Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Symptom domain	Criteria
Separation distress	The patient has ≥1 of the following 4 symptoms: 1) Persistent, intense yearning or longing for the deceased 2) Frequent feelings of intense loneliness or emptiness 3) Recurrent negative thoughts about life without the deceased or recurrent urge to join the deceased 4) Preoccupying thoughts about the deceased that impair daily functioning
Thoughts	The patient has ≥2 of the following 8 symptoms: 1) Rumination about circumstances of the death 2) Frequent disbelief or inability to accept the death
Feelings	3) Persistent feeling of being shocked, stunned, or emotionally numb since the death 4) Recurrent feelings of anger or bitterness regarding the death 5) Difficulty trusting or caring about others since the loss 6) Experiencing pain or other somatic symptoms the deceased person had, hearing the voice of the deceased, or seeing the deceased person 7) Intense emotional reactions to memories of the deceased
Behaviors	8) Excessive avoidance or excessive preoccupation with places, people, and things related to the deceased or death
Source: Adapted from reference 6

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

 

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

 

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

 

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Symptom domain	Criteria
Separation distress	The patient has ≥1 of the following 4 symptoms: 1) Persistent, intense yearning or longing for the deceased 2) Frequent feelings of intense loneliness or emptiness 3) Recurrent negative thoughts about life without the deceased or recurrent urge to join the deceased 4) Preoccupying thoughts about the deceased that impair daily functioning
Thoughts	The patient has ≥2 of the following 8 symptoms: 1) Rumination about circumstances of the death 2) Frequent disbelief or inability to accept the death
Feelings	3) Persistent feeling of being shocked, stunned, or emotionally numb since the death 4) Recurrent feelings of anger or bitterness regarding the death 5) Difficulty trusting or caring about others since the loss 6) Experiencing pain or other somatic symptoms the deceased person had, hearing the voice of the deceased, or seeing the deceased person 7) Intense emotional reactions to memories of the deceased
Behaviors	8) Excessive avoidance or excessive preoccupation with places, people, and things related to the deceased or death
Source: Adapted from reference 6

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

 

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

 

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

 

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Symptom domain	Criteria
Separation distress	The patient has ≥1 of the following 4 symptoms: 1) Persistent, intense yearning or longing for the deceased 2) Frequent feelings of intense loneliness or emptiness 3) Recurrent negative thoughts about life without the deceased or recurrent urge to join the deceased 4) Preoccupying thoughts about the deceased that impair daily functioning
Thoughts	The patient has ≥2 of the following 8 symptoms: 1) Rumination about circumstances of the death 2) Frequent disbelief or inability to accept the death
Feelings	3) Persistent feeling of being shocked, stunned, or emotionally numb since the death 4) Recurrent feelings of anger or bitterness regarding the death 5) Difficulty trusting or caring about others since the loss 6) Experiencing pain or other somatic symptoms the deceased person had, hearing the voice of the deceased, or seeing the deceased person 7) Intense emotional reactions to memories of the deceased
Behaviors	8) Excessive avoidance or excessive preoccupation with places, people, and things related to the deceased or death
Source: Adapted from reference 6

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

 

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

 

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

 

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:

Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.¹ Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.

Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.

Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.

Rating scales. When in doubt, use rating scales to assess for ADHD.² Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.

Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.

Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.

When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.

There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”

When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.

Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.

Disclosure

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

There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:

Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.¹ Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.

Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.

Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.

Rating scales. When in doubt, use rating scales to assess for ADHD.² Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.

Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.

Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.

When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.

There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”

When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.

Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.

Disclosure

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

There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:

Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.¹ Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.

Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.

Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.

Rating scales. When in doubt, use rating scales to assess for ADHD.² Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.

Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.

Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.

When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.

There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”

When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.

Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

You’ve been treating Mr. H, a 54-year-old factory worker and tobacco user, for depression that developed after a work-related back injury and subsequent disability. His depression has had a fair response to an antidepressant. He also has been maintained on chronic opioids (morphine and oxycodone/acetaminophen) for 18 months by his primary care physician (PCP). At the end of your appointment, he asks you for a refill of the opioids because he “ran out” early because of increased night pain and resultant insomnia and “stress.” He clarifies he has asked for early refills before from his PCP, but lately he has been denied. Because you “seem to listen to me more,” he asks for your help. How should you manage Mr. H?

Opioids are among the most commonly misused prescription drugs in the United States.¹ In 2008, poisoning was the leading cause of death from injury in the United States; roughly 90% of poisonings resulted from drug exposure, and >40% of these drug poisonings were from prescription opioids.² The Centers for Disease Control and Prevention estimates that the number of emergency department (ED) visits for nonmedical use of opioids increased 111% between 2004 and 2008, from 144,600 to 305,900 visits.³ The highest number of visits were for use of oxycodone, hydrocodone, and methadone.³

Increased prescribing of opioids and overdose deaths attributable to prescribed opioids have raised concern among physicians about how to effectively treat pain as well as prevent, recognize, and manage aberrant medication-taking behaviors (AMTBs). Psychiatrists are well-positioned to screen and manage their own patients for prescription opioid use disorder (POUD) or collaborate with opioid prescribers to accomplish the same.

Clarifying terminology

Terminology used to describe POUD and related conditions often is poorly defined or loosely applied. Because emotions often enter discussions between patients and physicians about problems related to opioid therapy, nonstigmatizing and more objective terminology is needed, and clinicians are working toward standardizing this. Relevant terms are defined in Table 1.⁴

The DSM-5 Substance Use Disorders Work Group has proposed using the term opioid use disorder (OUD) to replace the term opioid dependence.⁵ The hope is that removing the word “dependence” from the diagnostic term will reduce confusion between “dependence” due to expected physical dependence (tolerance, withdrawal) on medically prescribed opioids vs true addiction (currently defined as “opioid dependence” in DSM-IV-TR). This Work Group also has proposed combining opioid abuse and opioid dependence criteria into a single diagnosis of OUD, and adding “craving” to the criteria. For the complete proposed criteria, see www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=460.These changes are still under review. In this article, we use the term POUD.

Table 1

Terminology related to prescription opioid use disorder

 

Term	Definition
Chronic paina	Pain that extends beyond the expected period for healing (6 months), initiated by tissue damage, but perpetrated by the interaction of physiologic, affective, and environmental factors
Chronic nonmalignant paina	Chronic pain associated with diverse diagnoses and syndromes that are not terminal but affect the patient’s function
Appropriate usea	Taking a prescription as prescribed, and only for the condition indicated
Misusea	Taking a prescription for a reason or at a dose or frequency other than for which it was prescribed; this may or may not reflect POUD
Drug-seeking behaviors	Patient behaviors directed toward obtaining controlled substances, driven not by amelioration of the condition for which the medication was indicated but rather by other maladaptive gains; this may or may not reflect POUD
Chemical coping	Taking a controlled substance medication to relieve psychological problems (eg, to relieve low mood, anxiety, insomnia) and for reasons other than the purpose for which it was prescribed; this may or may not reflect POUD
Aberrant medication-taking behaviorsa	Taking a controlled substance medication in a manner that is not prescribed; causes for this may include: lack of understanding about how to take the opioid appropriately external pressures, such as to give to another person for his or her pain chemical coping pseudoaddiction (see below), including: addiction or substance use disorder (such as POUD) diversion
Pseudoaddiction	An iatrogenic syndrome of “addiction-like” behaviors in which the patient seeks opioids to relieve pain—such as seeking different doctors, self-adjusting the opioid dose, early refills of opioids, etc.—rather than to achieve pleasure or other nonpain-related effect. At times mistaken for true addiction, these behaviors tend to resolve and function improves once analgesia is better addressed
a These terms and definitions are adapted from reference 4. The remaining terms and definitions were developed by the authors POUD: prescription opioid use disorder

POUD and chronic pain

The incidence of POUD during opioid therapy for pain is unknown.⁶ Some researchers have suggested it may be as low as 0.2%,⁷ while others estimate that rates of POUD in patients with chronic pain may be similar to those in the general population: 3% to 16%.⁸ When applying the proposed DSM-5 criteria to patients receiving long-term opioid therapy for noncancer pain, the lifetime prevalence of POUD may be as high as 35%.⁹

 

 

Prescribers may be contributing to POUD. Roughly 76% of opioids used for nonmedical purposes were prescribed to someone else, 20% were prescribed to the user, and 4% came from other sources.¹ Strategies to reduce POUD risk may be underused. In a retrospective cohort study of 1,612 patient electronic medical records from 8 primary care clinics that managed patients with long-term opioids for chronic noncancer pain (average prescribing duration of 2 years duration, ≥3 monthly prescriptions in 6 months), researchers evaluated how often prescribers used 3 risk reduction practices:

 

• urine drug tests
• regular office visits (≥1 every 6 months and within 30 days of changing opioid treatment)
• restricted early refills (≤1 opioid refill more than a week early).¹⁰

Risk factors for opioid misuse included age 1 early refill. Researchers found that even for high-risk patients, these strategies were used infrequently. Less than one-quarter of patients with ≥3 risk factors ever had a drug test, and those at increased risk were more likely to receive >1 early refill but no more likely to have more frequent visits. Issues such as patient entitlement, lack of physician education, and time constraints may explain why these strategies are not used more often.¹¹

No one procedure or set of variables is sufficient to identify chronic pain patients who may be at risk for POUD. However, a history of drug or alcohol use disorders may be a significant risk factor.^12,13

 

Few tools have been developed to help identify those at risk of AMTBs or POUD, and all have limitations.^4,14 Recommended self-report measures include the Current Opioid Misuse Measure and the Opioid Risk Tool.¹⁵ A review of studies in which these kinds of tools were developed revealed limited evidence for their use; most studies had methodological shortcomings, did not use standardized AMTB criteria, and provided little assessment of whether these tools changed clinician behaviors or improved patient outcomes.¹⁶

Evaluating AMTBs

Although diagnosing POUD in pain patients receiving chronic opioids can be challenging, assessing for AMTBs typically is helpful. Once AMTBs are identified, they can be examined to determine what drives their expression (Table 1⁴ and Table 2¹⁷). However, often it is easier to identify AMTBs than to interpret their origins; as much as 30% to 50% of patients who complain of chronic pain may have primary substance dependence to sedatives, opioids, or both.¹¹

Table 2

Aberrant medication-taking behaviors and POUD risk

 

Behaviors more suggestive of POUD
Deterioration in function (work, social)
Illegal activities (selling medication, forging prescriptions, buying from non-medical sources)
Altering the route of administration (snorting, injecting)
Multiple episodes of ‘lost’ or ‘stolen’ prescriptions
Resistance to change therapy despite negative outcomes
Refusal to comply with toxicology testing
Concurrent, active abuse of alcohol, illegal drugs
Use of multiple physicians or pharmacies to obtain the prescription
Behaviors less suggestive of POUD
Complaints for more medication
Medication hoarding
Requesting specific pain medications
Openly acquiring similar medications from other providers
Occasional unsanctioned dose escalation
Nonadherence to other recommendations for pain therapy
POUD: prescription opioid use disorder Source: Reference 17

Although AMTBs are common among chronic nonmalignant pain patients,^18,19 how often AMTBs reflect underlying POUD is uncertain.⁷ It is critical to interpret AMTBs with a balance of caution and care: “react therapeutically, not punitively.”²⁰ Categorizing a patient’s AMTB as more or less likely to support a POUD diagnosis can be helpful, but is not conclusive (Table 2).¹⁷ Clinical correlation often is required. No single AMTB alone is indicative of POUD. When evaluating AMTBs, the treating provider should use a nonjudgmental stance, and consider obtaining collateral data from people who can provide differing perspectives of the patient’s behaviors, such as other clinicians, significant others, family, etc. (a release of information from the patient may be required). Another source of collateral data is prescription monitoring databases. These databases typically are state-based and provide electronic access to prescription information, allowing you to search for patterns—ie, use of multiple prescribers or pharmacies, undisclosed prescriptions, etc. Interest in establishing a single, federal database has been increasing, but striking a balance between carefully monitoring for AMTBs and protecting privacy remains unresolved.

 

DSM-IV-TR diagnostic criteria for opioid dependence²¹ can be challenging to interpret in patients who are prescribed opioids for pain (Table 3

 

).⁶ To clarify interpretation, the Liaison Committee on Pain and Addiction of the American Society of Addiction Medicine (ASAM) has provided an outline of possible indicators of addiction in pain patients (Table 4).⁶ This was a consensus statement from the American Pain Society, the American Academy of Pain Medicine, and ASAM.

Assessment is primarily clinical and requires an awareness of appropriate terminology, an index of clinical suspicion, and expertise teasing apart pain, addiction, and pseudoaddiction. In our experience, it is helpful to ask a chronic pain patient whom you suspect might have POUD, “Have you ever used your prescribed opioids for reasons other than improving function or reducing pain, such as for getting a ‘high,’ managing stress, escaping from problems, etc.?” An affirmative response suggests an underlying problem with use of prescribed opioids, indicating a need for more careful questioning to determine if AMTBs or POUD coexist with chronic pain.

Drug testing can help determine if a patient is taking opioids that are not prescribed—as well as illicit drugs or alcohol—and confirm the presence of those that are prescribed. Toxicology screening should include opioids typically screened for (eg, morphine, codeine, heroin) and those for which additional tests may be required (eg, semi-synthetics such as oxycodone and hydrocodone and synthetics such as fentanyl).

