, hate crimes, and discrimination at school, work, and the communities in which they live.² This population may experience feelings of anger as well as rejection and abandonment by the country they call home. They may also wrestle with conforming to American social norms while maintaining their Muslim identity.

When providing psychiatric care to American Muslim patients, clinicians need to understand these patients’ specific stressors. American Muslim patients may experience a variety of mental health conditions, including posttraumatic stress disorder, major depressive disorder, generalized anxiety disorder, panic attacks, adjustment disorder, and somatization.² Unfortunately, American Muslims may be less likely to seek psychiatric help because the stigma of mental illness remains a barrier to care in this community.³ In addition, entrenched cultural beliefs about mental illness may discourage many from seeking treatment. Because of a paucity of data on the psychiatric care of American Muslim patients, there is a great need to understand how to treat this vulnerable, often marginalized population.

Suggestions for improving care

Based on my clinical experience, I recommend the following practices for clinicians to consider when caring for American Muslim patients:

• Ensure that your assessment accounts for religious and cultural factors to help understand your patient’s perception of his/her illness.⁴ Consider using the DSM-IV Outline for Culture Formulation,⁵ DSM-5 Cultural Formulation Interview,⁶ or the American Academy of Child and Adolescent Psychiatry Practice Parameter for Cultural Competence in Child and Adolescent Psychiatric Practice.⁷
• Be sensitive to your patient’s family hierarchy and history. Often, extended family members will accompany an American Muslim patient for input and support during a clinical visit.
• Provide appropriate psychoeducation, because some patients may shun medication, especially those who think that medication should be reserved for severe illness that requires long-term inpatient stays.
• Listen for somatic symptoms that may mask distress.⁸
• Be mindful of your patient’s preferences regarding gender roles. For example, a female patient may prefer to receive care from a female clinician.
• Align therapy with your patient’s religious and cultural beliefs. Some research shows that for Muslim patients, modified short-term psychodynamic therapy fares better than classic long-term psychoanalysis.⁹ Therapy should focus on family dynamics, conflicts, and relationships.⁹
• Consider employing cognitive-behavioral therapy, solution-focused therapy, modeling, and behavioral techniques such as behavioral modification, systemic desensitization, and flooding because these may be effective for Muslim patients.^9,10
• Suggest guided imagery and relaxation techniques because some Muslim patients may find that these could be a natural extension of prayer and meditation.⁹
• Work with local Imams (Muslim spiritual leaders) to recognize mental illness, overcome stigma in the community, dispel misinformation, and refer patients.¹¹
• If the patient has a “traditional healer,” such as a Sheikh or Imam, understand the extent of this individual’s involvement. Some healers may tell patients that mental illness is a problem of faith or being possessed by a spirit (ie, “jinn” or Satan-like spirits).
• Use an interpreter if English is not the patient’s primary language.
• Respect the patient’s religious practices. When possible, offer alternative treatments to medication formulations that include pork (most gelatins). Also, patients may want to adjust their medication schedule during Ramadan, when many Muslims fast from dawn to dusk.

Future goals: Increasing access, reducing stigma

More research on the mental health needs of American Muslim patients is needed, especially as discrimination and hate crimes against this population continue to rise. Clinicians should tailor their assessments and recommended treatments to these patients’ preferences, and address how religious and cultural connectedness may impact their patient’s mental health. Increasing access to services and reducing stigma associated with mental health care are critical for improving outcomes among Muslim patients.

As clinicians, we increasingly communicate with each other via social media platforms to network, collaborate on research, find professional and personal support, refer patients, or hold academic conversations.^1,2 Although it is convenient, this form of online communication directly and indirectly breaks down barriers between our professional and personal lives, which can make it challenging to avoid behavior that could negatively affect one’s professional image.²

Although some medical organizations have offered guidelines on health care professionals’ use of social media,^2,3 these are subjective and not evidence-based. Here I offer some suggestions for appropriately interacting with your colleagues (ie, individuals who are not your personal friends) on social media.

Think before you post. Consider the potential professional ramifications of what you are about to post, and don’t post anything that may have adverse consequences on your image or that of psychiatry as a whole.

Don’t post derogatory or defamatory statements about colleagues. Such actions may violate professional codes of conduct. Disagreeing with colleagues on social media is common, but your posts should be respectful, friendly, and reflect positively on the profession.² Avoid making negative statements—even in jest—about your colleagues’ skills or professional experience, because such communication is not appropriate for public dissemination.²

If you notice colleagues posting unprofessional content that could negatively affect their careers or the public’s trust in psychiatry, tactfully express your concerns to them, and suggest that they take appropriate measures to rectify the situation.² Be aware of your state’s laws and regulations about mandated reporting if you discover a colleague’s online content violates the scope of clinical practice or ethical standards.¹ If the content is in violation of the law or medical board regulations, you may have a legal obligation to report that colleague to law enforcement, the licensing board, and/or his/her employer.^1,2

Avoid online snooping into the personal lives of colleagues. Respect their privacy when viewing their posts about personal activities that are not germane to their professional services.¹ If you find videos, images, or messages that reveal private, confidential, or sensitive information about a colleague, do not distribute that information without the colleague’s consent.¹

Be careful when accepting friend requests. Conflicts could arise if you accept friend requests from some but not all of your colleagues; this could be interpreted as favoritism and potentially create problematic work relationships.² Be consistent in accepting or rejecting colleagues’ friend requests. Consider using an employment-oriented social media platform to connect with colleagues outside of the workplace.²

As clinicians, we increasingly communicate with each other via social media platforms to network, collaborate on research, find professional and personal support, refer patients, or hold academic conversations.^1,2 Although it is convenient, this form of online communication directly and indirectly breaks down barriers between our professional and personal lives, which can make it challenging to avoid behavior that could negatively affect one’s professional image.²

Although some medical organizations have offered guidelines on health care professionals’ use of social media,^2,3 these are subjective and not evidence-based. Here I offer some suggestions for appropriately interacting with your colleagues (ie, individuals who are not your personal friends) on social media.

Think before you post. Consider the potential professional ramifications of what you are about to post, and don’t post anything that may have adverse consequences on your image or that of psychiatry as a whole.

