Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.

As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.

Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.

But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:

• Cerebral pathology
• Circuit disruptions of neural connections
• Chemical imbalance
• Cytokine inflammatory con­flagration
• Cognitive impairment
• Chronic course
• Crippled functioning.

My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:

• Connect with patients
• Correct diagnosis
• Course-specific intervention
• Choose the appropriate medication
• Combine cognitive-behavioral therapy with medication
• Cognitive assessment at baseline
• Compliance/concordance with treatment
• Continuity of care
• Comorbidities, physical and psychiatric
• Collaborative care with other medical specialists
• Comprehensive treatment plan with other mental health professionals.

A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.¹ Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psych­iatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or involuntary use of curse words that begin with a “C,” or any other letter, psychiatry has a clinical term for it: coprolalia.

Editor's note: How many C words are there in this editorial? Email answers to henry.nasrallah@currentpsychiatry.com

Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.

As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.

Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.

But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:

• Cerebral pathology
• Circuit disruptions of neural connections
• Chemical imbalance
• Cytokine inflammatory con­flagration
• Cognitive impairment
• Chronic course
• Crippled functioning.

My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:

• Connect with patients
• Correct diagnosis
• Course-specific intervention
• Choose the appropriate medication
• Combine cognitive-behavioral therapy with medication
• Cognitive assessment at baseline
• Compliance/concordance with treatment
• Continuity of care
• Comorbidities, physical and psychiatric
• Collaborative care with other medical specialists
• Comprehensive treatment plan with other mental health professionals.

A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.¹ Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psych­iatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or involuntary use of curse words that begin with a “C,” or any other letter, psychiatry has a clinical term for it: coprolalia.

Editor's note: How many C words are there in this editorial? Email answers to henry.nasrallah@currentpsychiatry.com

Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.

As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.

Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.

But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:

• Cerebral pathology
• Circuit disruptions of neural connections
• Chemical imbalance
• Cytokine inflammatory con­flagration
• Cognitive impairment
• Chronic course
• Crippled functioning.

My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:

• Connect with patients
• Correct diagnosis
• Course-specific intervention
• Choose the appropriate medication
• Combine cognitive-behavioral therapy with medication
• Cognitive assessment at baseline
• Compliance/concordance with treatment
• Continuity of care
• Comorbidities, physical and psychiatric
• Collaborative care with other medical specialists
• Comprehensive treatment plan with other mental health professionals.

A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.¹ Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psych­iatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or involuntary use of curse words that begin with a “C,” or any other letter, psychiatry has a clinical term for it: coprolalia.

Editor's note: How many C words are there in this editorial? Email answers to henry.nasrallah@currentpsychiatry.com

“Was this your first one?”

You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.

As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”

The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:

• “I saw this patient daily for weeks, and I was close to him.”
• “There was an element of suicidality in this case, so it was different.”
• “After all, this was my first experience like this.”

In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.

These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.

These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.

Continue to: This is not to diminish...

This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.

“Was this your first one?”

You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.

As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”

The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:

• “I saw this patient daily for weeks, and I was close to him.”
• “There was an element of suicidality in this case, so it was different.”
• “After all, this was my first experience like this.”

In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.

These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.

These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.

Continue to: This is not to diminish...

This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.

“Was this your first one?”

You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.

As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”

The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:

• “I saw this patient daily for weeks, and I was close to him.”
• “There was an element of suicidality in this case, so it was different.”
• “After all, this was my first experience like this.”

In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.

These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.

These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.

Continue to: This is not to diminish...

This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.

I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.

It is 3 AM. I am an intern in psychiatry, 2 months out of medical school, and tonight I am on crash working the trauma bay. The attending is an uncompromising intellectual who graces the ER like Meryl Streep on the red carpet. She smiles at me with only a slight movement from the corner of her mouth, “You know you’re gonna have to do some sutures before you finish your rotation.”

4 AM. I am feeling gross, and I hate wearing scrubs. I scan the patient list, looking for more psychiatry cases. Three more hours. A nurse approaches me with a gravid look on her face. “Dr. Brown, we have a code blue coming in. I think he overdosed on something. We’re going to need all the hands we can get.” Less than 2 minutes later, I am running toward a man who had been rolled in. Clothes drenched in vomit, matted hair. And CPR starts. The attending runs the code like a ballad, her central nervous system bathed in adrenaline, crimson blood boiling in her veins. I’m observing in the corner of the room, praying that this guy does not die. I am so uncomfortable; this is not a comfortable feeling. “Dr. Brown, you’re up.”

Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.

I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.

This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.

She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”

That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.

I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.

It is 3 AM. I am an intern in psychiatry, 2 months out of medical school, and tonight I am on crash working the trauma bay. The attending is an uncompromising intellectual who graces the ER like Meryl Streep on the red carpet. She smiles at me with only a slight movement from the corner of her mouth, “You know you’re gonna have to do some sutures before you finish your rotation.”

4 AM. I am feeling gross, and I hate wearing scrubs. I scan the patient list, looking for more psychiatry cases. Three more hours. A nurse approaches me with a gravid look on her face. “Dr. Brown, we have a code blue coming in. I think he overdosed on something. We’re going to need all the hands we can get.” Less than 2 minutes later, I am running toward a man who had been rolled in. Clothes drenched in vomit, matted hair. And CPR starts. The attending runs the code like a ballad, her central nervous system bathed in adrenaline, crimson blood boiling in her veins. I’m observing in the corner of the room, praying that this guy does not die. I am so uncomfortable; this is not a comfortable feeling. “Dr. Brown, you’re up.”

Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.

I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.

This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.

She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”

That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.

I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.

It is 3 AM. I am an intern in psychiatry, 2 months out of medical school, and tonight I am on crash working the trauma bay. The attending is an uncompromising intellectual who graces the ER like Meryl Streep on the red carpet. She smiles at me with only a slight movement from the corner of her mouth, “You know you’re gonna have to do some sutures before you finish your rotation.”

4 AM. I am feeling gross, and I hate wearing scrubs. I scan the patient list, looking for more psychiatry cases. Three more hours. A nurse approaches me with a gravid look on her face. “Dr. Brown, we have a code blue coming in. I think he overdosed on something. We’re going to need all the hands we can get.” Less than 2 minutes later, I am running toward a man who had been rolled in. Clothes drenched in vomit, matted hair. And CPR starts. The attending runs the code like a ballad, her central nervous system bathed in adrenaline, crimson blood boiling in her veins. I’m observing in the corner of the room, praying that this guy does not die. I am so uncomfortable; this is not a comfortable feeling. “Dr. Brown, you’re up.”

Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.

I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.

This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.

She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”

That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.

Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.

Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.

CYP2D6

The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.¹Table 1² lists some of the most common CYP2D6 alleles.

Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 2²). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.

Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.² Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 3^2-5) and/or substrates (Table 4^2,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.⁷ Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.

Phenoconversion

Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.⁸ In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.⁸ While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.

Continue to: Determining CYP2D6 phenotype

 

 

Determining CYP2D6 phenotype

Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.^3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (paliperidone). The risperidone-to-9-hydroxyrisperidone (R-to-9-OHR) concentration ratio is an indicator of CYP2D6 phenotype.³ While considerable overlap may exist using R-to-9-OHR concentration ratios as a predictor of CYP2D6 phenotype, this provides a practical and economically viable option for guiding drug therapy and recommending CYP2D6 genetic testing. The median R-to-9-OHR concentration ratios with the 25th to 75th percentiles are listed below as indicators of CYP2D6 phenotypes⁹:

• Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
• Extensive metabolizer: 0.08 (0.04 to 0.17)
• Intermediate metabolizer: 0.56 (0.30 to 1.0)
• Poor metabolizer: 2.5 (1.8 to 4.1).

Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.⁹

When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (desvenlafaxine) is the active metabolite of venlafaxine. The O-desmethylvenlafaxine-to-venlafaxine concentration ratio is an indicator of CYP2D6 phenotype.⁸ In this instance, a ratio ≥1 indicates an extensive metabolizer, whereas <1 indicates a poor metabolizer.

CYP1A2

While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.² Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 5²), and inducibility in the presence of environmental factors.

Continue to: CYP1A2 inhibiton

 

 

CYP1A2 inhibition

A variety of medications and environmental factors may inhibit CYP1A2.

Medications. Medications that may inhibit CYP1A2 include atazanavir, ciprofloxacin, ethinyl estradiol, and fluvoxamine.³

Caffeine. A significant increase in caffeine consumption can result in inhibition.³ Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.³ However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.

Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.¹⁰ Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.

Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.⁸

Continue to: CYP1A2 induction

 

 

CYP1A2 induction

A variety of medications and environmental factors may induce CYP1A2.

Medications. Certain medications may induce CYP1A2, including carbamazepine, phenytoin, rifampin, and primidone.

Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.³ Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.¹¹

Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.³ Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.¹⁰ Grilled meat also plays a role in induction.¹⁰

Related Resource

• Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.

Drug Brand Names

Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz  
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban  
Carbamazepine • Carbatrol, Tegretol  
Chlorpromazine • Thorazine  
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin  
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol  
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd  
Vortioxetine • Trintellix
Ziprasidone • Geodon

Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.

Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.

CYP2D6

The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.¹Table 1² lists some of the most common CYP2D6 alleles.

Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 2²). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.

Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.² Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 3^2-5) and/or substrates (Table 4^2,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.⁷ Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.

Phenoconversion

Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.⁸ In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.⁸ While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.

Continue to: Determining CYP2D6 phenotype

 

 

Determining CYP2D6 phenotype

Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.^3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (paliperidone). The risperidone-to-9-hydroxyrisperidone (R-to-9-OHR) concentration ratio is an indicator of CYP2D6 phenotype.³ While considerable overlap may exist using R-to-9-OHR concentration ratios as a predictor of CYP2D6 phenotype, this provides a practical and economically viable option for guiding drug therapy and recommending CYP2D6 genetic testing. The median R-to-9-OHR concentration ratios with the 25th to 75th percentiles are listed below as indicators of CYP2D6 phenotypes⁹:

• Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
• Extensive metabolizer: 0.08 (0.04 to 0.17)
• Intermediate metabolizer: 0.56 (0.30 to 1.0)
• Poor metabolizer: 2.5 (1.8 to 4.1).

Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.⁹

When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (desvenlafaxine) is the active metabolite of venlafaxine. The O-desmethylvenlafaxine-to-venlafaxine concentration ratio is an indicator of CYP2D6 phenotype.⁸ In this instance, a ratio ≥1 indicates an extensive metabolizer, whereas <1 indicates a poor metabolizer.

CYP1A2

While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.² Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 5²), and inducibility in the presence of environmental factors.

Continue to: CYP1A2 inhibiton

 

 

CYP1A2 inhibition

A variety of medications and environmental factors may inhibit CYP1A2.

Medications. Medications that may inhibit CYP1A2 include atazanavir, ciprofloxacin, ethinyl estradiol, and fluvoxamine.³

Caffeine. A significant increase in caffeine consumption can result in inhibition.³ Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.³ However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.

Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.¹⁰ Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.

Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.⁸

Continue to: CYP1A2 induction

 

 

CYP1A2 induction

A variety of medications and environmental factors may induce CYP1A2.

Medications. Certain medications may induce CYP1A2, including carbamazepine, phenytoin, rifampin, and primidone.

Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.³ Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.¹¹

Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.³ Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.¹⁰ Grilled meat also plays a role in induction.¹⁰

Related Resource

• Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.

Drug Brand Names

Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz  
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban  
Carbamazepine • Carbatrol, Tegretol  
Chlorpromazine • Thorazine  
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin  
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol  
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd  
Vortioxetine • Trintellix
Ziprasidone • Geodon

Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.

Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.

CYP2D6

The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.¹Table 1² lists some of the most common CYP2D6 alleles.

Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 2²). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.

Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.² Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 3^2-5) and/or substrates (Table 4^2,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.⁷ Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.

Phenoconversion

Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.⁸ In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.⁸ While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.

Continue to: Determining CYP2D6 phenotype

 

 

Determining CYP2D6 phenotype

Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.^3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (paliperidone). The risperidone-to-9-hydroxyrisperidone (R-to-9-OHR) concentration ratio is an indicator of CYP2D6 phenotype.³ While considerable overlap may exist using R-to-9-OHR concentration ratios as a predictor of CYP2D6 phenotype, this provides a practical and economically viable option for guiding drug therapy and recommending CYP2D6 genetic testing. The median R-to-9-OHR concentration ratios with the 25th to 75th percentiles are listed below as indicators of CYP2D6 phenotypes⁹:

• Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
• Extensive metabolizer: 0.08 (0.04 to 0.17)
• Intermediate metabolizer: 0.56 (0.30 to 1.0)
• Poor metabolizer: 2.5 (1.8 to 4.1).

Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.⁹

When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (desvenlafaxine) is the active metabolite of venlafaxine. The O-desmethylvenlafaxine-to-venlafaxine concentration ratio is an indicator of CYP2D6 phenotype.⁸ In this instance, a ratio ≥1 indicates an extensive metabolizer, whereas <1 indicates a poor metabolizer.

CYP1A2

While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.² Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 5²), and inducibility in the presence of environmental factors.

Continue to: CYP1A2 inhibiton

 

 

CYP1A2 inhibition

A variety of medications and environmental factors may inhibit CYP1A2.

Medications. Medications that may inhibit CYP1A2 include atazanavir, ciprofloxacin, ethinyl estradiol, and fluvoxamine.³

Caffeine. A significant increase in caffeine consumption can result in inhibition.³ Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.³ However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.

Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.¹⁰ Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.

Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.⁸

Continue to: CYP1A2 induction

 

 

CYP1A2 induction

A variety of medications and environmental factors may induce CYP1A2.

Medications. Certain medications may induce CYP1A2, including carbamazepine, phenytoin, rifampin, and primidone.

Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.³ Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.¹¹

Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.³ Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.¹⁰ Grilled meat also plays a role in induction.¹⁰

Related Resource

• Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.

Drug Brand Names

Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz  
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban  
Carbamazepine • Carbatrol, Tegretol  
Chlorpromazine • Thorazine  
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin  
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol  
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd  
Vortioxetine • Trintellix
Ziprasidone • Geodon

CASE Attempted suicide?

Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.

During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.

During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.

Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.

[polldaddy:10040204]

Continue to: The authors' observation

 

 

The authors’ observation

The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 1¹). Ms. S also denied having a history of depressive episodes or previous suicidal ideation, intention, or attempt, despite having said during the initial evaluation that she had a previous suicide attempt.

Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further, because she denied having any anxiety, worry, or stress related to her life in Yemen, her move to the United States, her parents’ health, school, or any other domains, she did not meet criteria for posttraumatic stress disorder, acute stress disorder (Table 2¹), or an anxiety disorder. Similarly, there was no evidence of a substance use disorder.

Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.

The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.² An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.

Continue to: Cultural factors and the clinical evaluation

 

 

Cultural factors and the clinical evaluation

Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.

The C-L team considered key cultural factors in its assessment of Ms. S (Table 3¹). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.³ Ms. S spoke English, but she often asked for the translation of words or questions, and her mother spoke only Arabic, and was assisted by a phone interpreter to communicate with the clinicians caring for her daughter. Conducting the interview with the phone interpreter added complexity to the interactions, interrupted the natural flow of the conversation, and was felt to hinder openness of disclosure.

Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.⁴ This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.

The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.

Continue to: Cultural attitudes to puberty

Cultural attitudes to puberty

Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.⁵ Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”

Family identification and attitudes toward mental health

Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.⁴ Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.⁶ Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness^7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo⁹ and a threat to family honor.¹⁰ Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems¹¹ and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”

Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.

The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”⁹ and suicidal ideation may not be disclosed because suicide is forbidden in Islam.¹² Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.¹³

Continue to: Directly asking Ms. S...

Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”¹² may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.

Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.⁴ Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.^7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.

[polldaddy:10040206]

The authors’ observations

Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.

Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.

Continue to: OUTCOME Culturally-appropriate outpatient therapy

 

 

OUTCOME Culturally-appropriate outpatient therapy

Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.

The authors’ observations

Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”

Bottom Line 

Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.

Related Resources

• Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
• Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.  
• Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821. 

Drug Brand Name

Naloxone • Narcan

CASE Attempted suicide?

Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.

During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.

During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.

Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.

[polldaddy:10040204]

Continue to: The authors' observation

 

 

The authors’ observation

The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 1¹). Ms. S also denied having a history of depressive episodes or previous suicidal ideation, intention, or attempt, despite having said during the initial evaluation that she had a previous suicide attempt.

Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further, because she denied having any anxiety, worry, or stress related to her life in Yemen, her move to the United States, her parents’ health, school, or any other domains, she did not meet criteria for posttraumatic stress disorder, acute stress disorder (Table 2¹), or an anxiety disorder. Similarly, there was no evidence of a substance use disorder.

Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.

The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.² An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.

Continue to: Cultural factors and the clinical evaluation

 

 

Cultural factors and the clinical evaluation

Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.

The C-L team considered key cultural factors in its assessment of Ms. S (Table 3¹). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.³ Ms. S spoke English, but she often asked for the translation of words or questions, and her mother spoke only Arabic, and was assisted by a phone interpreter to communicate with the clinicians caring for her daughter. Conducting the interview with the phone interpreter added complexity to the interactions, interrupted the natural flow of the conversation, and was felt to hinder openness of disclosure.

Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.⁴ This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.

The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.