Table 3

Identifying addiction in pain patients: Limitations of DSM-IV-TR

 

DSM-IV-TR substance dependence criteria	Challenges in using criterion to diagnose prescription opioid use disorder
Tolerance	Expected with prolonged opioid compliance
Physical dependence, withdrawal	Expected with prolonged opioid compliance
Use of larger amounts or longer than initially intended	Emergence of pain may demand increased dose or prolonged use
Multiple failed attempts to cut down or control	Emergence of pain may deter dose reduction or cessation
Time spent finding, using, or recovering	Difficulty finding adequate pain treatment may increase time spent pursuing analgesics. However, time spent recovering from overuse may suggest addiction
Given up or reduced important activities	Valid criteria—engaging in activities is expected to increase, not decline, with effective pain treatment
Continued use despite knowledge of negative consequences	Valid criteria—no harm is anticipated from analgesic opioid use for pain (see Table 4)
Source: Adapted from reference 6

Table 4

Possible indicators of addiction in pain patients

 

ASAM-APS-AAPM behavioral criteria	Examples of specific behaviors in opioid therapy for pain
Impaired control over opioid use	Patient requests early refills, frequently reports loss or theft of medication. Withdrawal noted at follow-up appointments despite having an adequate quantity of medication prescribed
Continued use despite harm from opioids	Patient exhibits declining function, opioid intoxication, persistent oversedation from opioids
Preoccupation with opioids	Patient ignores non-opioid interventions for pain, makes recurrent requests for opioid dose escalation (or complains of increasing pain) despite absence of disease progression or despite opioid dose increase by provider
AAPM: American Academy of Pain Medicine; APS: American Pain Society; ASAM: American Society of Addiction Medicine Source: Adapted from reference 6

Helping POUD patients

Goals of treatment include establishing a therapeutic alliance, educating patients about POUD, reducing relapse risk, and optimizing overall health (including pain and physical function). The ASAM Patient Placement Criteria²² provide guidance regarding level-of-care decisions. Treatment ideally includes a combination of education about POUD and its relationship to chronic pain, pharmacotherapy, psychotherapy—such as motivational enhancement therapy, 12-step facilitation therapy, cognitive-behavioral therapy, and relapse prevention—and referral to self-help groups such as Narcotics Anonymous or Pills Anonymous. Importantly, if pain is genuine, it requires treatment.

 

Pharmacotherapy. Methadone is recommended as the standard of care for OUD by the National Institutes of Health. Methadone is a full opioid agonist that decreases illicit opioid use, mortality, and related problems and requires highly structured treatment approaches under federal and state regulation. POUD patients may have higher rates of methadone maintenance treatment retention than heroin-dependent patients.²³ Published trials of buprenorphine for OUD have shown good treatment retention and reduction in illicit drug use and adverse events.²⁴ Buprenorphine also decreases mortality among OUD patients.

 

The first large-scale, randomized clinical trial of buprenorphine specifically for POUD included 653 treatment-seeking outpatients.²⁵ This study was designed to approximate clinical practice and included buprenorphine/naloxone, recommended abstinence, and self-help; one-half of participants received intensive addiction counseling. POUD patients were most likely to reduce prescription opioid misuse during buprenorphine/naloxone treatment. If tapered off buprenorphine/naloxone, even after 12 weeks of treatment, the likelihood of an unsuccessful outcome was high. Moreover, opioid dependence counseling did not seem to afford any difference in outcomes. However, despite clinical effectiveness, over the last decade only 19% of patients admitted primarily for OUD treatment (other than heroin) were planned to be offered buprenorphine or methadone.²⁶

 

 

A Cochrane review of oral naltrexone for OUD found that the drug was no better than placebo but concluded that available evidence does not allow an adequate evaluation.²⁷ Opioid antagonists may be of value to patients who do not want to take agonists or partial agonists. Extended-release naltrexone also is available to treat OUD.

See the Box below that details steps the FDA and others have taken to prevent POUD and Table 5 for precautions to incorporate when prescribing opioids long-term.

Box

 

Table 5

Universal precautions with chronic opioid management

 

Goals of therapy: partial pain relief and improvement in physical, emotional, and/or social functioning
Requirement for a single prescribing provider or treatment team
Limitation on dose and number of prescribed medications
Prohibition of changing dosage without discussion with the provider first
Monitoring patient adherence; discuss the use of ‘pill counts’
Prohibition of use with alcohol, other sedating medications, or illegal drugs without discussion with the provider
Agreement not to drive or operate heavy machinery until abatement of medication-related drowsiness
Responsibility to keep medication safe and secure
Prohibition of selling, lending, sharing, or giving medication to others
Limitations on refills—only by appointment, in person, and no extra refills for running out early
Compliance with all components of overall treatment plan (including consultations and referrals)
Biological testing to screen for drugs of abuse or alcohol as well as to confirm the presence of prescribed opioids
Adverse effects and safety issues, such as the risk of physical dependence and addiction behaviors
The option of sharing information with family members and other providers, as necessary, with the patient’s consent
Need for periodic reevaluation of treatment
Reasons for stopping opioid therapy
Consequences of nonadherence with the treatment agreement
Source: Gourlay DL, Heit HA, Almahrezi A. Universal precautions in pain medicine: a rational approach to the treatment of chronic pain. Pain Med. 2005;6(2):107-112.

CASE CONTINUED: A closer evaluation

After expressing your appreciation for Mr. H’s kind words and empathy for his chronic pain, you redirect him to his PCP. You ask him to sign a release of information so you and his other clinicians can coordinate his care. When discussing Mr. H with his PCP, you learn the patient has made limited requests for early refills and dose escalation primarily in relation to inadequate pain control and function, has genuine pain pathology, and is greatly distressed over his inability to work. No other AMTBs are present, and a check of the state prescribing database reveals that Mr. H did receive a small quantity of opioids from an ED on 1 occasion.

You and Mr. H’s PCP agree this is “pseudo-addiction” but want to watch Mr. H more closely and look for ways to coordinate his care. The PCP agrees to implement a prescribing agreement, start drug testing (including for the prescribed opioids), and reassess maximizing Mr. H’s function and pain management while you address his combined pain, depression, insomnia, and tobacco use.

 

Related Resources

 

• Ries RK, Fiellin D, Miller SC, et al, eds. Principles of addiction medicine. 4th ed. Hagerstown, MD: Lippincott Williams & Wilkins; 2009.
• Department of Veterans Affairs. Department of Defense. VA/DoD clinical practice guideline for management of opioid therapy for chronic pain. Appendix C: sample opioid pain care agreement. http://www.healthquality.va.gov/COT_312_Full-er.pdf. Published May 2010. Accessed June 21, 2012.
• Weaver M, Schnoll S. Addiction issues in prescribing opioids for chronic non-malignant pain. J Addiction Med. 2007;1(1):2-10.
• Weaver M, Heit HA, Savage S, et al. Clinical case discussion: chronic pain management. J Addiction Med. 2007;1(1):11-14.

Drug Brand Names

 

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Codeine • Tylenol with codeine, others
• Fentanyl • Duragesic, Actiq
• Hydrocodone • Lortab, Vicodin, others
• Methadone • Dolophine, Methadose
• Morphine • Roxanol
• Naltrexone extended-release • Vivitrol
• Oxycodone • OxyContin, Roxicodone

Disclosures

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

Dr. Frankowski’s time toward this project was provided by the American Board of Addiction Medicine-accredited Cincinnati VA Addiction Medicine Research Fellowship, affiliated with the CeTREAD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH.

The statements in this publication do not necessarily reflect the views or opinions of the Department of Veterans Affairs.

Acknowledgement

The authors thank Catherine Constance and Sandra Mason at the Cincinnati VA Medical Center for their administrative assistance.

Discuss this article at www.facebook.com/CurrentPsychiatry

You’ve been treating Mr. H, a 54-year-old factory worker and tobacco user, for depression that developed after a work-related back injury and subsequent disability. His depression has had a fair response to an antidepressant. He also has been maintained on chronic opioids (morphine and oxycodone/acetaminophen) for 18 months by his primary care physician (PCP). At the end of your appointment, he asks you for a refill of the opioids because he “ran out” early because of increased night pain and resultant insomnia and “stress.” He clarifies he has asked for early refills before from his PCP, but lately he has been denied. Because you “seem to listen to me more,” he asks for your help. How should you manage Mr. H?

Opioids are among the most commonly misused prescription drugs in the United States.¹ In 2008, poisoning was the leading cause of death from injury in the United States; roughly 90% of poisonings resulted from drug exposure, and >40% of these drug poisonings were from prescription opioids.² The Centers for Disease Control and Prevention estimates that the number of emergency department (ED) visits for nonmedical use of opioids increased 111% between 2004 and 2008, from 144,600 to 305,900 visits.³ The highest number of visits were for use of oxycodone, hydrocodone, and methadone.³

Increased prescribing of opioids and overdose deaths attributable to prescribed opioids have raised concern among physicians about how to effectively treat pain as well as prevent, recognize, and manage aberrant medication-taking behaviors (AMTBs). Psychiatrists are well-positioned to screen and manage their own patients for prescription opioid use disorder (POUD) or collaborate with opioid prescribers to accomplish the same.

Clarifying terminology

Terminology used to describe POUD and related conditions often is poorly defined or loosely applied. Because emotions often enter discussions between patients and physicians about problems related to opioid therapy, nonstigmatizing and more objective terminology is needed, and clinicians are working toward standardizing this. Relevant terms are defined in Table 1.⁴

The DSM-5 Substance Use Disorders Work Group has proposed using the term opioid use disorder (OUD) to replace the term opioid dependence.⁵ The hope is that removing the word “dependence” from the diagnostic term will reduce confusion between “dependence” due to expected physical dependence (tolerance, withdrawal) on medically prescribed opioids vs true addiction (currently defined as “opioid dependence” in DSM-IV-TR). This Work Group also has proposed combining opioid abuse and opioid dependence criteria into a single diagnosis of OUD, and adding “craving” to the criteria. For the complete proposed criteria, see www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=460.These changes are still under review. In this article, we use the term POUD.

Table 1

Terminology related to prescription opioid use disorder

 

Term	Definition
Chronic paina	Pain that extends beyond the expected period for healing (6 months), initiated by tissue damage, but perpetrated by the interaction of physiologic, affective, and environmental factors
Chronic nonmalignant paina	Chronic pain associated with diverse diagnoses and syndromes that are not terminal but affect the patient’s function
Appropriate usea	Taking a prescription as prescribed, and only for the condition indicated
Misusea	Taking a prescription for a reason or at a dose or frequency other than for which it was prescribed; this may or may not reflect POUD
Drug-seeking behaviors	Patient behaviors directed toward obtaining controlled substances, driven not by amelioration of the condition for which the medication was indicated but rather by other maladaptive gains; this may or may not reflect POUD
Chemical coping	Taking a controlled substance medication to relieve psychological problems (eg, to relieve low mood, anxiety, insomnia) and for reasons other than the purpose for which it was prescribed; this may or may not reflect POUD
Aberrant medication-taking behaviorsa	Taking a controlled substance medication in a manner that is not prescribed; causes for this may include: lack of understanding about how to take the opioid appropriately external pressures, such as to give to another person for his or her pain chemical coping pseudoaddiction (see below), including: addiction or substance use disorder (such as POUD) diversion
Pseudoaddiction	An iatrogenic syndrome of “addiction-like” behaviors in which the patient seeks opioids to relieve pain—such as seeking different doctors, self-adjusting the opioid dose, early refills of opioids, etc.—rather than to achieve pleasure or other nonpain-related effect. At times mistaken for true addiction, these behaviors tend to resolve and function improves once analgesia is better addressed
a These terms and definitions are adapted from reference 4. The remaining terms and definitions were developed by the authors POUD: prescription opioid use disorder

POUD and chronic pain

The incidence of POUD during opioid therapy for pain is unknown.⁶ Some researchers have suggested it may be as low as 0.2%,⁷ while others estimate that rates of POUD in patients with chronic pain may be similar to those in the general population: 3% to 16%.⁸ When applying the proposed DSM-5 criteria to patients receiving long-term opioid therapy for noncancer pain, the lifetime prevalence of POUD may be as high as 35%.⁹

 

 

Prescribers may be contributing to POUD. Roughly 76% of opioids used for nonmedical purposes were prescribed to someone else, 20% were prescribed to the user, and 4% came from other sources.¹ Strategies to reduce POUD risk may be underused. In a retrospective cohort study of 1,612 patient electronic medical records from 8 primary care clinics that managed patients with long-term opioids for chronic noncancer pain (average prescribing duration of 2 years duration, ≥3 monthly prescriptions in 6 months), researchers evaluated how often prescribers used 3 risk reduction practices:

 

• urine drug tests
• regular office visits (≥1 every 6 months and within 30 days of changing opioid treatment)
• restricted early refills (≤1 opioid refill more than a week early).¹⁰

Risk factors for opioid misuse included age 1 early refill. Researchers found that even for high-risk patients, these strategies were used infrequently. Less than one-quarter of patients with ≥3 risk factors ever had a drug test, and those at increased risk were more likely to receive >1 early refill but no more likely to have more frequent visits. Issues such as patient entitlement, lack of physician education, and time constraints may explain why these strategies are not used more often.¹¹