Don’t post derogatory or defamatory statements about colleagues. Such actions may violate professional codes of conduct. Disagreeing with colleagues on social media is common, but your posts should be respectful, friendly, and reflect positively on the profession.² Avoid making negative statements—even in jest—about your colleagues’ skills or professional experience, because such communication is not appropriate for public dissemination.²

If you notice colleagues posting unprofessional content that could negatively affect their careers or the public’s trust in psychiatry, tactfully express your concerns to them, and suggest that they take appropriate measures to rectify the situation.² Be aware of your state’s laws and regulations about mandated reporting if you discover a colleague’s online content violates the scope of clinical practice or ethical standards.¹ If the content is in violation of the law or medical board regulations, you may have a legal obligation to report that colleague to law enforcement, the licensing board, and/or his/her employer.^1,2

Avoid online snooping into the personal lives of colleagues. Respect their privacy when viewing their posts about personal activities that are not germane to their professional services.¹ If you find videos, images, or messages that reveal private, confidential, or sensitive information about a colleague, do not distribute that information without the colleague’s consent.¹

Be careful when accepting friend requests. Conflicts could arise if you accept friend requests from some but not all of your colleagues; this could be interpreted as favoritism and potentially create problematic work relationships.² Be consistent in accepting or rejecting colleagues’ friend requests. Consider using an employment-oriented social media platform to connect with colleagues outside of the workplace.²

As clinicians, we increasingly communicate with each other via social media platforms to network, collaborate on research, find professional and personal support, refer patients, or hold academic conversations.^1,2 Although it is convenient, this form of online communication directly and indirectly breaks down barriers between our professional and personal lives, which can make it challenging to avoid behavior that could negatively affect one’s professional image.²

Although some medical organizations have offered guidelines on health care professionals’ use of social media,^2,3 these are subjective and not evidence-based. Here I offer some suggestions for appropriately interacting with your colleagues (ie, individuals who are not your personal friends) on social media.

Think before you post. Consider the potential professional ramifications of what you are about to post, and don’t post anything that may have adverse consequences on your image or that of psychiatry as a whole.

Don’t post derogatory or defamatory statements about colleagues. Such actions may violate professional codes of conduct. Disagreeing with colleagues on social media is common, but your posts should be respectful, friendly, and reflect positively on the profession.² Avoid making negative statements—even in jest—about your colleagues’ skills or professional experience, because such communication is not appropriate for public dissemination.²

If you notice colleagues posting unprofessional content that could negatively affect their careers or the public’s trust in psychiatry, tactfully express your concerns to them, and suggest that they take appropriate measures to rectify the situation.² Be aware of your state’s laws and regulations about mandated reporting if you discover a colleague’s online content violates the scope of clinical practice or ethical standards.¹ If the content is in violation of the law or medical board regulations, you may have a legal obligation to report that colleague to law enforcement, the licensing board, and/or his/her employer.^1,2

Avoid online snooping into the personal lives of colleagues. Respect their privacy when viewing their posts about personal activities that are not germane to their professional services.¹ If you find videos, images, or messages that reveal private, confidential, or sensitive information about a colleague, do not distribute that information without the colleague’s consent.¹

Be careful when accepting friend requests. Conflicts could arise if you accept friend requests from some but not all of your colleagues; this could be interpreted as favoritism and potentially create problematic work relationships.² Be consistent in accepting or rejecting colleagues’ friend requests. Consider using an employment-oriented social media platform to connect with colleagues outside of the workplace.²

GRAPEVINE, TEX. – Early postpartum glucose tolerance testing for women with gestational diabetes resulted in a 99% adherence rate, with similar sensitivity and specificity as the currently recommended 4- to 12-week postpartum testing schedule.

“Two-day postpartum glucose tolerance testing has similar diagnostic utility as the 4- to 12-week postpartum glucose tolerance test to identify impaired glucose metabolism and diabetes at 1 year postpartum,” said Erika Werner, MD, speaking at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Overall, 29% of women studied had impaired glucose metabolism at 2 days postpartum, as did 25% in the 4- to 12-weeks postpartum window. At 1 year, that figure was 35%. The number of women meeting diagnostic criteria for diabetes held steady at 4% for all three time points.

The findings warrant “consideration for the 2-day postpartum glucose tolerance test (GTT) as the initial postpartum test for women who have gestational diabetes, with repeat testing at 1 year,” said Dr. Werner, a maternal-fetal medicine physician at Brown University, Providence, R.I.

Glucose testing for women with gestational diabetes mellitus (GDM) is recommended at 4-12 weeks postpartum by both the American Diabetes Association and the American College of Obstetricians and Gynecologists.

Testing can allow detection and treatment of impaired glucose metabolism, seen in 15%-40% of women with a history of GDM. Up to 1 in 20 women with GDM will receive a postpartum diagnosis of type 2 diabetes.

However, fewer than one in five women will actually have postpartum glucose testing, representing a large missed opportunity, said Dr. Werner.

Several factors likely contribute to those screening failures, she added. In addition to the potential for public insurance to lapse at 6 weeks postpartum, the logistical realities and time demands of parenting a newborn are themselves a significant barrier.

“What if we changed the timing?” and shifted glucose testing to the early postpartum days, before hospital discharge, asked Dr. Werner. Several pilot studies had already compared glucose screening in the first few days postpartum with the routine schedule, finding good correlation between the early and routine GTT schedule.

Importantly, the earlier studies achieved an adherence rate of more than 90% for early GTT. By contrast, fewer than half of the participants in the usual-care arms actually returned for postpartum GTT in the 4- to 12-week postpartum window, even under the optimized conditions associated with a medical study.

The single-center prospective cohort study conducted by Dr. Werner and collaborators enrolled 300 women with GDM. Women agreed to participate in glucose tolerance testing as inpatients, at 2 days postpartum, in addition to receiving a GTT between 4 and 12 weeks postpartum, and additional screening that included a glycosylated hemoglobin (HbA_1c) test at 1 year postpartum.

The investigators obtained postpartum day 2 GTTs for all but four of the patients. A total of 201 patients returned in the 4- to 12-week postpartum window, and 168 of those participants returned for HbA1c testing at 1 year. Of the 95 patients who didn’t come back for the 4- to 12-week test, 33 did return at 1 year for HbA_1c testing.

Dr. Werner and her coinvestigators included adult women who spoke either fluent Spanish or English and had GDM diagnosed by the Carpenter-Coustan criteria, or by having a blood glucose level of 200 mg/dL or more in a 1-hour glucose challenge test.