Continue to: Cultural attitudes to puberty

Cultural attitudes to puberty

Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.⁵ Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”

Family identification and attitudes toward mental health

Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.⁴ Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.⁶ Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness^7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo⁹ and a threat to family honor.¹⁰ Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems¹¹ and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”

Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.

The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”⁹ and suicidal ideation may not be disclosed because suicide is forbidden in Islam.¹² Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.¹³

Continue to: Directly asking Ms. S...

Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”¹² may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.

Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.⁴ Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.^7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.

[polldaddy:10040206]

The authors’ observations

Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.

Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.

Continue to: OUTCOME Culturally-appropriate outpatient therapy

 

 

OUTCOME Culturally-appropriate outpatient therapy

Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.

The authors’ observations

Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”

Bottom Line 

Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.

Related Resources

• Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
• Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.  
• Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821. 

Drug Brand Name

Naloxone • Narcan

CASE Attempted suicide?

Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.

During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.

During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.

Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.

[polldaddy:10040204]

Continue to: The authors' observation

 

 

The authors’ observation

The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 1¹). Ms. S also denied having a history of depressive episodes or previous suicidal ideation, intention, or attempt, despite having said during the initial evaluation that she had a previous suicide attempt.

Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further, because she denied having any anxiety, worry, or stress related to her life in Yemen, her move to the United States, her parents’ health, school, or any other domains, she did not meet criteria for posttraumatic stress disorder, acute stress disorder (Table 2¹), or an anxiety disorder. Similarly, there was no evidence of a substance use disorder.

Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.

The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.² An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.

Continue to: Cultural factors and the clinical evaluation

 

 

Cultural factors and the clinical evaluation

Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.

The C-L team considered key cultural factors in its assessment of Ms. S (Table 3¹). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.³ Ms. S spoke English, but she often asked for the translation of words or questions, and her mother spoke only Arabic, and was assisted by a phone interpreter to communicate with the clinicians caring for her daughter. Conducting the interview with the phone interpreter added complexity to the interactions, interrupted the natural flow of the conversation, and was felt to hinder openness of disclosure.

Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.⁴ This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.

The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.

Continue to: Cultural attitudes to puberty

Cultural attitudes to puberty

Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.⁵ Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”

Family identification and attitudes toward mental health

Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.⁴ Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.⁶ Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness^7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo⁹ and a threat to family honor.¹⁰ Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems¹¹ and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”

Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.

The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”⁹ and suicidal ideation may not be disclosed because suicide is forbidden in Islam.¹² Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.¹³

Continue to: Directly asking Ms. S...

Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”¹² may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.

Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.⁴ Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.^7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.

[polldaddy:10040206]

The authors’ observations

Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.

Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.

Continue to: OUTCOME Culturally-appropriate outpatient therapy

 

 

OUTCOME Culturally-appropriate outpatient therapy

Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.

The authors’ observations

Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”

Bottom Line 

Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.

Related Resources

• Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
• Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.  
• Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821. 

Drug Brand Name

Naloxone • Narcan

I read your editorial with appreciation this morning. In my practice, I have worked with adolescents and young adults for more than 30 years, so the fact that many mass shooters are so young has caught my attention.

Of course, there is never just one cause for such horrific actions. But it seems to me that there are two recurring themes in these situations: (1) many shooters are socially isolated and (2) in our culture, the use of guns is glorified as a representation of power and a source of satisfaction. Here are my thoughts on each:

1. Shooters are often loners who exhibit behavior that is deviant or in some way socially unacceptable; this varies from public masturbation or the voicing of scary thoughts and ideas to simply exhibiting social awkwardness. When the lonely, shunned child has access to powerful, multiple-shot weapons, this is a setup for a shooting.

Perhaps society inadvertently causes harm by forcing classroom integration. About 30 years ago, with the hope to normalize abnormal social interactions and to help students understand and accept those who are different from them, schools began to mainstream students with serious learning difficulties, including students with mental illnesses. These children lost their “group,” their classroom community of those similar to themselves. They are still assigned personalized curricula and work one-on-one with special education teachers, but they do not have much of a peer group anymore. These students are put with a group of students—normal kids—that frequently rejects them.

Part of the problem has to do with the demonization of the term “normal”; it is now politically incorrect to designate a student as normal or not, despite the persistence of the bell-shaped curve. If normal, nonviolent behavior is desired, we need to be able to name abnormal behaviors as such.

Parents, understandably, want this type of social integration for their child. But when these students are bullied throughout the day, it takes a toll. We, as parents or providers, may not fully recognize how children experience this bullying, and those affected may not be able to describe it. They then withdraw, not finding anyone to share their feelings and experiences with, to cope. Some of these kids live as loners in school, and around ages 16 to 25, this lifestyle can become intolerable. They may become depressed from the emotional pain, seek revenge, and wish to die.

The desire to die—and to get lots of attention from it—is recognized in many adolescents. Lonely, troubled teens imagine what others will say about them when they are dead, and think of themselves looking down from heaven or somewhere, watching the grief and surprise overtake their peers.

Continue to: To take out others with themselves...

To take out others with themselves makes dying less of a lonely act. Killing themselves and either people they hate or someone they love, to keep them company in the afterlife or to make sure they both suffer together, both make some sense. And both are tragic.

We need to better identify these lonely teens and help them find a friend. They need regular social interaction and monitoring by the same people daily. Red flags often exist. If they are depressed, more intense care and monitoring are needed.

2. The glorification of guns stems from the need of every civilization for warriors to protect them from invaders. Soldiers, war, and weapons of destruction thus become known—to young men, in particular—because there is a need for youth to join the military and train, even if just for a few years. We honor brave soldiers who die in the line of duty.

Some of these men develop expertise in the use of military machine guns—rapid-fire weapons that can kill many people from afar in minutes. They may wish to continue using their skills upon separating from the military; they want military-grade guns at home. This makes sense, for they mastered and practiced this skill for years and can handle guns safely.

Gun shows allow the purchase of military-grade weapons fairly easily in many states. In the right hands, no problem. But our laws about guns are minimal and do not check to ensure that the buyer is one of these healthy, normal, skilled men.

Continue to: This accessibility is compounded with...

This accessibility is compounded with the popularity of violent video games among teens and young adults, which often involve shooting animated characters and animals in realistic scenarios. There is apparently a sense of adventure, satisfaction, and power that comes from this.

The desire to hunt in the real world, with real weapons, for a heightened sense of accomplishment or power as a follow-up to this fantastical activity seems a normal progression of behavior. Shooting ranges, wild animal hunting farms, and deer hunting in autumn are usual and customary ways to fulfill this desire. Families in western New York, where I live, often teach their sons and daughters to use a gun starting at age 12 and take them on annual hunting trips. This is not a problem.

When a teen or young person becomes despondent and lonely, the feelings of power and satisfaction from hunting or killing something can act as an antidote to the negative feelings. If anger or jealousy are part of the problem, the weapon can be turned on the perceived source of those feelings. The shooters in these devastating massacres seem to be able to use their chosen weapon competently. Where does this familiarity come from? Often, the weapon was accessible in their own home.

Teens and young adults with depression or feelings of loneliness, anger, or jealousy should be evaluated for access to weapons, and for their knowledge of use of these weapons, as part of the care plan. Parents and other adults should be queried and warned to keep weapons away from them until their mood has stabilized. There is reluctance to do this in our society. Health care and law enforcement professionals need to put out public announcements that give this warning to everyone.

Alone, these two ideas I’ve outlined will not prevent all mass shootings. But a more rapid reaction to the red flags of loneliness, mood changes, and social changes in a young person, and seeking to change that dynamic, might reduce the prevalence. Public health is at stake, and prevention will require a willingness to see and react to troubled people—before the police need to be called for a crime.

Sandra Glantz, MSN, MPA, FNP-BC
Pittsford, NY

I read your editorial with appreciation this morning. In my practice, I have worked with adolescents and young adults for more than 30 years, so the fact that many mass shooters are so young has caught my attention.

Of course, there is never just one cause for such horrific actions. But it seems to me that there are two recurring themes in these situations: (1) many shooters are socially isolated and (2) in our culture, the use of guns is glorified as a representation of power and a source of satisfaction. Here are my thoughts on each:

1. Shooters are often loners who exhibit behavior that is deviant or in some way socially unacceptable; this varies from public masturbation or the voicing of scary thoughts and ideas to simply exhibiting social awkwardness. When the lonely, shunned child has access to powerful, multiple-shot weapons, this is a setup for a shooting.

Perhaps society inadvertently causes harm by forcing classroom integration. About 30 years ago, with the hope to normalize abnormal social interactions and to help students understand and accept those who are different from them, schools began to mainstream students with serious learning difficulties, including students with mental illnesses. These children lost their “group,” their classroom community of those similar to themselves. They are still assigned personalized curricula and work one-on-one with special education teachers, but they do not have much of a peer group anymore. These students are put with a group of students—normal kids—that frequently rejects them.