No one procedure or set of variables is sufficient to identify chronic pain patients who may be at risk for POUD. However, a history of drug or alcohol use disorders may be a significant risk factor.^12,13

 

Few tools have been developed to help identify those at risk of AMTBs or POUD, and all have limitations.^4,14 Recommended self-report measures include the Current Opioid Misuse Measure and the Opioid Risk Tool.¹⁵ A review of studies in which these kinds of tools were developed revealed limited evidence for their use; most studies had methodological shortcomings, did not use standardized AMTB criteria, and provided little assessment of whether these tools changed clinician behaviors or improved patient outcomes.¹⁶

Evaluating AMTBs

Although diagnosing POUD in pain patients receiving chronic opioids can be challenging, assessing for AMTBs typically is helpful. Once AMTBs are identified, they can be examined to determine what drives their expression (Table 1⁴ and Table 2¹⁷). However, often it is easier to identify AMTBs than to interpret their origins; as much as 30% to 50% of patients who complain of chronic pain may have primary substance dependence to sedatives, opioids, or both.¹¹

Table 2

Aberrant medication-taking behaviors and POUD risk

 

Behaviors more suggestive of POUD
Deterioration in function (work, social)
Illegal activities (selling medication, forging prescriptions, buying from non-medical sources)
Altering the route of administration (snorting, injecting)
Multiple episodes of ‘lost’ or ‘stolen’ prescriptions
Resistance to change therapy despite negative outcomes
Refusal to comply with toxicology testing
Concurrent, active abuse of alcohol, illegal drugs
Use of multiple physicians or pharmacies to obtain the prescription
Behaviors less suggestive of POUD
Complaints for more medication
Medication hoarding
Requesting specific pain medications
Openly acquiring similar medications from other providers
Occasional unsanctioned dose escalation
Nonadherence to other recommendations for pain therapy
POUD: prescription opioid use disorder Source: Reference 17

Although AMTBs are common among chronic nonmalignant pain patients,^18,19 how often AMTBs reflect underlying POUD is uncertain.⁷ It is critical to interpret AMTBs with a balance of caution and care: “react therapeutically, not punitively.”²⁰ Categorizing a patient’s AMTB as more or less likely to support a POUD diagnosis can be helpful, but is not conclusive (Table 2).¹⁷ Clinical correlation often is required. No single AMTB alone is indicative of POUD. When evaluating AMTBs, the treating provider should use a nonjudgmental stance, and consider obtaining collateral data from people who can provide differing perspectives of the patient’s behaviors, such as other clinicians, significant others, family, etc. (a release of information from the patient may be required). Another source of collateral data is prescription monitoring databases. These databases typically are state-based and provide electronic access to prescription information, allowing you to search for patterns—ie, use of multiple prescribers or pharmacies, undisclosed prescriptions, etc. Interest in establishing a single, federal database has been increasing, but striking a balance between carefully monitoring for AMTBs and protecting privacy remains unresolved.

 

DSM-IV-TR diagnostic criteria for opioid dependence²¹ can be challenging to interpret in patients who are prescribed opioids for pain (Table 3

 

).⁶ To clarify interpretation, the Liaison Committee on Pain and Addiction of the American Society of Addiction Medicine (ASAM) has provided an outline of possible indicators of addiction in pain patients (Table 4).⁶ This was a consensus statement from the American Pain Society, the American Academy of Pain Medicine, and ASAM.

Assessment is primarily clinical and requires an awareness of appropriate terminology, an index of clinical suspicion, and expertise teasing apart pain, addiction, and pseudoaddiction. In our experience, it is helpful to ask a chronic pain patient whom you suspect might have POUD, “Have you ever used your prescribed opioids for reasons other than improving function or reducing pain, such as for getting a ‘high,’ managing stress, escaping from problems, etc.?” An affirmative response suggests an underlying problem with use of prescribed opioids, indicating a need for more careful questioning to determine if AMTBs or POUD coexist with chronic pain.

Drug testing can help determine if a patient is taking opioids that are not prescribed—as well as illicit drugs or alcohol—and confirm the presence of those that are prescribed. Toxicology screening should include opioids typically screened for (eg, morphine, codeine, heroin) and those for which additional tests may be required (eg, semi-synthetics such as oxycodone and hydrocodone and synthetics such as fentanyl).

Table 3

Identifying addiction in pain patients: Limitations of DSM-IV-TR

 

DSM-IV-TR substance dependence criteria	Challenges in using criterion to diagnose prescription opioid use disorder
Tolerance	Expected with prolonged opioid compliance
Physical dependence, withdrawal	Expected with prolonged opioid compliance
Use of larger amounts or longer than initially intended	Emergence of pain may demand increased dose or prolonged use
Multiple failed attempts to cut down or control	Emergence of pain may deter dose reduction or cessation
Time spent finding, using, or recovering	Difficulty finding adequate pain treatment may increase time spent pursuing analgesics. However, time spent recovering from overuse may suggest addiction
Given up or reduced important activities	Valid criteria—engaging in activities is expected to increase, not decline, with effective pain treatment
Continued use despite knowledge of negative consequences	Valid criteria—no harm is anticipated from analgesic opioid use for pain (see Table 4)
Source: Adapted from reference 6

Table 4

Possible indicators of addiction in pain patients

 

ASAM-APS-AAPM behavioral criteria	Examples of specific behaviors in opioid therapy for pain
Impaired control over opioid use	Patient requests early refills, frequently reports loss or theft of medication. Withdrawal noted at follow-up appointments despite having an adequate quantity of medication prescribed
Continued use despite harm from opioids	Patient exhibits declining function, opioid intoxication, persistent oversedation from opioids
Preoccupation with opioids	Patient ignores non-opioid interventions for pain, makes recurrent requests for opioid dose escalation (or complains of increasing pain) despite absence of disease progression or despite opioid dose increase by provider
AAPM: American Academy of Pain Medicine; APS: American Pain Society; ASAM: American Society of Addiction Medicine Source: Adapted from reference 6

Helping POUD patients

Goals of treatment include establishing a therapeutic alliance, educating patients about POUD, reducing relapse risk, and optimizing overall health (including pain and physical function). The ASAM Patient Placement Criteria²² provide guidance regarding level-of-care decisions. Treatment ideally includes a combination of education about POUD and its relationship to chronic pain, pharmacotherapy, psychotherapy—such as motivational enhancement therapy, 12-step facilitation therapy, cognitive-behavioral therapy, and relapse prevention—and referral to self-help groups such as Narcotics Anonymous or Pills Anonymous. Importantly, if pain is genuine, it requires treatment.

 

Pharmacotherapy. Methadone is recommended as the standard of care for OUD by the National Institutes of Health. Methadone is a full opioid agonist that decreases illicit opioid use, mortality, and related problems and requires highly structured treatment approaches under federal and state regulation. POUD patients may have higher rates of methadone maintenance treatment retention than heroin-dependent patients.²³ Published trials of buprenorphine for OUD have shown good treatment retention and reduction in illicit drug use and adverse events.²⁴ Buprenorphine also decreases mortality among OUD patients.

 

The first large-scale, randomized clinical trial of buprenorphine specifically for POUD included 653 treatment-seeking outpatients.²⁵ This study was designed to approximate clinical practice and included buprenorphine/naloxone, recommended abstinence, and self-help; one-half of participants received intensive addiction counseling. POUD patients were most likely to reduce prescription opioid misuse during buprenorphine/naloxone treatment. If tapered off buprenorphine/naloxone, even after 12 weeks of treatment, the likelihood of an unsuccessful outcome was high. Moreover, opioid dependence counseling did not seem to afford any difference in outcomes. However, despite clinical effectiveness, over the last decade only 19% of patients admitted primarily for OUD treatment (other than heroin) were planned to be offered buprenorphine or methadone.²⁶

 

 

A Cochrane review of oral naltrexone for OUD found that the drug was no better than placebo but concluded that available evidence does not allow an adequate evaluation.²⁷ Opioid antagonists may be of value to patients who do not want to take agonists or partial agonists. Extended-release naltrexone also is available to treat OUD.

See the Box below that details steps the FDA and others have taken to prevent POUD and Table 5 for precautions to incorporate when prescribing opioids long-term.

Box

 

Table 5

Universal precautions with chronic opioid management

 

Goals of therapy: partial pain relief and improvement in physical, emotional, and/or social functioning
Requirement for a single prescribing provider or treatment team
Limitation on dose and number of prescribed medications
Prohibition of changing dosage without discussion with the provider first
Monitoring patient adherence; discuss the use of ‘pill counts’
Prohibition of use with alcohol, other sedating medications, or illegal drugs without discussion with the provider
Agreement not to drive or operate heavy machinery until abatement of medication-related drowsiness
Responsibility to keep medication safe and secure
Prohibition of selling, lending, sharing, or giving medication to others
Limitations on refills—only by appointment, in person, and no extra refills for running out early
Compliance with all components of overall treatment plan (including consultations and referrals)
Biological testing to screen for drugs of abuse or alcohol as well as to confirm the presence of prescribed opioids
Adverse effects and safety issues, such as the risk of physical dependence and addiction behaviors
The option of sharing information with family members and other providers, as necessary, with the patient’s consent
Need for periodic reevaluation of treatment
Reasons for stopping opioid therapy
Consequences of nonadherence with the treatment agreement
Source: Gourlay DL, Heit HA, Almahrezi A. Universal precautions in pain medicine: a rational approach to the treatment of chronic pain. Pain Med. 2005;6(2):107-112.

CASE CONTINUED: A closer evaluation

After expressing your appreciation for Mr. H’s kind words and empathy for his chronic pain, you redirect him to his PCP. You ask him to sign a release of information so you and his other clinicians can coordinate his care. When discussing Mr. H with his PCP, you learn the patient has made limited requests for early refills and dose escalation primarily in relation to inadequate pain control and function, has genuine pain pathology, and is greatly distressed over his inability to work. No other AMTBs are present, and a check of the state prescribing database reveals that Mr. H did receive a small quantity of opioids from an ED on 1 occasion.

You and Mr. H’s PCP agree this is “pseudo-addiction” but want to watch Mr. H more closely and look for ways to coordinate his care. The PCP agrees to implement a prescribing agreement, start drug testing (including for the prescribed opioids), and reassess maximizing Mr. H’s function and pain management while you address his combined pain, depression, insomnia, and tobacco use.

 

Related Resources

 

• Ries RK, Fiellin D, Miller SC, et al, eds. Principles of addiction medicine. 4th ed. Hagerstown, MD: Lippincott Williams & Wilkins; 2009.
• Department of Veterans Affairs. Department of Defense. VA/DoD clinical practice guideline for management of opioid therapy for chronic pain. Appendix C: sample opioid pain care agreement. http://www.healthquality.va.gov/COT_312_Full-er.pdf. Published May 2010. Accessed June 21, 2012.
• Weaver M, Schnoll S. Addiction issues in prescribing opioids for chronic non-malignant pain. J Addiction Med. 2007;1(1):2-10.
• Weaver M, Heit HA, Savage S, et al. Clinical case discussion: chronic pain management. J Addiction Med. 2007;1(1):11-14.

Drug Brand Names

 

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Codeine • Tylenol with codeine, others
• Fentanyl • Duragesic, Actiq
• Hydrocodone • Lortab, Vicodin, others
• Methadone • Dolophine, Methadose
• Morphine • Roxanol
• Naltrexone extended-release • Vivitrol
• Oxycodone • OxyContin, Roxicodone

Disclosures

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

Dr. Frankowski’s time toward this project was provided by the American Board of Addiction Medicine-accredited Cincinnati VA Addiction Medicine Research Fellowship, affiliated with the CeTREAD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH.

The statements in this publication do not necessarily reflect the views or opinions of the Department of Veterans Affairs.

Acknowledgement

The authors thank Catherine Constance and Sandra Mason at the Cincinnati VA Medical Center for their administrative assistance.

Discuss this article at www.facebook.com/CurrentPsychiatry

You’ve been treating Mr. H, a 54-year-old factory worker and tobacco user, for depression that developed after a work-related back injury and subsequent disability. His depression has had a fair response to an antidepressant. He also has been maintained on chronic opioids (morphine and oxycodone/acetaminophen) for 18 months by his primary care physician (PCP). At the end of your appointment, he asks you for a refill of the opioids because he “ran out” early because of increased night pain and resultant insomnia and “stress.” He clarifies he has asked for early refills before from his PCP, but lately he has been denied. Because you “seem to listen to me more,” he asks for your help. How should you manage Mr. H?

Opioids are among the most commonly misused prescription drugs in the United States.¹ In 2008, poisoning was the leading cause of death from injury in the United States; roughly 90% of poisonings resulted from drug exposure, and >40% of these drug poisonings were from prescription opioids.² The Centers for Disease Control and Prevention estimates that the number of emergency department (ED) visits for nonmedical use of opioids increased 111% between 2004 and 2008, from 144,600 to 305,900 visits.³ The highest number of visits were for use of oxycodone, hydrocodone, and methadone.³

Increased prescribing of opioids and overdose deaths attributable to prescribed opioids have raised concern among physicians about how to effectively treat pain as well as prevent, recognize, and manage aberrant medication-taking behaviors (AMTBs). Psychiatrists are well-positioned to screen and manage their own patients for prescription opioid use disorder (POUD) or collaborate with opioid prescribers to accomplish the same.