The early GTT results weren’t shared with patients or their health care providers. For outpatient visits, participants were offered financial incentives and received multiple reminder phone calls and the offer of free transportation.

For the purposes of the study, impaired glucose metabolism was defined as fasting blood glucose of 100 mg/dL or greater, a 2-hour GTT blood glucose level of 140 mg/dL or greater, or HbA_1c of 5.7% or greater.

Participants were diagnosed with diabetes if they had a fasting blood glucose of 126 mg/dL or greater, a 2-hour GTT blood glucose level of 200 mg/dL or greater, or HbA_1c of 6.5% or greater.

Dr. Werner and colleagues conducted two analyses of their results. In the first, they included only women in both arms who had complete data. In the second analysis, they looked at all women who had data for the 1-year postpartum mark, assuming that interval GTTs were negative for women who were missing these values.

The statistical analysis showed that, for women with complete data, both early and later postpartum GTTs were similar in predicting impaired glucose metabolism at 1 year postpartum (areas under the receiver operating curve [AUC], 0.63 and 0.60, respectively).

For identifying diabetes at 1 year, both early and late testing had high negative predictive value (98% and 99%, respectively), but the later testing strategy had higher sensitivity and specificity, yielding an AUC of 0.83, compared with 0.65 for early testing.

Turning to the second analysis that included all women who had 1-year postpartum HbA_1c values, negative predictive values for diabetes were similarly high (98%) for both the early and late testing strategies. For identifying impaired glucose metabolism at 1 year in this group, both the positive and negative predictive value of the early and late strategies were similar.

Patients were about 32 years old at baseline, with a mean body mass index of 31.7 kg/m². More than half of patients (52.3%) had private insurance, and 22% had GDM in a pregnancy prior to the index pregnancy. Black patients made up about 9% of the study population; 54% of participants were white, and 23% Hispanic. About one-third of patients were nulliparous, and two-thirds had education beyond high school.

During their pregnancies, about 44% of patients managed GDM by diet alone, 40% required insulin, with an additional 1% also requiring an oral agent. The remainder required oral agents alone. Patients delivered at a mean 38.3 weeks gestation, with about 40% receiving cesarean deliveries.

Some of the study’s strengths included its prospective nature, the diverse population recruited, and the fact that participants and providers were both blinded to the 2-day GTT results. Although more than half of participants completed the study – besting the previous pilots – 44% of patients still had incomplete data, noted Dr. Werner.

The American Diabetes Association sponsored the study. Dr. Werner reported no other conflicts of interest.

koakes@mdedge.com

SOURCE: Werner E et al. SMFM 2020. Abstract 72.

GRAPEVINE, TEX. – Early postpartum glucose tolerance testing for women with gestational diabetes resulted in a 99% adherence rate, with similar sensitivity and specificity as the currently recommended 4- to 12-week postpartum testing schedule.

“Two-day postpartum glucose tolerance testing has similar diagnostic utility as the 4- to 12-week postpartum glucose tolerance test to identify impaired glucose metabolism and diabetes at 1 year postpartum,” said Erika Werner, MD, speaking at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Overall, 29% of women studied had impaired glucose metabolism at 2 days postpartum, as did 25% in the 4- to 12-weeks postpartum window. At 1 year, that figure was 35%. The number of women meeting diagnostic criteria for diabetes held steady at 4% for all three time points.

The findings warrant “consideration for the 2-day postpartum glucose tolerance test (GTT) as the initial postpartum test for women who have gestational diabetes, with repeat testing at 1 year,” said Dr. Werner, a maternal-fetal medicine physician at Brown University, Providence, R.I.

Glucose testing for women with gestational diabetes mellitus (GDM) is recommended at 4-12 weeks postpartum by both the American Diabetes Association and the American College of Obstetricians and Gynecologists.

Testing can allow detection and treatment of impaired glucose metabolism, seen in 15%-40% of women with a history of GDM. Up to 1 in 20 women with GDM will receive a postpartum diagnosis of type 2 diabetes.

However, fewer than one in five women will actually have postpartum glucose testing, representing a large missed opportunity, said Dr. Werner.

Several factors likely contribute to those screening failures, she added. In addition to the potential for public insurance to lapse at 6 weeks postpartum, the logistical realities and time demands of parenting a newborn are themselves a significant barrier.

“What if we changed the timing?” and shifted glucose testing to the early postpartum days, before hospital discharge, asked Dr. Werner. Several pilot studies had already compared glucose screening in the first few days postpartum with the routine schedule, finding good correlation between the early and routine GTT schedule.

Importantly, the earlier studies achieved an adherence rate of more than 90% for early GTT. By contrast, fewer than half of the participants in the usual-care arms actually returned for postpartum GTT in the 4- to 12-week postpartum window, even under the optimized conditions associated with a medical study.

The single-center prospective cohort study conducted by Dr. Werner and collaborators enrolled 300 women with GDM. Women agreed to participate in glucose tolerance testing as inpatients, at 2 days postpartum, in addition to receiving a GTT between 4 and 12 weeks postpartum, and additional screening that included a glycosylated hemoglobin (HbA_1c) test at 1 year postpartum.

The investigators obtained postpartum day 2 GTTs for all but four of the patients. A total of 201 patients returned in the 4- to 12-week postpartum window, and 168 of those participants returned for HbA1c testing at 1 year. Of the 95 patients who didn’t come back for the 4- to 12-week test, 33 did return at 1 year for HbA_1c testing.

Dr. Werner and her coinvestigators included adult women who spoke either fluent Spanish or English and had GDM diagnosed by the Carpenter-Coustan criteria, or by having a blood glucose level of 200 mg/dL or more in a 1-hour glucose challenge test.

The early GTT results weren’t shared with patients or their health care providers. For outpatient visits, participants were offered financial incentives and received multiple reminder phone calls and the offer of free transportation.

For the purposes of the study, impaired glucose metabolism was defined as fasting blood glucose of 100 mg/dL or greater, a 2-hour GTT blood glucose level of 140 mg/dL or greater, or HbA_1c of 5.7% or greater.

Participants were diagnosed with diabetes if they had a fasting blood glucose of 126 mg/dL or greater, a 2-hour GTT blood glucose level of 200 mg/dL or greater, or HbA_1c of 6.5% or greater.