Part of the problem has to do with the demonization of the term “normal”; it is now politically incorrect to designate a student as normal or not, despite the persistence of the bell-shaped curve. If normal, nonviolent behavior is desired, we need to be able to name abnormal behaviors as such.

Parents, understandably, want this type of social integration for their child. But when these students are bullied throughout the day, it takes a toll. We, as parents or providers, may not fully recognize how children experience this bullying, and those affected may not be able to describe it. They then withdraw, not finding anyone to share their feelings and experiences with, to cope. Some of these kids live as loners in school, and around ages 16 to 25, this lifestyle can become intolerable. They may become depressed from the emotional pain, seek revenge, and wish to die.

The desire to die—and to get lots of attention from it—is recognized in many adolescents. Lonely, troubled teens imagine what others will say about them when they are dead, and think of themselves looking down from heaven or somewhere, watching the grief and surprise overtake their peers.

Continue to: To take out others with themselves...

To take out others with themselves makes dying less of a lonely act. Killing themselves and either people they hate or someone they love, to keep them company in the afterlife or to make sure they both suffer together, both make some sense. And both are tragic.

We need to better identify these lonely teens and help them find a friend. They need regular social interaction and monitoring by the same people daily. Red flags often exist. If they are depressed, more intense care and monitoring are needed.

2. The glorification of guns stems from the need of every civilization for warriors to protect them from invaders. Soldiers, war, and weapons of destruction thus become known—to young men, in particular—because there is a need for youth to join the military and train, even if just for a few years. We honor brave soldiers who die in the line of duty.

Some of these men develop expertise in the use of military machine guns—rapid-fire weapons that can kill many people from afar in minutes. They may wish to continue using their skills upon separating from the military; they want military-grade guns at home. This makes sense, for they mastered and practiced this skill for years and can handle guns safely.

Gun shows allow the purchase of military-grade weapons fairly easily in many states. In the right hands, no problem. But our laws about guns are minimal and do not check to ensure that the buyer is one of these healthy, normal, skilled men.

Continue to: This accessibility is compounded with...

This accessibility is compounded with the popularity of violent video games among teens and young adults, which often involve shooting animated characters and animals in realistic scenarios. There is apparently a sense of adventure, satisfaction, and power that comes from this.

The desire to hunt in the real world, with real weapons, for a heightened sense of accomplishment or power as a follow-up to this fantastical activity seems a normal progression of behavior. Shooting ranges, wild animal hunting farms, and deer hunting in autumn are usual and customary ways to fulfill this desire. Families in western New York, where I live, often teach their sons and daughters to use a gun starting at age 12 and take them on annual hunting trips. This is not a problem.

When a teen or young person becomes despondent and lonely, the feelings of power and satisfaction from hunting or killing something can act as an antidote to the negative feelings. If anger or jealousy are part of the problem, the weapon can be turned on the perceived source of those feelings. The shooters in these devastating massacres seem to be able to use their chosen weapon competently. Where does this familiarity come from? Often, the weapon was accessible in their own home.

Teens and young adults with depression or feelings of loneliness, anger, or jealousy should be evaluated for access to weapons, and for their knowledge of use of these weapons, as part of the care plan. Parents and other adults should be queried and warned to keep weapons away from them until their mood has stabilized. There is reluctance to do this in our society. Health care and law enforcement professionals need to put out public announcements that give this warning to everyone.

Alone, these two ideas I’ve outlined will not prevent all mass shootings. But a more rapid reaction to the red flags of loneliness, mood changes, and social changes in a young person, and seeking to change that dynamic, might reduce the prevalence. Public health is at stake, and prevention will require a willingness to see and react to troubled people—before the police need to be called for a crime.

Sandra Glantz, MSN, MPA, FNP-BC
Pittsford, NY

I read your editorial with appreciation this morning. In my practice, I have worked with adolescents and young adults for more than 30 years, so the fact that many mass shooters are so young has caught my attention.

Of course, there is never just one cause for such horrific actions. But it seems to me that there are two recurring themes in these situations: (1) many shooters are socially isolated and (2) in our culture, the use of guns is glorified as a representation of power and a source of satisfaction. Here are my thoughts on each:

1. Shooters are often loners who exhibit behavior that is deviant or in some way socially unacceptable; this varies from public masturbation or the voicing of scary thoughts and ideas to simply exhibiting social awkwardness. When the lonely, shunned child has access to powerful, multiple-shot weapons, this is a setup for a shooting.

Perhaps society inadvertently causes harm by forcing classroom integration. About 30 years ago, with the hope to normalize abnormal social interactions and to help students understand and accept those who are different from them, schools began to mainstream students with serious learning difficulties, including students with mental illnesses. These children lost their “group,” their classroom community of those similar to themselves. They are still assigned personalized curricula and work one-on-one with special education teachers, but they do not have much of a peer group anymore. These students are put with a group of students—normal kids—that frequently rejects them.

Part of the problem has to do with the demonization of the term “normal”; it is now politically incorrect to designate a student as normal or not, despite the persistence of the bell-shaped curve. If normal, nonviolent behavior is desired, we need to be able to name abnormal behaviors as such.

Parents, understandably, want this type of social integration for their child. But when these students are bullied throughout the day, it takes a toll. We, as parents or providers, may not fully recognize how children experience this bullying, and those affected may not be able to describe it. They then withdraw, not finding anyone to share their feelings and experiences with, to cope. Some of these kids live as loners in school, and around ages 16 to 25, this lifestyle can become intolerable. They may become depressed from the emotional pain, seek revenge, and wish to die.

The desire to die—and to get lots of attention from it—is recognized in many adolescents. Lonely, troubled teens imagine what others will say about them when they are dead, and think of themselves looking down from heaven or somewhere, watching the grief and surprise overtake their peers.

Continue to: To take out others with themselves...

To take out others with themselves makes dying less of a lonely act. Killing themselves and either people they hate or someone they love, to keep them company in the afterlife or to make sure they both suffer together, both make some sense. And both are tragic.

We need to better identify these lonely teens and help them find a friend. They need regular social interaction and monitoring by the same people daily. Red flags often exist. If they are depressed, more intense care and monitoring are needed.

2. The glorification of guns stems from the need of every civilization for warriors to protect them from invaders. Soldiers, war, and weapons of destruction thus become known—to young men, in particular—because there is a need for youth to join the military and train, even if just for a few years. We honor brave soldiers who die in the line of duty.

Some of these men develop expertise in the use of military machine guns—rapid-fire weapons that can kill many people from afar in minutes. They may wish to continue using their skills upon separating from the military; they want military-grade guns at home. This makes sense, for they mastered and practiced this skill for years and can handle guns safely.

Gun shows allow the purchase of military-grade weapons fairly easily in many states. In the right hands, no problem. But our laws about guns are minimal and do not check to ensure that the buyer is one of these healthy, normal, skilled men.

Continue to: This accessibility is compounded with...

This accessibility is compounded with the popularity of violent video games among teens and young adults, which often involve shooting animated characters and animals in realistic scenarios. There is apparently a sense of adventure, satisfaction, and power that comes from this.

The desire to hunt in the real world, with real weapons, for a heightened sense of accomplishment or power as a follow-up to this fantastical activity seems a normal progression of behavior. Shooting ranges, wild animal hunting farms, and deer hunting in autumn are usual and customary ways to fulfill this desire. Families in western New York, where I live, often teach their sons and daughters to use a gun starting at age 12 and take them on annual hunting trips. This is not a problem.

When a teen or young person becomes despondent and lonely, the feelings of power and satisfaction from hunting or killing something can act as an antidote to the negative feelings. If anger or jealousy are part of the problem, the weapon can be turned on the perceived source of those feelings. The shooters in these devastating massacres seem to be able to use their chosen weapon competently. Where does this familiarity come from? Often, the weapon was accessible in their own home.

Teens and young adults with depression or feelings of loneliness, anger, or jealousy should be evaluated for access to weapons, and for their knowledge of use of these weapons, as part of the care plan. Parents and other adults should be queried and warned to keep weapons away from them until their mood has stabilized. There is reluctance to do this in our society. Health care and law enforcement professionals need to put out public announcements that give this warning to everyone.

Alone, these two ideas I’ve outlined will not prevent all mass shootings. But a more rapid reaction to the red flags of loneliness, mood changes, and social changes in a young person, and seeking to change that dynamic, might reduce the prevalence. Public health is at stake, and prevention will require a willingness to see and react to troubled people—before the police need to be called for a crime.