Clarifying terminology

Terminology used to describe POUD and related conditions often is poorly defined or loosely applied. Because emotions often enter discussions between patients and physicians about problems related to opioid therapy, nonstigmatizing and more objective terminology is needed, and clinicians are working toward standardizing this. Relevant terms are defined in Table 1.⁴

The DSM-5 Substance Use Disorders Work Group has proposed using the term opioid use disorder (OUD) to replace the term opioid dependence.⁵ The hope is that removing the word “dependence” from the diagnostic term will reduce confusion between “dependence” due to expected physical dependence (tolerance, withdrawal) on medically prescribed opioids vs true addiction (currently defined as “opioid dependence” in DSM-IV-TR). This Work Group also has proposed combining opioid abuse and opioid dependence criteria into a single diagnosis of OUD, and adding “craving” to the criteria. For the complete proposed criteria, see www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=460.These changes are still under review. In this article, we use the term POUD.

Table 1

Terminology related to prescription opioid use disorder

 

Term	Definition
Chronic paina	Pain that extends beyond the expected period for healing (6 months), initiated by tissue damage, but perpetrated by the interaction of physiologic, affective, and environmental factors
Chronic nonmalignant paina	Chronic pain associated with diverse diagnoses and syndromes that are not terminal but affect the patient’s function
Appropriate usea	Taking a prescription as prescribed, and only for the condition indicated
Misusea	Taking a prescription for a reason or at a dose or frequency other than for which it was prescribed; this may or may not reflect POUD
Drug-seeking behaviors	Patient behaviors directed toward obtaining controlled substances, driven not by amelioration of the condition for which the medication was indicated but rather by other maladaptive gains; this may or may not reflect POUD
Chemical coping	Taking a controlled substance medication to relieve psychological problems (eg, to relieve low mood, anxiety, insomnia) and for reasons other than the purpose for which it was prescribed; this may or may not reflect POUD
Aberrant medication-taking behaviorsa	Taking a controlled substance medication in a manner that is not prescribed; causes for this may include: lack of understanding about how to take the opioid appropriately external pressures, such as to give to another person for his or her pain chemical coping pseudoaddiction (see below), including: addiction or substance use disorder (such as POUD) diversion
Pseudoaddiction	An iatrogenic syndrome of “addiction-like” behaviors in which the patient seeks opioids to relieve pain—such as seeking different doctors, self-adjusting the opioid dose, early refills of opioids, etc.—rather than to achieve pleasure or other nonpain-related effect. At times mistaken for true addiction, these behaviors tend to resolve and function improves once analgesia is better addressed
a These terms and definitions are adapted from reference 4. The remaining terms and definitions were developed by the authors POUD: prescription opioid use disorder

POUD and chronic pain

The incidence of POUD during opioid therapy for pain is unknown.⁶ Some researchers have suggested it may be as low as 0.2%,⁷ while others estimate that rates of POUD in patients with chronic pain may be similar to those in the general population: 3% to 16%.⁸ When applying the proposed DSM-5 criteria to patients receiving long-term opioid therapy for noncancer pain, the lifetime prevalence of POUD may be as high as 35%.⁹

 

 

Prescribers may be contributing to POUD. Roughly 76% of opioids used for nonmedical purposes were prescribed to someone else, 20% were prescribed to the user, and 4% came from other sources.¹ Strategies to reduce POUD risk may be underused. In a retrospective cohort study of 1,612 patient electronic medical records from 8 primary care clinics that managed patients with long-term opioids for chronic noncancer pain (average prescribing duration of 2 years duration, ≥3 monthly prescriptions in 6 months), researchers evaluated how often prescribers used 3 risk reduction practices:

 

• urine drug tests
• regular office visits (≥1 every 6 months and within 30 days of changing opioid treatment)
• restricted early refills (≤1 opioid refill more than a week early).¹⁰

Risk factors for opioid misuse included age 1 early refill. Researchers found that even for high-risk patients, these strategies were used infrequently. Less than one-quarter of patients with ≥3 risk factors ever had a drug test, and those at increased risk were more likely to receive >1 early refill but no more likely to have more frequent visits. Issues such as patient entitlement, lack of physician education, and time constraints may explain why these strategies are not used more often.¹¹

No one procedure or set of variables is sufficient to identify chronic pain patients who may be at risk for POUD. However, a history of drug or alcohol use disorders may be a significant risk factor.^12,13

 

Few tools have been developed to help identify those at risk of AMTBs or POUD, and all have limitations.^4,14 Recommended self-report measures include the Current Opioid Misuse Measure and the Opioid Risk Tool.¹⁵ A review of studies in which these kinds of tools were developed revealed limited evidence for their use; most studies had methodological shortcomings, did not use standardized AMTB criteria, and provided little assessment of whether these tools changed clinician behaviors or improved patient outcomes.¹⁶

Evaluating AMTBs

Although diagnosing POUD in pain patients receiving chronic opioids can be challenging, assessing for AMTBs typically is helpful. Once AMTBs are identified, they can be examined to determine what drives their expression (Table 1⁴ and Table 2¹⁷). However, often it is easier to identify AMTBs than to interpret their origins; as much as 30% to 50% of patients who complain of chronic pain may have primary substance dependence to sedatives, opioids, or both.¹¹

Table 2

Aberrant medication-taking behaviors and POUD risk

 

Behaviors more suggestive of POUD
Deterioration in function (work, social)
Illegal activities (selling medication, forging prescriptions, buying from non-medical sources)
Altering the route of administration (snorting, injecting)
Multiple episodes of ‘lost’ or ‘stolen’ prescriptions
Resistance to change therapy despite negative outcomes
Refusal to comply with toxicology testing
Concurrent, active abuse of alcohol, illegal drugs
Use of multiple physicians or pharmacies to obtain the prescription
Behaviors less suggestive of POUD
Complaints for more medication
Medication hoarding
Requesting specific pain medications
Openly acquiring similar medications from other providers
Occasional unsanctioned dose escalation
Nonadherence to other recommendations for pain therapy
POUD: prescription opioid use disorder Source: Reference 17

Although AMTBs are common among chronic nonmalignant pain patients,^18,19 how often AMTBs reflect underlying POUD is uncertain.⁷ It is critical to interpret AMTBs with a balance of caution and care: “react therapeutically, not punitively.”²⁰ Categorizing a patient’s AMTB as more or less likely to support a POUD diagnosis can be helpful, but is not conclusive (Table 2).¹⁷ Clinical correlation often is required. No single AMTB alone is indicative of POUD. When evaluating AMTBs, the treating provider should use a nonjudgmental stance, and consider obtaining collateral data from people who can provide differing perspectives of the patient’s behaviors, such as other clinicians, significant others, family, etc. (a release of information from the patient may be required). Another source of collateral data is prescription monitoring databases. These databases typically are state-based and provide electronic access to prescription information, allowing you to search for patterns—ie, use of multiple prescribers or pharmacies, undisclosed prescriptions, etc. Interest in establishing a single, federal database has been increasing, but striking a balance between carefully monitoring for AMTBs and protecting privacy remains unresolved.

 

DSM-IV-TR diagnostic criteria for opioid dependence²¹ can be challenging to interpret in patients who are prescribed opioids for pain (Table 3

 

).⁶ To clarify interpretation, the Liaison Committee on Pain and Addiction of the American Society of Addiction Medicine (ASAM) has provided an outline of possible indicators of addiction in pain patients (Table 4).⁶ This was a consensus statement from the American Pain Society, the American Academy of Pain Medicine, and ASAM.

Assessment is primarily clinical and requires an awareness of appropriate terminology, an index of clinical suspicion, and expertise teasing apart pain, addiction, and pseudoaddiction. In our experience, it is helpful to ask a chronic pain patient whom you suspect might have POUD, “Have you ever used your prescribed opioids for reasons other than improving function or reducing pain, such as for getting a ‘high,’ managing stress, escaping from problems, etc.?” An affirmative response suggests an underlying problem with use of prescribed opioids, indicating a need for more careful questioning to determine if AMTBs or POUD coexist with chronic pain.

Drug testing can help determine if a patient is taking opioids that are not prescribed—as well as illicit drugs or alcohol—and confirm the presence of those that are prescribed. Toxicology screening should include opioids typically screened for (eg, morphine, codeine, heroin) and those for which additional tests may be required (eg, semi-synthetics such as oxycodone and hydrocodone and synthetics such as fentanyl).

Table 3

Identifying addiction in pain patients: Limitations of DSM-IV-TR

 

DSM-IV-TR substance dependence criteria	Challenges in using criterion to diagnose prescription opioid use disorder
Tolerance	Expected with prolonged opioid compliance
Physical dependence, withdrawal	Expected with prolonged opioid compliance
Use of larger amounts or longer than initially intended	Emergence of pain may demand increased dose or prolonged use
Multiple failed attempts to cut down or control	Emergence of pain may deter dose reduction or cessation
Time spent finding, using, or recovering	Difficulty finding adequate pain treatment may increase time spent pursuing analgesics. However, time spent recovering from overuse may suggest addiction
Given up or reduced important activities	Valid criteria—engaging in activities is expected to increase, not decline, with effective pain treatment
Continued use despite knowledge of negative consequences	Valid criteria—no harm is anticipated from analgesic opioid use for pain (see Table 4)
Source: Adapted from reference 6

Table 4

Possible indicators of addiction in pain patients

 

ASAM-APS-AAPM behavioral criteria	Examples of specific behaviors in opioid therapy for pain
Impaired control over opioid use	Patient requests early refills, frequently reports loss or theft of medication. Withdrawal noted at follow-up appointments despite having an adequate quantity of medication prescribed
Continued use despite harm from opioids	Patient exhibits declining function, opioid intoxication, persistent oversedation from opioids
Preoccupation with opioids	Patient ignores non-opioid interventions for pain, makes recurrent requests for opioid dose escalation (or complains of increasing pain) despite absence of disease progression or despite opioid dose increase by provider
AAPM: American Academy of Pain Medicine; APS: American Pain Society; ASAM: American Society of Addiction Medicine Source: Adapted from reference 6

Helping POUD patients

Goals of treatment include establishing a therapeutic alliance, educating patients about POUD, reducing relapse risk, and optimizing overall health (including pain and physical function). The ASAM Patient Placement Criteria²² provide guidance regarding level-of-care decisions. Treatment ideally includes a combination of education about POUD and its relationship to chronic pain, pharmacotherapy, psychotherapy—such as motivational enhancement therapy, 12-step facilitation therapy, cognitive-behavioral therapy, and relapse prevention—and referral to self-help groups such as Narcotics Anonymous or Pills Anonymous. Importantly, if pain is genuine, it requires treatment.

 

Pharmacotherapy. Methadone is recommended as the standard of care for OUD by the National Institutes of Health. Methadone is a full opioid agonist that decreases illicit opioid use, mortality, and related problems and requires highly structured treatment approaches under federal and state regulation. POUD patients may have higher rates of methadone maintenance treatment retention than heroin-dependent patients.²³ Published trials of buprenorphine for OUD have shown good treatment retention and reduction in illicit drug use and adverse events.²⁴ Buprenorphine also decreases mortality among OUD patients.

 

The first large-scale, randomized clinical trial of buprenorphine specifically for POUD included 653 treatment-seeking outpatients.²⁵ This study was designed to approximate clinical practice and included buprenorphine/naloxone, recommended abstinence, and self-help; one-half of participants received intensive addiction counseling. POUD patients were most likely to reduce prescription opioid misuse during buprenorphine/naloxone treatment. If tapered off buprenorphine/naloxone, even after 12 weeks of treatment, the likelihood of an unsuccessful outcome was high. Moreover, opioid dependence counseling did not seem to afford any difference in outcomes. However, despite clinical effectiveness, over the last decade only 19% of patients admitted primarily for OUD treatment (other than heroin) were planned to be offered buprenorphine or methadone.²⁶

 

 

A Cochrane review of oral naltrexone for OUD found that the drug was no better than placebo but concluded that available evidence does not allow an adequate evaluation.²⁷ Opioid antagonists may be of value to patients who do not want to take agonists or partial agonists. Extended-release naltrexone also is available to treat OUD.

See the Box below that details steps the FDA and others have taken to prevent POUD and Table 5 for precautions to incorporate when prescribing opioids long-term.

Box

 

Table 5

Universal precautions with chronic opioid management

 

Goals of therapy: partial pain relief and improvement in physical, emotional, and/or social functioning
Requirement for a single prescribing provider or treatment team
Limitation on dose and number of prescribed medications
Prohibition of changing dosage without discussion with the provider first
Monitoring patient adherence; discuss the use of ‘pill counts’
Prohibition of use with alcohol, other sedating medications, or illegal drugs without discussion with the provider
Agreement not to drive or operate heavy machinery until abatement of medication-related drowsiness
Responsibility to keep medication safe and secure
Prohibition of selling, lending, sharing, or giving medication to others
Limitations on refills—only by appointment, in person, and no extra refills for running out early
Compliance with all components of overall treatment plan (including consultations and referrals)
Biological testing to screen for drugs of abuse or alcohol as well as to confirm the presence of prescribed opioids
Adverse effects and safety issues, such as the risk of physical dependence and addiction behaviors
The option of sharing information with family members and other providers, as necessary, with the patient’s consent
Need for periodic reevaluation of treatment
Reasons for stopping opioid therapy
Consequences of nonadherence with the treatment agreement
Source: Gourlay DL, Heit HA, Almahrezi A. Universal precautions in pain medicine: a rational approach to the treatment of chronic pain. Pain Med. 2005;6(2):107-112.