Dr. Werner and colleagues conducted two analyses of their results. In the first, they included only women in both arms who had complete data. In the second analysis, they looked at all women who had data for the 1-year postpartum mark, assuming that interval GTTs were negative for women who were missing these values.

The statistical analysis showed that, for women with complete data, both early and later postpartum GTTs were similar in predicting impaired glucose metabolism at 1 year postpartum (areas under the receiver operating curve [AUC], 0.63 and 0.60, respectively).

For identifying diabetes at 1 year, both early and late testing had high negative predictive value (98% and 99%, respectively), but the later testing strategy had higher sensitivity and specificity, yielding an AUC of 0.83, compared with 0.65 for early testing.

Turning to the second analysis that included all women who had 1-year postpartum HbA_1c values, negative predictive values for diabetes were similarly high (98%) for both the early and late testing strategies. For identifying impaired glucose metabolism at 1 year in this group, both the positive and negative predictive value of the early and late strategies were similar.

Patients were about 32 years old at baseline, with a mean body mass index of 31.7 kg/m². More than half of patients (52.3%) had private insurance, and 22% had GDM in a pregnancy prior to the index pregnancy. Black patients made up about 9% of the study population; 54% of participants were white, and 23% Hispanic. About one-third of patients were nulliparous, and two-thirds had education beyond high school.

During their pregnancies, about 44% of patients managed GDM by diet alone, 40% required insulin, with an additional 1% also requiring an oral agent. The remainder required oral agents alone. Patients delivered at a mean 38.3 weeks gestation, with about 40% receiving cesarean deliveries.

Some of the study’s strengths included its prospective nature, the diverse population recruited, and the fact that participants and providers were both blinded to the 2-day GTT results. Although more than half of participants completed the study – besting the previous pilots – 44% of patients still had incomplete data, noted Dr. Werner.

The American Diabetes Association sponsored the study. Dr. Werner reported no other conflicts of interest.

koakes@mdedge.com

SOURCE: Werner E et al. SMFM 2020. Abstract 72.

GRAPEVINE, TEX. – Early postpartum glucose tolerance testing for women with gestational diabetes resulted in a 99% adherence rate, with similar sensitivity and specificity as the currently recommended 4- to 12-week postpartum testing schedule.

“Two-day postpartum glucose tolerance testing has similar diagnostic utility as the 4- to 12-week postpartum glucose tolerance test to identify impaired glucose metabolism and diabetes at 1 year postpartum,” said Erika Werner, MD, speaking at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Overall, 29% of women studied had impaired glucose metabolism at 2 days postpartum, as did 25% in the 4- to 12-weeks postpartum window. At 1 year, that figure was 35%. The number of women meeting diagnostic criteria for diabetes held steady at 4% for all three time points.

The findings warrant “consideration for the 2-day postpartum glucose tolerance test (GTT) as the initial postpartum test for women who have gestational diabetes, with repeat testing at 1 year,” said Dr. Werner, a maternal-fetal medicine physician at Brown University, Providence, R.I.

Glucose testing for women with gestational diabetes mellitus (GDM) is recommended at 4-12 weeks postpartum by both the American Diabetes Association and the American College of Obstetricians and Gynecologists.

Testing can allow detection and treatment of impaired glucose metabolism, seen in 15%-40% of women with a history of GDM. Up to 1 in 20 women with GDM will receive a postpartum diagnosis of type 2 diabetes.

However, fewer than one in five women will actually have postpartum glucose testing, representing a large missed opportunity, said Dr. Werner.

Several factors likely contribute to those screening failures, she added. In addition to the potential for public insurance to lapse at 6 weeks postpartum, the logistical realities and time demands of parenting a newborn are themselves a significant barrier.

“What if we changed the timing?” and shifted glucose testing to the early postpartum days, before hospital discharge, asked Dr. Werner. Several pilot studies had already compared glucose screening in the first few days postpartum with the routine schedule, finding good correlation between the early and routine GTT schedule.

Importantly, the earlier studies achieved an adherence rate of more than 90% for early GTT. By contrast, fewer than half of the participants in the usual-care arms actually returned for postpartum GTT in the 4- to 12-week postpartum window, even under the optimized conditions associated with a medical study.

The single-center prospective cohort study conducted by Dr. Werner and collaborators enrolled 300 women with GDM. Women agreed to participate in glucose tolerance testing as inpatients, at 2 days postpartum, in addition to receiving a GTT between 4 and 12 weeks postpartum, and additional screening that included a glycosylated hemoglobin (HbA_1c) test at 1 year postpartum.

The investigators obtained postpartum day 2 GTTs for all but four of the patients. A total of 201 patients returned in the 4- to 12-week postpartum window, and 168 of those participants returned for HbA1c testing at 1 year. Of the 95 patients who didn’t come back for the 4- to 12-week test, 33 did return at 1 year for HbA_1c testing.

Dr. Werner and her coinvestigators included adult women who spoke either fluent Spanish or English and had GDM diagnosed by the Carpenter-Coustan criteria, or by having a blood glucose level of 200 mg/dL or more in a 1-hour glucose challenge test.

The early GTT results weren’t shared with patients or their health care providers. For outpatient visits, participants were offered financial incentives and received multiple reminder phone calls and the offer of free transportation.

For the purposes of the study, impaired glucose metabolism was defined as fasting blood glucose of 100 mg/dL or greater, a 2-hour GTT blood glucose level of 140 mg/dL or greater, or HbA_1c of 5.7% or greater.

Participants were diagnosed with diabetes if they had a fasting blood glucose of 126 mg/dL or greater, a 2-hour GTT blood glucose level of 200 mg/dL or greater, or HbA_1c of 6.5% or greater.

Dr. Werner and colleagues conducted two analyses of their results. In the first, they included only women in both arms who had complete data. In the second analysis, they looked at all women who had data for the 1-year postpartum mark, assuming that interval GTTs were negative for women who were missing these values.

The statistical analysis showed that, for women with complete data, both early and later postpartum GTTs were similar in predicting impaired glucose metabolism at 1 year postpartum (areas under the receiver operating curve [AUC], 0.63 and 0.60, respectively).

For identifying diabetes at 1 year, both early and late testing had high negative predictive value (98% and 99%, respectively), but the later testing strategy had higher sensitivity and specificity, yielding an AUC of 0.83, compared with 0.65 for early testing.