Sandra Glantz, MSN, MPA, FNP-BC
Pittsford, NY

EVIDENCE SUMMARY

A 2016 systematic review and meta-analysis of 3 RCTs that included 3200 women with late preterm labor (between 34 weeks 0 days and 36 weeks 6 days) found that women who were given betamethasone had a significantly lower incidence of transient tachypnea of the newborn (number needed to treat [NNT]=37; relative risk [RR]=0.72; 95% confidence interval [CI], 0.56-0.92), severe respiratory distress syndrome (NNT=114; RR=0.60; 95% CI, 0.33-0.94), and use of surfactant (NNT=92; RR=0.61; 95% CI, 0.38-0.99).¹

A composite outcome measure also favors betamethasone

In addition to these 3 outcomes, the largest RCT in the meta-analysis evaluated a composite outcome and found that betamethasone improved it by 20%. The RCT, comparing 1427 women in the experimental arm with 1400 controls, found benefit to administering 12 mg betamethasone intramuscularly every 24 hours for 2 days for women at high risk of late preterm delivery.² Enrollment criteria included women with 3 cm dilation or 75% effacement, preterm premature rupture of membranes, or a planned delivery scheduled in the late preterm period.

The primary outcome was a composite score based on one or more of the following within 72 hours after birth: continuous positive airway pressure or high-flow nasal cannula for at least 2 continuous hours, supplemental oxygen with a fraction of inspired oxygen of 0.30 or more for at least 4 continuous hours, mechanical ventilation, stillbirth or neonatal death, or the need for extracorporeal circulation membrane oxygenation. The betamethasone group had 165 women (11.6%) with the primary outcome compared with 202 (14.4%) in the control arm (NNT=34; RR=0.80; 95% CI, 0.66–0.97; P<.02).

Neonatal hypoglycemia may increase, but not dangerously

The same RCT explored the risks of late preterm betamethasone. There was no increase in chorioamnionitis nor neonatal sepsis in the betamethasone group.² Although neonatal hypoglycemia increased (24% vs 15%; number needed to harm=11.1; RR=1.60; 95% CI, 1.37-1.87; P<.001), no increase was seen in intermediate care nursery or ICU stays (41.8% vs 44.9%; RR=0.93; 95% CI, 0.85-1.01; P=.09) nor length of hospital stay (7 vs 8 days; P=.20).

Three letters to the editor questioned whether hypoglycemia from late-term corticosteroids may lead to long-term neurocognitive delays.³ The authors responded that meta-analyses of RCTs haven’t found an association between antenatal steroid use and neurocognitive delay and that studies that have found an association between hypoglycemia and neurocognitive delay looked at profound and prolonged hypoglycemia, which wasn’t seen in the late preterm betamethasone study.

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

Both the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine have published recommendations supporting corticosteroids for threatened late preterm delivery with certain caveats.^4-6 Because of a lack of evidence, maternity care providers shouldn’t give corticosteroids for threatened late preterm delivery to women with multiple gestation, diabetes, previous exposure to steroids during pregnancy, or pregnancies with major nonlethal fetal malformations.^4-6 Evidence doesn’t support tocolysis when steroids are given in the late preterm period.^4,5

EVIDENCE SUMMARY

A 2016 systematic review and meta-analysis of 3 RCTs that included 3200 women with late preterm labor (between 34 weeks 0 days and 36 weeks 6 days) found that women who were given betamethasone had a significantly lower incidence of transient tachypnea of the newborn (number needed to treat [NNT]=37; relative risk [RR]=0.72; 95% confidence interval [CI], 0.56-0.92), severe respiratory distress syndrome (NNT=114; RR=0.60; 95% CI, 0.33-0.94), and use of surfactant (NNT=92; RR=0.61; 95% CI, 0.38-0.99).¹

A composite outcome measure also favors betamethasone

In addition to these 3 outcomes, the largest RCT in the meta-analysis evaluated a composite outcome and found that betamethasone improved it by 20%. The RCT, comparing 1427 women in the experimental arm with 1400 controls, found benefit to administering 12 mg betamethasone intramuscularly every 24 hours for 2 days for women at high risk of late preterm delivery.² Enrollment criteria included women with 3 cm dilation or 75% effacement, preterm premature rupture of membranes, or a planned delivery scheduled in the late preterm period.

The primary outcome was a composite score based on one or more of the following within 72 hours after birth: continuous positive airway pressure or high-flow nasal cannula for at least 2 continuous hours, supplemental oxygen with a fraction of inspired oxygen of 0.30 or more for at least 4 continuous hours, mechanical ventilation, stillbirth or neonatal death, or the need for extracorporeal circulation membrane oxygenation. The betamethasone group had 165 women (11.6%) with the primary outcome compared with 202 (14.4%) in the control arm (NNT=34; RR=0.80; 95% CI, 0.66–0.97; P<.02).

Neonatal hypoglycemia may increase, but not dangerously

The same RCT explored the risks of late preterm betamethasone. There was no increase in chorioamnionitis nor neonatal sepsis in the betamethasone group.² Although neonatal hypoglycemia increased (24% vs 15%; number needed to harm=11.1; RR=1.60; 95% CI, 1.37-1.87; P<.001), no increase was seen in intermediate care nursery or ICU stays (41.8% vs 44.9%; RR=0.93; 95% CI, 0.85-1.01; P=.09) nor length of hospital stay (7 vs 8 days; P=.20).

Three letters to the editor questioned whether hypoglycemia from late-term corticosteroids may lead to long-term neurocognitive delays.³ The authors responded that meta-analyses of RCTs haven’t found an association between antenatal steroid use and neurocognitive delay and that studies that have found an association between hypoglycemia and neurocognitive delay looked at profound and prolonged hypoglycemia, which wasn’t seen in the late preterm betamethasone study.

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

Both the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine have published recommendations supporting corticosteroids for threatened late preterm delivery with certain caveats.^4-6 Because of a lack of evidence, maternity care providers shouldn’t give corticosteroids for threatened late preterm delivery to women with multiple gestation, diabetes, previous exposure to steroids during pregnancy, or pregnancies with major nonlethal fetal malformations.^4-6 Evidence doesn’t support tocolysis when steroids are given in the late preterm period.^4,5

EVIDENCE SUMMARY

A 2016 systematic review and meta-analysis of 3 RCTs that included 3200 women with late preterm labor (between 34 weeks 0 days and 36 weeks 6 days) found that women who were given betamethasone had a significantly lower incidence of transient tachypnea of the newborn (number needed to treat [NNT]=37; relative risk [RR]=0.72; 95% confidence interval [CI], 0.56-0.92), severe respiratory distress syndrome (NNT=114; RR=0.60; 95% CI, 0.33-0.94), and use of surfactant (NNT=92; RR=0.61; 95% CI, 0.38-0.99).¹

A composite outcome measure also favors betamethasone

In addition to these 3 outcomes, the largest RCT in the meta-analysis evaluated a composite outcome and found that betamethasone improved it by 20%. The RCT, comparing 1427 women in the experimental arm with 1400 controls, found benefit to administering 12 mg betamethasone intramuscularly every 24 hours for 2 days for women at high risk of late preterm delivery.² Enrollment criteria included women with 3 cm dilation or 75% effacement, preterm premature rupture of membranes, or a planned delivery scheduled in the late preterm period.

The primary outcome was a composite score based on one or more of the following within 72 hours after birth: continuous positive airway pressure or high-flow nasal cannula for at least 2 continuous hours, supplemental oxygen with a fraction of inspired oxygen of 0.30 or more for at least 4 continuous hours, mechanical ventilation, stillbirth or neonatal death, or the need for extracorporeal circulation membrane oxygenation. The betamethasone group had 165 women (11.6%) with the primary outcome compared with 202 (14.4%) in the control arm (NNT=34; RR=0.80; 95% CI, 0.66–0.97; P<.02).

Neonatal hypoglycemia may increase, but not dangerously

The same RCT explored the risks of late preterm betamethasone. There was no increase in chorioamnionitis nor neonatal sepsis in the betamethasone group.² Although neonatal hypoglycemia increased (24% vs 15%; number needed to harm=11.1; RR=1.60; 95% CI, 1.37-1.87; P<.001), no increase was seen in intermediate care nursery or ICU stays (41.8% vs 44.9%; RR=0.93; 95% CI, 0.85-1.01; P=.09) nor length of hospital stay (7 vs 8 days; P=.20).

Three letters to the editor questioned whether hypoglycemia from late-term corticosteroids may lead to long-term neurocognitive delays.³ The authors responded that meta-analyses of RCTs haven’t found an association between antenatal steroid use and neurocognitive delay and that studies that have found an association between hypoglycemia and neurocognitive delay looked at profound and prolonged hypoglycemia, which wasn’t seen in the late preterm betamethasone study.