CASE CONTINUED: A closer evaluation

After expressing your appreciation for Mr. H’s kind words and empathy for his chronic pain, you redirect him to his PCP. You ask him to sign a release of information so you and his other clinicians can coordinate his care. When discussing Mr. H with his PCP, you learn the patient has made limited requests for early refills and dose escalation primarily in relation to inadequate pain control and function, has genuine pain pathology, and is greatly distressed over his inability to work. No other AMTBs are present, and a check of the state prescribing database reveals that Mr. H did receive a small quantity of opioids from an ED on 1 occasion.

You and Mr. H’s PCP agree this is “pseudo-addiction” but want to watch Mr. H more closely and look for ways to coordinate his care. The PCP agrees to implement a prescribing agreement, start drug testing (including for the prescribed opioids), and reassess maximizing Mr. H’s function and pain management while you address his combined pain, depression, insomnia, and tobacco use.

 

Related Resources

 

• Ries RK, Fiellin D, Miller SC, et al, eds. Principles of addiction medicine. 4th ed. Hagerstown, MD: Lippincott Williams & Wilkins; 2009.
• Department of Veterans Affairs. Department of Defense. VA/DoD clinical practice guideline for management of opioid therapy for chronic pain. Appendix C: sample opioid pain care agreement. http://www.healthquality.va.gov/COT_312_Full-er.pdf. Published May 2010. Accessed June 21, 2012.
• Weaver M, Schnoll S. Addiction issues in prescribing opioids for chronic non-malignant pain. J Addiction Med. 2007;1(1):2-10.
• Weaver M, Heit HA, Savage S, et al. Clinical case discussion: chronic pain management. J Addiction Med. 2007;1(1):11-14.

Drug Brand Names

 

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Codeine • Tylenol with codeine, others
• Fentanyl • Duragesic, Actiq
• Hydrocodone • Lortab, Vicodin, others
• Methadone • Dolophine, Methadose
• Morphine • Roxanol
• Naltrexone extended-release • Vivitrol
• Oxycodone • OxyContin, Roxicodone

Disclosures

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

Dr. Frankowski’s time toward this project was provided by the American Board of Addiction Medicine-accredited Cincinnati VA Addiction Medicine Research Fellowship, affiliated with the CeTREAD, Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH.

The statements in this publication do not necessarily reflect the views or opinions of the Department of Veterans Affairs.

Acknowledgement

The authors thank Catherine Constance and Sandra Mason at the Cincinnati VA Medical Center for their administrative assistance.

Discuss this article at www.facebook.com/CurrentPsychiatry

The rate of off-label prescribing of second-generation antipsychotics (SGAs) is estimated to have doubled in the past decade.^1,2 In 2010, quetiapine was the most commonly used SGA in the United States with >10 million prescriptions dispensed.² Clinical experience and reports from patients indicate quetiapine may be useful for treating anxiety. When making medication choices, it can be useful to combine anecdotal evidence with the facts (or lack thereof). Does evidence support or contradict the use of quetiapine for anxiety?

What the research shows

Quetiapine is FDA-approved for treating:

• adults and adolescents with schizophrenia
• adults, children, and adolescents with acute manic episodes associated with bipolar I disorder (BDI) as monotherapy or as an adjunct to lithium or divalproex
• adults with an acute depressive episode associated with bipolar disorder
• adjunctive treatment of major depressive disorder (MDD) in adults
• maintenance treatment of BDI as an adjunct to lithium or divalproex in adults.³

In addition, quetiapine extended-release (XR) is approved as an adjunctive treatment for MDD in adults.⁴

Neither the immediate-release or XR formulation is indicated for treating anxiety, but quetiapine has been studied as a treatment for several anxiety disorders, including posttraumatic stress disorder, social phobia, obsessive-compulsive disorder, and anxiety secondary to mood disorders. It has been most extensively studied as treatment for generalized anxiety disorder (GAD).

Three trials that involved >2,100 patients found quetiapine XR monotherapy is effective for GAD in doses of 50 to 300 mg/d.^5-7 In 2 of the studies, quetiapine XR was as effective as paroxetine and escitalopram for GAD.^5,6 Reviews of off-label SGA use have found that compared with placebo, quetiapine XR monotherapy is effective for GAD (number needed to treat=8).^8,9 Side effects reported in clinical trials of quetiapine included headache, somnolence, sedation, fatigue, dizziness, dry mouth, weight gain, hyperlipidemia, and elevated glucose levels.

What did the FDA say?

In April 2009, the FDA’s Psychopharmacologic Drugs Advisory Committee reviewed whether evidence supported quetiapine XR for treating MDD and GAD.¹⁰ Although the committee found that quetiapine XR monotherapy effectively treated GAD, it concluded it was not acceptably safe.¹¹ The committee expressed concerns over exposing a greatly expanded population to a drug with substantial metabolic side effects, including weight gain (incidence 3% to 23%), increased cholesterol (incidence 7% to 18%), and hyperglycemia.^12-14 Weight gain and metabolic effects have been reported even when quetiapine is prescribed at low doses (≤100 mg/d).^15,16 The FDA did not approve expanding the indication of quetiapine XR to include treatment of GAD.

Our opinion

Quetiapine XR is effective for treating GAD. However, even at low doses, it is associated with substantial side effects and should be reserved for patients with poor response or contraindications (eg, mania) to traditional GAD treatments such as selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. Published studies assessed quetiapine XR only when used on a scheduled basis, and did not address use of quetiapine immediate release or XR on an as-needed basis for GAD.

Related Resources

• AstraZeneca. Seroquel prescribing information. www1.astrazeneca-us.com/pi/seroquel.pdf.
• AstraZeneca. Seroquel XR prescribing information. www1.astrazeneca-us.com/pi/seroquelxr.pdf.

Drug Brand Names

• Divalproex • Depakote
• Paroxetine • Paxil
• Escitalopram • Lexapro
• Quetiapine • Seroquel
• Lithium • Eskalith, Lithobid

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

The rate of off-label prescribing of second-generation antipsychotics (SGAs) is estimated to have doubled in the past decade.^1,2 In 2010, quetiapine was the most commonly used SGA in the United States with >10 million prescriptions dispensed.² Clinical experience and reports from patients indicate quetiapine may be useful for treating anxiety. When making medication choices, it can be useful to combine anecdotal evidence with the facts (or lack thereof). Does evidence support or contradict the use of quetiapine for anxiety?

What the research shows

Quetiapine is FDA-approved for treating:

• adults and adolescents with schizophrenia
• adults, children, and adolescents with acute manic episodes associated with bipolar I disorder (BDI) as monotherapy or as an adjunct to lithium or divalproex
• adults with an acute depressive episode associated with bipolar disorder
• adjunctive treatment of major depressive disorder (MDD) in adults
• maintenance treatment of BDI as an adjunct to lithium or divalproex in adults.³

In addition, quetiapine extended-release (XR) is approved as an adjunctive treatment for MDD in adults.⁴

Neither the immediate-release or XR formulation is indicated for treating anxiety, but quetiapine has been studied as a treatment for several anxiety disorders, including posttraumatic stress disorder, social phobia, obsessive-compulsive disorder, and anxiety secondary to mood disorders. It has been most extensively studied as treatment for generalized anxiety disorder (GAD).

Three trials that involved >2,100 patients found quetiapine XR monotherapy is effective for GAD in doses of 50 to 300 mg/d.^5-7 In 2 of the studies, quetiapine XR was as effective as paroxetine and escitalopram for GAD.^5,6 Reviews of off-label SGA use have found that compared with placebo, quetiapine XR monotherapy is effective for GAD (number needed to treat=8).^8,9 Side effects reported in clinical trials of quetiapine included headache, somnolence, sedation, fatigue, dizziness, dry mouth, weight gain, hyperlipidemia, and elevated glucose levels.

What did the FDA say?

In April 2009, the FDA’s Psychopharmacologic Drugs Advisory Committee reviewed whether evidence supported quetiapine XR for treating MDD and GAD.¹⁰ Although the committee found that quetiapine XR monotherapy effectively treated GAD, it concluded it was not acceptably safe.¹¹ The committee expressed concerns over exposing a greatly expanded population to a drug with substantial metabolic side effects, including weight gain (incidence 3% to 23%), increased cholesterol (incidence 7% to 18%), and hyperglycemia.^12-14 Weight gain and metabolic effects have been reported even when quetiapine is prescribed at low doses (≤100 mg/d).^15,16 The FDA did not approve expanding the indication of quetiapine XR to include treatment of GAD.

Our opinion

Quetiapine XR is effective for treating GAD. However, even at low doses, it is associated with substantial side effects and should be reserved for patients with poor response or contraindications (eg, mania) to traditional GAD treatments such as selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. Published studies assessed quetiapine XR only when used on a scheduled basis, and did not address use of quetiapine immediate release or XR on an as-needed basis for GAD.

Related Resources

• AstraZeneca. Seroquel prescribing information. www1.astrazeneca-us.com/pi/seroquel.pdf.
• AstraZeneca. Seroquel XR prescribing information. www1.astrazeneca-us.com/pi/seroquelxr.pdf.

Drug Brand Names

• Divalproex • Depakote
• Paroxetine • Paxil
• Escitalopram • Lexapro
• Quetiapine • Seroquel
• Lithium • Eskalith, Lithobid

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

The rate of off-label prescribing of second-generation antipsychotics (SGAs) is estimated to have doubled in the past decade.^1,2 In 2010, quetiapine was the most commonly used SGA in the United States with >10 million prescriptions dispensed.² Clinical experience and reports from patients indicate quetiapine may be useful for treating anxiety. When making medication choices, it can be useful to combine anecdotal evidence with the facts (or lack thereof). Does evidence support or contradict the use of quetiapine for anxiety?

What the research shows

Quetiapine is FDA-approved for treating:

• adults and adolescents with schizophrenia
• adults, children, and adolescents with acute manic episodes associated with bipolar I disorder (BDI) as monotherapy or as an adjunct to lithium or divalproex
• adults with an acute depressive episode associated with bipolar disorder
• adjunctive treatment of major depressive disorder (MDD) in adults
• maintenance treatment of BDI as an adjunct to lithium or divalproex in adults.³

In addition, quetiapine extended-release (XR) is approved as an adjunctive treatment for MDD in adults.⁴

Neither the immediate-release or XR formulation is indicated for treating anxiety, but quetiapine has been studied as a treatment for several anxiety disorders, including posttraumatic stress disorder, social phobia, obsessive-compulsive disorder, and anxiety secondary to mood disorders. It has been most extensively studied as treatment for generalized anxiety disorder (GAD).

Three trials that involved >2,100 patients found quetiapine XR monotherapy is effective for GAD in doses of 50 to 300 mg/d.^5-7 In 2 of the studies, quetiapine XR was as effective as paroxetine and escitalopram for GAD.^5,6 Reviews of off-label SGA use have found that compared with placebo, quetiapine XR monotherapy is effective for GAD (number needed to treat=8).^8,9 Side effects reported in clinical trials of quetiapine included headache, somnolence, sedation, fatigue, dizziness, dry mouth, weight gain, hyperlipidemia, and elevated glucose levels.

What did the FDA say?

In April 2009, the FDA’s Psychopharmacologic Drugs Advisory Committee reviewed whether evidence supported quetiapine XR for treating MDD and GAD.¹⁰ Although the committee found that quetiapine XR monotherapy effectively treated GAD, it concluded it was not acceptably safe.¹¹ The committee expressed concerns over exposing a greatly expanded population to a drug with substantial metabolic side effects, including weight gain (incidence 3% to 23%), increased cholesterol (incidence 7% to 18%), and hyperglycemia.^12-14 Weight gain and metabolic effects have been reported even when quetiapine is prescribed at low doses (≤100 mg/d).^15,16 The FDA did not approve expanding the indication of quetiapine XR to include treatment of GAD.

Our opinion

Quetiapine XR is effective for treating GAD. However, even at low doses, it is associated with substantial side effects and should be reserved for patients with poor response or contraindications (eg, mania) to traditional GAD treatments such as selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. Published studies assessed quetiapine XR only when used on a scheduled basis, and did not address use of quetiapine immediate release or XR on an as-needed basis for GAD.

Related Resources

• AstraZeneca. Seroquel prescribing information. www1.astrazeneca-us.com/pi/seroquel.pdf.
• AstraZeneca. Seroquel XR prescribing information. www1.astrazeneca-us.com/pi/seroquelxr.pdf.

Drug Brand Names

• Divalproex • Depakote
• Paroxetine • Paxil
• Escitalopram • Lexapro
• Quetiapine • Seroquel
• Lithium • Eskalith, Lithobid

Disclosure

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

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

The Advisory Committee on Immunization Practices (ACIP) is evaluating whether to recommend the use of meningococcal vaccines for infants and children <2 years.¹ The decision may be made within the next 4 to 8 months. In its deliberation, ACIP must consider several issues, which I review here.