Turning to the second analysis that included all women who had 1-year postpartum HbA_1c values, negative predictive values for diabetes were similarly high (98%) for both the early and late testing strategies. For identifying impaired glucose metabolism at 1 year in this group, both the positive and negative predictive value of the early and late strategies were similar.

Patients were about 32 years old at baseline, with a mean body mass index of 31.7 kg/m². More than half of patients (52.3%) had private insurance, and 22% had GDM in a pregnancy prior to the index pregnancy. Black patients made up about 9% of the study population; 54% of participants were white, and 23% Hispanic. About one-third of patients were nulliparous, and two-thirds had education beyond high school.

During their pregnancies, about 44% of patients managed GDM by diet alone, 40% required insulin, with an additional 1% also requiring an oral agent. The remainder required oral agents alone. Patients delivered at a mean 38.3 weeks gestation, with about 40% receiving cesarean deliveries.

Some of the study’s strengths included its prospective nature, the diverse population recruited, and the fact that participants and providers were both blinded to the 2-day GTT results. Although more than half of participants completed the study – besting the previous pilots – 44% of patients still had incomplete data, noted Dr. Werner.

The American Diabetes Association sponsored the study. Dr. Werner reported no other conflicts of interest.

koakes@mdedge.com

SOURCE: Werner E et al. SMFM 2020. Abstract 72.

LAS VEGAS – Between 2010 and 2017, the proportion of newly diagnosed cases of acute hepatitis C virus infection rose threefold, driven largely by the concomitant opioid epidemic.

Doug Brunk/MDedge News

That makes efforts to screen, diagnose, and cure high-risk populations more important than ever, Stevan A. Gonzalez, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

About 70% of HCV cases are related to injection drug use,” said Dr. Gonzalez, medical director of liver transplantation at the Baylor Simmons Transplant Institute at the Baylor Scott & White All Saints Medical Center in Fort Worth, Tex. “This is affecting whites as much as blacks and Hispanics, females as much as males, and in nonurban areas as much as in urban areas.”

Data from the Centers for Disease Control and Prevention and the Substance Abuse and Mental Health Services Administration indicate that during 2004-2014, the number of acute HCV cases among those aged 18-29 years increased 400%, and the use of injection opioids rose 600%.

At the same time, the number of HCV cases among those aged 30-39 years increased 325%, and the use of injection opioids rose 83%.

“We’re starting to see a pattern overlapping between HCV exposure and opioid injection,” Dr. Gonzalez said. Other high-risk populations include homeless and incarcerated individuals.

More than 70 million people worldwide have chronic HCV infection, Dr. Gonzalez noted, with possibly as many as 5 million cases in the United States. It remains the nation’s most common blood-borne infection.

Chronic disease develops in up to 85% of people who are exposed, infection is asymptomatic, and HCV remains one of the leading indications for liver transplantation and causes of liver cancer.

From a geographic standpoint, the prevalence of HCV in young adults is eclipsing that of Baby Boomers in several states in the Appalachian region and in Northeast, which have long been trouble spots for opioid use disorder (Gastroenterol. 2018 May;154[6]:1850-1).

Surprising exposure risk

The primary risk of transmission is through contaminated blood and the exposure through needles.

“It really doesn’t matter whether it’s a needle that has a small amount of dead space where a little bit of blood can remain or needles that have a larger amount of blood,” Dr. Gonzalez said.

“I’ve had patients who come to me and say, ‘I can’t believe I have HCV. It’s impossible. I always use my own needles. They’re always brand new; I’ve never shared with anybody,’” he continued.

“This is where education and awareness is so critical, because it’s not just the needles,” Dr. Gonzalez explained. “HCV can survive on inanimate objects. For example, on a tabletop surface or a water container, HCV can remain viable up to 3 weeks. In a syringe, 2 months. For that reason, HCV can also be transmitted through crack pipes and nasal drug use, where the prevalence can be up to 35%.”

The duration of a person’s HCV infection drives the transmission.

“That’s important to think about, because people who have chronic hepatitis C are infectious until they’re treated,” Dr. Gonzalez said. “If they don’t know that they have hepatitis C, they continue to transmit the virus to others.”

One study found that half of people living with HCV are unaware of their infection (PLoS One. 2014 Jul 2;9[7]:e101554). According to Dr. Gonzalez, forthcoming guidelines from the U.S. Preventive Services Task Force are expected to recommend a one-time screening for HCV infection in all adults aged 18-79 years, a Grade B recommendation. “That’s a big deal,” he said. (The draft recommendations are available here.)

HCV infection disproportionately affects individuals in correctional institutions. In fact, an estimated one in three inmates in the United States has chronic HCV.

“This is sort of a forgotten population with a lot of substance use and mental illness,” Dr. Gonzalez said. “Injection drug use in that setting is the most common risk factor: It’s about 60% in terms of the risk of transmission within correctional settings. HCV-associated liver disease has now surpassed HIV as a cause of death within correctional settings.”
 

Weighing treatment options

The most common oral regimens for chronic HCV include sofosbuvir/ledipasvir, sofosbuvir/velpatasvir, and glecaprevir/pibrentasvir. They achieve cure in 93%-100% of cases.

“HCV can be cured; it can be eradicated from the body long term,” Dr. Gonzalez said. “The choice of regimen, treatment duration, and use of ribavirin depends on the presence/absence of cirrhosis, prior treatment experience, and the genotype.”

All six forms of the HCV genotype can be treated with oral medication, he added, and methadone, bupropion, and naloxone are safe to use during therapy.

Reinfection following HCV treatment occurs infrequently. Dr. Gonzalez cited a randomized, controlled trial presented as an abstract at the 2018 annual meeting of the American Association for the Study of Liver Diseases. That study’s researchers found that – among 199 patients on opioid-replacement therapy who were receiving direct-acting antiviral therapy, in whom greater than 50% were actively using drugs – the rate of reinfection at 3 years was 1.8 reinfections/100 person-years.

“That’s lower than people expect,” Dr. Gonzalez said.
 

How to boost screening

Electronic health record systems can be used as an important tool to increase HCV screening in health care settings.