Continue to: RECOMMENDATIONS

 

 

RECOMMENDATIONS

Both the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine have published recommendations supporting corticosteroids for threatened late preterm delivery with certain caveats.^4-6 Because of a lack of evidence, maternity care providers shouldn’t give corticosteroids for threatened late preterm delivery to women with multiple gestation, diabetes, previous exposure to steroids during pregnancy, or pregnancies with major nonlethal fetal malformations.^4-6 Evidence doesn’t support tocolysis when steroids are given in the late preterm period.^4,5

EVIDENCE SUMMARY

Three meta-analyses that included only randomized controlled trials (RCTs) compared various CBT delivery methods with controls (wait-listed for treatment or general sleep hygiene education) to assess sleep outcomes for adults with insomnia.^1-3 TABLE 1^1-3 summarizes the results.

CBT is comparable to pharmacotherapy

A 2002 comparative meta-analysis of 21 RCTs with a total of 470 patients examined the effectiveness of CBT (stimulus control and/or sleep restriction) compared with pharmacotherapy (benzodiazepines or benzodiazepine agonists) for treating primary insomnia of longer than one month’s duration in adults with no comorbid medical or psychiatric diagnoses.⁴ The CBT group received intervention over an average of 5 weeks, and the pharmacotherapy group received intervention over an average of 2 weeks.

CBT produced greater reductions in sleep onset latency than pharmacotherapy based on mean weighted effect size (1.05 vs 0.45 weighted effect size; 95% confidence interval, 0.17-1.04; P=.01). Although both CBT and pharmacotherapy improved sleep outcomes, no statistical differences were found in wake after sleep onset time, total sleep time, number of awakenings, or sleep quality ratings (TABLE 2⁴).

Continue to: CBT has significant benefit for comorbid insomnia

 

 

CBT has significant benefit for comorbid insomnia

A 2015 meta-analysis of 23 studies enrolling a total of 1379 adults with a number of illnesses (chronic pain, alcohol dependence, breast cancer, psychiatric disorders, chronic obstructive pulmonary disease, fibromyalgia) and comorbid insomnia investigated the qualitative effectiveness of individual or group CBT therapy.⁵ Subjects received at least 4 face-to-face sessions and at least 2 components of CBT.

The primary outcome showed that sleep quality improved, as measured by a 6.36-point reduction in the Insomnia Severity Index (ISI; a 7-question scale on which 0=no insomnia and 28=severe insomnia) and a 3.3-point reduction in the Pittsburgh Sleep Quality Index (PSQI; a 7-category assessment tool on which 0=perfect quality and 21=poor quality). The effect size was large for both ISI and PSQI, as indicated by standard mean differences greater than 0.8 (1.22 and 0.88, respectively) and was sustained for as long as 18 months.

RECOMMENDATIONS

The American College of Physicians strongly recommends that all adult patients receive CBT as initial treatment for chronic insomnia disorder. It can be performed in multiple settings, including the primary care setting. Compared with hypnotics, CBT is unlikely to have any adverse effects.⁶

EVIDENCE SUMMARY

Three meta-analyses that included only randomized controlled trials (RCTs) compared various CBT delivery methods with controls (wait-listed for treatment or general sleep hygiene education) to assess sleep outcomes for adults with insomnia.^1-3 TABLE 1^1-3 summarizes the results.

CBT is comparable to pharmacotherapy

A 2002 comparative meta-analysis of 21 RCTs with a total of 470 patients examined the effectiveness of CBT (stimulus control and/or sleep restriction) compared with pharmacotherapy (benzodiazepines or benzodiazepine agonists) for treating primary insomnia of longer than one month’s duration in adults with no comorbid medical or psychiatric diagnoses.⁴ The CBT group received intervention over an average of 5 weeks, and the pharmacotherapy group received intervention over an average of 2 weeks.

CBT produced greater reductions in sleep onset latency than pharmacotherapy based on mean weighted effect size (1.05 vs 0.45 weighted effect size; 95% confidence interval, 0.17-1.04; P=.01). Although both CBT and pharmacotherapy improved sleep outcomes, no statistical differences were found in wake after sleep onset time, total sleep time, number of awakenings, or sleep quality ratings (TABLE 2⁴).

Continue to: CBT has significant benefit for comorbid insomnia

 

 

CBT has significant benefit for comorbid insomnia

A 2015 meta-analysis of 23 studies enrolling a total of 1379 adults with a number of illnesses (chronic pain, alcohol dependence, breast cancer, psychiatric disorders, chronic obstructive pulmonary disease, fibromyalgia) and comorbid insomnia investigated the qualitative effectiveness of individual or group CBT therapy.⁵ Subjects received at least 4 face-to-face sessions and at least 2 components of CBT.

The primary outcome showed that sleep quality improved, as measured by a 6.36-point reduction in the Insomnia Severity Index (ISI; a 7-question scale on which 0=no insomnia and 28=severe insomnia) and a 3.3-point reduction in the Pittsburgh Sleep Quality Index (PSQI; a 7-category assessment tool on which 0=perfect quality and 21=poor quality). The effect size was large for both ISI and PSQI, as indicated by standard mean differences greater than 0.8 (1.22 and 0.88, respectively) and was sustained for as long as 18 months.

RECOMMENDATIONS

The American College of Physicians strongly recommends that all adult patients receive CBT as initial treatment for chronic insomnia disorder. It can be performed in multiple settings, including the primary care setting. Compared with hypnotics, CBT is unlikely to have any adverse effects.⁶

EVIDENCE SUMMARY

Three meta-analyses that included only randomized controlled trials (RCTs) compared various CBT delivery methods with controls (wait-listed for treatment or general sleep hygiene education) to assess sleep outcomes for adults with insomnia.^1-3 TABLE 1^1-3 summarizes the results.

CBT is comparable to pharmacotherapy

A 2002 comparative meta-analysis of 21 RCTs with a total of 470 patients examined the effectiveness of CBT (stimulus control and/or sleep restriction) compared with pharmacotherapy (benzodiazepines or benzodiazepine agonists) for treating primary insomnia of longer than one month’s duration in adults with no comorbid medical or psychiatric diagnoses.⁴ The CBT group received intervention over an average of 5 weeks, and the pharmacotherapy group received intervention over an average of 2 weeks.

CBT produced greater reductions in sleep onset latency than pharmacotherapy based on mean weighted effect size (1.05 vs 0.45 weighted effect size; 95% confidence interval, 0.17-1.04; P=.01). Although both CBT and pharmacotherapy improved sleep outcomes, no statistical differences were found in wake after sleep onset time, total sleep time, number of awakenings, or sleep quality ratings (TABLE 2⁴).

Continue to: CBT has significant benefit for comorbid insomnia

 

 

CBT has significant benefit for comorbid insomnia

A 2015 meta-analysis of 23 studies enrolling a total of 1379 adults with a number of illnesses (chronic pain, alcohol dependence, breast cancer, psychiatric disorders, chronic obstructive pulmonary disease, fibromyalgia) and comorbid insomnia investigated the qualitative effectiveness of individual or group CBT therapy.⁵ Subjects received at least 4 face-to-face sessions and at least 2 components of CBT.

The primary outcome showed that sleep quality improved, as measured by a 6.36-point reduction in the Insomnia Severity Index (ISI; a 7-question scale on which 0=no insomnia and 28=severe insomnia) and a 3.3-point reduction in the Pittsburgh Sleep Quality Index (PSQI; a 7-category assessment tool on which 0=perfect quality and 21=poor quality). The effect size was large for both ISI and PSQI, as indicated by standard mean differences greater than 0.8 (1.22 and 0.88, respectively) and was sustained for as long as 18 months.

RECOMMENDATIONS

The American College of Physicians strongly recommends that all adult patients receive CBT as initial treatment for chronic insomnia disorder. It can be performed in multiple settings, including the primary care setting. Compared with hypnotics, CBT is unlikely to have any adverse effects.⁶

A 44-year-old African-American woman with sickle cell trait presented to the clinic to establish care. She complained of polyarthralgias that she’d had since adolescence; the pain was worst in her right shoulder. She reported morning stiffness that lasted up to 8 hours, an intermittent facial rash, oral ulcers, joint edema (of which she had pictures on her phone), and photosensitivity. She took ibuprofen and acetaminophen as needed for pain. She once worked as a medical assistant but hadn’t been able to work since 2014 due to pain. She reported having been told as a teenager that she might have juvenile arthritis, but she didn’t recall ever having diagnostic tests performed or receiving treatment other than anti-inflammatories.

A couple of weeks after an initial visit with a rheumatologist, the patient returned to the family medicine clinic. She said she was upset that the specialist had x-rayed her hands, but had not checked her shoulder, which was the primary source of her pain. She also had pain in her hands, hips, feet, and knees.