Current and impending vaccine options. Two quadrivalent meningococcal conjugate vaccines (MCV4) are licensed by the US Food and Drug Administration (FDA) for use in the United States: Men ACWY-CRM (Menveo, Novartis) and Men ACWY-D (Menactra, Sanofi Pasteur).² Both vaccines protect against 4 meningococcal serogroups (A, C, Y, and W-135) and are approved for use among those ages 2 to 55 years. In addition, Menactra was recently licensed as a 2-dose series for children ages 9 to 23 months. ACIP recommends routine use of MCV4 for adolescents ages 11 to 18 years, with a preference for the first dose at ages 11 to 12 years; and for all individuals between the ages of 2 and 55 years who are at increased risk for meningococcal disease ( TABLE ).

Complicating matters is the pending availability of more formulations. In addition to the 2-dose Menactra option for children 9 to 23 months, Novartis has an application before the FDA for a 4-dose schedule with Menveo, given at ages 2, 4, 6, and 12 months. GlaxoSmithKline has just received approval from the FDA for MenHibrix, a combination vaccine that contains antigens against Haemophilus influenzae type b (Hib) and 2 meningococcal serogroups, C and Y, licensed as a 4-dose series given at ages 2, 4, 6, and 12 months.

These vaccines have proven to be immunogenic in infants without diminishing the effectiveness of other, co-administered vaccines in normal infant populations. They also appear to be safe, although the studies to date have not been sufficiently large to detect uncommon adverse events.^3-7

Table
Patients at high risk for meningococcal disease

Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D People with functional or anatomical asplenia Microbiologists working with Neisseria meningitidis Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic
Source: CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011;60:72-76.

Meningococcal disease incidence and prevalence are declining

One major consideration for ACIP is the changing epidemiology of meningococcal disease and the low prevalence of disease in all age groups, including infants. The incidence of meningococcal disease has declined in the United States since 1980, with a marked and sustained decline since 2000 ( FIGURE 1 ).⁸ This decline has occurred in all age groups including infants, who have the highest rate of infection ( FIGURE 2 ).⁸ This decline in incidence occurred for all serogroups, including serogroup B.⁸

Serogroup B. Among children <5 years, including infants, half of meningococcal disease is caused by serogroup B,⁸ and these infections would not be prevented by any of the currently licensed vaccines or by those under review. Furthermore, half of all infections occur before age 9 months⁸ —an age range for which Menactra in not approved.

Serogroup C and Y. One-third of infections with serogroups C and Y occur before the age of 6 months⁸ and would not be prevented by any of the new products. Also of note: From 2007 to 2009, the mean number of cases of serotype A or C infection occurring each year in children <5 years was 77.⁸

The impact on children vs adults. Meningococcal disease in children is generally less severe than that occurring in older age groups. Overall case fatality in children is 6%; 10% in those with serogroup B and 1% in those with serogroup Y.⁸ The disease in children does result in significant sequelae, however, with 10% suffering hearing loss and 1% to 2% requiring amputation. From 2007 to 2009, there were 4 to 8 deaths per year among children under age 5, and 8 to 12 children per year experienced serious sequelae.⁸

FIGURE 1
The incidence of meningococcal disease has declined steadily since 2000⁸

1970-1996 National Notifiable Diseases Surveillance System data. 1997-2009 Active Bacterial Core surveillance data estimated to the US population.

FIGURE 2
Meningococcal disease has declined among infants and other age groups⁸

Active Bacterial Core surveillance cases from 1993-2009 estimated to the US population with 18% correction for underreporting.

ACIP’s dilemma

The low morbidity and mortality associated with meningococcal disease is one issue to consider when deciding whether to recommend new vaccines as part of the routine infant and child immunization schedule. The vaccine schedule is already crowded and complex, and parents increasingly are questioning the need for additional antigens.

 

In addition, the cost of vaccines for children has escalated over the past decade due mainly to the new, more expensive formulations.

The reason for a declining incidence of meningococcal disease is not fully known. It may be partly explained by increasing rates of vaccination among adolescents. However, the overall low rate of disease in the population makes assessing herd immunity difficult.

If ACIP decides to recommend vaccinating infants against meningococcal disease, it is unclear how long immunity will last, potentially necessitating a booster dose before the currently recommended adolescent dose.

Finally, in children at high risk, it is not fully known how meningococcal vaccines will affect the immune response to pneumococcal conjugate vaccine. This is an important consideration because the incidence of pneumococcal disease among these children is much higher than that of meningococcal disease.

Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m², which is the diagnostic for obesity.¹ If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.² In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.³

*For a PDF of the full article, click on the link to the left of this introduction.

Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m², which is the diagnostic for obesity.¹ If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.² In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.³

*For a PDF of the full article, click on the link to the left of this introduction.

Obesity has reached epidemic proportions in the United States in the past 2 decades. According to a recent report, 36% of the adult population currently has a body mass index of more than 30 kg/m², which is the diagnostic for obesity.¹ If we focus only on the US adult cancer survivor population, then the magnitude of being overweight or obese is notably higher, ranging from 52% to 68%.² In adult survivors of childhood cancer, several factors are associated with increased risk for obesity, such as hypothalamic or pituitary radiation, the use of certain antidepressants, and lifestyle factors.³

*For a PDF of the full article, click on the link to the left of this introduction.

Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.

Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.

Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.

Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.

Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.

*For a PDF of the full article, click on the link to the left of this introduction.

Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.

Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.

Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.

Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.

Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.

*For a PDF of the full article, click on the link to the left of this introduction.

Background: A direct correlation between the preoperative prostate cancer antigen 3 (PCA3) gene and total tumor volume in postprostatectomy specimens has recently been reported. This suggests that the PCA3 score could serve as a surrogate for tumor burden in patients with prostate cancer. Accordingly, the PCA3 density (that is, the ratio of the PCA3 score to prostate volume) is representative of the degree of prostate volume occupied by tumor.

Objective: To show that the PCA3 density would be directly related to the likelihood of finding cancer on prostate biopsy, given that larger tumors in smaller glands would be more likely to be detected through prostate biopsy.

Methods: We identified 288 men referred for prostate biopsy for an elevated prostate-specific antigen (PSA) level, high PSA velocity, low free- to total-PSA ratio, or suspicious digital rectal exam. All of the patients had had a urinary PCA3 test performed no more than 4 weeks before biopsy, and prostate volume was recorded by transrectal ultrasound determination at the time of biopsy. The diagnostic yield of PSA level, PSA density (PSAD), PCA3 score, and PCA3 density in detecting cancer was evaluated using a receiver operating characteristic (ROC) curve.

Results: Of the 288 patients included for analysis, 183 (63.5%) underwent an initial prostate biopsy and 105 (36.5%) had at least 1 previous negative biopsy. Cancer was detected in 74 (25.7%) patients. The area under the curve was 0.486 for PSA level, 0.590 for PSAD, 0.687 for PCA3 score, and 0.717 for PCA3 density.

Conclusion: PCA3 density is strongly correlated with cancer detection and may be useful in selecting patients for biopsy.

*For a PDF of the full article, click on the link to the left of this introduction.

The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.

*For a PDF of the full article, click on the link to the left of this introduction.

The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.

*For a PDF of the full article, click on the link to the left of this introduction.

The concept of maintenance therapy has been well studied in hematologic malignancies, and now, an increasing number of clinical trials explore the role of maintenance therapy in solid cancers. Both biological and lower-intensity chemotherapeutic agents are currently being evaluated as maintenance therapy. However, despite the increase in research in this area, there has not been consensus about the definition and timing of maintenance therapy. In this review, we will focus on continuation maintenance therapy and switch maintenance therapy in patients with metastatic solid tumors who have achieved stable disease, partial response, or complete response after first-line treatment.

*For a PDF of the full article, click on the link to the left of this introduction.

It’s been about 15 years since the last surge of interest in primary care as a career, when U.S. medical graduates temporarily reversed a long decline by flocking to family medicine, general internal medicine, and pediatrics. Newly minted doctors responded enthusiastically to a widely held perception in the mid-1990s that primary care would be central to a brave new paradigm of managed healthcare delivery.

That profound change never materialized, and the primary-care workforce has since resumed a downward slide that is sounding alarm bells throughout the country. Even more distressing, the medical profession’s recent misfortunes have spread far beyond the doctor’s office.

“What we’re looking at now is that there’s a shortage of somewhere around 90,000 physicians in the next 10 years, increasing in the five years beyond that to 125,000 or more,” says Atul Grover, MD, PhD, chief public policy officer of the Association of American Medical Colleges. The association’s estimates suggest that the 10- and 15-year shortfalls will be split nearly evenly between primary care and other specialties.

Hospitalists could feel that widening gap as well. With increasing numbers of aging baby boomers reaching Medicare eligibility and 32 million Americans set to join the ranks of the insured by 2019 through the Affordable Care Act, primary care’s difficulties arguably are the closest to a full-blown crisis. “Primary care in the United States needs a lifeline,” began a 2009 editorial in the New England Journal of Medicine.¹ And that was before an estimate suggesting that new insurance mandates will require an additional 4,307 to 6,940 primary-care physicians to meet demand before the end of the decade contributing about 15% to the expected shortfall.²

Why should hospitalists care about the fate of their counterparts? For starters, what’s good for outpatient providers is good for a sound healthcare system. Researchers have linked strong

primary care to lower overall spending, fewer health disparities, and higher quality of care.³

Hospitalists and primary-care physicians (PCPs) also are inexorably linked. They follow similar training and education pathways, and need each other to ensure safe transitions of care. And despite the evidence pointing to a slew of contributing factors, HM regularly is blamed for many of primary care’s mounting woes.

Based on well-functioning healthcare systems around the world, analysts say the ideal primary-care-to-specialty-care-provider ratio should be roughly 40:60 or 50:50. According to Kathleen Klink, MD, director of the Division of Medicine and Dentistry in the Health Resources and Services Administration (HRSA), only about 32% of physicians in the U.S. are practicing primary care. Unless something changes, that percentage will erode even further. “We’re going in the wrong direction,” Dr. Klink says.

 

Opinions differ on the extent of the current PCP shortage. Nevertheless, there is clearly a “huge maldistribution problem,” says Robert Phillips, MD, MSPH, director of the Washington, D.C.-based Robert Graham Center, a primary-care research center. Rural and underserved areas already are being shortchanged as more doctors locate in more affluent and desirable areas, he says.

That phenomenon is hardly unique to primary care, but Dr. Phillips says the deficit in frontline doctors could cause disproportionately more hardships in rural and underserved communities given the shrinking pipeline for medical trainees. A decade ago, almost a third of all medical graduates were placed into primary-care residency training slots. Now, he says, that figure is a bit less than 22%. “We can’t even replace the primary-care workforce we have now with that kind of output,” Dr. Phillips says.

Already, many doctors are no longer accepting new Medicaid or Medicare patients because their practices are losing money from low reimbursement rates. The Affordable Care Act’s significant expansion of insurance benefits, Dr. Grover says, will effectively accelerate the timetable of growing imbalances between supply and demand. “I think the challenge you face is, Will the ACA efforts to expand access fail because you’re giving people an insurance card but you have nobody there to take care of them?”

click for large version

Reasons Aplenty

Some medical students simply aren’t interested in primary care. For the rest, however, interviews with doctors, analysts, and federal officials suggest that the pipeline has been battered throughout its length. Of all the contributing factors, Dr. Phillips says, the main one might be income disparity. In a 2009 study, the center found that the growing gulf in salaries between primary care and subspecialty medicine “cuts in half the likelihood that a student will choose to go into primary care,” he says. Over a career, that gap translates into a difference of $3.5 million. “It dissuades them strongly,” Dr. Phillips says.

At the same time, medical school tuitions have increased at a rate far outstripping the consumer price index. “What we found is that when you hit somewhere between $200,000 and $250,000 in debt, that’s where you see the dropoff really happen,” he says. “Because it becomes almost unfathomable that you can, on a primary-care income, pay off your debts without it severely cutting into your lifestyle.”

Lori Heim, MD, former president of the American Academy of Family Physicians and a hospitalist at Scotland Memorial Hospital in Laurinburg, N.C., says the prevailing fee-for-service payment model has failed primary-care providers, requiring them to work more to meet soaring outpatient demand but reimbursing them less. “People talk about the hamster wheel,” she says. “And that has created more workplace dissatisfaction. Not only does it impact students, but it also impacts the number of primary-care physicians who want to stay in the community, practicing.”

Frederick Chen, MD, MPH, associate professor of family medicine at the University of Washington in Seattle, can relate. “I came from community practice, where you’re seeing 30 to 35 patients a day, and the pressure was entirely on your productivity, and that’s not fun,” he says. “So we’re burning out a lot of primary-care physicians, and students are seeing that very easily.”

The larger theme, several doctors say, is one of perceived worth. Leora Horwitz, MD, assistant professor of internal medicine at Yale School of Medicine in New Haven, Conn., says she has to think holistically about her patients’ symptoms, medication lists, family history, home situation, and other factors during her limited time with them. She bristles at the notion that specialists might spend their time considering only one aspect of her patients’ care yet bill twice as much.

 

“Realistically, I am providing better value to the healthcare system than a specialist does, and yet we pay specialists much more,” she says. “And until that’s different, people go where the money is and they also go where the respect is, and I think it’s going to be very hard to recruit more people to primary care.”