In 2017, researchers published an analysis of three randomized trials carried out at three separate primary care settings to improve screening for HCV: repeated mailings, an EHR best practice alert (BPA), and patient solicitation (Hepatology 2017 Jan;65[1]:44-53). They evaluated HCV antibody testing, diagnosis, and costs for each of the interventions, compared with standard-of-care testing.

The investigators found that the BPA intervention had the lowest incremental cost per completed test – $24 with fixed start-up costs, including technical design and development of the BPA system; $3 without fixed start-up costs. The BPA intervention also had the lowest incremental cost per new case identified.

Other efforts to expand access to screening and treatment are underway.

In 2019, Louisiana health officials negotiated a one-time fee for unlimited access for 5 years to sofosbuvir/velpatasvir (Epclusa) to treat the estimated 30,000 patients on Louisiana Medicaid and in that state’s department of corrections who have HCV.

“The goal is 90% cure; the burden is on the state health department to screen, diagnose, and dispense medication,” Dr. Gonzalez said.

Also in 2019, the state of Washington used an open bidding process to negotiate access to glecaprevir/pibrentasvir (Mavyret) for the state’s Medicaid population who have HCV.

“Those states are setting the pace,” Dr. Gonzalez said. “They are showing examples of how we can start implementing a process to treat these vulnerable populations.”

Meanwhile, the World Health Organization set a goal of eliminating viral hepatitis as a major public health threat by 2030.

“That sounds ambitious, but I think it’s possible,” Dr. Gonzalez said. “It’s important to address these high-risk populations: the incarcerated, people who use drugs, and the homeless, because those are the groups that have a high prevalence of HCV – mainly through injection drug use.

“If we don’t address that population, and we only target the general population, we’re going to have a continual source of transmission,” Dr. Gonzalez warned. “In that case, we would never be able to achieve elimination.”

Dr. Gonzalez disclosed that he is a member of the speakers bureau for AbbVie and Salix.

dbrunk@mdedge.com

LAS VEGAS – Between 2010 and 2017, the proportion of newly diagnosed cases of acute hepatitis C virus infection rose threefold, driven largely by the concomitant opioid epidemic.

Doug Brunk/MDedge News

That makes efforts to screen, diagnose, and cure high-risk populations more important than ever, Stevan A. Gonzalez, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

About 70% of HCV cases are related to injection drug use,” said Dr. Gonzalez, medical director of liver transplantation at the Baylor Simmons Transplant Institute at the Baylor Scott & White All Saints Medical Center in Fort Worth, Tex. “This is affecting whites as much as blacks and Hispanics, females as much as males, and in nonurban areas as much as in urban areas.”

Data from the Centers for Disease Control and Prevention and the Substance Abuse and Mental Health Services Administration indicate that during 2004-2014, the number of acute HCV cases among those aged 18-29 years increased 400%, and the use of injection opioids rose 600%.

At the same time, the number of HCV cases among those aged 30-39 years increased 325%, and the use of injection opioids rose 83%.

“We’re starting to see a pattern overlapping between HCV exposure and opioid injection,” Dr. Gonzalez said. Other high-risk populations include homeless and incarcerated individuals.

More than 70 million people worldwide have chronic HCV infection, Dr. Gonzalez noted, with possibly as many as 5 million cases in the United States. It remains the nation’s most common blood-borne infection.

Chronic disease develops in up to 85% of people who are exposed, infection is asymptomatic, and HCV remains one of the leading indications for liver transplantation and causes of liver cancer.

From a geographic standpoint, the prevalence of HCV in young adults is eclipsing that of Baby Boomers in several states in the Appalachian region and in Northeast, which have long been trouble spots for opioid use disorder (Gastroenterol. 2018 May;154[6]:1850-1).

Surprising exposure risk

The primary risk of transmission is through contaminated blood and the exposure through needles.

“It really doesn’t matter whether it’s a needle that has a small amount of dead space where a little bit of blood can remain or needles that have a larger amount of blood,” Dr. Gonzalez said.

“I’ve had patients who come to me and say, ‘I can’t believe I have HCV. It’s impossible. I always use my own needles. They’re always brand new; I’ve never shared with anybody,’” he continued.

“This is where education and awareness is so critical, because it’s not just the needles,” Dr. Gonzalez explained. “HCV can survive on inanimate objects. For example, on a tabletop surface or a water container, HCV can remain viable up to 3 weeks. In a syringe, 2 months. For that reason, HCV can also be transmitted through crack pipes and nasal drug use, where the prevalence can be up to 35%.”

The duration of a person’s HCV infection drives the transmission.

“That’s important to think about, because people who have chronic hepatitis C are infectious until they’re treated,” Dr. Gonzalez said. “If they don’t know that they have hepatitis C, they continue to transmit the virus to others.”

One study found that half of people living with HCV are unaware of their infection (PLoS One. 2014 Jul 2;9[7]:e101554). According to Dr. Gonzalez, forthcoming guidelines from the U.S. Preventive Services Task Force are expected to recommend a one-time screening for HCV infection in all adults aged 18-79 years, a Grade B recommendation. “That’s a big deal,” he said. (The draft recommendations are available here.)

HCV infection disproportionately affects individuals in correctional institutions. In fact, an estimated one in three inmates in the United States has chronic HCV.

“This is sort of a forgotten population with a lot of substance use and mental illness,” Dr. Gonzalez said. “Injection drug use in that setting is the most common risk factor: It’s about 60% in terms of the risk of transmission within correctional settings. HCV-associated liver disease has now surpassed HIV as a cause of death within correctional settings.”
 

Weighing treatment options

The most common oral regimens for chronic HCV include sofosbuvir/ledipasvir, sofosbuvir/velpatasvir, and glecaprevir/pibrentasvir. They achieve cure in 93%-100% of cases.

“HCV can be cured; it can be eradicated from the body long term,” Dr. Gonzalez said. “The choice of regimen, treatment duration, and use of ribavirin depends on the presence/absence of cirrhosis, prior treatment experience, and the genotype.”

All six forms of the HCV genotype can be treated with oral medication, he added, and methadone, bupropion, and naloxone are safe to use during therapy.

Reinfection following HCV treatment occurs infrequently. Dr. Gonzalez cited a randomized, controlled trial presented as an abstract at the 2018 annual meeting of the American Association for the Study of Liver Diseases. That study’s researchers found that – among 199 patients on opioid-replacement therapy who were receiving direct-acting antiviral therapy, in whom greater than 50% were actively using drugs – the rate of reinfection at 3 years was 1.8 reinfections/100 person-years.