On physical exam, the patient looked fatigued. A musculoskeletal exam revealed no joint effusions or edema, but was significant for right shoulder pain with reduced abduction to 90°. Gross motor strength was 5/5 in all 4 extremities. Laboratory testing revealed an antinuclear antibody titer of 1:160 and was negative for double-stranded DNA. Bilateral hand and foot x-rays showed no joint erosions. An x-ray of the right shoulder was obtained, which showed evidence of osteopenia and an erosion in the humeral head (FIGURES 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Rheumatoid arthritis

The patient’s history of morning stiffness and the joint erosion observed on x-ray were highly suggestive of rheumatoid arthritis (RA).

Joint stiffness due to osteoarthritis is worse with activity and generally lasts only a few minutes, while joint stiffness due to rheumatoid arthritis is worse at rest and lasts 30 minutes or more.

RA is a symmetric, inflammatory, peripheral polyarthritis of unknown etiology. It is the most common form of inflammatory arthritis, affecting 1% of the population worldwide.¹ It causes cartilage and bone to erode, leading to the deformation and destruction of joints. If RA is left untreated or is unresponsive to therapy, it can eventually lead to loss of physical function.

Making the diagnosis

The distinctive signs of RA are joint erosions and rheumatoid nodules, which are often absent on initial presentation.

Classification criteria. The 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria for RA² are based on the presence of synovitis in at least one joint, the absence of an alternative diagnosis that better explains the synovitis, and a cumulative score of at least 6/10 from the following 4 domains:

1. Number and site of involved joints
   • 2 to 10 large joints (shoulders, elbows, hips, knees, ankles)=1 point
   • 1 to 3 small joints (metacarpophalangeal [MCP] joints, proximal interphalangeal [PIP] joints, 2nd-5th metatarsophalangeal joints, thumb interphalangeal joints, wrists)=2 points
   • 4 to 10 small joints=3 points
   • More than 10 joints (including at least 1 small joint)=5 points
2. Serologic abnormality (rheumatoid factor [RF] and anti-cyclic citrullinated peptide)
   • Low positive=2 points
   • High positive=3 points
3. Elevated acute phase response (erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP])=1 point
4. Symptom duration of at least 6 weeks=1 point.

These criteria are best suited for early disease. For patients with longstanding symptoms, diagnosis is based on an erosive disease with a history of criteria fulfillment, or a currently inactive longstanding disease, with or without treatment, that has previously fulfilled the criteria.³

Continue to: The differential Dx is extensive

 

 

The differential Dx is extensive

The differential includes polyarthralgias such as viral polyarthritis, systemic rheumatic diseases, and osteoarthritis.

Viral polyarthritis is caused by rubella, parvovirus B19⁴, alphaviruses, and hepatitis B. Symptoms can last from 3 days to several weeks, but rarely persist beyond 6 weeks; alphaviruses, however, can last 3 to 6 months.⁵ The common symptom triad includes fever, arthritis, and rash. Chikungunya is an example of an alphavirus that has become a global disease. Alphavirus arthritis can mimic seronegative RA and even satisfy the classification criteria for RA if the initial symptoms of fever and rash and history of travel to endemic regions are not appreciated.⁵

Systemic rheumatic diseases. Early RA may mimic the arthritis of systemic lupus erythematosus (SLE), Sjögren’s syndrome, dermatomyositis, or mixed connective tissue disease.⁶ In contrast to RA, these disorders generally have systemic features, such as rashes, dry mouth and eyes, myositis, or nephritis, and generate autobodies, which are not seen with RA. The CRP is often normal in patients with active SLE, even when the ESR is elevated.

Immediate treatment with disease-modifying antirheumatic drugs is important to achieve disease control and prevent disability.

Osteoarthritis (OA) can be confused with RA, particularly when small joints are involved. A thorough history helps elucidate the diagnosis. For example, OA of the fingers affects distal interphalangeal joints and is associated with Heberden’s nodes, while RA more commonly affects MCP and PIP joints. Swelling from OA is typically firm, while swelling due to RA is warm, boggy, and tender. Joint stiffness due to OA is worse with activity and generally lasts only a few minutes, while joint stiffness due to RA is worse at rest and lasts 30 minutes or more. X-rays show joint-space narrowing with OA, but no erosions or cysts. RF may be present at low levels in older patients with OA, while it is usually associated with high levels in patients with seropositive RA.

Continue to: Treat with disease-modifying antirheumatic drugs

 

 

Treat with disease-modifying antirheumatic drugs

Immediate treatment of RA with disease-modifying antirheumatic drugs (DMARDs) is important to achieve control of the disease and prevent disability.

Our patient. We ordered a purified protein derivative skin test in preparation for the patient to start therapy with a DMARD. Our patient followed up with Rheumatology and was started on indomethacin, with an initial dose of 25 mg bid. (DMARDs are first-line therapy; indomethacin is a second-line choice. In this case, the patient declined DMARDs after hearing they lowered the body’s ability to fight infection.) An RF level measured 6.74 IU/ml, which is within normal limits. The patient was subsequently lost to follow-up.

CORRESPONDENCE
Barbara Kiersz, DO, 6835 Austin Center Blvd., Austin, TX 78731; bmkiersz@gmail.com.

A 44-year-old African-American woman with sickle cell trait presented to the clinic to establish care. She complained of polyarthralgias that she’d had since adolescence; the pain was worst in her right shoulder. She reported morning stiffness that lasted up to 8 hours, an intermittent facial rash, oral ulcers, joint edema (of which she had pictures on her phone), and photosensitivity. She took ibuprofen and acetaminophen as needed for pain. She once worked as a medical assistant but hadn’t been able to work since 2014 due to pain. She reported having been told as a teenager that she might have juvenile arthritis, but she didn’t recall ever having diagnostic tests performed or receiving treatment other than anti-inflammatories.

A couple of weeks after an initial visit with a rheumatologist, the patient returned to the family medicine clinic. She said she was upset that the specialist had x-rayed her hands, but had not checked her shoulder, which was the primary source of her pain. She also had pain in her hands, hips, feet, and knees.

On physical exam, the patient looked fatigued. A musculoskeletal exam revealed no joint effusions or edema, but was significant for right shoulder pain with reduced abduction to 90°. Gross motor strength was 5/5 in all 4 extremities. Laboratory testing revealed an antinuclear antibody titer of 1:160 and was negative for double-stranded DNA. Bilateral hand and foot x-rays showed no joint erosions. An x-ray of the right shoulder was obtained, which showed evidence of osteopenia and an erosion in the humeral head (FIGURES 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Rheumatoid arthritis

The patient’s history of morning stiffness and the joint erosion observed on x-ray were highly suggestive of rheumatoid arthritis (RA).

Joint stiffness due to osteoarthritis is worse with activity and generally lasts only a few minutes, while joint stiffness due to rheumatoid arthritis is worse at rest and lasts 30 minutes or more.

RA is a symmetric, inflammatory, peripheral polyarthritis of unknown etiology. It is the most common form of inflammatory arthritis, affecting 1% of the population worldwide.¹ It causes cartilage and bone to erode, leading to the deformation and destruction of joints. If RA is left untreated or is unresponsive to therapy, it can eventually lead to loss of physical function.

Making the diagnosis

The distinctive signs of RA are joint erosions and rheumatoid nodules, which are often absent on initial presentation.

Classification criteria. The 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria for RA² are based on the presence of synovitis in at least one joint, the absence of an alternative diagnosis that better explains the synovitis, and a cumulative score of at least 6/10 from the following 4 domains:

1. Number and site of involved joints
   • 2 to 10 large joints (shoulders, elbows, hips, knees, ankles)=1 point
   • 1 to 3 small joints (metacarpophalangeal [MCP] joints, proximal interphalangeal [PIP] joints, 2nd-5th metatarsophalangeal joints, thumb interphalangeal joints, wrists)=2 points
   • 4 to 10 small joints=3 points
   • More than 10 joints (including at least 1 small joint)=5 points
2. Serologic abnormality (rheumatoid factor [RF] and anti-cyclic citrullinated peptide)
   • Low positive=2 points
   • High positive=3 points
3. Elevated acute phase response (erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP])=1 point
4. Symptom duration of at least 6 weeks=1 point.

These criteria are best suited for early disease. For patients with longstanding symptoms, diagnosis is based on an erosive disease with a history of criteria fulfillment, or a currently inactive longstanding disease, with or without treatment, that has previously fulfilled the criteria.³

Continue to: The differential Dx is extensive

 

 

The differential Dx is extensive

The differential includes polyarthralgias such as viral polyarthritis, systemic rheumatic diseases, and osteoarthritis.