Despite research pointing to financial concerns, lifestyle perceptions, and training inadequacies as key factors in the decline of primary care, perceptions that HM is poaching young talent have been hard to shake. A recent article in The Atlantic asserts that HM might be a “rational choice” given the profession’s more favorable training, lifestyle, and financial considerations.⁴ The author, a general internist, contrasts those enticements “to the realities of office practice: Fifteen-minute visits with patients on multiple medications, oodles of paperwork that cause office docs to run a gauntlet just to get through their day, and more documentation and regulatory burdens than ever before.”

Nevertheless, the article describes PCPs who resist hospitals’ calls to move to a hospitalist system as honorable “holdouts” who are committed to being directly involved in their patients’ care.

In her blog post at KevinMD.com, “Hospitalists are Killing Primary Care, and other Myths Debunked,” Vineet Arora, MD, MPP, FHM, a hospitalist at the University of Chicago, addresses those perceptions head-on. “If hospitalists did not exist, there would still be declining interest in primary care among medical students and residents,” she writes.

In a subsequent interview, Dr. Arora contends that both primary care and HM instead might be losing out to higher-paying subspecialties, especially the “ROAD” quartet of radiology, ophthalmology, anesthesiology, and dermatology. She also questions the notion that the professions draw from the same talent pool. “Anecdotally, I can tell you that I don’t see a lot of people choosing between primary care and hospital medicine,” she says. “They’re thinking, ‘Do I want to do critical care, hospital medicine, or cardiology?’ Because the type of person who does hospital medicine is more attracted to that inpatient, acute environment.”

Dr. Horwitz agrees that the choice between a career in primary care and HM might not be as clear-cut as some detractors have suggested. Even so, she describes hospitalists as a “double-edged sword” for PCPs. “On the one hand, primary-care docs get paid so little for their outpatient visits that most need to see a high volume of patients in a day just to break even. So they have less and less time to go to the hospital to see hospitalizations,” Dr. Horwitz says. “The hospitalist movement was really a godsend in that respect, because it allowed primary-care docs to focus on their outpatient practice and not spend all that travel time going to the hospital.”

Other PCPs have lamented the erosion of their inpatient roles while recognizing that current economic realities are gradually pushing them out of the hospital. In fact, Dr. Horwitz says, PCPs often don’t know when their patients have been hospitalized, leading to a breakdown in the continuity of care. A weak primary-care infrastructure in a community, hospitalists say, can likewise imperil safe transitions. With the partitioning of inpatient and outpatient responsibilities, the potential for such miscommunications and lapses has clearly grown.

“We’re all in the same workforce; we’re all trying to take care of patients,” Dr. Heim says. “The discussion needs to be on how do we coordinate, not over turf wars.”

Signs of Life

Experts are focusing more on team-based approaches among the few potential short-term solutions, a common theme in HM circles. Advanced-practice registered nurses, physician assistants, and other providers can be trained more quickly than doctors, potentially extending the reach of primary care. In turn, the concept of team-based care could be beefed up during medical residencies.

 

Primary-care advocates say more equitable reimbursements also could help to ease the crisis, as would more federal support of residency training. But with many politicians focused on deficit reduction, new government incentives are debuting even as existing programs are being threatened or dismantled.

The Affordable Care Act, for example, more than doubled the capacity of the well-regarded National Health Service Corps, which provides scholarships and loan repayments to doctors who agree to practice in underserved communities. The law also created primary-care incentive payments that added $500 million to physician incomes in 2011. “So that’s a pretty strong message of value, and it’s some real value, too,” Dr. Phillips says.

The Affordable Care Act, however, cuts $155 billion to hospital payments over 10 years, adding to the downward pressure on reimbursements. And President Obama’s fiscal-year 2013 budget proposal trims an additional $1 billion, or 10%, from Medicare’s annual payments for patient care, which could impact graduate medical education as hospitals seek to balance out the cuts.

Amid the challenges, primary care is showing some encouraging signs of life. Medical school enrollments are on pace to increase by 30% over their 2002 levels within the next three to five years. In both 2010 and 2011, the number of U.S. medical graduates going into family medicine increased by roughly 10% (followed by a more modest increase of 1% this year). Residency matches in general internal medicine also have been climbing. Dr. Heim and others say it’s no coincidence that students’ interest in primary care began rising again amid public discussions on healthcare reform that focused on the value of primary care.

In the end, the profession’s fate could depend in large part on whether the affirmations continue this time around. “There are some rock stars and heroes of primary care that are not as well-known to medical students as they should be,” says Elbert Huang, MD, associate professor of medicine at the University of Chicago. Highlighting some of those individual leaders, Dr. Huang believes, might significantly improve the profession’s standing among students.

“We need a Michael Jordan of primary care,” he says.

Bryn Nelson is a freelance medical writer in Seattle.

References

1. Bodenheimer T, Grumbach K, Berenson RA. A lifeline for primary care. New Engl J Med. 2009;360(26):2693-2696.
2. Hofer AN, Abraham JM, Moscovice I. Expansion of coverage under the Patient Protection and Affordable Care Act and primary care utilization. Milbank Q. 2011;89(1):69-89.
3. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83(3):457-502.
4. Henning Schumann, J. The doctor is out: young talent is turning away from primary care. The Atlantic; March 12, 2012.

It’s been about 15 years since the last surge of interest in primary care as a career, when U.S. medical graduates temporarily reversed a long decline by flocking to family medicine, general internal medicine, and pediatrics. Newly minted doctors responded enthusiastically to a widely held perception in the mid-1990s that primary care would be central to a brave new paradigm of managed healthcare delivery.

That profound change never materialized, and the primary-care workforce has since resumed a downward slide that is sounding alarm bells throughout the country. Even more distressing, the medical profession’s recent misfortunes have spread far beyond the doctor’s office.

“What we’re looking at now is that there’s a shortage of somewhere around 90,000 physicians in the next 10 years, increasing in the five years beyond that to 125,000 or more,” says Atul Grover, MD, PhD, chief public policy officer of the Association of American Medical Colleges. The association’s estimates suggest that the 10- and 15-year shortfalls will be split nearly evenly between primary care and other specialties.

Hospitalists could feel that widening gap as well. With increasing numbers of aging baby boomers reaching Medicare eligibility and 32 million Americans set to join the ranks of the insured by 2019 through the Affordable Care Act, primary care’s difficulties arguably are the closest to a full-blown crisis. “Primary care in the United States needs a lifeline,” began a 2009 editorial in the New England Journal of Medicine.¹ And that was before an estimate suggesting that new insurance mandates will require an additional 4,307 to 6,940 primary-care physicians to meet demand before the end of the decade contributing about 15% to the expected shortfall.²

Why should hospitalists care about the fate of their counterparts? For starters, what’s good for outpatient providers is good for a sound healthcare system. Researchers have linked strong

primary care to lower overall spending, fewer health disparities, and higher quality of care.³

Hospitalists and primary-care physicians (PCPs) also are inexorably linked. They follow similar training and education pathways, and need each other to ensure safe transitions of care. And despite the evidence pointing to a slew of contributing factors, HM regularly is blamed for many of primary care’s mounting woes.

Based on well-functioning healthcare systems around the world, analysts say the ideal primary-care-to-specialty-care-provider ratio should be roughly 40:60 or 50:50. According to Kathleen Klink, MD, director of the Division of Medicine and Dentistry in the Health Resources and Services Administration (HRSA), only about 32% of physicians in the U.S. are practicing primary care. Unless something changes, that percentage will erode even further. “We’re going in the wrong direction,” Dr. Klink says.

 

Opinions differ on the extent of the current PCP shortage. Nevertheless, there is clearly a “huge maldistribution problem,” says Robert Phillips, MD, MSPH, director of the Washington, D.C.-based Robert Graham Center, a primary-care research center. Rural and underserved areas already are being shortchanged as more doctors locate in more affluent and desirable areas, he says.

That phenomenon is hardly unique to primary care, but Dr. Phillips says the deficit in frontline doctors could cause disproportionately more hardships in rural and underserved communities given the shrinking pipeline for medical trainees. A decade ago, almost a third of all medical graduates were placed into primary-care residency training slots. Now, he says, that figure is a bit less than 22%. “We can’t even replace the primary-care workforce we have now with that kind of output,” Dr. Phillips says.

Already, many doctors are no longer accepting new Medicaid or Medicare patients because their practices are losing money from low reimbursement rates. The Affordable Care Act’s significant expansion of insurance benefits, Dr. Grover says, will effectively accelerate the timetable of growing imbalances between supply and demand. “I think the challenge you face is, Will the ACA efforts to expand access fail because you’re giving people an insurance card but you have nobody there to take care of them?”

click for large version

Reasons Aplenty

Some medical students simply aren’t interested in primary care. For the rest, however, interviews with doctors, analysts, and federal officials suggest that the pipeline has been battered throughout its length. Of all the contributing factors, Dr. Phillips says, the main one might be income disparity. In a 2009 study, the center found that the growing gulf in salaries between primary care and subspecialty medicine “cuts in half the likelihood that a student will choose to go into primary care,” he says. Over a career, that gap translates into a difference of $3.5 million. “It dissuades them strongly,” Dr. Phillips says.

At the same time, medical school tuitions have increased at a rate far outstripping the consumer price index. “What we found is that when you hit somewhere between $200,000 and $250,000 in debt, that’s where you see the dropoff really happen,” he says. “Because it becomes almost unfathomable that you can, on a primary-care income, pay off your debts without it severely cutting into your lifestyle.”

Lori Heim, MD, former president of the American Academy of Family Physicians and a hospitalist at Scotland Memorial Hospital in Laurinburg, N.C., says the prevailing fee-for-service payment model has failed primary-care providers, requiring them to work more to meet soaring outpatient demand but reimbursing them less. “People talk about the hamster wheel,” she says. “And that has created more workplace dissatisfaction. Not only does it impact students, but it also impacts the number of primary-care physicians who want to stay in the community, practicing.”

Frederick Chen, MD, MPH, associate professor of family medicine at the University of Washington in Seattle, can relate. “I came from community practice, where you’re seeing 30 to 35 patients a day, and the pressure was entirely on your productivity, and that’s not fun,” he says. “So we’re burning out a lot of primary-care physicians, and students are seeing that very easily.”

The larger theme, several doctors say, is one of perceived worth. Leora Horwitz, MD, assistant professor of internal medicine at Yale School of Medicine in New Haven, Conn., says she has to think holistically about her patients’ symptoms, medication lists, family history, home situation, and other factors during her limited time with them. She bristles at the notion that specialists might spend their time considering only one aspect of her patients’ care yet bill twice as much.

 

“Realistically, I am providing better value to the healthcare system than a specialist does, and yet we pay specialists much more,” she says. “And until that’s different, people go where the money is and they also go where the respect is, and I think it’s going to be very hard to recruit more people to primary care.”

Despite research pointing to financial concerns, lifestyle perceptions, and training inadequacies as key factors in the decline of primary care, perceptions that HM is poaching young talent have been hard to shake. A recent article in The Atlantic asserts that HM might be a “rational choice” given the profession’s more favorable training, lifestyle, and financial considerations.⁴ The author, a general internist, contrasts those enticements “to the realities of office practice: Fifteen-minute visits with patients on multiple medications, oodles of paperwork that cause office docs to run a gauntlet just to get through their day, and more documentation and regulatory burdens than ever before.”

Nevertheless, the article describes PCPs who resist hospitals’ calls to move to a hospitalist system as honorable “holdouts” who are committed to being directly involved in their patients’ care.

In her blog post at KevinMD.com, “Hospitalists are Killing Primary Care, and other Myths Debunked,” Vineet Arora, MD, MPP, FHM, a hospitalist at the University of Chicago, addresses those perceptions head-on. “If hospitalists did not exist, there would still be declining interest in primary care among medical students and residents,” she writes.

In a subsequent interview, Dr. Arora contends that both primary care and HM instead might be losing out to higher-paying subspecialties, especially the “ROAD” quartet of radiology, ophthalmology, anesthesiology, and dermatology. She also questions the notion that the professions draw from the same talent pool. “Anecdotally, I can tell you that I don’t see a lot of people choosing between primary care and hospital medicine,” she says. “They’re thinking, ‘Do I want to do critical care, hospital medicine, or cardiology?’ Because the type of person who does hospital medicine is more attracted to that inpatient, acute environment.”

Dr. Horwitz agrees that the choice between a career in primary care and HM might not be as clear-cut as some detractors have suggested. Even so, she describes hospitalists as a “double-edged sword” for PCPs. “On the one hand, primary-care docs get paid so little for their outpatient visits that most need to see a high volume of patients in a day just to break even. So they have less and less time to go to the hospital to see hospitalizations,” Dr. Horwitz says. “The hospitalist movement was really a godsend in that respect, because it allowed primary-care docs to focus on their outpatient practice and not spend all that travel time going to the hospital.”

Other PCPs have lamented the erosion of their inpatient roles while recognizing that current economic realities are gradually pushing them out of the hospital. In fact, Dr. Horwitz says, PCPs often don’t know when their patients have been hospitalized, leading to a breakdown in the continuity of care. A weak primary-care infrastructure in a community, hospitalists say, can likewise imperil safe transitions. With the partitioning of inpatient and outpatient responsibilities, the potential for such miscommunications and lapses has clearly grown.

“We’re all in the same workforce; we’re all trying to take care of patients,” Dr. Heim says. “The discussion needs to be on how do we coordinate, not over turf wars.”