“That’s lower than people expect,” Dr. Gonzalez said.
 

How to boost screening

Electronic health record systems can be used as an important tool to increase HCV screening in health care settings.

In 2017, researchers published an analysis of three randomized trials carried out at three separate primary care settings to improve screening for HCV: repeated mailings, an EHR best practice alert (BPA), and patient solicitation (Hepatology 2017 Jan;65[1]:44-53). They evaluated HCV antibody testing, diagnosis, and costs for each of the interventions, compared with standard-of-care testing.

The investigators found that the BPA intervention had the lowest incremental cost per completed test – $24 with fixed start-up costs, including technical design and development of the BPA system; $3 without fixed start-up costs. The BPA intervention also had the lowest incremental cost per new case identified.

Other efforts to expand access to screening and treatment are underway.

In 2019, Louisiana health officials negotiated a one-time fee for unlimited access for 5 years to sofosbuvir/velpatasvir (Epclusa) to treat the estimated 30,000 patients on Louisiana Medicaid and in that state’s department of corrections who have HCV.

“The goal is 90% cure; the burden is on the state health department to screen, diagnose, and dispense medication,” Dr. Gonzalez said.

Also in 2019, the state of Washington used an open bidding process to negotiate access to glecaprevir/pibrentasvir (Mavyret) for the state’s Medicaid population who have HCV.

“Those states are setting the pace,” Dr. Gonzalez said. “They are showing examples of how we can start implementing a process to treat these vulnerable populations.”

Meanwhile, the World Health Organization set a goal of eliminating viral hepatitis as a major public health threat by 2030.

“That sounds ambitious, but I think it’s possible,” Dr. Gonzalez said. “It’s important to address these high-risk populations: the incarcerated, people who use drugs, and the homeless, because those are the groups that have a high prevalence of HCV – mainly through injection drug use.

“If we don’t address that population, and we only target the general population, we’re going to have a continual source of transmission,” Dr. Gonzalez warned. “In that case, we would never be able to achieve elimination.”

Dr. Gonzalez disclosed that he is a member of the speakers bureau for AbbVie and Salix.

dbrunk@mdedge.com

LAS VEGAS – Between 2010 and 2017, the proportion of newly diagnosed cases of acute hepatitis C virus infection rose threefold, driven largely by the concomitant opioid epidemic.

Doug Brunk/MDedge News

That makes efforts to screen, diagnose, and cure high-risk populations more important than ever, Stevan A. Gonzalez, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association.

About 70% of HCV cases are related to injection drug use,” said Dr. Gonzalez, medical director of liver transplantation at the Baylor Simmons Transplant Institute at the Baylor Scott & White All Saints Medical Center in Fort Worth, Tex. “This is affecting whites as much as blacks and Hispanics, females as much as males, and in nonurban areas as much as in urban areas.”

Data from the Centers for Disease Control and Prevention and the Substance Abuse and Mental Health Services Administration indicate that during 2004-2014, the number of acute HCV cases among those aged 18-29 years increased 400%, and the use of injection opioids rose 600%.

At the same time, the number of HCV cases among those aged 30-39 years increased 325%, and the use of injection opioids rose 83%.

“We’re starting to see a pattern overlapping between HCV exposure and opioid injection,” Dr. Gonzalez said. Other high-risk populations include homeless and incarcerated individuals.

More than 70 million people worldwide have chronic HCV infection, Dr. Gonzalez noted, with possibly as many as 5 million cases in the United States. It remains the nation’s most common blood-borne infection.

Chronic disease develops in up to 85% of people who are exposed, infection is asymptomatic, and HCV remains one of the leading indications for liver transplantation and causes of liver cancer.

From a geographic standpoint, the prevalence of HCV in young adults is eclipsing that of Baby Boomers in several states in the Appalachian region and in Northeast, which have long been trouble spots for opioid use disorder (Gastroenterol. 2018 May;154[6]:1850-1).

Surprising exposure risk

The primary risk of transmission is through contaminated blood and the exposure through needles.

“It really doesn’t matter whether it’s a needle that has a small amount of dead space where a little bit of blood can remain or needles that have a larger amount of blood,” Dr. Gonzalez said.

“I’ve had patients who come to me and say, ‘I can’t believe I have HCV. It’s impossible. I always use my own needles. They’re always brand new; I’ve never shared with anybody,’” he continued.

“This is where education and awareness is so critical, because it’s not just the needles,” Dr. Gonzalez explained. “HCV can survive on inanimate objects. For example, on a tabletop surface or a water container, HCV can remain viable up to 3 weeks. In a syringe, 2 months. For that reason, HCV can also be transmitted through crack pipes and nasal drug use, where the prevalence can be up to 35%.”

The duration of a person’s HCV infection drives the transmission.

“That’s important to think about, because people who have chronic hepatitis C are infectious until they’re treated,” Dr. Gonzalez said. “If they don’t know that they have hepatitis C, they continue to transmit the virus to others.”

One study found that half of people living with HCV are unaware of their infection (PLoS One. 2014 Jul 2;9[7]:e101554). According to Dr. Gonzalez, forthcoming guidelines from the U.S. Preventive Services Task Force are expected to recommend a one-time screening for HCV infection in all adults aged 18-79 years, a Grade B recommendation. “That’s a big deal,” he said. (The draft recommendations are available here.)

HCV infection disproportionately affects individuals in correctional institutions. In fact, an estimated one in three inmates in the United States has chronic HCV.

“This is sort of a forgotten population with a lot of substance use and mental illness,” Dr. Gonzalez said. “Injection drug use in that setting is the most common risk factor: It’s about 60% in terms of the risk of transmission within correctional settings. HCV-associated liver disease has now surpassed HIV as a cause of death within correctional settings.”
 

Weighing treatment options

The most common oral regimens for chronic HCV include sofosbuvir/ledipasvir, sofosbuvir/velpatasvir, and glecaprevir/pibrentasvir. They achieve cure in 93%-100% of cases.

“HCV can be cured; it can be eradicated from the body long term,” Dr. Gonzalez said. “The choice of regimen, treatment duration, and use of ribavirin depends on the presence/absence of cirrhosis, prior treatment experience, and the genotype.”