Viral polyarthritis is caused by rubella, parvovirus B19⁴, alphaviruses, and hepatitis B. Symptoms can last from 3 days to several weeks, but rarely persist beyond 6 weeks; alphaviruses, however, can last 3 to 6 months.⁵ The common symptom triad includes fever, arthritis, and rash. Chikungunya is an example of an alphavirus that has become a global disease. Alphavirus arthritis can mimic seronegative RA and even satisfy the classification criteria for RA if the initial symptoms of fever and rash and history of travel to endemic regions are not appreciated.⁵

Systemic rheumatic diseases. Early RA may mimic the arthritis of systemic lupus erythematosus (SLE), Sjögren’s syndrome, dermatomyositis, or mixed connective tissue disease.⁶ In contrast to RA, these disorders generally have systemic features, such as rashes, dry mouth and eyes, myositis, or nephritis, and generate autobodies, which are not seen with RA. The CRP is often normal in patients with active SLE, even when the ESR is elevated.

Immediate treatment with disease-modifying antirheumatic drugs is important to achieve disease control and prevent disability.

Osteoarthritis (OA) can be confused with RA, particularly when small joints are involved. A thorough history helps elucidate the diagnosis. For example, OA of the fingers affects distal interphalangeal joints and is associated with Heberden’s nodes, while RA more commonly affects MCP and PIP joints. Swelling from OA is typically firm, while swelling due to RA is warm, boggy, and tender. Joint stiffness due to OA is worse with activity and generally lasts only a few minutes, while joint stiffness due to RA is worse at rest and lasts 30 minutes or more. X-rays show joint-space narrowing with OA, but no erosions or cysts. RF may be present at low levels in older patients with OA, while it is usually associated with high levels in patients with seropositive RA.

Continue to: Treat with disease-modifying antirheumatic drugs

 

 

Treat with disease-modifying antirheumatic drugs

Immediate treatment of RA with disease-modifying antirheumatic drugs (DMARDs) is important to achieve control of the disease and prevent disability.

Our patient. We ordered a purified protein derivative skin test in preparation for the patient to start therapy with a DMARD. Our patient followed up with Rheumatology and was started on indomethacin, with an initial dose of 25 mg bid. (DMARDs are first-line therapy; indomethacin is a second-line choice. In this case, the patient declined DMARDs after hearing they lowered the body’s ability to fight infection.) An RF level measured 6.74 IU/ml, which is within normal limits. The patient was subsequently lost to follow-up.

CORRESPONDENCE
Barbara Kiersz, DO, 6835 Austin Center Blvd., Austin, TX 78731; bmkiersz@gmail.com.

A 44-year-old African-American woman with sickle cell trait presented to the clinic to establish care. She complained of polyarthralgias that she’d had since adolescence; the pain was worst in her right shoulder. She reported morning stiffness that lasted up to 8 hours, an intermittent facial rash, oral ulcers, joint edema (of which she had pictures on her phone), and photosensitivity. She took ibuprofen and acetaminophen as needed for pain. She once worked as a medical assistant but hadn’t been able to work since 2014 due to pain. She reported having been told as a teenager that she might have juvenile arthritis, but she didn’t recall ever having diagnostic tests performed or receiving treatment other than anti-inflammatories.

A couple of weeks after an initial visit with a rheumatologist, the patient returned to the family medicine clinic. She said she was upset that the specialist had x-rayed her hands, but had not checked her shoulder, which was the primary source of her pain. She also had pain in her hands, hips, feet, and knees.

On physical exam, the patient looked fatigued. A musculoskeletal exam revealed no joint effusions or edema, but was significant for right shoulder pain with reduced abduction to 90°. Gross motor strength was 5/5 in all 4 extremities. Laboratory testing revealed an antinuclear antibody titer of 1:160 and was negative for double-stranded DNA. Bilateral hand and foot x-rays showed no joint erosions. An x-ray of the right shoulder was obtained, which showed evidence of osteopenia and an erosion in the humeral head (FIGURES 1A and 1B).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

 

 

Diagnosis: Rheumatoid arthritis

The patient’s history of morning stiffness and the joint erosion observed on x-ray were highly suggestive of rheumatoid arthritis (RA).

Joint stiffness due to osteoarthritis is worse with activity and generally lasts only a few minutes, while joint stiffness due to rheumatoid arthritis is worse at rest and lasts 30 minutes or more.

RA is a symmetric, inflammatory, peripheral polyarthritis of unknown etiology. It is the most common form of inflammatory arthritis, affecting 1% of the population worldwide.¹ It causes cartilage and bone to erode, leading to the deformation and destruction of joints. If RA is left untreated or is unresponsive to therapy, it can eventually lead to loss of physical function.

Making the diagnosis

The distinctive signs of RA are joint erosions and rheumatoid nodules, which are often absent on initial presentation.

Classification criteria. The 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria for RA² are based on the presence of synovitis in at least one joint, the absence of an alternative diagnosis that better explains the synovitis, and a cumulative score of at least 6/10 from the following 4 domains:

1. Number and site of involved joints
   • 2 to 10 large joints (shoulders, elbows, hips, knees, ankles)=1 point
   • 1 to 3 small joints (metacarpophalangeal [MCP] joints, proximal interphalangeal [PIP] joints, 2nd-5th metatarsophalangeal joints, thumb interphalangeal joints, wrists)=2 points
   • 4 to 10 small joints=3 points
   • More than 10 joints (including at least 1 small joint)=5 points
2. Serologic abnormality (rheumatoid factor [RF] and anti-cyclic citrullinated peptide)
   • Low positive=2 points
   • High positive=3 points
3. Elevated acute phase response (erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP])=1 point
4. Symptom duration of at least 6 weeks=1 point.

These criteria are best suited for early disease. For patients with longstanding symptoms, diagnosis is based on an erosive disease with a history of criteria fulfillment, or a currently inactive longstanding disease, with or without treatment, that has previously fulfilled the criteria.³

Continue to: The differential Dx is extensive

 

 

The differential Dx is extensive

The differential includes polyarthralgias such as viral polyarthritis, systemic rheumatic diseases, and osteoarthritis.

Viral polyarthritis is caused by rubella, parvovirus B19⁴, alphaviruses, and hepatitis B. Symptoms can last from 3 days to several weeks, but rarely persist beyond 6 weeks; alphaviruses, however, can last 3 to 6 months.⁵ The common symptom triad includes fever, arthritis, and rash. Chikungunya is an example of an alphavirus that has become a global disease. Alphavirus arthritis can mimic seronegative RA and even satisfy the classification criteria for RA if the initial symptoms of fever and rash and history of travel to endemic regions are not appreciated.⁵

Systemic rheumatic diseases. Early RA may mimic the arthritis of systemic lupus erythematosus (SLE), Sjögren’s syndrome, dermatomyositis, or mixed connective tissue disease.⁶ In contrast to RA, these disorders generally have systemic features, such as rashes, dry mouth and eyes, myositis, or nephritis, and generate autobodies, which are not seen with RA. The CRP is often normal in patients with active SLE, even when the ESR is elevated.

Immediate treatment with disease-modifying antirheumatic drugs is important to achieve disease control and prevent disability.

Osteoarthritis (OA) can be confused with RA, particularly when small joints are involved. A thorough history helps elucidate the diagnosis. For example, OA of the fingers affects distal interphalangeal joints and is associated with Heberden’s nodes, while RA more commonly affects MCP and PIP joints. Swelling from OA is typically firm, while swelling due to RA is warm, boggy, and tender. Joint stiffness due to OA is worse with activity and generally lasts only a few minutes, while joint stiffness due to RA is worse at rest and lasts 30 minutes or more. X-rays show joint-space narrowing with OA, but no erosions or cysts. RF may be present at low levels in older patients with OA, while it is usually associated with high levels in patients with seropositive RA.

Continue to: Treat with disease-modifying antirheumatic drugs

 

 

Treat with disease-modifying antirheumatic drugs

Immediate treatment of RA with disease-modifying antirheumatic drugs (DMARDs) is important to achieve control of the disease and prevent disability.

Our patient. We ordered a purified protein derivative skin test in preparation for the patient to start therapy with a DMARD. Our patient followed up with Rheumatology and was started on indomethacin, with an initial dose of 25 mg bid. (DMARDs are first-line therapy; indomethacin is a second-line choice. In this case, the patient declined DMARDs after hearing they lowered the body’s ability to fight infection.) An RF level measured 6.74 IU/ml, which is within normal limits. The patient was subsequently lost to follow-up.

CORRESPONDENCE
Barbara Kiersz, DO, 6835 Austin Center Blvd., Austin, TX 78731; bmkiersz@gmail.com.