Signs of Life

Experts are focusing more on team-based approaches among the few potential short-term solutions, a common theme in HM circles. Advanced-practice registered nurses, physician assistants, and other providers can be trained more quickly than doctors, potentially extending the reach of primary care. In turn, the concept of team-based care could be beefed up during medical residencies.

 

Primary-care advocates say more equitable reimbursements also could help to ease the crisis, as would more federal support of residency training. But with many politicians focused on deficit reduction, new government incentives are debuting even as existing programs are being threatened or dismantled.

The Affordable Care Act, for example, more than doubled the capacity of the well-regarded National Health Service Corps, which provides scholarships and loan repayments to doctors who agree to practice in underserved communities. The law also created primary-care incentive payments that added $500 million to physician incomes in 2011. “So that’s a pretty strong message of value, and it’s some real value, too,” Dr. Phillips says.

The Affordable Care Act, however, cuts $155 billion to hospital payments over 10 years, adding to the downward pressure on reimbursements. And President Obama’s fiscal-year 2013 budget proposal trims an additional $1 billion, or 10%, from Medicare’s annual payments for patient care, which could impact graduate medical education as hospitals seek to balance out the cuts.

Amid the challenges, primary care is showing some encouraging signs of life. Medical school enrollments are on pace to increase by 30% over their 2002 levels within the next three to five years. In both 2010 and 2011, the number of U.S. medical graduates going into family medicine increased by roughly 10% (followed by a more modest increase of 1% this year). Residency matches in general internal medicine also have been climbing. Dr. Heim and others say it’s no coincidence that students’ interest in primary care began rising again amid public discussions on healthcare reform that focused on the value of primary care.

In the end, the profession’s fate could depend in large part on whether the affirmations continue this time around. “There are some rock stars and heroes of primary care that are not as well-known to medical students as they should be,” says Elbert Huang, MD, associate professor of medicine at the University of Chicago. Highlighting some of those individual leaders, Dr. Huang believes, might significantly improve the profession’s standing among students.

“We need a Michael Jordan of primary care,” he says.

Bryn Nelson is a freelance medical writer in Seattle.

References

1. Bodenheimer T, Grumbach K, Berenson RA. A lifeline for primary care. New Engl J Med. 2009;360(26):2693-2696.
2. Hofer AN, Abraham JM, Moscovice I. Expansion of coverage under the Patient Protection and Affordable Care Act and primary care utilization. Milbank Q. 2011;89(1):69-89.
3. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83(3):457-502.
4. Henning Schumann, J. The doctor is out: young talent is turning away from primary care. The Atlantic; March 12, 2012.

It’s been about 15 years since the last surge of interest in primary care as a career, when U.S. medical graduates temporarily reversed a long decline by flocking to family medicine, general internal medicine, and pediatrics. Newly minted doctors responded enthusiastically to a widely held perception in the mid-1990s that primary care would be central to a brave new paradigm of managed healthcare delivery.

That profound change never materialized, and the primary-care workforce has since resumed a downward slide that is sounding alarm bells throughout the country. Even more distressing, the medical profession’s recent misfortunes have spread far beyond the doctor’s office.

“What we’re looking at now is that there’s a shortage of somewhere around 90,000 physicians in the next 10 years, increasing in the five years beyond that to 125,000 or more,” says Atul Grover, MD, PhD, chief public policy officer of the Association of American Medical Colleges. The association’s estimates suggest that the 10- and 15-year shortfalls will be split nearly evenly between primary care and other specialties.

Hospitalists could feel that widening gap as well. With increasing numbers of aging baby boomers reaching Medicare eligibility and 32 million Americans set to join the ranks of the insured by 2019 through the Affordable Care Act, primary care’s difficulties arguably are the closest to a full-blown crisis. “Primary care in the United States needs a lifeline,” began a 2009 editorial in the New England Journal of Medicine.¹ And that was before an estimate suggesting that new insurance mandates will require an additional 4,307 to 6,940 primary-care physicians to meet demand before the end of the decade contributing about 15% to the expected shortfall.²

Why should hospitalists care about the fate of their counterparts? For starters, what’s good for outpatient providers is good for a sound healthcare system. Researchers have linked strong

primary care to lower overall spending, fewer health disparities, and higher quality of care.³

Hospitalists and primary-care physicians (PCPs) also are inexorably linked. They follow similar training and education pathways, and need each other to ensure safe transitions of care. And despite the evidence pointing to a slew of contributing factors, HM regularly is blamed for many of primary care’s mounting woes.

Based on well-functioning healthcare systems around the world, analysts say the ideal primary-care-to-specialty-care-provider ratio should be roughly 40:60 or 50:50. According to Kathleen Klink, MD, director of the Division of Medicine and Dentistry in the Health Resources and Services Administration (HRSA), only about 32% of physicians in the U.S. are practicing primary care. Unless something changes, that percentage will erode even further. “We’re going in the wrong direction,” Dr. Klink says.

 

Opinions differ on the extent of the current PCP shortage. Nevertheless, there is clearly a “huge maldistribution problem,” says Robert Phillips, MD, MSPH, director of the Washington, D.C.-based Robert Graham Center, a primary-care research center. Rural and underserved areas already are being shortchanged as more doctors locate in more affluent and desirable areas, he says.

That phenomenon is hardly unique to primary care, but Dr. Phillips says the deficit in frontline doctors could cause disproportionately more hardships in rural and underserved communities given the shrinking pipeline for medical trainees. A decade ago, almost a third of all medical graduates were placed into primary-care residency training slots. Now, he says, that figure is a bit less than 22%. “We can’t even replace the primary-care workforce we have now with that kind of output,” Dr. Phillips says.

Already, many doctors are no longer accepting new Medicaid or Medicare patients because their practices are losing money from low reimbursement rates. The Affordable Care Act’s significant expansion of insurance benefits, Dr. Grover says, will effectively accelerate the timetable of growing imbalances between supply and demand. “I think the challenge you face is, Will the ACA efforts to expand access fail because you’re giving people an insurance card but you have nobody there to take care of them?”

click for large version

Reasons Aplenty

Some medical students simply aren’t interested in primary care. For the rest, however, interviews with doctors, analysts, and federal officials suggest that the pipeline has been battered throughout its length. Of all the contributing factors, Dr. Phillips says, the main one might be income disparity. In a 2009 study, the center found that the growing gulf in salaries between primary care and subspecialty medicine “cuts in half the likelihood that a student will choose to go into primary care,” he says. Over a career, that gap translates into a difference of $3.5 million. “It dissuades them strongly,” Dr. Phillips says.

At the same time, medical school tuitions have increased at a rate far outstripping the consumer price index. “What we found is that when you hit somewhere between $200,000 and $250,000 in debt, that’s where you see the dropoff really happen,” he says. “Because it becomes almost unfathomable that you can, on a primary-care income, pay off your debts without it severely cutting into your lifestyle.”

Lori Heim, MD, former president of the American Academy of Family Physicians and a hospitalist at Scotland Memorial Hospital in Laurinburg, N.C., says the prevailing fee-for-service payment model has failed primary-care providers, requiring them to work more to meet soaring outpatient demand but reimbursing them less. “People talk about the hamster wheel,” she says. “And that has created more workplace dissatisfaction. Not only does it impact students, but it also impacts the number of primary-care physicians who want to stay in the community, practicing.”

Frederick Chen, MD, MPH, associate professor of family medicine at the University of Washington in Seattle, can relate. “I came from community practice, where you’re seeing 30 to 35 patients a day, and the pressure was entirely on your productivity, and that’s not fun,” he says. “So we’re burning out a lot of primary-care physicians, and students are seeing that very easily.”

The larger theme, several doctors say, is one of perceived worth. Leora Horwitz, MD, assistant professor of internal medicine at Yale School of Medicine in New Haven, Conn., says she has to think holistically about her patients’ symptoms, medication lists, family history, home situation, and other factors during her limited time with them. She bristles at the notion that specialists might spend their time considering only one aspect of her patients’ care yet bill twice as much.

 

“Realistically, I am providing better value to the healthcare system than a specialist does, and yet we pay specialists much more,” she says. “And until that’s different, people go where the money is and they also go where the respect is, and I think it’s going to be very hard to recruit more people to primary care.”

Despite research pointing to financial concerns, lifestyle perceptions, and training inadequacies as key factors in the decline of primary care, perceptions that HM is poaching young talent have been hard to shake. A recent article in The Atlantic asserts that HM might be a “rational choice” given the profession’s more favorable training, lifestyle, and financial considerations.⁴ The author, a general internist, contrasts those enticements “to the realities of office practice: Fifteen-minute visits with patients on multiple medications, oodles of paperwork that cause office docs to run a gauntlet just to get through their day, and more documentation and regulatory burdens than ever before.”

Nevertheless, the article describes PCPs who resist hospitals’ calls to move to a hospitalist system as honorable “holdouts” who are committed to being directly involved in their patients’ care.

In her blog post at KevinMD.com, “Hospitalists are Killing Primary Care, and other Myths Debunked,” Vineet Arora, MD, MPP, FHM, a hospitalist at the University of Chicago, addresses those perceptions head-on. “If hospitalists did not exist, there would still be declining interest in primary care among medical students and residents,” she writes.

In a subsequent interview, Dr. Arora contends that both primary care and HM instead might be losing out to higher-paying subspecialties, especially the “ROAD” quartet of radiology, ophthalmology, anesthesiology, and dermatology. She also questions the notion that the professions draw from the same talent pool. “Anecdotally, I can tell you that I don’t see a lot of people choosing between primary care and hospital medicine,” she says. “They’re thinking, ‘Do I want to do critical care, hospital medicine, or cardiology?’ Because the type of person who does hospital medicine is more attracted to that inpatient, acute environment.”

Dr. Horwitz agrees that the choice between a career in primary care and HM might not be as clear-cut as some detractors have suggested. Even so, she describes hospitalists as a “double-edged sword” for PCPs. “On the one hand, primary-care docs get paid so little for their outpatient visits that most need to see a high volume of patients in a day just to break even. So they have less and less time to go to the hospital to see hospitalizations,” Dr. Horwitz says. “The hospitalist movement was really a godsend in that respect, because it allowed primary-care docs to focus on their outpatient practice and not spend all that travel time going to the hospital.”

Other PCPs have lamented the erosion of their inpatient roles while recognizing that current economic realities are gradually pushing them out of the hospital. In fact, Dr. Horwitz says, PCPs often don’t know when their patients have been hospitalized, leading to a breakdown in the continuity of care. A weak primary-care infrastructure in a community, hospitalists say, can likewise imperil safe transitions. With the partitioning of inpatient and outpatient responsibilities, the potential for such miscommunications and lapses has clearly grown.

“We’re all in the same workforce; we’re all trying to take care of patients,” Dr. Heim says. “The discussion needs to be on how do we coordinate, not over turf wars.”

Signs of Life

Experts are focusing more on team-based approaches among the few potential short-term solutions, a common theme in HM circles. Advanced-practice registered nurses, physician assistants, and other providers can be trained more quickly than doctors, potentially extending the reach of primary care. In turn, the concept of team-based care could be beefed up during medical residencies.

 

Primary-care advocates say more equitable reimbursements also could help to ease the crisis, as would more federal support of residency training. But with many politicians focused on deficit reduction, new government incentives are debuting even as existing programs are being threatened or dismantled.

The Affordable Care Act, for example, more than doubled the capacity of the well-regarded National Health Service Corps, which provides scholarships and loan repayments to doctors who agree to practice in underserved communities. The law also created primary-care incentive payments that added $500 million to physician incomes in 2011. “So that’s a pretty strong message of value, and it’s some real value, too,” Dr. Phillips says.

The Affordable Care Act, however, cuts $155 billion to hospital payments over 10 years, adding to the downward pressure on reimbursements. And President Obama’s fiscal-year 2013 budget proposal trims an additional $1 billion, or 10%, from Medicare’s annual payments for patient care, which could impact graduate medical education as hospitals seek to balance out the cuts.

Amid the challenges, primary care is showing some encouraging signs of life. Medical school enrollments are on pace to increase by 30% over their 2002 levels within the next three to five years. In both 2010 and 2011, the number of U.S. medical graduates going into family medicine increased by roughly 10% (followed by a more modest increase of 1% this year). Residency matches in general internal medicine also have been climbing. Dr. Heim and others say it’s no coincidence that students’ interest in primary care began rising again amid public discussions on healthcare reform that focused on the value of primary care.

In the end, the profession’s fate could depend in large part on whether the affirmations continue this time around. “There are some rock stars and heroes of primary care that are not as well-known to medical students as they should be,” says Elbert Huang, MD, associate professor of medicine at the University of Chicago. Highlighting some of those individual leaders, Dr. Huang believes, might significantly improve the profession’s standing among students.

“We need a Michael Jordan of primary care,” he says.

Bryn Nelson is a freelance medical writer in Seattle.

References

1. Bodenheimer T, Grumbach K, Berenson RA. A lifeline for primary care. New Engl J Med. 2009;360(26):2693-2696.
2. Hofer AN, Abraham JM, Moscovice I. Expansion of coverage under the Patient Protection and Affordable Care Act and primary care utilization. Milbank Q. 2011;89(1):69-89.
3. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83(3):457-502.
4. Henning Schumann, J. The doctor is out: young talent is turning away from primary care. The Atlantic; March 12, 2012.