All six forms of the HCV genotype can be treated with oral medication, he added, and methadone, bupropion, and naloxone are safe to use during therapy.

Reinfection following HCV treatment occurs infrequently. Dr. Gonzalez cited a randomized, controlled trial presented as an abstract at the 2018 annual meeting of the American Association for the Study of Liver Diseases. That study’s researchers found that – among 199 patients on opioid-replacement therapy who were receiving direct-acting antiviral therapy, in whom greater than 50% were actively using drugs – the rate of reinfection at 3 years was 1.8 reinfections/100 person-years.

“That’s lower than people expect,” Dr. Gonzalez said.
 

How to boost screening

Electronic health record systems can be used as an important tool to increase HCV screening in health care settings.

In 2017, researchers published an analysis of three randomized trials carried out at three separate primary care settings to improve screening for HCV: repeated mailings, an EHR best practice alert (BPA), and patient solicitation (Hepatology 2017 Jan;65[1]:44-53). They evaluated HCV antibody testing, diagnosis, and costs for each of the interventions, compared with standard-of-care testing.

The investigators found that the BPA intervention had the lowest incremental cost per completed test – $24 with fixed start-up costs, including technical design and development of the BPA system; $3 without fixed start-up costs. The BPA intervention also had the lowest incremental cost per new case identified.

Other efforts to expand access to screening and treatment are underway.

In 2019, Louisiana health officials negotiated a one-time fee for unlimited access for 5 years to sofosbuvir/velpatasvir (Epclusa) to treat the estimated 30,000 patients on Louisiana Medicaid and in that state’s department of corrections who have HCV.

“The goal is 90% cure; the burden is on the state health department to screen, diagnose, and dispense medication,” Dr. Gonzalez said.

Also in 2019, the state of Washington used an open bidding process to negotiate access to glecaprevir/pibrentasvir (Mavyret) for the state’s Medicaid population who have HCV.

“Those states are setting the pace,” Dr. Gonzalez said. “They are showing examples of how we can start implementing a process to treat these vulnerable populations.”

Meanwhile, the World Health Organization set a goal of eliminating viral hepatitis as a major public health threat by 2030.

“That sounds ambitious, but I think it’s possible,” Dr. Gonzalez said. “It’s important to address these high-risk populations: the incarcerated, people who use drugs, and the homeless, because those are the groups that have a high prevalence of HCV – mainly through injection drug use.

“If we don’t address that population, and we only target the general population, we’re going to have a continual source of transmission,” Dr. Gonzalez warned. “In that case, we would never be able to achieve elimination.”

Dr. Gonzalez disclosed that he is a member of the speakers bureau for AbbVie and Salix.

dbrunk@mdedge.com

Physicians in internal medicine struggle to find happiness both in and outside the workplace, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Only 22% of internists reported that they were very happy at work, with only neurologists reporting a worse at-work happiness rate, according to the Medscape report.

The news wasn’t much better when it came to happiness outside the office, as only 48% of internists reported they were very happy. Once again, neurologists had the lowest happiness rate outside the office, at 44%.

The rate of burnout among internists, at 43%, was similar to that of physicians overall at 41%; 14% of internists reported that they were both burned out and depressed. The most common contributing factors to burnout for internists were having too many bureaucratic tasks (62%), receiving a lack of respect from colleagues (34%), and spending too many hours at work (33%).

Internists dealt with burnout by isolating themselves from others (47%), talking with family/friends (45%), and exercising (41%). In addition, only 41% of internists took 3-4 weeks’ vacation, less than the 44% for physicians overall, and 43% took less than 3 weeks of vacation.

About 14% of internists said that they’d contemplated suicide, and 1% reported that they’d attempted it; 80% said they’d never thought about suicide. Only 16% said that they were seeking or planning to seek professional help for symptoms of burnout or depression, and 64% said they weren’t planning on seeking help and had never done so in the past.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

lfranki@mdedge.com

Physicians in internal medicine struggle to find happiness both in and outside the workplace, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Only 22% of internists reported that they were very happy at work, with only neurologists reporting a worse at-work happiness rate, according to the Medscape report.

The news wasn’t much better when it came to happiness outside the office, as only 48% of internists reported they were very happy. Once again, neurologists had the lowest happiness rate outside the office, at 44%.

The rate of burnout among internists, at 43%, was similar to that of physicians overall at 41%; 14% of internists reported that they were both burned out and depressed. The most common contributing factors to burnout for internists were having too many bureaucratic tasks (62%), receiving a lack of respect from colleagues (34%), and spending too many hours at work (33%).

Internists dealt with burnout by isolating themselves from others (47%), talking with family/friends (45%), and exercising (41%). In addition, only 41% of internists took 3-4 weeks’ vacation, less than the 44% for physicians overall, and 43% took less than 3 weeks of vacation.

About 14% of internists said that they’d contemplated suicide, and 1% reported that they’d attempted it; 80% said they’d never thought about suicide. Only 16% said that they were seeking or planning to seek professional help for symptoms of burnout or depression, and 64% said they weren’t planning on seeking help and had never done so in the past.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

lfranki@mdedge.com

Physicians in internal medicine struggle to find happiness both in and outside the workplace, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Only 22% of internists reported that they were very happy at work, with only neurologists reporting a worse at-work happiness rate, according to the Medscape report.

The news wasn’t much better when it came to happiness outside the office, as only 48% of internists reported they were very happy. Once again, neurologists had the lowest happiness rate outside the office, at 44%.

The rate of burnout among internists, at 43%, was similar to that of physicians overall at 41%; 14% of internists reported that they were both burned out and depressed. The most common contributing factors to burnout for internists were having too many bureaucratic tasks (62%), receiving a lack of respect from colleagues (34%), and spending too many hours at work (33%).

Internists dealt with burnout by isolating themselves from others (47%), talking with family/friends (45%), and exercising (41%). In addition, only 41% of internists took 3-4 weeks’ vacation, less than the 44% for physicians overall, and 43% took less than 3 weeks of vacation.

About 14% of internists said that they’d contemplated suicide, and 1% reported that they’d attempted it; 80% said they’d never thought about suicide. Only 16% said that they were seeking or planning to seek professional help for symptoms of burnout or depression, and 64% said they weren’t planning on seeking help and had never done so in the past.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

lfranki@mdedge.com